NAVLE

STUDY
GUIDE
- 2020 -
TABLE OF CONTENTS
TOXICOLOGY……………………………………………………………………………………………………………………………………………………..1
CLINICAL PATHOLOGY….…………………………………………………………………………………………………………………….………………5
HYPERSENSITIVITIES…………………………………………………………………………………………………………………………….…………….6
CARDIOLOGY….………………………………………………………………………………………………………………………………………….………7
RESPIRATORY….…………………………………………………………………………………………………………………………………………………10
NEUROLOGY….………………………………………………………………………………………………………………………………….….…………..11
HEPATOLOGY….……………………………………………………………………………………………………………………………………….………13
TICK BORNE DISEASES….………………………………………………………………………………………………………………………………….13
FUNGAL DISEASES….……………………………………………………………………………………………………………………….……………….14
PARASITOLOGY….……………………………………………………………………………………………………………………………….……………15
ONCOLOGY….…………………………………………………………………………………………………………………………………………………..20
RENAL….………………………………………………………………………………………………………………………………………………………….22
UROLITHIASIS….………………………………………………………………………………………………………………………………………………23
RINGWORM….…………………………………………………………………………………………………………………………………………………24
LEPTOSPIRA INTERROGANS SEROVAR….………………………………………………………………………………………………………….24
CLOSTRIDIAL DISEASES….…………………………………………………………………………………………………………………….…………..24
DENTISTRY….………………………………………………………………………………………………………………………………….………………..25
REPRODUCTION….…………………………………………………………………………………………………………………………………………..26
ORTHOPEDICS….……………………………………………………………………………………………………………………………….……………..29
OPHTHALMOLOGY….………………………………………………………………………………………………………………………………….……29
ANTIBIOTICS….……………………………………………………………………………………………………………………………….….……………..31
FOOD POISONING….…………………………………………………………………………………………………………………….………………….32
RABIES….………………………………………………………………………………………………………………………………………………………….32
SENSITIVITY AND SPECIFICITY….……………………………………………………………………………………………………………………….33
CAMELID DISEASES….………………………………………………………………………………………………………………………………………33
FISH DISEASES….………………………………………………………………………………………………………………………………………………34
PRIMATE DISEASES….………………………………………………………………………………………………………………………………………35
SMALL RODENT/RABBIT DISEASES….………………………………………………………………………………………………….……………35
FERRET DISEASES….…………………………………………………………………………………………………………………………………………38
REPTILE DISEASES….………………………………………………………………………………………………………………………………………..39
EXOTIC BIRD DISEASES….………………………………………………………………………………………………………………………………….41
CHICKEN DISEASES….……………………………………………………………………………………………………………………………………….43
TURKEY DISEASES….…………………………………………………………………………………………………………………………………………46
PIG DISEASES….……………………………………………………………………………………………………………………………………………….47
CERVID DISEASES…………………………………………………………………………………………………………………………………………….51
RUMINANT DISEASES….…………………………………………………………………………………………………………………………………..51
GOAT & SHEEP DISEASES….……………………………………………………………………………………………………………………………..53
BOVINE DISEASES….…………………………………………….……………………………………...56
EQUINE DISEASES….………………………………………………………………….…………………65
CANINE AND FELINE DISEASES….……………..…………………………............................78
CANINE DISEASES….…………………………………………………………………………………....83
FELINE DISEASES….…………………………………………………………………........................91
 TOXICOLOGY
SMALL ANIMALS
- Xylitol – DOGS – rapid insulin release → hypoglycemia
o Vomit, weakness, ataxia, depression, ↓ K, seizures, coma
o Less common – liver issues (run coags and liver values, start SAMe)
o Tx = fluids + dextrose
- Bleach – dilute w/ milk (don’t force vomiting! Causes more damage)
o Tx: gastric protectants
- Black widow – L atrodectans, L Hesperus
o Acetylcholine – binds Ca channels → ascending motor paralysis + destroyed peripheral nerves
o Recumbent, vocalization, pain, rigidity w/ mm spasms
o Death: respiratory/cardiovascular failure
- Rodenticides
o Warfarin – anticoagulant (2/7/9/10) – give Vit K1, plasma transfusion
▪ PT (prothrombin time) = prolonged (factor 7 – shortest ½ life, extrinsic system)
o Brodifacoum – Vit K antagonist (epoxide reductase) – give Vit K1, monitor PT
o Cholecalciferol – active Vit D – fatal hypercalcemia
▪ Chem: ↑ Ca, ↑ P → metastatic mineralization of soft tissues
• Renal/cardiac/GI damage
▪ Tx: diuresis, pred, bisphosphonates, salmon calcitonin
o Bromethalin – CNS toxin (uncouples oxidative phosphorylation)
▪ Give MANNITOL, IV lipids to bind in blood
▪ Grave prognosis once symptomatic
- Ethylene glycol
o Ataxia, nausea, PUPD, at 24-72 hours show signs of renal failure
o Ca oxalate crystals, ↑ anion gap, azotemia, metabolic acidosis
o ↑ glucose, ↓ Ca
o Tx: 4-MP (4-methylpyrazole) or ethanol (if no 4-MP) – if tx within 8-12 hours of ingestion, good prognosis; if after
that point, poor/grave prognosis
- Organophosphate
o Inhibits acetylcholinesterase → muscarinic signs (hypersalivation, incoordination, bloat)
o Tx: atropine or 2-PAM (pralidoxime = anticholinesterase)
- Fleet enemas – high in phosphorus
o ↑ P and ↑ Na (colon absorption), ↓ Ca – weakness, shock, tremors, seizures
o Tx: Ca gluconate, P binders, if severe ↑ K – insulin + dextrose
- Strychnine (snail bait)
o Antagonizes glycine – lose impulse contractility of spinal cord/brainstem
o Affects striated muscle → tremors!
o Tx: methocarbamol (for convulsions), ↓ stimulation
- Chocolate – methylxanthines (theobromine, caffeine)
o CNS excitation, tachycardia, vasoconstriction
o Highest concentration in unsweetened baking chocolate
- Pyrethrins – CATS
o Alters Na channels – ↑ depolarization length
o Depression, hypersalivation, ataxia, mm tremors
o Tx: methocarbamol, bathe (remove product)
- Acetaminophen – CATS
o Lack glutathione and glucoronyl transferase → methemoglobinemia (dark brown blood – oxidative damage to Hg)
o Heinz bodies
o Tx: N-acetylcysteine
- Heinz Body Anemia
o Methylene blue, molybdenum deficiency, rye grass, brassica family
o Zinc – pennies after 1983
o Onions – causes hemolytic anemia, hemoglobinemia/uria, Heinz body anemia (oxidative damage)

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 - Renal Failure
o Grapes and raisins – don’t know why
o Lilies
▪ Acute renal failure = CATS (Stargazer lily)
▪ Ca oxalate = peace, cala
▪ Renal toxin = day, Easter, tiger
▪ Cardiotoxin = lily of the valley
- Ma Huang
o Hyperthermia, tachycardia, tremors
o Contains pseudoephedrine and ephedrine
▪ Same presentation as ingestion of Sudafed
o Major component of herbal supplements marketed for weight loss and athletic performance – now banned
o Ma Huang alone – ok for use in traditional Chinese medicine – for respiratory problems
LARGE ANIMALS
- Heinz Body Anemia
o Methylene blue, molybdenum deficiency, Rye grass, brassica family
o Red Maple Leaves – HORSES – icterus (↓ O2 in blood) + colic
- Zearalenone – PIGS – Fusarium
o Potent estrogenic metabolite → hyperestrogenism, pseudopregnancy, vulvovaginitis
- Salt Poisoning
o LESION = perivascular eosinophil infiltration
o ↑ blood Na means water diffuses out of brain which creates idiogenic osmoles to draw water back
o REHYDRATE SLOWLY of brain gets water too fast
o Head pressing, stargazing, blindness, seizures, hemolysis (water swells RBC and lyses them)
- Copper
o Toxicity = SHEEP → fed cow/horse feed
▪ Hemolytic anemia/icterus, methemoglobinemia, hemoglobinemia/uria
o Deficiency = SHEEP → enzootic ataxia/swayback
▪ Primary (low Cu intake) or Secondary (high molybdenum, S, Fe, Se intake)
▪ Enzootic ataxia = lambs 1-2 months old
▪ Swayback = congenital, very young lambs = progressive ascending paralysis
- Grass Tetany/staggers = HYPOMAGNESEMIA
o Phalaris – canary grasses
▪ Stiff legged gait, bellowing, hyperexcitability, nystagmus, head tremors, falling/flailing, restless, death
▪ Tx: remove from pasture, give IV Mg and Ca SLOWLY
o Lactating animals – early spring – lush pastures (↑ nitrogen/K – inhibit Mg absorption)
- Black Walnut (Juglans nigra) – HORSES – LAMINITIS
GI TOXINS
- Slaframine – Moldy Red Clover
o Slobbers! (hypersalivation)
- Oak (leaves/acorns) – Quercus spp.
o Hemorrhagic diarrhea, abd pain, tenesmus, colic, death
▪ Goats are most resistant to Quercus
o Cattle only – renal damage (tubular nephrosis)
▪ Cattle are most commonly affected
- Cantharidin – Blister Beetles – COLICKING HORSES
o Cardiovascular shock, endotoxic shock, renal failure, mouth/tongue vesicles, watery diarrhea
o Renal tubular damage (hematuria), cardiac arrhythmias
o Abrupt colic, fever, hypersalivation, frequent urination, hematuria
- Claviceps purpura – ERGOTISM (parasitic fungus)
o On rye, oats, wheat, KY bluegrass (ergot in grain!)
o Alkaloids – vascular constriction, thrombosis, gangrene, vomit, colic, diarrhea

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NEUROTOXINS
- Blue-green algae – Anabaena, Microcystis, Aphanizomenon
o Nicotinic agonists – mimics acetylcholine
o Acetylcholinesterase inhibitor
o Dead animals next to pond! Miosis, ptyalism, ↓ HR, diarrhea, ataxia, convulsions, death in minutes
- Nightshade
o Atropine (CNS signs = mydriasis, progressive paralysis, depression)
- Water Hemlock
o TOXIC LEAVES (grand mal seizures, salivation, tachypnea, death, lupine-like birth defects)
- Perennial Ryegrass
o Endophytic fungus (Epichloe) – activated GABA rcptrs → ataxia, tremors
- Lead Poisoning – petroleum products (used motor oil)
o Acute blindness, dullness, recumbent, vocalizing, unaware
▪ Dog: vomiting, intermittent seizures, abnormal behavior, pale
o Rumen contents w/ oily sheen
o CBC: microcytic, hypochromic anemia, ↑ nRBC
o Tx: Ca EDTA to chelate – Ca prevents hypocalcemia (Na EDTA binds Ca → hypocalcemia)
- Sorghum
o Myelomalacia of lower spinal cord → pelvic limb incoordination, urine dribbling, DEATH
- Yellow Star Thistle (Centaurea solstitialis)
o Nigropallidal myelomalacia (loss of globus pallidus and substantia nigra)
o LOSS OF PREHENSION – dystonia of lip mm and tongue, dysphagia, unable to prehend fee
o GRAVE prognosis – recommend euthanasia (will die of starvation or dehydration)
REPRO TOXINS
- False Hellebore (Veratrum californicum)
o Teratogen = Cyclopamine
o Day 14 of gestation: craniofacial deformities (0-1 eye, cleft palate)
o Day 30 of gestation: metacarpal hypoplasia (limb/bone shortening)
- Locoweeds
o Swainsonine toxic – cerebral disease = locoism in livestock
▪ Behavior change, aggression, ataxia, depression, circling, vision loss
▪ High altitudes = cattle = “high mountain disease” = pulmonary hypertension
o Abortion, weak lambs, bent legs, ataxia
o Inhibits α-mannosidases = neurovascular cytoplasmic vacuolation
o WEST! Dry conditions, scarce forages, Rocky Mountains
- Fescue (Neotyphodium coenophialum)
o Ergopeptine alkaloids – dopamine agonist
o Prolactin suppression – inhibits lactation, thick placenta, dystocia, agalactia, prolonged gestation, weak/stillborn
foals
▪ REPRO FAILURE IN MARES (no congenital defects)
o Lameness, rear hoof sloughing, ↓ weight gain, fat necrosis
- Lupine = “Crooked Calf Disease”
o Arthrogryposis (crooked limbs), cleft palate, malpositioning in uterus
- Ponderosa Pine Needles
o LAST trimester abortion, retained placenta
COAGULOPATHY
- Bracken fern
o Bone marrow suppression (↓ neutrophils and lymphocytes)
o Toxic glycoside (ptaquiloside) and thiaminase
o Enzootic hematuria – hemorrhagic cystitis → progresses to bladder neoplasia
o Polioencephalomalacia – due to thiaminase (HORSES)

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 - Cyanide
o Choke cherry – arrow grass, Sudan grass, Johnson grass, Sorghum
o Bright red MM – cyanide block oxidative transport → Hg can't release O2 (venous blood stays oxygenated)
o Tx: Na thiosulfate, Na nitrate, methylene blue (NOT supplemental O2)
- Carbon monoxide
o Cherry red MM – if no almond smell, RO cyanide
- Nitrates – BROWN blood
- Moldy Sweet Clover
o Vit K antagonist = dicumarol (like Warfarin)
o Hemorrhage!! Not hemolysis
o Test PT (prothrombin time) – factor 7 is 1st to go
- Anthrax
o HORSES/COWS – sudden death, colic, fever, SQ edema
▪ Horses – no rigor mortis + unclotted blood exuding from orifices
o DO NOT NECROPSY!!! – could release spores!! CONTACT AUTHORITIES – ZOONOTIC (human forms = intestinal,
pulmonary, cutaneous)
o Dx: vitreous humor or blood from ear scrape
CARDIO TOXINS
- Milkweed, gossypol (cottonseeds), oleander, rhododendron, foxglove, white snakeroot
o Acute death, arrhythmias
- Ionophores (i.e. monensin) – toxic to HORSES
o Coccidiostat used in cattle
o Myocardial necrosis, DCM – heart murmur, resp distress, staggering, profuse sweating, hemoglobinuria
o Dx: echocardiogram = fractional shortening to determine prognosis
o Tx: empty GI tract (mineral oil, activated charcoal, fluid therapy)
- Locoweeds (Astragalus, Oxytropis)
o BRISKET DISEASE – swainsonine toxin → ↑ severity of congestive heart failure – high altitude
PULMONARY TOXINS
- Perilla mint
o Type 1 pneumocytes, bronchiolar epithelial cells
o Dyspnea, frothing at mouth – wet, emphysematous lungs on necropsy
o High mortality (permanent lung fibrosis)
- Brassica plants – rape, kale, turnips
o FOG FEVER – acute bovine pulmonary edema and emphysema, grunts
o Lots of tryptophan – converted to 3-MI (3-methyl-indole) → atypical interstitial pneumonia, emphysema, cyanosis
o Cattle on lush forage – frothy nasal discharge, SQ emphysema, loud cough, open mouth breathing, wheezes,
crackles
- Moldy Sweet Potatoes (Fusarium solani)
o 4-IP (4-ipomeanol) – atypical interstitial pneumonia
o Grunting, frothing at mouth, deep cough, resp distress, death in 2-5 days
o Wet lungs, firm, fail to collapse – same lesions as 3-MI
HEPATIC TOXINS
- Pyrrolizidine alkaloids – fiddleneck (Amsinkia intermedia), common groundsel, ragwort, Senecio, Larkspur
o Inhibits hepatocyte mitosis – no replication – acute liver failure, hepatic encephalopathy, icterus
o Dx: megalocytosis, periportal fibrosis, bile duct hyperplasia
▪ Presents similar to Theiler’s disease in horses – use histopath to differentiate
o Secondary photosensitization (sunburned white skin)
▪ Chlorophyll metabolite (phylloerythrin) normally cleared by liver → w/ liver damage, it accumulates in
skin
▪ Vs. PRIMARY PHOTOSENSITIZATION = St. John’s Wort, Erodium, Brassica, Hypericum
• Hypericin – causes large areas of skin sloughing (mainly unpigmented areas)

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 - Aflatoxin = mycotoxin (Aspergillus)
o Similar lesions to PA, but no megalocytes
o Subacute hepatic necrosis/fibrosis
o Moldy grain!
- Tetradymia (Horsebrush)
o Tetradymol toxin = hepatic photosensitization
▪ Exposed to sunlight → develop full body edema (swollen eyelids, ears, lips, throat region (“bighead”)
▪ Mortality = liver damage
o SHEEP – most commonly affected

***4 hour general rule: if past 4 hours after ingestion, don’t force emesis (past the stomach at that point)
- Don’t induce vomiting for bleach, petroleum products, if they are not conscious/fully aware (may regurg)

Human Toxins
- TILCOMISIN – fatal to humans if injected
o If accidental injection, ICE and call ER

CLINICAL PATHOLOGY
Misc. Facts
- Lactate – assess perfusion (normal <2.5 mmol/L) → reflects anaerobic metabolism
o Produced from pyruvate in anaerobic environments to keep glycolysis running
- Stress response: ↑ neutrophils, ↑ monocytes, ↓ lymphocytes
- Polychromasia = regenerative anemia (fewer mature RBC released into circulation)
o Reticulocyte counts: regenerative vs non-regenerative
▪ Canine: nonregenerative: <95,000 / Feline: nonregenerative: <60,000
Blood Transfusions
- Acute blood loss w/ PCV <20%
o ↑ PCV 1% = 1ml/kg packed RBC
- Crossmatching
o Major = donor RBC + recipient plasma
o Minor = donor plasma + recipient RBC
- Transfusion reactions in cats: anaphylaxis (common in Type B cats – Abyssinians, English Shorthairs, Cornish/Devon Rex)
o Type B = anti-A antibodies (giving B to A is not as bad as A to B; Type A is more common)

- Bovine Blood Types

o B and J = most clinically relevant
o Transfusion reaction: tachycardia, dyspnea, ptyalism, harsh lung sounds
o Tx: dexamethasone, epinephrine, antihistamine, O2
Bleeding Tests
- PTT = partial thromboplastin time = intrinsic and common
- PT = prothrombin time = extrinsic and common
- TT = thrombin time = measure final steps of coagulation (fibrinogen → fibrin)
- Buccal mucosal bleeding test = platelet function
- Template bleeding time = determine functional ability of platelets to plug a minute wound
o (helpful for petechial and ecchymotic hemorrhage)
- Antithrombin activity = measured when DIC (disseminated intravascular coagulation) is concern
Calcium
- Hypocalcemia – check hypoproteinemia (Ca bound to albumin) → check ionized Ca
- Hypercalcemia – neoplasia (lymphoma, AGASACA), primary hyperparathyroidism, chronic renal failure (renal 2˚
hyperparathyroidism), hypervitaminosis D, nutritional 2˚ hyperparathyroidism

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Joint Fluid
- Normal – small mononuclear cells w/o neutrophils
- Suppurative – neutrophils
- Granulomatous – mononuclear (lymphocytes, macrophages, plasma cells)
- Pyogranulomatous – neutrophils and mononuclear cells
Immune Mediated Thrombocytopenia
- Spherocytes on blood smear → tx w/ azathioprine
IMHA
- Spherocytes on blood smear, polychromasia → regenerative anemia, autoagglutination, positive Coombs
o Dogs: Lethargy, weakness, pale, tachypnea, icteric
o Tx: pred, blood transfusion, aspirin (prevent thromboembolism)
- Tx w/ prednisone! Can also use azathioprine, cyclosporine, mycophenolate, or leflunomide if not responsive enough to pred
o 20% can relapse! (if taper meds too soon!)
Von Willebrand
- Factor 8 related antigen deficiency → abnormal platelet function (can't adhere to subendothelial collagen)
- Doberman pinschers!!
Hemophilia A
- Factor 8 deficiency → prolonged ACT and PTT
- Tx: plasma
Canine Thrombopathia
- Inherited – platelets fail to aggregate and secrete granules
- Coag and Platelet numbers = NORMAL
- Basset hounds!!

Iron Deficiency
- Hypochromic RBC (less red) and microcytic (smaller) – less volume
- Microcytic hypochromic non-regenerative anemia
DIC
- Severe coagulopathy – thrombosis + hemorrhage
- Lethargy, anorexia, bleeding from gums
- Prolonged PT/PTT, ↓ PLATELET, positive D dimer (fibrinogen degradation product), ↓ antithrombin III activity
o 2 of the above are enough to diagnose
SIRS (systemic inflammatory response syndrome)
- Fever, ↑ HR, leukopenia
- IL-1 (interleukin 1) – most important in SIRS – major up-stream inflammatory response cytokine (causes tremendous
amplification of inflammatory response)

HYPERSENSITIVITIES
Type 1 = IgE mediated, immune mediated
- Causes: vaccinations
Type 2 = antibody dependent reaction
- IgG or IgM made against normal self-antigens and some foreign antigens that resemble some molecules on the surface of
host cells
Type 3 = immune complex mediated reaction
- Soluble antigen-antibody complexes form in large amounts and overwhelm body instead of being normally removed by
macrophages in spleen and liver
- Results: immune complex disease (arthritis, nephritis, uveitis)
- Causes: sulfa drugs in Doberman pinschers
Type 4 = delayed hypersensitivity → cell mediated
- T8 lymphocytes – sensitized to antigen and differentiate into cytotoxic T lymphocytes
- T helper 1 type T4 lymphocytes become sensitized to antigen and produce cytokines

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 CARDIOLOGY
ECG
- P pulmonale = tall/slender P wave = RIGHT atrial enlargement
- P mitrale = ↑ duration of P wave = LEFT atrial enlargement
Physiology
- Stroke vol x HR = cardiac output (CO)
o Stroke vol determined by preload, afterload, and contractility rate
- Cardiac output x O2 content = O2 delivery
- Response to acute blood loss
o ↑ CO – catecholamines induce vasoconstriction
o ADH releases causing water and Na resorption by kidney
o Splenic contraction occurs – inject stored RBC into circulation
ECF vs ICF
- 2/3 body weight = water (total body water = 60% body weight)
- ECF: ICF = 1:2
o ECF = plasma, interstitial fluid, CSF, synovial fluid
Shock
- Hypovolemic Shock
o Critical ↓ in IV volume (dehydration, hemorrhage, 3rd spacing)
o ↓ IV vol (preload) = ↓ stroke vol/CO = ↓ tissue perfusion/oxygenation
o Vomiting, diarrhea, dehydration, dry MM, prolonged CRT, ↑ HR, weak femoral pulses
o Central venous pression = direct measure of BP in cranial vena cava (preload estimate): -5-5 is hypovolemia
- Cardiogenic Shock
o ↓ myocardial contractility w/ ↓ O2 delivery
o ALWAYS associated w/ primary heart disease
- Obstructive Shock
o Abnormal blood distribution – impairs blood return (GDV obstructed vena cava, pericardial tamponade)
- Distributive/Vasogenic Shock
o Secondary to sepsis and anaphylactic reactions causing vasodilation
Heart Sounds
- S1 = ventricular contraction and closure of AV valves
- S2 = closure of pulmonic/aortic valves (beginning of diastole)
- S3 = ventricular relaxation (very subtle – only heard occasionally during mid-diastole)
- S4 = atrial contraction (very subtle – only heard at end of diastole)
Murmurs
- Left = PAM (3rd ICS = pulmonic, 4th = aortic, 5th = mitral)
o Left heart base = pulmonic stenosis, PDA, subaortic stenosis
o Heart apex = mitral valve dysplasia
- Right = 3-4th ICS = tricuspid
o Systolic at right mid-thorax = tricuspid dysplasia
Failure of Foramen Ovale Closure
- Small slit = shunting btw R and L atrium in fetus
- When born, lungs expand (↓ R atrial pressure) and L atrium becomes high pressure system – should close foramen ovale
- If not closed in 48h → blood shunting from L atrium to R atrium
VSD (ventricular septal defect)
- CATTLE – most common congenital heart defect (failure to thrive by 2-3 months, pulmonary edema, 2˚ pneumonia)
- HORSES – most common congenital defect! (some are normal, some go into heart failure)
- Pathogenesis: oxygenated blood is pushed into R atrium/ventricle → R ventricle dilatation and hypertrophy → ↑ flow to R
side causing pulmonic stenosis (left sided murmur at pulmonic valve(
- Murmur = loud holosystolic or constant murmur heard on BOTH sides (blood shunting from L to R)
- Echo = small turbulent jet flowing L to R through septum
- Tx: small – none (good prognosis); large – surgical correction

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Tetralogy of Fallot
- 1) overriding aorta 2) pulmonic valve stenosis 3) VSD 4) Right ventricular hypertrophy
- Right sided heart failure, cyanosis, 2˚ bacterial endocarditis, exercise intolerance, failure to thrive, syncope, bilateral basilar
murmur, POLYCYTHEMIA (venous blood to arterial circulation → hypoxemia, ↑ EPO
o R → L Shunt = Polycythemia (dark red MM, hypoxemia – ↑ drive for erythropoietin due to hypoxemia)
- Breeds: Keeshonds, bulldogs
Patent Ductus Arteriosus (PDA)
- L (aorta) → R (pulmonary artery) shunt (failure to close after birth)
o Excess vol in pulmonary aa, vv, L atrium/ventricle, aortic arth
o Washing machine murmur – continuous, both sides of chest
o Water hammer pulses – large bounding pulse + sharp peak and rapid decline
- Radiographs – enlarged L heart/pulmonary vasculature + aneurismal bridge of aorta near PDA on DV
o R ventricle enlarged w/ R→L PDA shunt
- MOST COMMON CONGENITAL DEFECT IN DOGS; rare in cats/cows/horses (which are VSD)
o Tiny fluffies, GSD, labs, Newfoundlands
- Tx: surgical ligation (large cylindrical PDA) or coil embolization (funnel shaped PDA)
o Don’t repair R→L PDA!
- Reverse PDA
o “red head, blue body” = R → L shunt (after the aorta branches to direct blood to the head = cyanotic caudal half
MM, pink gingiva
Valvular Endocarditis
- Heart valve infection → OLDER animals
- Small Animals + Horses = aortic valve most common (also mitral)
o Mitral regurg (DDx = degenerative thickening, ruptured chordae tendonae)
o Aortic regurg – no impact on performance!! (harsh decrescendo holodiastolic murmur @ L heart base) – HORSES
- Cause: foot abscess, sepsis (FUO, lethargy, systemic illness)
- Dx: vegetative lesions on heart valves, positive blood culture
Pericardial Effusion
- Causes: HSA, chemodectoma, idiopathic, L atrial rupture (chronic mitral regurg), trauma, PPDH (hernia), infectious
pericarditis, foreign body, coagulopathy, heart base tumor (BLV in cows)
o Muffled heart sounds, ↓ milk, lethargy, anorexia, cough, collapse, pale MM
o Pulsus paradoxicus – pulse exaggerations during resp, weak as inhales, strong as exhales
o Electrical alternans – different QRS amplitudes (heart shifting in free fluid)
- Rads – enlarged globoid heart
- Necrospy – nutmeg liver (R heart failure from pericardial effusion)
- Tx: pericardiocentesis (NOT FUROSEMIDE – will ↓ R heart preload → circulatory failure)
Atrial Premature Complexes
- Causes pulse deficits – clinically insignificant
Atrial Fibrillation
- Most common supraventricular arrhythmia in cattle – from digestive disturbance of abnormal electrolytes → vagal tone,
hypo/hyperkalemia, Ca therapy
- Most common pathologic arrhythmia in horses (2nd Degree AV block most common non-pathologic)
o Poor performance, exercise intolerance – if acute, more treatable
- PULSUS ALTERANS – 2 quick normal pulses then no pulse, irregular HR
- ECG – no P waves (SA not working), high frequency/low amplitude F waves, irregular QRS intervals
- Auscultation – irregularly irregular rhythm w/ variable heart sounds
- Tx (horse): quinidine (Class 1A Na channel blocker – prolong myocardium refractory period)
o Toxicosis – ↑ QRS duration >25%, colic, ataxia, hypotension, diarrhea, edema
o Try Digoxin as adjunctive tx – if quinidine causes ↑ ventricular response rate, resting HR >90 bpm, low vagal tone,
no conversion in 24 hours
- Prognosis – good if HR converts to <60 bpm, A fib < 4min duration, murmur < Grade 3/6
- Tx (dog): diltiazem, atenolol, digoxin, procainamide
o Digoxin – cardiac glycoside = positive inotrope, slows HR

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Ventricular Premature Complexes
- Tx when HR >180 bpm, pulse deficits, clinical signs, VPCs >20 sec in duration
- R starts overlapping T → TREAT! Can cause fibrillation!
Ventricular Fibrillation
- Chaotic electrical and mechanical activity during cardiac arrest
Ventricular Tachycardia
- LIDOCAINE!! If no response, try procainamide and quinidine
Ventricular Asystole
- No electrical or mechanical activity
Hyperkalemia
- NO P WAVE, ↑ P-R interval, wide QRS, tall tented T waves
- May see atrial standstill 2˚ to this – ABSENT P WAVES
AV Blocks
- First Degree
o Takes longer to get through AV node
o ECG: ↑ P-R interval, no dropped QRS
o 1st and 2nd – NORMAL in horse (high vagal tone – no tx needed)
- Second Degree
o Refractory AV node responding to delayed atrial depolarization – exercise intolerance, syncope (dogs/cats)
▪ Can be normal in horses
o Mobits Type 1 = P-R progressively longer until there is dropped QRS
o Mobits Type 2 = P-R unchanged and occasionally see P w/o QRS
- Third Degree
o No impulses from atria to ventricles
o Subservient pacemaker (AV node or ventricle) causes ventricular contraction
o Clinical Signs: exercise intolerance, syncope w/ excitement
o P waves unassociated with QRS
o Tx: pacemaker (chronic cases) or atropine to ↑ HR
▪ NEVER LIDOCAINE – will abolish ventricular escape beat
Heart Failure
- Right Heart Failure
o Cows: traumatic reticulopericarditis (anorexia, bottle jaw/brisket edema, true jugular pulses, ↑HR/RR, depression)
o Clinical Signs: tachypnea/dyspnea (pleural effusion), hepatomegaly (venous congestion), mm wasting (protein lost
into effusions), lethargy, weakness, venous distension, ascites, peripheral edema
o Rads – large heart, hepatomegaly
- Left Heart Failure
o Clinical Signs: cough (pulmonary edema), difficulty breathing
o Rads – large heart, L atrial enlargement, large pulmonary aa, hepatomegaly, alveolar pattern (perihilar region to R
and L caudal lung lobes)
- Tx: furosemide (↓ blood vol/edema/ascites), nitroprusside (vasodilator), Na restricted diet, enalapril (ACEi – vasodilator to
combat vasoconstriction/↑ vascular resistance)

Sick Sinus Syndrome (SSS)

- Severe bradycardia/tachycardia, sinoatrial arrest → exercise intolerance, syncope
- Breeds: mini schnauzers, westies, cockers
- Dx: Holter harness (evaluate frequency and severity)
- If severe – tx = pacemaker (don’t treat unless causing clinical signs)

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 RESPIRATORY
Pulse Oximetry – O2 saturation curve
- Intervene when % drops
- 98-100% = >100 mmHg O2 in arterial blood (anesthetized pt breathing 100% O2 should be >300 mmHg)
o If not >300 mmHg, not exchanging O2 normally (V/Q mismatch, barrier to diffusion)
- 95% = 80mmHg / 90% = 60mmHg / 50% = 30mmHg / 10% = 10mmHg
Acid-Base Status
- Metabolic Acidosis
o Saliva loss – cattle (rumen saliva rich in bicar)
o Dehydrated calf – sunken eyes, nonresponsive → give fluids w/ bicarb
- Metabolic Alkalosis
o Saliva loss – horses (lots of Cl in saliva)
o Sweating horses – horse sweat high in Cl and K – renal retention of bicarb
o Vomiting – lose Cl from stomach acid
- Respiratory Acidosis
o Causes: hypoventilation (buildup of CO2), airway obstruction, pneumothorax, flail chest, neuromuscular dz,
abdominal enlargement, pleural space dz, bicarb therapy
- Respiratory Alkalosis
o Hyperventilation
- Hypoxemia
o Low PO2 – V/Q mismatch, diffusion impairment, low inspired O2, hypoventilation, shunt
- To Determine: primary is whichever goes w/ pH, low bicard = metabolic acidosis, low PaCO2 = resp alkalosis
Ventilation/Oxygenation
- Measure w/ arterial blood gas
- Hyperventilation: PaCO2 <30 mmHg / Hypoventilation: PaCO2 >30 mmHg
o Normal: 35-45 = appropriate ventilation
o ↑ PaCO2 = horse is underventilating (not blowing off enough CO2) → resp acidosis
- Oxygenation
o Hypoxemia = hypoventilation, low FiO2 (not enough O2), venous/arterial blood mixing (↓ oxygenation)
o Cyanosis = PaO2 <50mmHg (check MM)
o Most common cause of cardiac arrest = systemic hypoxemia
- Base Excess – how much base you need to add to solution (ie plasma) to get normal pH (normal HCO3 = 22-24mEq/L)
o Calculation: 0.3 to 0.4 x BW x base deficit (23-pt’s HCO3) = __mEq
o May only fix half – then reassess
Stridor vs Stertor
- Both audible w/o stethoscope – indicate extra-thoracic problem
- Stridor = high pitched, generated near larynx / Stertor = gurgling noise, generated in nasal passages
Pneumothorax
- No dorsal sounds, yes ventral sounds – free air moves dorsally when lungs collapse
- Causes: trauma, damaged lung, ruptured bulla, migrating foxtail, pneumomediastinum,
o NEVER from pulmonary hypertension (causes heart failure)
o Look for rib fractures, diaphragmatic hernia, pulmonary contusions, pleural effusion
- Resp Distress: dyspnea, tachypnea
- Tx: THORACOCENTESIS – DON’T GIVE O2 (worsens pneumothorax!)
Aspiration Pneumonia
- Harsh lung sounds/crackles cranioventral, fever, anorexia, lethargy, depression
- Causes (cows/horses) = mineral oil drenches (tasteless, often aspirated), pharyngeal paralysis, leaking bottle nipples, gastric
reflux, improper intubation
- Causes (dogs/cats) = megaesophagus (myasthenia, congenital), after anesthesai
- Rads = alveolar pattern – R cranial + middle lobes if sternal (depends on pt position when aspiration occurred bc gravity)
Atelectasis
- Incomplete expansion of lung lobe – loss of air from alveoli
- Common w/ prolonged recumbency and inhalant anesthesia (also ↓ pulmonary surfactant in newborns, ARDS, drowning)

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Neurogenic Pulmonary Edema
- Causes: head trauma, seizures, electrocution, upper airway obstruction
- Rapid onset resp difficulty after CNS insult – CAUDODORSAL distribution
Lung Lobe Torsion
- Tx = Lung lobectomy (use iso + injectable succinylcholine – critical that dog stays completely still – no resp motion)
o Can also use nondepolarizing neuromuscular blockers (pancuronium, atracurium, d-tubocurarine)
Smoke Inhalation (from fire)
- CO inhalation – carboxyhemoglobin formation + O2 displacement → severe acidosis
- Laryngeal edema – heat damage to larynx → swelling, upper airway obstruction
- Smoke can inhibit pulmonary macrophage function
- Prognosis: skin burns worsen prognosis
o 1st degree = superficial, epidermis only
o 2nd degree = partial thickness, epidermis, may go to deep dermis
o 3rd degree = epidermis, dermis, and adnexal structures
o 4th degree = total destruction of skin, fat, fascia, bone, and muscle

NEUROLOGY
UMN vs LMN – Lesion Localization
- UMN = hyperreflexia of spinal reflexes, ↑ mm tone
- LMN = hyporeflexia of spinal reflexes, ↓ mm tone
o C1-C5 → all 4 limbs are UMN
o C6-T2 → LMN thoracic limbs, UMN pelvic limbs
o T3-L3 → normal thoracic limbs, UMN pelvic limbs
o L4-S4 → normal thoracic limbs, LMN pelvic limbs (anus/bladder – dribbling urine, dropping feces, no anal tone)
- Prognosis = POOR if no deep pain for 24h
Cranial Nerves
- CN I = Olfactory
- CN II = Optic
o PLR, dazzle
- CN III = Oculomotor
o Closes eyes (levator palpebrae superioris), raises upper eyelid (palpebral levator)
o Lesion = strabismus – movement of eye in horizontal and vertical planes
o Iris sphincter – parasympathetic innervation
- CN IV = Trochlear
o Oblique muscle of eyeball → lesion = medial strabismus
- CN V = Trigeminal
o Mandibular branch – motor to mastication mm (pterygoid, masseter, temporalis) → lesion = can't close mouth
o Ophthalmic branch – sensory to eyes, eyelids, cornea
o Maxillary branch – sensory to face, pinnae, nasal septum
- CN VI = Abducens
o Motor to lateral rectus → lesion = medial strabismus
o Motor to retractor bulbi – not involved w/ PLR, only movement of eye
- CN VII = Facial
o Opens eyes – orbicularis oculi mm
o Motor to mm of facial expression
o Taste in rostral 2/3 of tongue
o Lesions = can't blink, corneal ulceration, muzzle deviation, ear droop, no menace or palpebral
▪ Deficits = exposure keratitis – lacrimation defects
▪ May see deficits in pts w/ otitis media (runs through middle ear)
- CN VIII = Vestibulocochlear
o Vestibular signs (ie nystagmus)
o May see deficits in pts w/ otitis media (runs through middle ear)
- CN IX = Glossopharyngeal

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 - CN X = Vagus
o Lesion = dysphonia, dysphagia, abnormal vocalization, inspiratory dyspnea, megaesophagus
- CN XI = Accessory
- CN XII = Hypoglossal
Cranial Nerve Tests
- Menace = CN 2 and 7
- Palpebral = CN 5 and 7
- PLR = CN 2 and 3
- Corneal = CN 5 and 6 → Always test! Always touch the globe!
Horner’s Syndrome
- 1) 3rd eyelid protrusion 2) enophthalmos (retracted globe) 3) ptosis (droopy eyelid) 4) miosis (small pupil)
o Cows: regional hyperthermia / Horses: SWEATING on ipsilateral head and neck
- Disrupted sympathetic fibers of eye (opposite of fight/flight)
- Causes: idiopathic (most common), chest neoplasia, chronic otitis, hypothyroidism, trauma, retrobulbar dz, guttural pouch
dz (horses)
Vestibular Disease
- Central = vertical nystagmus + conscious proprioceptive deficits
- Clinical Signs: head tilt, nystagmus, circling TOWARD side of lesion
o PARADOXICAL – circling AWAY from lesion (peripheral signs in 1 direction, central in other – lesion on central side)
o Vestibular signs + CP deficits → lesion on same side as CP deficits
Cerebellar Disease
- Ataxia, hypermetric/exaggerated gait, sway
- Cerebellar hypoplasia – congenital defect, non-progressive disease; incoordination, abnormal posture/balance
Listeriosis vs TEME (thromboembolic meningitis)
- Listeria monocytogenes
o Goats/cattle fed spoiled silage (microaerophilic, low pH environment)
o Unilateral – dropped lip, no menace/palpebral, ptosis, drooling, fever, dysphagia, circling
▪ ↓ FACIAL SENSATION
▪ Asymmetric CN V/XII signs – ascending infection
▪ Abortion in cattle → fetus is autolyzed
o MONONUCLEAR PLEOCYTOSIS on CSF tap, microabscesses in brainstem/CN roots
o Tx: procaine penicillin
o ZOONOTIC – foodborne illness, abortions/stillbirths in humans
- TEME = Histophilus somnus
o High fever (unlike Polioencephalomalacia), resp signs before CNS signs
o NEUTROPHILIC PLEOCYTOSIS on CSF tap, xanthochromia/cloudy due to ↑ neutrophils
▪ Xanthochromia = evidence of prior hemorrhage (yellow discoloration)
o TEME = thromboembolic meningoencephalitis
o High risk calves
▪ Histophilus somnus infection = pleuritis and myocardial abscess
o Involved in bovine respiratory disease complex (BRDC) – most common in recently weaned calves esp. during high
stress periods (like weaning and transportation to a feedlot)
Status Epilepticus
- If in active epilepticus, DIAZEPAM RECTALLY – even in cats
- Idiopathic epilepsy = Beagles, Keeshonds, Dachshunds, Labs, Goldens, Shelties, Irish Wolfhounds, Vizslas
o 1-5y animal, generalized tonic-clonic seizures w/o interictal abnormalities
Head Trauma
- Obtunded, most of PE normal
- Tx goal = minimize intracranial pressure (ICP) + need high PaO2 → keep cerebral blood flow low w/o causing hypoxia
Cushing’s Reflex
- ↑ ICP (ie brain trauma) → ↑ systemic BP to overcome the pressure to perfuse the brain via vasoconstriction → ↓ HR
- DO NOT INTERVENE TO ↓ BP – may eliminate cerebral blood flow and kill the pt!!

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 HEPATOLOGY
Liver Bloodwork
- ALT/AST – liver leakage enzyme (damage, not function)
o AST – also RBC, cardiac/skeletal mm
- ALP/GGT – liver inducible enzyme (cholestasis)
o ALP – liver, intestine, kidney, bone
- SHD – liver specific in cow, horse, sheep, goat
- LDH – muscle, heart, liver
- Liver Products: bilirubin, bile acids, fibrinogen, albumin, antithrombin III, BUN (best measure of liver function), cholesterol,
glucose, coag factors (do coags if think have liver dz)
- Bilirubin in HORSES – ↑ bilirubin from fasting (can become icteric)
o Hemolysis = ↑ bilirubin (damaged RBC removed, Hg processed)
o Liver failure → hemolytic crisis (more fragile RBC from toxic metabolites in blood) → TERMINAL LIVER DISEASE
Portosystemic Shunt
- Cats – BRIGHT ORANGE IRISES (pathognomonic), ptyalism
o Other congenital issue in cats w/ PSS: heart murmurs
- Dogs – YORKIES
o Other congenital issue in dogs w/ PSS: runt, retained deciduous teeth, cryptorchidism
- Both – depression, lethargy, salivation, poor weight gain, aggression, failure to thrive, hepatic encephalopathy (head
pressing, seizures, wandering, tonic-clonic seizures after eating, circling), underweight, poor-doer
- Rads – small liver (cranial shifted gastric axis)
- Bloodwork – microcytic anemia, ↑ pre/post-prandial bile acids (shunt = BA p=bypass liver, enter systemic circulation)
o Normal liver enzymes!
- UA – urate stones
- Phrenicoabdominal vv = ONLY veins that should enter vena cava btw hepatic and renal vv
- Tx:
o Lactulose – easily fermented carbs – metabolized to acid in gut (↓ colonic pH – keeps ammonia in ionized form
(NH4+) rather than NH3 and is excreted
▪ Cathartic – ↓ GI transit time (↓ ammonia absorption)
▪ Carb source used by colonic flora as protein alternative
o Sub dairy/veggie proteins instead of meat – feed max protein they will tolerate w/o clinical signs (encephalopathy)
o Oral neomycin – kill urease producing bacteria in gut → ↓ ammonia production in gut
Hepatoencephalopathy
- Chronic weight loss, frequent yawning, unaware of surroundings, UTD on vaccines, neuro signs
- Cause: ↑ ammonia, aromatic amino acids, metacaptans to brain (causes CNS signs)

TICK BORNE DISEASES

Lyme Disease (Borrelia burgdorferi)
- Vector = ixodes (from white footed mouse)
- Humans = erythema migrans (cutaneous rash)
- Dogs = arthritis, lymphadenopathy, fever, anorexia
Ehrlichia
- Canine granulocytic ehrlichiosis = E. ewingii, Anaplasma phagocytophilia; Vector = Amblyomma
- Canine monocytic ehrlichiosis = E. canis; Vector = Rhipicephalus
- Clinical Signs = fever, anorexia, limb edema, depression, oral vesicles, petechiation, joint pain/swelling, aqueous
flare/retinitis, hypoalbuminemia, ↑ ALP
Rocky Mountain Spotted Fever (Rickettsia rickettsia)
- Vector = Dermacentor
- Clinical Signs = SAME AS EHRLICHIA – differentiate bc RMSF course is over in 2 weeks
- Pathogenesis = vasculitis

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Franciella tularensis (Tularemia)
- Cats and dogs – infected by close contact w/ rodents and RABBITS; Vector = ticks
- ZOONOTIC – potential bio warfare (ulceroglandular, pneumonic, typhoidal)
- Dogs – relatively resistant (Clinical Signs = depression, fever, lymphadenopathy, oral ulceration)
Cytauxzoon felis (CATS)
- Vector = Dermacentor
- Rapidly progressive, almost 100% fatal
- Clinical Signs = dark urine, icterus, fever, prolonged CRT, death (DIC), anemia
- Ring-shaped organisms in RBC / Schizonts in spleen, liver, blood, bone marrow, lymph nodes
COWS
- Anaplasma marginale
o Ticks but also any blood feeding insect (and iatrogenic – needles, instruments)
o EXTRAVASCULAR HEMOLYSIS – NO HEMOGLOBINURIA (different from lepto, bacillary Hg-uria, anthrax)
▪ New additions to herd – weak, depressed, staring into space, pale, icteris, fever
- Babesia
o Also DOGS (Greyhounds, pitbulls predisposed) and HORSES (malaria-like parasite)
o Vector = Boophilus ticks
o Tx: imidocarb
- Heartwater disease (Ehrlichia ruminatium)
o Vector = Amblyomma (seen in Africa, West Indies)
o Fatal encephalitis in sheep, goats, cattle
- Epizootic Bovine Abortion (EBA)
o Aka foothills abortion (California foothills)
o Vector = Ornithodoros coriaceus (soft ticks)
o Aborted fetus shows enlarged lymph nodes and spleen, destructive thymus lesion
- Otobius megnini
o Soft tick that likes ears (cattle will rub/scratch at their ears)

FUNGAL DISEASES
Blastomycosis = Blastomyces dermatidis
- OH, MS, MO River Valleys – HUNTING DOGS
- BELLS – bone, eyes, lnn, lungs, skin → skin lesions, lymphadenopathy, cough, uveitis, boney lesions
o NOT cats
- Broad based budding yeast
- Tx: systemic antifungals (itraconazole)
Histoplasma
- OH, MS, MO River Valleys
- Large bowel diarreha
- Small intracellular yeast (small round bodies, basophilic center, in mononuclear phagocytes)
- Smaller than a RBC, round to oval, eccentric purple cresent-shaped nucleus w/ thin clear halo
Cryptococcus = Cryptococcus neoformans
- Resp and ocular dz, facial swelling, nose distortion (“roman nose” in cats), lymphadenopathy
- Pigeon droppings!
- Small yeast w/ large capsule, narrow based budding; dx by latex agglutination Histoplasma
Aspergillus
- Branching fungal hyphae on HISTOPATH (not cytology), rhinoscopy (fungal plaques)
- Doliocephalics = nasal aspergillus; GSD = disseminated
- Tx: Clotrimazole (post recovery = severe laryngeal edema)
Coccidiomycosis = Coccidiodes immitis
- West Coast
- Similar clinical signs to Blasto – cough, lameness, draining lesions, pneumonia, lymphadenopathy
o CATS – SKIN lesions

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 - Spherule – double walled structure containing endospores
- Tx: Antifungals (don’t use ketoconazole in cats → causes vomiting)
o Ketoconazole + Amphotericin B (potentiated activity) = systemic antifungal treatment
Sporotrichosis
- Contagious, ZOONOTIC (esp w/ cat lesions!!)
- Looks like Histoplasma – smaller than RBC, clear thin halo

PARASITOLOGY
SMALL ANIMAL GI PARASITES
- Hookworms = Ancylostoma caninum
o Thin walls, 2-8 cells
o Dogs = anemia / Humans = cutaneous larval migrans
o Tx: any dewormer other than praziquantel
- Roundworms = Toxocara canis (dog), T. cati (cat)
o Dog = young puppy, cough
o Transmission: transplacental (puppies), transmammary (kittens)
o Humans = visceral and ocular larval migrans
- Tapeworm
o Echinococcus granulosis
▪ Non pathogenic in animals, FATAL in humans (hydatid cyst disease)
o Dipylidium caninum
▪ Fleas = intermediate host / proglottids in feces (rice grains)
▪ Treat for fleas, give praziquantel for tapes
o Taenia taeniaeformis
▪ From eating infected prey, rarely causes clinical signs
▪ Tx: praziquantel
- Whipworms = Trichuris vulpis
o Football shaped eggs
o Tx: fenbendazole, milbemycin oxime
- Coccidia
o Eimeria – 4 sporocysts
▪ From eating rabbit feces – parasitic in birds/reptiles/herbivores; don’t need to tx in dogs/cats
o Isospora
▪ Tx: sulfadimethoxine (Albon)
o Crytosporidium
▪ Round, slightly smaller than RBC, acid-fast or IFA stain to dx
▪ Resistant to disinfectants, humans get from water contamination
▪ Tx: clindamycin, azithromycin, tylosin
- Giardia
o Binucleate, outlined by adhesive discs, swims in “falling leaf” motion, pear shaped
o ZOONOTIC
o Tx: metronidazole, fenbendazole
o Dx: trophozoites in fecal smear, IFA, giardia ELISA, cysts in fecal float
- Tritrichomonas foetus
o Flagellated parasite (looks like giardia but w/ 1 nucleus and undulating membrane)
o Kittens w/ unresponsive diarrhea
o Tx: ronidazole
- Strongyloides stercoralis = Threadworm
o Mucoid diarrhea, possible anemia (puppies, kittens)
o Dx: Baermann fecal technique (best way to recover larvae)

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 - Gnathostoma = Stomach worm
o 3cm long nematodes w/ spine covered heads – vomited up!
o Need copepods (near fresh water) – adults live in stomach, cause gastritis
o ZOONOTIC – ingestion of undercooked fish (gastritis, peritonitis, cutaneous/neural migration)
o Tx: albendazole
OTHER SMALL ANIMAL PARASITES
- Paragnonimus kellicotti – Lung Worm (dogs, cats)
o Crawfish, snails = intermediate hosts
o Dx: fecal sedimentation, tracheal wash – single operculum
o Tx: fenbendazole, praziquantel

- Capillaria aerophile – Lung Worm

o Asymmetric terminal plugs (similar to trichuris eggs)
- Aelurostrongylus abstrusus – Common Lung Worm in Cats
o Dx: Baermann / Tx: fenbendazole
- Toxoplasma gondii – CATS (definitive host)
o ZOONOTIC – infants infected in utero = chorioretinitis, mental retardation
▪ Pregnant women – don’t change cat litter box! (if cleaning feces right away, its ok – takes 1-5 days after
shedding for oocysts to sporulate and become infectious)
o SHEEP, kittens, pigs, dogs (NOT cows) → ABORTION, stillbirth, diarrhea, cough, dyspnea, seizures, chorioretinitis,
meningoencephalomyelitis, myositis
o Tx: clindamycin
- Heartworm – Dirofilaria immitis
o Cats = lower adult worm burdens, cat larvae more likely to migrate to ectopic locations, often microfilaria negative
▪ Sometimes male-only infection; worms don’t live as long
o Wolbachia – symbiotic bacteria → doxycycline
o Prevention: ivermectin, milbemycin oxime
o Dx: antigen test (dogs), heat treated antigen test/antibody test (cats), blood smear for microfilaria (dogs)
o Tx:
▪ Cats – corticosteroids (NOT ADULTICIDE – could cause embolization/death)
▪ Dogs – melarsamine (immiticide/adulticide) + ivermectin (kill microfilaria)
▪ STRICT ACTIVITY REST – ↓ chance of pulmonary thromboembolism
- Dipetalonema reconditum
o Looks similar to Dirofilaria immitis – not pathogenic, have to differentiate!
- Raccoon roundworm – Baylisascaris procyonis
o ZOONOTIC – larval migrans to brain → CNS disease
o Ocular disease
- Leishmania – Trypanosoma
o Transmitted by sand flies
- Cuterebra – Botfly
o Cats – fistulous swelling on ventrum, erythematous, exudes small amount purulent material
o Eggs in environment – get on animal → heat hatches eggs → larva migrate to SQ (leave pore for breathing) → exit
o Remove in ONE PIECE – rupturing larvae could cause anaphylaxis
- Ctenocephalides felis – CAT FLEA
o Pruritis and inflammation, possible flea allergy dermatitis, anemia, skin lesions, tapeworm infestation
o Dogs – flea allergy dermatitis on CAUDAL HALF of animal
o Generalized miliary dermatitis, dark brown flecks in fur, eosinophilic plaques
▪ Alopecia, ulceration, erythema, pruritis (inguinal, caudal thigh)
o Tx: flea products, steroids, antihistamines, abx, sometimes hypo-sensitization is helpful
- Demodex canis – Demodex mange (D. gatoi – cats)
o Young animals (INHERITED DEFECT) – don’t breed, will clear on its own
o Adults – IMMUNE SUPRESSED – look for underlying systemic problem
▪ Tx: ivermectin, amitraz, milbemycin, abx (2˚ infection)
▪ Amitraz (Mitaban) – only FDA approved tx → dip must be done in hospital

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 o Non-contagious: focal areas of circumscribed alopecia and scaling (face, muzzle, periorbital, thoracic limbs)
o Dx: DEEP skin scrap (cigar shaped mite)
- Scabies ascariasis – mite
o ZOONOTIC – but fairly host specific
o Severe pruritis around pinna, ventral thorax/abdomen, legs → alopecia, crusting, erythema
o Tx: ivermectin, amitraz, milbemycin, Selamectin
- Ollulanus tricuspis
o CATS →Mild erosive gastritis – vomiting a few minutes/hours after eating
o Worms are usually digested and passed in feces
o Dx: check vomit/stomach contents for larvae and adult worms
RUMINANT GI PARASITES
- Haemonchus contortus
o Anemia & hypoproteinemia – SHEEP and GOATS (abomasum blood sucker)
o Chronic weight loss, poor doer, NO DIARRHEA, appear pale
o Dx: inch long worms in abomasum (barber pole appearance)
o Tx: fenbendazole – if resistant, change to ivermectin; only treat if pale enough (4-5/5)
- Nematodirus
o Young animals – profuse watery diarrhea, anorexia, weight loss, dehydration
▪ Spring – coccidiosis season
o Elliptical appearance, sharply curved poles, 2-8 blastomeres surrounded by fluid filled cavity
- Ostertagia ostertagii – Roundworm
o Type 1
▪ Acute weight loss (anorexia, poor growth), diarrhea – NAÏVE cows
▪ Diarrhea - <2y olds on pasture – chronic dz
▪ Winter and Spring – infection w/ large numbers of L3 from contaminated pastures
▪ HIGH EGG COUNTS, not assoc. w/ large numbers of larvae w/ few adults in abomasum
o Type 2
▪ Chronic weight loss, diarrhea – OLDER cows
▪ Fall and Winter – LOW EGG COUNTS
▪ Lots of inhibited L4 that rapidly change – THOUSANDS OF LARVAE IN ABOMASUM
▪ “Moroccan Leather” abomasum appearance
o Tx: ivermectin – kills all life stages; fenbendazole
- Coccidiosis – Eimeria
o **Isospora only affects carnivores
o CALF dz – nervous coccidiosis – calves <1yr (older than 21 days)
o Heat labile neurotoxin – diarrhea (bloody + tenesmus) → neuro signs
o Tx: amprolium (Monensin, sulfa drugs)
- Strongyloides – Intestinal Threadworm
o Penetrate oral mucosa or skin → bloodstream → heart → lungs → trachea → coughed up and swallowed
o Live in intestines
- Monezia – Tapeworm
o Rectangular or triangular structure; Non-pathogenic but can cause initial stasis
EQUINE GI PARASITES
- Oxyuris equi – Pinworm
o Anal pruritis, tail rubbing, alopecia around tail/perineal area
o Female worms crawl out of anus → cement eggs to perineal region (larvae hatch, cause discomfort)
o Scotch tape prep – look for eggs
- Parascaris equorum – Roundworm (ascarid)
o Respiratory signs (migrate through lungs, predisposes to infection), weight loss, diarrhea
▪ FOALS – colic from intestinal impaction
▪ ADULTS – can cause immune mediated hypersensitivity
• “Verminous pneumonia” and “summer colds”
o Tx: anthelmintics, kill SLOWLY of cause massive die-off and impaction
▪ If horse recently dewormed and is now colicking → likely roundworms

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 - Tapeworm – Anoplocephala magna/perfliata, Paranoplocephala mamillana
o Gi disturbance, ulceration, unthriftiness, anemia, colic
▪ Alters peristalsis → INTUSSUSCEPTION, ileal impaction
o Tx: praziquantel, pyrantel (only for Anoplocephala)
- Strongyloides westeri
o FOAL diarrhea – parasite transmitted in milk
o Tx: ivermectin, oxibendazole – give ivermectin to pregnant mare (prevent infection in foals)
- Strongylus vulgaris
o Verminous arteritis → larval migration through cranial mesenteric artery → thrombosis and arteritis
- Trichostrongylus axei – Small Stomach Worm (Hairworm)
o Chronic gastritis, weight loss – penetrate mucosa, cause ulceration/thickening
o Ruminants, horses housed near cattle
- Gasterophilus intestinalis - Stomach bot fly larvae
o Yellowish eggs on medial aspect of forelimb cannon bones; no clinical signs usually (gastritis, stomach rupture
possible)
- Habronema/Draschia megatoma = Cutaneous Habronemiasis
o “Summer Sores”
o Dx: nonhealing reddish-brown greasy skin granulomas w/ yellow calcified material (rice grain looking things)
▪ Larvae: spiny knobs on tails
o Most tx = poor results → ivermectin, moxidectin, fly control
- Small Stronglyes (Cyathostomes) and Roundworms (Ascarids)
o Significant resistance to macrocyclic lactones (ivermectin, moxidectin)
o Death from parasitic infections in sheep/goats = becoming more common
o Do fecal egg count prior to deworming (only deworm if have high egg counts)
RUMINANT & EQUINE DERMATOLOGY PARASITES
- Hypoderma lineatum vs Hypoderma bovis – cattle grub, heel/warble fly
o Eggs on feet hairs – L1 hatch and burrow into skin
▪ H. bovis → epidural fat in spinal column
▪ H. lineatum → esophagus
▪ L2: migrate into SQ tissue on back → L3 → nodules on dorsum w/ top pore (breathing hole)
o Tx: ivermectin in early fatt – emerge in spring but crucial to tx in fall!
o Huge economic losses – hide damage (mainly cattle); can happen to horses
- Onchocerca cervicallis
o Dermatitis – hypersensitivity to dying microfilaria
o Diamond shape lesions (“bull’s eye” head lesion), ocular lesions (UVEITIS, conjunctivitis, keratitis) – aberrant
migration of microfilaria; ventral midline dermatitis
o Vector = Culicoides
o NONSEASONAL – nonpruritic / Tx: ivermectin (microfilaria), no tx for adults
- Culicoides hypersensitivity – “Sweet itch”
o Gnat saliva = Type 1 hypersensitivity (very pruritic diffuse lesions)
o Warm months (SEASONAL), worse w/ age
o Tx: ↓ exposure, steroids; antihistamines may help, topical shampoos are USELESS!
o Vector for Bluetongue, Onchocerca
- Haematobia irritans – horn/face fly
o Bigger cow problem (repro in cow feces), also affects horses (who are housed near cattle)
o Ventral midline dermatitis, focal lesions w/ wheals and crusts (NONPRURITIC ventral midline crusting)
- Habronema muscae – Summer Sores
o Larvae migrate from stomach and emerge – create granulomatous lesions (eye, genitalia, lower extremeties)
▪ Calcified larvae in lesion, gastritis, eosinophilic granulomas (summer sores)
- Sarcoptes scabei – Sarcoptic Mange
o Most economically important in PIGS – severely pruritic, hyperkeratotic ear lesiosn
▪ ↓ growth, ↓ milk in cows, hide damage / head, neck, and ears in horses
o ZOONOTIC & REPORTABLE – skin lesions in humans (most spp can get this!!)
o Tx: ivermectin

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 - Chorioptes equi – Equine Mange
o Lesions near foot & fetlock (draft horses) – pruritic dermatitis
o Tx: ivermectin
- Demodex
o Rare in horses (not really pruritic) – head, neck, withers – dx w/ skin scrape
o No tx in horses → amitraz = colic/death in horses
o Only form of mange that isn’t reportable
- Thelazia lacrymalis – Eye Worm
o Vector = Musca autumnalis (horse face fly)
o Tx: remove manually + 10% levamisole drops
- Sheep Keds – Melophagus ovinus
o 6 legs – wingless flies; adults feed on blood
o Clinical Signs: pruritis, stained wool, potentially anemia
RUMINANT & EQUINE OTHER PARASITES
- Lungworms
o Dictyocaulus arnfeldi – HORSE lungworm
▪ Definitive Host = DONKEY – horses housed near donkeys
▪ Dx: Baermann (L1 hatched in feces), transtracheal wash
o Dictyocaulus viviparous – HORSE lungworm
▪ Ingest L3 → hatch in small intestine → go via lymphatics to lungs → L4 → adult → coughed up and
swallowed → molt in intestines → molt on ground after being defecated
▪ Dx: tracheal wash, Baermann fecal analysis (not float – too heavy to float)
▪ Tx: fenbendazole, ivermectin, levamisole, albendazole

o Dictyocaulus filarial – GOAT lungworm

▪ Bronchitis in goats (also Muellerius capillaris, Protostrongylus refescens)
o Lungworm Dx: BAERMANN sedimentation
- Cochiomyia hominovorax – Screw worms
o REPORTABLE – eradicated in US by releasing lots of sterile males
o Clinical Signs: myiasis (eggs laid on wounds, maggots feeding on live flesh – create huge wound)
▪ Metallic blue-green fly leaving the wound
▪ Sarcophaga (flesh flies) also does this to wounds
- Oestrus ovis – SHEEP
o Fly deposits larvae at nostrils → migrate to nose
o Sneeze, head shaking, nose rubbing, nasal discharge, stridor
▪ Hypersensitivity response w/ heavy infestation
o Nasal discharge cytology = eosinophils + mast cells
o Tx: ivermectin
- Hematopinus spp – COW blood-sucking lice
o Severe ANEMIA – calves 2-7 months (become susceptible to pneumonia)
o Dx: skin scrape – lice have 6 legs
- Neospora caninum
o ABORTION @4-6 months in CATTLE + dog w/ diffuse mm atrophy, trouble walking on hind limbs (neuro and
muscular abnormalities); DOG = definitive host
▪ Most other abortions are later in gestation: Brucella, Listeria, Lepto
o Autolysis of fetus + granulomas in brain
- Sarcocystis
o S. hirsute = CAT / S. hominis = human / S. cruzi = dog
▪ All affect cattle as intermediate host!
o Carnivore eats cow w/ muscle cyst → form sporocysts → shed in feces, eaten by cows → sporocysts hatch and
invade muscle, form cysts / takes 10 weeks
o Cows: fever, anorexia, salivation, weakness, muscle fasciculations, weight loss
o Prevention: prevent carnivore feces from contaminating the area

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 - Tsetse fly – Trypanosomiasis
o Nagana in cattle / African Sleeping Sickness in humans
o Fever, anemia, weight loss, sleeping sickness = Trypanosoma brucei
- Reduvid Beetle – Chagas Disease = Trypanosoma cruzi
o Nervous, GI, cardiac
o South America, parts of US (vs Nagana in Africa)
PORCINE PARASITES
- Ascaris suis – Roundworm
o Migrates through liver (“milk spots”) / migrates through lungs (“thumps” – coughs)
o Sporadically die due to impaction, but usually not many clinical signs
o Necropsy = “milk spots” in liver, condemnation of meat, 20-40cm worms in intestines (large bowel diarrhea)
- Trichuris suis – Whipworm (MUCOHEMORRHAGIC DIARRHEA)
o ALL AGES – usually weaned pigs → MUCOHEMORRHAGIC DIARRHEA
o Double operculated egg – fecal float / Necropsy – eggs in cecum/colon
o Prevention: anthelmintics 1 week before farrowing, move to clean pasture
- Taenia solium – Pork Tapeworm
o ZOONOTIC – cysticercosis from eating undercooked pork!
▪ Pig = intermediate host (eating infected human feces) – cycsticerci form in pigs’ cardiac/skeletal mm →
humans eat meat w/ cysts → adult tapes form in intestines
- Isospora suis – Coccidiosis
o Diarrhea – nursing and weaning pigs – HIGH MORBIDITY – 1-3 week old pigs
o Watery diarrhea, ill thrift, failure to gain weight, dehydration → Other DDx (age and signs) = E. coli
▪ Differentiate: coccidia doesn’t respond to antibiotics
o Tx: amprolium – IMPROVE SANITATION
- Strongyloides randomi – Threadworm
o Trans-colostrum transmission – worms reside in small intestines – SUCKLING piglets
o Heavy infestation = diarrhea, anemia, emaciation, death
o Tx: ivermectin, benzimidazoles
- Metastrongylus – Lungworm
o EARTHWORMS – intermediate host (prevention = keep away from soil that contains earthworms)
o Coughing, unthriftiness = 2˚ pneumonia and thumps
- Stephanarus dentatis – Kidney Worm
o EARTHWORMS – intermediate host (no earthworm soil!)
o Unthriftiness, slow growth, death, posterior ataxia/paralysis (larvae migrating at spinal cord)
o Dx: Urinalysis / Necrospy = worms in kidneys, ureters, perirenal fat
- Trichinella spiralis
o Can affect most animals – bears, horses, rats, marine mammals, pigs
o Transmission: ingestion of encysted larvae in muscles / pig infection from eating garbage (or rats that fell in feed)
▪ Prevention: cook pigs’ food, prevent cannibalism
▪ Tx: NOT PRACTICAL – can kill by cooking
o ZOONOTIC – humans get from eating undercooked pork!

ONCOLOGY
Chemo Drugs
- Doxorubicin = adiamycin
o Dogs – cardiotoxic (cumulative), irreversible tissue sloughing if perivascularized
o Cats – renal toxicity
- Cyclophosphamide
o Sterile hemorrhagic cystitis – encourage animals to drink lots of water, give fluids, urinate frequently (prevent the
compound from sitting in bladder)
- Vincristine: Paralytic ileus / CURES TVT
- L-asparaginase (Elspar): Anaphylaxis (foreign protein that illicits immune response); only can use 3x max

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 - Cisplatin
o Dogs – nephrotoxicity
o Cats – fatal pulmonary edema (“cisplat splats cats”) – NEVER USE IN CATS
- Carboplatin
o Not used as much anymore; safe in cats
o GI signs 2 WEEKS after (vs 3-5 days in the others)
- 5-fluorouracil (5-FU – fucks up cats)
o Neurotoxic to CATS (irreversible)
- Chemotherapy effects:
o 10h → 10d → 4months
▪ Neutrophils life span = 10h / platelet life span = 10d / RBC life span = 4 months
▪ Bone marrow suppression: when you expect to see drops in counts
o Common side effects: GI (diarrhea, nausea) in 5-7 days (how long it takes for cells to go from crypt to tip of villi)
o Alopecia: poodles!
Common Tumor Locations
- HORSE
o Bladder – SCC
o Kidney – renal carcinoma
o Stomach – SCC (weight loss, colic)
o Intestines – lymphoma (VERY POOR PROGNOSIS)
o Ocular – SCC (lack pigment in eyelids, older Hereford cattle)
▪ Also lymphoma – EUTHANIZE – meat is condemned
- CAT
o Striated muscle – rhabdomyosarcoma
o Intranasal – lymphoma (dyspnea from lnn compressing trachea)
o Nasal Planum – SCC
o Intraocular – melanoma (2nd = lymphoma; ciliary body adenomas and HSA less common)
o Oral – SCC (2nd = fibrosarcoma)
o Skin – basal cell tumor (older cats)
o Cat lymphoma = GI small cell lymphoma (vs IBD)
- DOG
o Oral – melanoma (1/3), SCC, fibrosarcoma, epulides
▪ Large cell w/ black pigment, ONCEPT melanoma vaccine
o Intranasal – adenocarcinoma
o Bone – osteosarcoma
▪ “away from elbow, toward the knee” – metaphysis (cell division location), met to diaphysis (blood supply)
▪ Amputate + chemo → at dx, there are already pulmonary mets
▪ Why so painful? Pushes periosteum off of bone = CODMAN’S TRIANGLE
o Kidney – renal carcinoma (polycythemia from EPO secretion)
o Ocular – meibomian adenoma
o Skin – sebaceous gland tumor (hyperplasia, epithelioma, adenoma/carcinoma)
▪ Mast cell tumors – like to recruit eosinophils, 10% of MCT wont stain granules on Diff Quick!! (will look
like histiocytoma unless very carefully look for a granulated cell which are very few in number)
• Low grade – brachycephalics (Boxers!)
• High grade – Sharpei
▪ SCC – non-pigmented areas
o Spleen – HSA (commonly find when develop acute hemoabdomen/sudden death)
o Dog lymphoma – large cell lymphoma (enlarged peripheral lymph nodes)
o Butt – AGASACA (neuroendocrine tumor, nuclear rowing), perianal adenoma (densely clumped, look like
hepatocytes w/ bright pink and blue cytoplasmic granulation)
o Bladder – TCC (transitional cell carcinoma)
- GOAT/SHEEP
o Nasal adenocarcinoma – ovine/caprine nasal adenocarcinoma virus
▪ Expansive, destructive, NOT metastatic → exercise intolerance, noisy breathing

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Types of Tumors
- Carcinoma – epithelial cells (salivary glands, mammary glands, cells lining most tissues)
o Cytology = COHESIVE CLUSTERS, tight cellular junctions, polygonal cells
- Sarcoma – mesenchymal cells (named by cell type: fibroblasts = fibrosarcoma, osteoblasts = osteosarcoma)
o Cytology = SPINDLE SHAPED, elongated cytoplasm, oval nucleicriter
- Round Cell Tumors – lymphoma, plasma cell, histiocytic, TVT, Mast cell
o Cytology = large populations of cells, NOT clusters, round cells, usually unique identifiable features (MCT = purple
granules)
Criteria of Malignancy
- Anisocytosis (different size cells), anisokaryosis (different size nuclei)
- Multinucleation, differences in size/number of nucleoli
- Open chromatin (normally very dense, very dark) – when open, means lots of protein synthesis – lighter, stippled/clumped

RENAL
Bloodwork/Diagnostics
- ↑ renal values, ↑ specific gravity (hyperconcentrated) = pre-renal azotemia (dehydration)
- Not fasted/high protein diet = ↑ BUN
- GFR – assessed by serum creatinine (↑ creatinine proportional to ↓ GFR)
- 65% renal function has to be lost before dog can't concentrate urine (75% in cats)
- 75% renal function has to be lost for azotemia to develop in dog
- HORSE – 66% of kidneys damaged before see lab indications of renal insufficiency (isosthenuria), azotemia at 75% damage
- USG: 1.001-1.007 = hyposthenuria = renal function can dilute urine (takes work to get this low)
- Urine Culture Indications: isosthenuria (urine too dilute to ID bacteria), WBC in urine, bacteria in urine, NOT bilirubinuria
- Water Deprivation Test: PUPD animals (ruled out DM, renal insufficiency, hypercalcemia, liver failure, Cushing's,
hyperthyroidism, etc.) to determine diabetes insipidus vs. psychogenic water consumption
o Only if have normal renal values and low specific gravity in face of adequate hydration
- Azotemia
o Pre-renal = hypovolemia, dehydration
o Renal = aminoglycoside toxicity, pigment nephropathy, oxalate plant consumption
o Post-renal = urinary obstruction, ruptured urinary bladder
- ADH
o Release stimulated by hyperosmolality and ↓ circulating blood vol
o ↑ renal water absorption/urine osmolality by ↑ permeability of collecting tubules
o Osmoreceptors in hypothalamus detect changes in plasma osmolality → release ADH accordingly
Embryology
- Umbilical aa → round ligament of bladder
- Urachus → middle ligament of bladder
- Umbilical v → falciform
Nervous Bladder Control
- Hypogastric = sympathetic (β rcptrs – detrusor muscle / α rcptrs – internal urethral sphincter)
- Pelvic = parasympathetic (detrusor muscle – bladder wall)
- Pudendal = somatic (external urethral sphincter)
- Voiding = parasympathetic stim + sympathetic inhib = detrusor muscle contracts bladder, expels urine
- Storage = sympathetic + somatic are active – hypogastric stims detrusor muscle → relax, also stims α rcptrs in internal
urethral sphincter / pudendal nerve stims external urethral sphincter → contract
Pyelonephritis – ascending UTI → kidney infection
- Bacterial/WBC casts in urine, ↑ renal values
- Fever, anorexia, depression, vomiting, abdominal pain on palpation, dysuria, pollakiuria, hematuria, PUPD
- US – hydronephrosis (dilated renal pelvis), hydronephrosis of ureters, lack of corticomedullary definition
- Definitive Dx = renal biopsy
- Tx: aggressive IV fluids + antibiotics → serious and life-threatening condition

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Renal Failure
- Acute vs Chronic
o Acute = anuria
o Chronic = anemia (↓ EPO)
o Both = ↑ P (impaired excretion), metabolic acidosis (↓ bicarb production by kidneys)
- Weight loss, PUPD, anorexia
- Tx:
o Weekly SQ fluids + renal diet (helpful for chronic renal failure(
o H2 rcptr antagonist – ↓ gastric acid secretion → prevent vomiting/gastric ulcers
o Oral phosphate binding agents (Aluminum hydroxide) – prevent P absorption in intestines
▪ NOT Ca based! Would exacerbate hypercalcemia
o K supplement – chronic renal failure often has ↓ K
o Restrict dietary protein and P – ↓ nitrogenous waste
o Ca channel blocking agents (amlodipine) – palliated hypertension
- Sequelae
o ↓ calcitriol formation (active VitD) – calcitriol is negative feedback to stop PTH → PTH ↑↑↑ → chronic weight
loss (only supplement calcitriol if P is <6mg/dl)
o Gastric ulcers – renal disease + uremia = ↓ mucosal blood flow → gastric hypersecretion
o 2˚ Hyperparathyroidism – body’s compensation for ↑ P (from ↓ GFR) → body upregulates PTH to ↓ P absorption
in kidneys allowing P to return to normal concentrations in early disease
Urethral incontinence
- Urethral hypotonicity (dogs more common)
- Tx: phenylpropanolamine (Proin) → doesn’t work well in males, much better results in females
Nephrotic Syndrome
- Protein losing nephropathies (glomerulonephritis, amyloidosis)
- Proteinuria + hypercholesterolemia + edema/ascites + hypoproteinemia
Renal Infarct (indicates thrombosis)
- Necropsy: triangle/pyramid shaped lesion fanning from medulla to cortex

UROLITHIASIS
EQUINE
- Ca carbonate and Ca phosphate – equine urine has lots of Ca; these form in alkaline urine
Ca Carbonate
- Most common equine urolith
- Sheep grazing in lush pasture – clover/alfalfa = lots of Ca and oxalates
Silica Stones
- Sheep – high intake of silica in range grasses; dehydrated animals
o Sheep/cattle – grazing western rangeland
Struvite
- Mg ammonium phosphate – made of Ca, Mg, phosphate
- ALKALINE urine – tx is acidifying diet (diet change to treat this has ↑ Ca oxalate stones)
- Maintain USG <1.020 (dilute to prevent precipitation), low protein diet (↓ urea)
- Cocci – urease positive bacteria, cleave urea to ammonia → ↑ pH, make conditions even more favorable (TREAT UTI)
Ca Oxalate
- ACIDIC urine – treat w/ alkalinizing diet, K citrate
Cysteine
- Can't see on rads; genetic defect in renal tubules (predominantly in MALES)
- Newfoundland, Dachshund, Labs, Bassets, Yorkies – genetic defect = cystinuria
Urate
- Can't see on rads; PSS, DALMATIANS (defect in urate metabolism)
o Genetic defect in making allitoin from urates in liver → ↑ urate buildup
- Tx: allopurinol (inhibits xanthine oxidase which metabolizes xanthine) – could lead to xanthine crystals

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 RINGWORM
DERMATOPHYTOSIS
- Common in winter (crowding) – healthy other than skin lesions + hair loss
- Dx: Wood’s Lamp, fungal culture w/ KOH prep (definitive), DTM (dermatophyte test media)
- Tx: topical – captan, diluted bleach, lime sulfur, miconazole shampoos
o Rarely need systemic antifungals
o DON’T USE KETOCONAZOLE IN CATS – makes them vomit, causes hepatotoxicity
Species
- Cattle =Trichophyton verrucosum, T. mentagrophytes
- Llama/pig = Microsporum nanum
- Cat/dog = Microsporum canis, M. gypseum, T. mentagrophytes
o Hair loss/face pruritis = common
- Goat = T. verrucosum
- Horse = T. equinum, T. mentagrophytes, M. gypseum
o Alopecia/pruritis on saddle/girth regions (head, neck, shoulders)

LEPTOSPIRA INTERROGANS SEROVAR

Gram NEGATIVE
- Stains poorly – have to use dark field microscopy, MAT (microscopic agglutination test)
- ZOONOTIC – careful when handling urine
- Tx: tetracycline, vaccination
Species Serovars
- Cattle = Hardjo (repro problems in herd)
- Swine (possums, skunks, raccoons) = Pomona
o ABORTION (late term)
o If infection after purchasing replacement gilts, cull the replacement gilts (maintained by renal carriers) + vaccine
remaining pigs
- Dogs = Canicola
o Most common serovars: Grippotyphosa, Bratislava, Pomona
o Acute renal failure; SHOULD BE A CORE VACCINE IN LOUISIANA (yorkies get it most commonly!)
- Rats = Icterohemorrhagic
- Swine, mice, horses = Bratislava
- Mice (raccoons, muskrats, squirrels) = Grippotyphosa

CLOSTRIDIAL DISEASES
Gram POSITIVE
Clostridium hemolyticum → REDWATER (Bacillary hemoglobinuria)
- Liver infection – migrating flukes (Fasciola hepatica) → anaerobic tracts that let clostridium bloom and cause disease
o Marshy areas: snail is part of liver fluke lifecycle
- Acute hemolysis, death, PORT WINE COLORED URINE, liver w/ anemic infarct, icteric/hemorrhagic body fluids
Clostridium chauvoei → BLACKLEG
- Ingest organism → enters bloodstream → deposits in muscle
- Acute lameness, depression, febrile, crepitant edematous swelling on shoulder muscles
Clostridium septicum → MALIGNANT EDEMA
- Pitting edema, infiltrates connective tissue and SQ tissue, necrosis of damaged tissue
o Similar to Blackleg but NO CREPITUS
o C novyi Type B, C. perfingens Type A, C. sodelli → all cause malignant edema
o C. novyi Type A = BIGHEAD (rams)
▪ Spores enter wound through head butting (young <9month rams) – swelling/edema of head and neck
▪ Tx: would debridement + penicillin (fatal if untreated)

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Clostridium tetani → TETANUS
- Inoculation though deep wound w/ sport → see signs in 10-14 days
o Ex: cow calved last week w/ dystocia; pig recently castrated without tetanus vaccine; lamb from invaccinated ewe
after tail docking/castration
- TRISMUS (sardonic grin) = erect ears, hyper-alert, stiff gait, pump-handle tail, sawhorse stance, lockjaw,3rd eyelid prolapse,
extensor rigidity
o Tetanus neurotoxin binds inhibitory rcptrs → binds postsynaptic rcptrs
- Prevention: tetanus antitoxin (immediate protection), tetanus toxoid (protection 14 days after vaccination)
- Tx: penicillin + muscle relaxants
Clostridium botulinum → BOTULISM
- Toxin blocks acetylcholine release (binds presynaptic membrane)
- Flaccid paralysis, rapid death (resp paralysis), tongue hanging out
- Shaker Foal Syndrome (2wks to 6 months) – ingest spore, grows in intestines → flaccid paralysis/paresis
o Adults: only show clinical signs if ingest preformed toxin
Clostridium perfringens → CLOSTRIDIAL DIARRHEA
- Types A, B, C
- Acute diarrhea (foals) – death in 48h if not treated – hemoconcentration (PCV >65%)
- Type C = PIGLETS <7 DAYS OLD – hemorrhagic and necrotic enteritis
o HIGH morbidity, HIGH mortality
- Type D = SHEEP – death in lambs 4-5 months old – clostridial entertoxemia (lambs on rich feed)
Clostridium piliformis → TYZZER’S DISEASE (acute necrotizing hepatitis)
- FOALS 1-6 weeks old – icterus, fever, diarrhea, convulsions
o Hyperfibrinogenemia, hypoglycemia, ↑ liver enzymes, acidosis
o Randomly distributed foci of liver necrosis + long slender rods in hepatocytes
- Vs Theiler’s Disease
o Serum hepatitis, serum sickness
o From administering tetanus antitoxin to ADULT horses – Type 3 HST
▪ Should only give after surgery or after wound in unvaccinated horse
▪ DO NOT give to horse previously vaccinated with toxoid
▪ Give toxoid at 3-4-12 months, then annually and 1-2 months prior to foaling
• Repeat after wounds/surgery in vaccinated horse
o Acute diffuse necrotizing hepatitis – severe widespread hepatic necrosis
o Icterus, Hepatoencephalopathy, malaise, weight loss → rapidly progressive and fatal

DENTISTRY
PIGS
- 44 permanent teeth
RUMINANTS
- 32 teeth → Dental Formula: 2(I 0/4, C 0/0, P 3/3, M 3/3)
o No maxillary incisors
- Aging:
o Erupt at…in wear at…(after eruption, take 6 months before is in wear)
o I1 = 18-24 months…1.5y
o I2 = 24-30 months…2.5y
o I3 = 33-36 months …3.5y
o I4 = 42-48 months…4.5y
- Fluoride toxicity
o Cattle exposed to lots of fluoride at young age – permanent damage to teeth
o Ameloblasts prematurely ↓ in size – enamel forms irregular matrix that doesn’t calicify
o Also affects bone – 1st palpable lesion on medial surface of 3rd metatarsals
▪ Articular surface NOT affected w/ osteoflurosis – helps rule in/out osteomyelitis, septic arthritis, OA

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HORSES
- 40-42 teeth → Dental Formula: 2(I 3/3, C 1/1, P 3-4/3, M 3/3)
- Aging
o 5-6 months = wolf tooth (P1 - 105) erupts (is OLDEST tooth, commonly removed so bit can fit)
o 1y = M1 erupts (109)
o 2.5y = I1 erupts (101)
o 3.5y = I2 erupts (102)
o 4.5y = I3 erupts (103)
o 4.5-5y = canines erupt (or not) (104)
o 6y = I1 cup starts to disappear
o 7y = I2 cup starts to disappear
o 8y = I3 cup starts to disappear
o 9y = Galvayne’s groove starts to appear (longitudinal groove on I3)
o 15y = groove is ½ way down each tooth
o 20y = groove is completely down each tooth
- Float teeth on → maxilla buccal and mandible lingual (mandible is narrower than maxilla)
o Teeth erupt ang grow throughout life
- Common: retained deciduous teeth, malocclusion, caudal hooks, rostral hooks, NOT CARIES
- Tooth root abscess → common cause of maxillary sinusitis (1st molars)
o Weight loss, quidding (dropping feed), halitosis, unilateral purulent nasal discharge
CATS
- 30 teeth → Dental Formula: 2(I 3/3, C 1/1, P 3/2, M 1/1)
- Feline odontoclastic resorptive lesions (FORL)
o Abnormal formation/mineralization of cementum = cemental resorption
▪ Diets w/ ↑ VitD, ↓ Ca/Mg/P/K
o Endodontic necrosis on rads – internal and external lesions
o Tx: alendronate (bisphosphonate inhibits demineralization of bone), extraction of affected teeth, avoid excess VitD
o Is likely that other teeth will be affected in future
DOGS
- 42 teeth → Dental Formula: 2(I 3/3, C 1/1, P 4/4, M 2/3)
- Underbite – mandibular prognathism and maxillary brachygnathism – common in brachycephalics
- Tertiary dentin – from aggressive chewing/allergy gnawing – stains easily, causes teeth to look brown but prevents pulp
cavity exposure from excessive wear

REPRODUCTION
CYCLE
- Proestrus – ↓ P4, ↑ E2 – vaginal bleeding, swollen vulva, attracts males but wont let them mount
- Estrus – lowest P4, highest E2 – only time female stands for mating, LH surge
o E2 – vaginal cells proliferate, form cornified epithelium
- Metestrus – ↑ P4
- Diestrus – high P4 – when pyometra can occur
o P4 promoted endometrial growth, suppresses myometrial activity, inhibits leukocyte response to infection
PIG
- Estrus cycle = 21 days
o Estrus: sow stands while being mounted by boar
o If using boar only for estrus detection → vasectomy or epididymectomy
o Synchronize pigs: batch wean at 3-4 weeks (wont ovulate while lactating) → estrus in 4-6 days
▪ True lactational anestrus – wont cycle until no longer lactating (cats too!)
▪ PGF2α doesn’t work – CL is only mature/responsive for short time in pigs
▪ Whitten effect – wont work during lactation
- Gestation = 113-114 (3 months, 3 week, 3 days)
o Pregnancy dependent on OVARIAN progesterone throughout gestation
- Sows: 14 teats (dogs 10, cats 8, cows 4, sheep/goat 2)

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GOAT/SHEEP
- GOAT estrus cycle = 21 days (duration of estrus = 1.5-3 days)
- SHEEP estrus cycle = 16 days
- Gestation = 150 days
o Placenta takes over progesterone production EARLY in pregnancy from CL
o COW – progesterone production is from CL then augmented by placenta
- Breeding: SHORT DAY LENGTH – seasonally polyestrus (fall/winter)
- Whitten effect = Buck effect = intro new buck causes sheep/goats to ovulate at same time (“buck in a jar”)
COW
- Estrus cycle = 21 days
- Estrus length = 8-18 hours (receptivity = 90 hours, ovulate 24-30 hours AFTER onset of estrus)
o Allows AI after estrus is over – post-estrual hemorrhage means too late to breed
o AI = INTRAUTERINE
- Gestation = 9.5 months
o Placenta – epithelia-chorial (sow, mare, ewe, goat)
▪ If not passed in 12 hours → retained! (usually passed in 2h)
o Placentomes – COTYLEDON (fetal: baby sleeps in COT), CARUNCLE (maternal: mom drives the CAR)
o Normal fetus position: anterior presentation, dorsosacral position, front limbs extended
o Takes 40-50 days for uterus to return to normal size (25-30) w/ complete histologic repair (up to 50)
- Dx of Pregnancy:
o US – 28 days (fetal gender @ 58-90 days)
o Chorioallantoic slip – 30-35 days
o Fetus palpable – 60 days (out of reach until 4-7 months)
o Placentomes palpable – 75-90 days
o Uterine artery fremitus on ipsilateral horn – 120 days
o Fremitus felt bilaterally – 7 months on
- Synchronizing Estrus
o 2 injections of PGF2α 11-14 days apart – if immature CL on 1st shot, now synchronized on 2nd shot
▪ Also those that were synchronized on 1st shot will have very responsive CL
o PGF2α – no affect to synchronize if given during anestrus – need mature CL
o When lyse a CL w/ PGF2α – see estrus in 3 days
- PGF2α + Dex = abortion/induction
o <4 months: PGF2a will lyse CL (main contributor of P4) → abortion
o 4-8 months: need PGF2a (CL and placenta both contribute P4) + dex → abortion
▪ Never use a corticosteroid in a pregnant cow unless want to induce abortion!!
o >8 months: only need PGF2a
▪ Placenta no longer contributes P4 – can induce
▪ Dex: mimics rise in fetal cortisol; takes 48 hours from dex induction to parturition
- Breeding soundness exam: sperm motility of 30%, sperm morphology of 70% normal
HORSE
- Estrus cycle = 19-26 days (estrus duration = 2-10 days; avg = 6 days)
o Estrus – tail raising, frequent urination, squatting
▪ Most effective way to start cycling: artificial light for 16 hours/day for 60 days prior to breeding
• Initiates ovarian activity
o Anestrus – winter – strike and avoid stallions
o As day length ↑ at end of winter, horse should return to breeding (vernal transition)
- Gestation = 345 days (330-360); premature is <320, prolonged if >365
o Most owners want foaling in mid-January (racing horses have artificial birthday as Jan 1st)
▪ Breeding: mid-February (start artificial light mid-December)
▪ Horse is seasonally polyestrus – normally start in April/May

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 o Maintenance of Pregnancy
▪ Ovarian P4 peaks early in gestation, gradually replaced by placental P4
▪ Parturition (normal position: anterior presentation, dorsosacral position w/ forelimbs extended)
• Stage 1 = fetal repositioning into dorsosacral position
• Stage 2 = starts w/ rupture of chorioallantois, ends with birth of foal
o 20-30 minutes – if >30 minutes, emergency!!!
• Stage 3 = passage of placenta
o Within 3 hours
- Dx Pregnancy
o US – 11-14 days
o Rectal palpation – Day 25 (day 20-30 vesicle forms bulge – can feel chorionic vesicle)
▪ Can see fetal heartbeat by day 25
o Rectal palpation – Day 90-120 can feel fetus
o Palpation of ovary location and enlarged uterine arteries – 7 months
- Uterine Biopsies – to determine if mare can carry foal to term
o Amount of fibrosis present in older mare’s uterus → indicates how able she is to carry a foal to term
o Kenney categories: 1 = minimal change / 3 = marked change (5% chance of carrying to term; can still get pregnant)
- Spermatogenesis
o Takes 60 days for spermatogonia to mature to sperm (stallion w/ poor semen quality should be reevaluated @2
months before final judgement)
o Oligozoospermatism: ↓ sperm numbers (old age, testicular derangement/hypoplasia/atrophy, fibrosis)
o Acute Orchitis: tends to cause morphologic/motility abnormalities in sperm
CAT/DOG
- DOGS
o Gestation = 63 days (larger litter = shorter gestation, smaller littler = longer gestation)
▪ See fetal skeletons on rads – Day 42
o Pregnancy Stages
▪ Stage 1 = 6-12 hours (up to 36) – pants, trembles, nesting behavior, restless, subclinical uterine
contractions, dilation of cervix
▪ Stage 2 = 6-12 hours (up to 36) – abdominal straining that goes w/ uterine contractions, puppy delivery
q30-60 minutes (up to 4 hours)
▪ Stage 3 = expulsion of fetal membranes, involution of uterus (passed 5-15 minutes after birth of pup
before another puppy can be delivered)
o Thich green discharge (lochia) – seen in all stages and up to 3 weeks
o Complete uterine involution/endometrial recovery = 3 months
o Vaginal bleeding = 4-6 weeks post-whelping normally; subinvolution = bleeding for 12-15 weeks
o Pseudopregnancy
▪ ↑ prolactin, ↓ progesterone – mammary gland hyperplasia, lactation, nesting, mothering of objects
- Dystocia
o Hours have passed since expulsion of last fetus? Give oxytocin (also Ca and check fetuses w/ US, rads to check for
malpositioning/malformation
o Brachycephalics (Bostons, bulldogs) – predisposed to large headed puppies + mothers w/ flat pelvic inlets
- Mammary Tumors = carcinomas (hormone dependent)
o 70-90% feline mammary tumors = malignant (majority will metastasize)
▪ 50% canine mammary tumors = malignant
o DDx = mammary hyperplasia (younger cats)
o Tx: radical bilateral mastectomy – spay when remove mammary tumor
▪ Do chest rads before operating – met check!
o Prevention – spay cat before 6 months old (↓ risk by 7x)
▪ OHA before heat cycle prevents hormonal effects on mammary glands that predispose to tumors
▪ Dogs spayed before estrus are 0.05% as likely to have mammary tumors as intact dog
• Risk ↑ to 8% (1 heat) and 26% (2 heats), and no ↓ in risk after 3 rd heat

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 o Prognosis in dogs – 50/50 benign and malignant
▪ Inflammatory carcinomas = poor prognosis, local inflammation
▪ Dogs w/ tumors >3cm = worse prognosis (>2cm in cats)
- Ovariohysterectomy (OHA)
o Most common complication = hemorrhage (left pedicle – use mesocolon to retract / right pedicle – use
mesoduodenum to retract)
o Prevention for uterine neoplasia, pyometra, mammary neoplasia (if before 1 st heat)
o Spay hook – to retrieve BROAD LIGAMENT of uterus
- Ovarian Remnant Syndrome
o If cat is spayed and showing signs of heat → check vaginal cytology (cornified epithelial cells = ovarian remnant)
▪ LH – if low, ovarian remnant likely; if high – does not rule it out
- Pyometra
o Dog under influence of progesterone
o E. coli → most common organism (normal in vagina, favorable environment during diestrus (↑P4, ↓E2)
o Common cause in dogs >8yr = cystic endometrial hyperplasia (CEH)
▪ Develop from repeated exposure to progesterone, progressive thickening, hypertrophies glands
o Lethargy, PUPD, fever, tumor in caudal glands (4th/5th)
o Tx: OHA!!! Don’t try to medically manage a closed pyometra! Surgical emergency w/ possible rupture!
▪ Open pyometra – can try prostaglandin + antibiotics
- Castration – ↓ ROAMING behavior, inter-male aggression, urine marking

ORTHOPEDICS
Anatomy (from middle outwards): diaphysis → metaphysis → epiphysis
Salter Harris Fractures (physeal fractures) – commonly lead to premature closure of physis
- Type 1 = Physis (S = straight through)
- Type 2 = Physis and metaphysis (A = above)
- Type 3 = Physis and epiphysis (L = lower)
- Type 4 = Metaphysis, physis, epiphysis (T = through)
- Type 5 = compression injury to physis (R = rammed)
Articular fractures
- Important: Rigid fixation, anatomic realignment, early return to function!
- Prolonged rest = fibrosis, ↓ range of motion of the joint
Hypertrophic Osteopathy vs. Osteodystrophy
- Osteopathy – due to thoracic mass (when mass removed, mass resolved)
o Distal extremeties to proximal (metacarpal/tarsal bones affected 1st, may progress to long bones)
o Periosteal proliferation in diaphysis
- Osteodystrophy
o Young, growing large breed dogs – may be correlated to Ca/P levels and balance
o VERY PAIFNUL – affects metaphysis (radiolucent lines w/in metaphysis: “double physis”)
o Analgesia + supportive care → usually resolves on its own

OPHTHALMOLOGY
Layers of Tear Film
- Mucus – conjunctival goblet cells → keep tear film adhered
- Aqueous – lacrimal gland/gland of 3rd eyelid → nutrition + immunological factors
- Lipid – meibomian gland → even spreading, prevents evaporation
Cataracts
- ↑ opacity of lens – diffuse changes
- Causes = trauma (disrupted lens fibers, causing uveitis), most common in cats is ANTERIOR UVEITIS, inherited cataracts rare
in cats, aging, intraocular disease, endocrine disease (dogs! Diabetes mellitus)
- Tx: phacoemulsification

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 - Incomplete – can see through; not completely ossified, tapetal reflections still seen through it
- Complete – completely opacified lens, can't see tapetal reflection
- Incipient – focal, only minor effect on vision, no need to remove lens
- Resorbing – degradation of lens proteins after cataract development
Glaucoma
- Breeds: purebreds, Cockers, Bassets, Beagles, Samoyeds
- Primary – iridocorneal angle compromised during 1st few years of life, eventually causes acute pressure spike → ↓ aqueous
outflow → ↑ pressure in eye (glaucoma)
- Secondary – anterior uveitis (inflammatory debris plug), intraocular neoplasia, diabetes
- Ocular pain, buphthalmos (big eye = CHRONIC), corneal edema (blue haze over cornea), mydriasis, fundic changes (retinal
vascular attenuation, tapetal hyperreflectivity), corneal fibrosis, lens luxation, pale optic discs
- Dx: measure intraocular pressures
o <10 mmHg = uveitis / >30 mmHg = glaucoma
- Tx: ↑ outflow / ↓ production of aqueous
o IV mannitol (↓ IOP via osmosis), oral/topical methazolamide/dorzolamide (carbonic anhydrase inhibitor – ↓
aqueous production), topical latanoprost (prostaglandin analog)
- Prognosis: glaucoma in 1 eye = glaucoma in other eye in 6-12 months
Anterior Uveitis
- Causes = immune mediated (lens-induced), traumatic, idiopathic, infectious, hypertension, neoplasia
- Rubiosis iridis, aqueous flare, hyphema (blood in anterior chamber), hypopyon, keratic precipitates, ↓ IOP
- Sequelae: cataracts (CATS) – inflam mediators break down lens proteins), glaucoma (debris clogs angle), corneal scarring
(NOT KCS – cannot extend to lacrimal gland)
- Tx: topical/systemic steroids (pred/dex, NOT hydrocortisone), topical NSAIDs (flurbiprofen, Voltaren), systemic NSAIDs
(carprofen, flunixin), topical atropine (relieve ciliary spasm, ↓ posterior synechia development), NOT topical abx (unless
infectious cause)
Chorioretinitis
- Causes = infectious (fungi, viral, bacterial, rickettsial, toxoplasma), autoimmune (uveodermatologic syndrome), systemic
hypertension, lymphoma, choroidal melanoma, coagulopathy
- Poorly defined grey spots throughout fundus (indicates cellular infiltration), retinal hemorrhage/separation (acute cases),
hyperreflectivity (indicates previous damage or chronic chorioretinitis)
Anisocoria
- 1 pupil dilated, 1 constricted → HEAD TRAUMA
Proptosis
- Trauma most common cause; common in BRACHYCEPHALICS
- Tx: replace globe, temporary tarsorrhaphy (protects eye, keeps in position while heals; left for 3 weeks)
Retrobulbar Abscess
- Acutely painful, unilateral exophthalmos, retropulsed with minimal resistance, systemically ill (fever, ↑ WBC, anorexia)
- Causes: penetrating wound, FB, spread from dental/sinus infection, hematogenous spread
Lens Luxation – TERRIERS
- Mechanically obstruct aqueous flow
- Anterior luxation = immediate lens removal (discomfort, uveitis, glaucoma) / posterior = left on vitreous floor
Nuclear Sclerosis
- Normal aging change to center of lens
Entropion
- Eyelid margin inverts INWARD → conjunctivitis/keratitis → blepharospasm, epiphora
- Fairly common (foals, other young animals) – usually resolves on its own as they grow
- Tx: sometimes spontaneous resolution / local anesthetic and evert lid and staple (temporary until it resolves) / surgical
correction rarely needed – overcorrection = long term problems
Ectropion
- Eyelid margin everts OUTWARD → exposure keratitis, very uncommon in horse
KCS (Keratoconjunctivitis sicca)
- Abnormality of lacrimal gland and gland of 3rd eyelid
- ↓ aqueous part of tear film → thick green ocular mucoid discharge, bilateral blepharospasm, 360˚ corneal vascularization
- Dx: Schirmer tear test (normal: 15mm/60sec)

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 - Tx: cyclosporine eye drops (reverses immune mediated process, stims tear production), topical steroids (↓ immune
destruction of lacrimal gland)
- Causes: immune mediated adenitis (75%), trauma to lacrimal nerve, skull irradiation, canine distemper
o Drugs: TMS, atropine, general anesthetics, EtoGesic (etodolac)
Cherry Eye
- Prolapse of 3rd eyelid – brachycephalics more common
- Tx: gland replacement (Morgan pocket technique/Kaswan anchoring technique)
o Removing gland = ↑ risk of KCS (3rd eyelid gland contributes significantly to tear production) – DON’T DO IT
Corneal Ulcers
- Uncomplicated takes DAYS to heal (<5 days) – if present longer, consider complicated (look for source of complication)
- Tx (complicated): conjunctival flap
- Tx (melting): always assume it’s infected → take swab for culture and cytology
Uveal Cyst vs Uveal Melanoma
- Cyst: brown round circular FREE FLOATING mass in anterior chamber – will TRANSILLUMINATE
o Very spherical/ovoid and smooth
- Melanoma: brown, round circular NON FREE FLOATING mass – will NOT transilluminate
o Fleshier appearing
Meibomian Glands
- Adenoma = mass attached to eyelid margin, most common ocular tumor of dogs – usually BENIGN
- Chalazion = obstruction of meibomian gland – appears as swelling within eyelids rather than from it

ANTIBIOTICS
NOT FOR FOOD ANIMALS:
- Diethyl stilbestrol, Chloramphenicol (aplastic anemia in humans), nitroimidazoles, clenbuterol, fluoroquinolones,
vancomycin, nitrofurans, phenylbutazone, most sulfas, dimetridazole
- OK to use: penicillin (10 day withdrawal), ionophores, sulfas (7 day withdrawal), tetracycline (28 day withdrawal), Ceftiofur
(SHORTEST withdrawal = 4 days)
Tetracyclines
- Doxycycline, tetracycline, minocycline, tigecycline
- Enamel hypoplasia and teeth staining (young animals), esophageal stricture (cats)
- Bacteriostatic – G+, G-, mycoplasma, protozoa
Fluoroquinolones
- Enrofloxacin, difloxacin, marbofloxacin, danofloxacin
- Enrofloxacin (Baytril) – cartilage abnormalities in young animals
- Bactericidal – inhibits DNA replication/transcription – G+, G-
Beta Lactams
- Penicillins: penicillin, ampicillin, amoxicillin (and Clavamox), methicillin, nafcillin, carbenicillin, ticarcillin
- Bactericidal – targets cell wall synthesis – G+, G-
Aminoglycoside
- Streptomycin, amikacin, gentamicin, neomycin
- Nephrotoxicity (reversible), ototoxicity (irreversible)
- Bactericidal – targets protein synthesis
Sulfonamides
- TMS, sulfadiazine
- Crystalluria, KCS (dogs)
Chloramphenicol
- Bone marrow suppression, aplastic anemia
- Bacteriostatic – inhibits protein synthesis – G+, G-, anaerobic, aerobic, intracellular
Macrolides
- Macrolide antibiotics - Fatal to horses/rabbits
- Bacteriostatic – inhibits protein synthesis – G+

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Lincosamides
- Clindamycin, lincomycin
- Bacteriostatic – inhibits protein synthesis – G+
Other Antibiotics
- Rifampin – causes orange/red urine (make sure owners know ahead of time)
- Bacitracin – serious nephrotoxicity
- Vancomycin – ototoxicity, nephrotoxicity

FOOD POISONING
Virus = 2/3 of foodborne illness in US
Staph aureus
- Heat stable enterotoxin – abd cramps/pain, vomiting, diarrhea, nausea, chills
- Usually mild illness – recovery in 1-2 days
Campylobacter jejuni
- UNDERCOOKED CHICKEN – also raw milk
- Diarrhea – young adults, neuro complications uncommon
- Guillian-Barre Syndrome – acute inflammatory polyneuropathy – autoimmune dz triggered after certain resp/GI infections
E. coli 0157:H7
- Enterohemorrhagic strain – produces Shiga-like toxins
- RAW GROUND BEEF – fecal contamination – recent outbreaks from veggies (spinach)
- Severe acute hemorrhagic diarrhea, abd cramps, hemolytic uremic syndrome (HUS)
o Illness resolves in 5-10 days usually
o Children/elderly predisposed to HUS – renal damage/failure
- Cattle: NO SYMPTOMS – usually get from nearby contaminated veggie farm
o ID carriers: send stool to lab for 0157:H7 fecal culture from random sampling of cattle
▪ Sorbitol-MacConkey agar (SMAC) – able to ferment sorbitol
Clostridium botulinum
- HONEY – clostridial spores → do not feed to infants (infant botulism)
- Persistent constipation, floppy arms/neck/legs, weak cry, weak suckling, lethargy, difficulty breathing, CNS signs
Listeria monocytogenes
- Grows slowly in refrigerated foods – psychrophilic (grow at low temps)
- Abortions/stillbirth in humans – also CNS signs (fever, muscle aches)
Yersinia enterocolitica
- Acute severe ABDOMINAL PAIN and fever (gastroenteritis) – less acute pain: think Trichenella spiralis
- PORK!
Mycobacterium bovis – TUBERCULOSIS IN CATTLE
- Humans get from drinking raw unpasteurized milk – controlled in US by pasteurization
o Others in milk: Mycobac. avium spp paratuberculosis, Brucella abortus, Salmonella Dublin, Listeria monocytogenes
Shigella
- Bacillary dysentery in humans – PRIMATE DISEASE
Vibrio cholera
- SHELLFISH – GI signs in humans
RABIES
Rhabdoviridae family, genus lyssavirus (bullet shaped, enveloped)
Wildlife reservoirs – skunks, raccoons, coyotes, foxes
- Transmit via saliva (biting)
Stages
- Prodromal stage – change in behavior, voice change, attacked by wild animal
- Furious/excitable stage (1-7 days) – irritable, excitable, photophobia, hyperesthesia, attacks imaginary objects, drooling,
seizures, coma/death
- Paralytic/dumb stage – flaccid paralysis
Clinical signs (farm animals) – anorexia, depression, ataxia, aggression, single region of pruritis/alopecia

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Dx: Negri bodies in carnivores, Purkinje cells in herbivores
- Definitive Dx: direct IFA
Vaccination Protocols
- Dogs: 3 months → booster at 1 year, then q1-3years
- Horses: vaccination NOT required by law, only recommended in endemic areas (booster annually)
Protocols
- Humans
o Unvaccinated: inject human rabies immunoglobulin + 5 injections of rabies vaccine over 1 month
o Vaccinated: 2 injections of rabies vaccine
- Cats/Dogs/Ferrets
o Pets suspected to have been bitten by wild animals
▪ Vaccinated: vaccinate immediately and quarantine for 45 days
▪ Unvaccinated: euthanize OR quarantine for 6 months then vaccinate 1 month before release
o Pets that have bitten humans
▪ Strays: euthanize and test
▪ Vaccinated: confine and observe for 10 days
▪ Unvaccinated: euthanize and test OR quarantine in 10 days in approved facility
▪ If unsure (pets only): confine 10 days and then vaccinate

SENSITIVITY AND SPECIFICITY

Sensitivity
- Disease + and test +
o LOW sensitivity = MOST false negative
o Looks at animals who DO have the disease (65% sensitive = 65% true positives, 35% false negatives)
- Used to find FALSE NEGATIVES
Specificity
- Disease – and test –
o Percentage of true negatives vs false positives
- Used to find FALSE POSITIVES
Positive Predictive Value = proportion of affected animals (disease positive) that test positive
Negative Predictive Value = proportions of unaffected animals (disease negative) that test negative

Tip: create this chart with the info given using made up
population size (ex. 1000 population size)
- Prevalence = 10%
o 900 are TN, 100 are TP
- 96% sensitive (100 have disease)
o 0.96 x 100 = 96
o 100 – 96 = 4 FN
- 98% specific (900 don’t have disease)
o 0.98 x 900 = 882
o 900 – 882 = 18 FP
Then just use the formulas to calculate what you are
looking for!

CAMELID DISEASES – 1%
Parelaphaostrongylus tenuis = MENINGEAL WORM (aka deer worm)
- LLAMA DISEASE – definitive host is white tailed deer
- Ataxia, hindlimb paresis that progresses to forelimbs, muscle weakness, paralysis, circling
- CSF tap = eosinophilia

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Choanal atresia
- ALPACA DISEASE – opening btw nasal and pharyngeal area blocked by membranous tissue/bone
- Young alpacas: difficulty breathing and nursing, cyanosis, lack of weight gain, aerophagia
- EUTHANIZE – usually also have polydactyly, cardiac/renal/other organ deficits
Cria – baby llama
- Born w/ adhesions btw free end of penis and prepuce – gradually detach during puberty
Ulcers
- Most common location = third compartment of stomach and proximal duodenum
- Clinical Signs – malaise, anorexia, repeated colic, some are asymptomatic until they suddenly die
- Tx: omeprazole (parenteral! Oral is not effective)
- Management: ↓ stress!!
Mycoplasma hemolamae
- Weight loss! (DDx = GI parasites, poor dentition/nutrition, Johne’s disease (paratuberculosis), M. hemolamae, eosinophilic
enteritis, BVD, GI ulcers, neoplasia – lymphoma, SCC)
- Weak/depressed cria – wean, do oral exam, do PCR for M. hemolamae
Selenium Supplementation
- Feed hay from selenium fertilized fields, add to the grain ration based on the region, inject supplement annually as needed
- Don’t use cattle Se supplement! Contains too much copper
Core Vaccines
- Tetanus, Clostridium perfringens C/D toxoids
- Rabies – only in rabies-endemic areas
Removing Canines
- Cut off crown just above the gingiva to disarm fighting teeth in South American camelid males
- Painful! – anesthesia needed! → has to be repeated as the teeth continue to grow
- After castration, canines of males stop growing

FISH DISEASES – <1%

General Fish Facts
- Anatomy: 2 chambered heart, nucleated RBC
- Gram negative = most common pathogen
- Biologic cycle: ammonia (toxic) → Nitrosomonas → nitrite (toxic) →Nitrobacter → nitrate
- Freshwater fish – DON’T drink water / Saltwater fish – DO drink water
FDA approved anesthetic: MS222 (tricaine methanosulfonate)
- 21 day withdrawal before fish can be eated
FDA regulates SALMON / USDA regulates CATFISH
Ich – Icthyophthirius multifilis
- Erratic swimming, white spots on skin/gills
- Tx: malachite green or formalin
Aeromonas salmonicidia
- Furunculosis of salmonids, goldfish ulcer disease, carp erythrodermatitis, trout ulcer disease
- Most common bacterial pathogen of fish worldwide
Whirling Disease – Myxobolus cerebralis
- Erratic swimming, deformed around head/spin – RAINBOW TROUT
- Histopath: diffuse necrosis of cartilage and spores in cartilage
Hole-in-the-Head Disease
- Herpes, Edwardsiella ictaluri
- CATFISH – swim erratically, spin around, eventually die
Gill Rot – Branchiomyces sanguinis/demigrans
- CARP/EELS – resp distress due to gill necrosis → caused by thrombosis of blood vessels in gills
Enteric Redmouth Disease – Yersinia ruckeri
- BENIGN, LOW MORTALITY

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Columnaris Disease – Flexibacter columnaris
- Peduncle disease, fin rot, black patch necrosis, cotton wool disease
- White plaques that have red peripheral zone which becomes erosions/ulcers; necrosis of skin
Mycobacteriosis
- Common chronic disease in aquarium fish – skeletal deformities, ulcerations/erosions of fins
Lymphcystis disease – iridovirus
- Saltwater and freshwater fish – CAULIFLOWER growths on skin/fins/gills
Saprolegnia
- Opportunistic fungus on fish; Winter die-off in catfish

MARINE MAMMALS:
- Counter current circulation to keep warm
- Dinoflagellates (brevotoxin) – high mortalities in Atlantic/Gulf – esp manatees
- Distemper (morbillivirus) – high mortalities in seals

PRIMATE DISEASES
Old World Monkeys – Colobus, Proboscis, Mandrill
- Sex skin, opposable thumbs, ischial callosities for sitting – NO PREHENSILE TAIL
New World Monkeys – lemur, squirrel moneys
- Wide nasal septum
Transmitted from primates → humans: Herpes B, Salmonella, Tuberculosis
- Herpes simiae (Herpes B) – nonpathogenic in macaques, fatal encephalitis in humans
o Bite/scratch transmission; macaques are most frequent carriers
o Causes mild cold sore like lesions in monkeys
Transmitted from humans → primates: Rubella (measles – fatal!), tuberculosis (Old World Monkeys)
- TB test in monkeys: intradermal in eyelid (so can read from a distance)

SMALL RODENT/RABBIT DISEASES – <1%

Antibiotics in Rodents
- DON’T USE: streptomycin, penicillin, ampicillin, bacitracin, lincomycin, vancomycin, erythromycin, clindamycin →
penicillins, cephalosporins, macrolides
o Clostridial enterotoxemia: GI tract is primarily Gram + → antibiotics w/ G+ coverage disrupts normal flora balance
o Allows growth of clostridial organisms → dysbiosis
- USE: enrofloxacin, chloramphenicol, TMS
RABBIT DISEASES
- Anatomy – induced ovulator, heat dissipation via ears (no sweat), 2 uterine hors, 2 cervixes, require 120ml/kg/day water
- Gestation: 29-35 days
- Dental Formula: 2(I 2/1, C 0/0, P 3/2, M 3/3) – diastema btw incisors and premolars
o All teeth – open roots, continuously growing, malocclusion common problem
o Malocclusion → anorexia
▪ Lethargy, inappetence, grinding teeth, absent GI sounds, painful abdomen w/ no formed feces
▪ Usually fed only pellet + occasional lettuce → change diet to leafy greens, ↓ pellets/seeds
▪ Rads – uneven occlusal surface (improper incisor angle), root elongation of molar/premolars
- Bladder Stones – Ca carbonate
o Absorb Ca through GI tract at same rate of ingestion, whether they need it or not
- Snuffles – Pasteurella multocida
o Upper resp signs: mucopurulent discharge, sneezing
o Also enzootic pneumonia, otitis media/interna, conjunctivitis, meningitis, encephalitis, repro tract infections,
abscesses, septicemia, rhinitis/sinusitis (NOT typhlitis)

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 - Vertebral Fracture
o Acutely down in hind limbs, dribbling urine, no withdrawal in hindlegs – usually dropped by children
o Common site = caudal lumbar region (L7)
- Uterine Adenocarcinoma
o Common neoplasia in female rabbits – very high in intact females → SPAY THEM
o Hematuria, anorexia, weight loss, depression, dysuria – distinguish hematuria from porphyrinuria
- Syphilis – Treponema paraluis cuniculi
o Sexually transmitted – skin lesions around vent, NO hematuria
- Psoroptes cuniculi – Rabbit Ear Mite
o ONLY NON-REPORTABLE Psoroptes species
o Scratching at ears, crusts, excoriations in ears – severe crusting/inflammation in external canals
o Tx: ivermectin, Selamectin – NOT NOT NOT FIPRONIL (Frontline) – VERY TOXIC to rabbits
- Cheyletiella parasitovorax – Rabbit Fur Mite
o White flakes (“walking dandruff”) – shedding, scaling, dandruff on dorsum
o Can infect dogs, cats, humans
- Encephalitozoon cuniculi
o Neurologic/renal disease – infects LENSES, causes phacoclastic cataracts (break through lens capsule), uveitis
o Remove lens w/ phacoemulsification (for cataracts), oral albendazole/topical steroids for uveitis

- Trichobezoar – hairball stuck in stomach

o Weight loss, anorexia, scant stool production – predisposed to development if have ↓ GI motility
o Supportive care, syringe feed high fiber foods, hope they pass without surgery
o Cannot vomit!!
- Head tilt in rabbits: Pasteurella, trauma, Encephalocytozoon cuniculi
CHINCHILLA DISEASES
- Dust baths – q1-2 days to maintain coat health (too frequent can cause conjunctivitis) – volcanic ash
- Heat Intolerance – no hotter than 80˚F → hyperthermia common
- No cedar shavings – cause resp irritation
- Don’t require supplemental VitC, no dental adjustments (though dental disease is common)
- Long life span – up to 20 years
- Penile ring in males, precocial young
GUINEA PIG DISEASES
- Gestation: 63 days, precocial young (fully furred, eyes open, more mature and mobile at birth)
o Pregnancy toxemia a problem – breed before 6 months (fused pelvis)
- Metastatic mineralization – incidental finding (necropsy)
- Dental abscess – associated with malocclusion
- Bordetella bronchiseptica – NEVER HOUSE RABBITS AND GUINEA PIGS TOGETHER
o Normal inhabitant in oropharynx of rabbits – pathogenic to GP (resp distress, weight loss, sudden death)
- Hypovitaminosis C = SCURVY
o Anorexia, painful swollen stifles, loose incisors/dental malocclusion, rough haircoat, petechiation
o Often fed only timothy hay – leads to collagen defects w/ painful/swollen stifles most common sign
o Lack enzyme to convert glucose to ascorbic acid → need Vit C in diet
o Tx: Vit C injections (NOT multivitamins – Vit A/D toxicosis), add leafy greens to diet
- Viral pododermatitis a problem
- Bacterial Pododermatitis
o Staph aureus
o Risk factors: obesity, poor sanitation, wire/abrasive floors
o Guarded prognosis: soft bedding, wound care/bandaging, parenteral antimicrobials
- Chlamydia caviae = infectious conjunctivitis
- Strep equi ssp. Zooepidemicus = suppurative lymphadenitis
- Trixacarus caviae (sarcoptic mange) = mange in guinea pigs
o Super itchy guinea pigs

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RAT DISEASES
- Lifespan – 2.5 years
- Tyzzers disease – Clostridium piliforme
o See in RABBITS, mice, hamsters – usually subclinical unless rodent is stressed/immunosuppressed
o Diarrha, kyphosis, poor haircoat, death
o Histopath – focal areas of hepatic necrosis and inflammation of terminal ileum
- Cilia associated respiratory bacillus (CAR) infection – Mycoplasma pulmonis
o Severe bronchiectasis, pulmonary abscesses, atelectasis – GOOD HUSBANDRY PREVENTS
- Murine respiratory mycoplasmosis (mice and rats) – Mycoplasma pulmonis
o Nasal discharge, ataxia, coughing, sneezing, dyspnea, head tilt, incoordination, circling
▪ Inflammation of respiratory tract/inner ear
o Tx: oxytetracycline in water
- Psuedotuberculosis (mice and rats) – Corynebacterium kutscheri
o Caseous purulent foci in lungs when stressed – dyspnea, oculonasal discharge, rough haircoat, hunched posture
o Cytology – “Chinese character” formation of impression smears
- Ringtail
o Annular constriction of tail (dry gangrene, fall off) – weanling rats kept in wire-bottom cages
o Prevention: keep temps btw 70-74˚F, ↑ humidity, DO NOT use wire bottom cage, provide nesting material
o Factors: ↑ temp, ↓ humidity, impaired blood supply tail, drafts
- Sialodacryoadenitis – Coronavirus
o Bleeding from eyes, exophthalmos, squinting, corneal drying → ulcers, swollen face/neck, red discharge from
eyes (porphyrin pigment – secreted from Harderian glands in times of stress)
o Inflammation/necrosis of salivary and nasolacrimal glands
o Tx: self limiting in 2 weeks
- Mammary Tumors
o BENIGN – fibroadenomas → can be anywhere based on extensive nature of mammary tissue (males and females)
o Surgical excision for well-being of rat
- Rats w/ resp dz → mycoplasma
- Normal age related change = yellowing fur, brownish granular sebaceous secretions at base of hair shafts
MICE DISEASES
- Lifespan – 1.5 years
- Gestation: 19-21 days
- Mammary tumors – RNA retrovirus
o MALIGNANT – anaplastic, invasive → surgical excision DOES NOT have good prognosis
o Extensive nature of mammary tissue means can be found anywhere (even dorsum)
- Barbering of hair by cagemate
o Common in pigmented mice (black mouse w/ alopecia that started on face→trunk, other mice are normal)
- Sendai Virus
o Respiratory disease → pneumonia, weight loss, dyspnea, chattering, death
▪ Usually subclinical in rats/hamsters
o VERY contagious, difficult to control
- Trychophyton mentagrophytes – RINGWORM (mice/rats)
o Patchy alopecia/flaking on head
o Tx: usually not necessary (self limiting) – antifungal = griseofluvin
- Lymphocytic choriomeningitis (LCM) – RNA arenavirus
o EUTHANIZE COLONY – ZOONOTIC
- Transmissible murine colonic hyperplasia – Citrobacter freundi strain 4280
o 2-4 weeks old (no signs in adults) → anorexia, dehydration, diarrhea
o Histopath: thickening and inflammation of colonic mucosa
o Highly contagious and self limiting – treat w/ neomycin or tetracyclines
- Rotavirus
o 1-3 weeks old → soft yellow diarrhea that stains/dries around anus – causes obstipation and death
o Electron microscopy to ID the virus
o Tx: clean and remove infected feces

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 - Pinworms – Syphacia obvelata, Aspicularis tetraptera
o Heavy parasite load → rectal prolapse; inhabits cecum, usually subclinical infection
o Tx: piperazine sulfate, ivermectin
HAMSTER DISEASES
- Lifespan – 2 years
- Gestation: 15-18 days
- NOT induced ovulator (unlike ferret, cat, rabbit)
- Bilaterally asymmetric intermittent swollen cheeks – FOOD STUFFED IN POUCHES
- Proliferative ileitis – Lawsonia intracellularis
o 3-10 weeks old – wet tail, lethargic, dehydrated, depressed
o AGGRESSIVE treatment – SQ fluids (50ml/kg – electrolyte/glucose solution), enrofloxacin and TMS to treat
bacteria, sometimes bismuth subsalicylate for persistent diarrhea
o GRAVE PROGNOSIS
- Amyloidosis – common renal disease in hamsters, no effective treatment
GERBIL DISEASES
- Prone to seizures when stimulated
- Glands on mid ventral abdomen
HEDGEHOG DISEASES
- Demyelinating Paralysis – Wobbly Hedgehog Syndrome
o Gradual progressive disease – hereditary
o Inability to roll into a ball → ataxia → seizures, tremors, severe muscle atrophy, weight loss, death
o NO TREATMENT
MINK DISEASES
- Aleutian Disease - parvovirus
o Chronic immunosuppressive wasting disease
o Aleutian (blue) coat color gene = most severely affected
- Transmissible Mink Encephalopathy = prion disease in minks

FERRET DISEASES - <1%

General
- INDUCED OVULATOR
o Estrogen toxicity if remain in estrus and not bred → aplastic anemia and bone marrow toxicity; Tx: SPAY
- Gestation: 42 days
- Vaccines: Require canine distemper (hyperkeratosis, ↑ mortality) and rabies (Imrab 3)
- Susceptible to heartworms (similar to cats – Proheart!), gastric ulcers (helicobacter – melena, vomiting, bruxism)
o Ulcer tx: amoxicillin + metronidazole + gastroprotectants (sucralfate, H2 blockers)
- Splenomegaly = NORMAL – unless there is distinct mass, leave spleen alone!
- Influenza – humans give to ferrets!!
Heat stroke
- Lethargic, inappetent, barely walking (other DDx = insulinoma but BG is normal)
Diet – STRICT carnivore
- Need meat proteins/fats, LOW FIBER (high plant proteins associated w/ urolithiasis, highly digestible due to short GI)
- FATAL hypoglycemia is have insulinoma and fasted longer than 6 hours
Cystic calculi
- STRUVITE most common, overall uncommon in ferrets
Proliferative bowel disease/Epizootic Catarrhal Enteritis
- Intracellular bacteria (formerly Campylobacter, related to Lawsonia in pigs)
- Prolapsed rectum, chronic diarrhea, weight loss, green stool containing mucus, bruxism (from GI ulcer pain)
- Histopath: thickening intestines, enlarged mesenteric lymph nodes
- Tx: antibiotics (susceptible to Chloramphenicol)

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Adrenal Tumor (#1 MOST COMMON FERRET DISEASE) → Bald ferret!
- Secrete ESTRADIOL – vulvar hyperplasia (females), hair loss (truncal alopecia), pruritis, behavioral changes
- Prostatitis/paraprostatic cysts (males) – stranguria, bilaterally symmetric alopecia, pruritic
- Tx: adrenalectomy, mitotane and ketoconazole NOT successful in reducing clinical signs; Deslorelin implant
o Trilostane – increases 17-hydroxyprogesterone which is already elevated in these pts
Insulinoma (#2 MOST COMMON FERRET DISEASE)
- HYPOGLYCEMIA – bouts of lethargy, dragging pelvic limbs, acute onset of ataxia, salivation, SEIZURES, glassy eyes
- Dx: take blood glucose levels when they present, then insulin level
- Primarily left sided
- Tx: surgery, diazoxide (better than prednisone)
Lymphoma
- Mediastinal, multicentric / GI = worst prognosis
- Common ferret tumors: insulinoma, adrenal tumor, mast cell tumor (benign/incidental), lymphoma, SCC (mandibles)
o Melanoma = rare
Urethral Obstruction
- Uncommon, but most likely from prostatic hypertrophy 2˚ to hyperadrenocorticism

REPTILE DISEASES - <1%

Anatomy
- Nucleated RBC, 3 chambered heart (2 atria, single ventricle w/ incomplete septum), heterophils (not neutrophils)
- No bladder (snakes)
- Renal portal system – blood from caudal half of body passes through kidney before going to heart
o DON’T GIVE GENTAMICIN IN CAUDAL HALF OF BODY – NEPRHOTOXIC!! (aminoglycosides)
Raw fish diet → neurologic signs
- Contain thiaminase → Vit B1 deficinecy (weight loss w/ good appetite + neurologic signs)
- Supplement w/ vitamins
Metabolic Bone Disease
- 2˚ nutritional hyperparathyroidism – imbalances in ↓ Ca, ↓ Vit D3, ↑ phosphorus
- Causes: low Ca, lack of UV light, Vit D deficieincy
o Ca gets resorbed from bone to maintain serum levels → weak/pliable bones
o Need full spectrum UV light for conversion of inactive Vit D to Vit D3 in skin
▪ UVB stimulates 7-dehydrochloesterol to form pre-Vit D
o Need Vit D3 for proper Ca absorption and metabolism
- Poor growth, osteopenia, fractures, pliable mandible/maxilla, bowing of long bones
- Tx: Vit D3 every 4 weeks (overdose → soft tissue mineralization)
Dysecdysis – inability to shed skin
- Usually from inadequate humidity, lack of abrasive substrate to rub against, stress (ectoparasitism), nutritional deficiencies,
systemic disease
- Snakes: retained spectacles – do not use forceps to peel off eyecaps or can cause corneal damage!
o Blue eyes = impending shed (7-10 days)
- Tx: ↑ humidity (humidity chamber, ophthalmic ointment, search for underlying cause
Cryptosporidium
- Regurg, weight loss, debilitation → NO effective tx, euthanize due to zoonoses
- Thickening of GI mucosa, loss of motility → acid-fast staining
Infectious Stomatitis – Aeromonas, Pseudomonas
- Petechiation, caseous material build up in mouth
- Tx: debridement, antibiotics
Salmonella – normal flora / Stomatitis – oral abscess

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TURTLE DISEASES
- NO IVERMECTIN – crosses BBB – causes neuro signs (paresis, paralysis, death)
- Integument
o Burned on dorsum from heat bulbs
o Chemical exposure wounds on ventrum when cage not rinsed after cleaning
o Prey wounds when fed live prey
o Ectoparasites uncommon in reptiles; mites – scale loss, erythema
- Hypovitaminosis A
o RESPIRATORY INFECTIONS – nasal discharge, dyspnea, open mouth breathing, edema of eyelids, 2˚ infections of
skin/eyes/resp systems (Aeromonas, Pseudomonas)
▪ May also see renal disease, squamous metaplasia of epithelium, swelling of ears, anorexia, lethargy
o Common in turtles fed imbalanced diet of fruits and insects
o Tx: nebulization, hotter temps, Vit A supplements, antibiotics, drain tympanic membranes
- Septicemic cutaneous ulcerative disease (SCUD) – Citrobacter freundii
o Pitted scutes that sloguh w/ underlying purulent exudate, petechia on skin, liver necrosis
o Prevention: good husbandry / Tx: chloramphenicol
- Malocclusion
o Difficulty eating, overgrown beak, hx of metabolic bone disease causing distortion of skull
o Tx: NOT supplementing calcium (wont help since skull is fully formed), long term corrective trimming bc usually
keeps recurring
SNAKE DISEASES
- Ulcerative dermatitis
o Predisposing factors: humid environment, skin lesions, exposure to feces, inadequate UV light
o Erythema, necrosis, ulceration of dermis; exudative discharge
o 2˚ infection w/ Aeromonas and Pseudomonas → septicemia and death
o Tx: improve hygiene; antibiotics
- Inclusion body disease – Retrovirus/arenavirus?
o Regurg, inability to right itself – transmitted by Ophionyssus natricus? Maybe?
o Affects boas and pythons – probably spread by mites → neurologic dz, vomiting → fatal
▪ Unthrifty, anorexia, ↓ weight, poor wound healing, dermal necrosis
o Dx: biopsy – kidneys, liver, spleen
- Meningitis – BACTERIAL
o Stargazing, mentally obtunded, twisted cervical positioning
o Supportive care, antibiotics, corticosteroids to ↓ inflammation
- Entamoeba invadens
o Severe GI signs and death – weight loss, vomiting, hemorrhagic diarrhea, anorexia
o Housed w/ TURTLES – carriers but unaffected – DON’T HOUSE TURTLES AND SNAKES TOGETHER
o Tx: metronidazole (protozoa)
- Infectious Stomatitis (Mouth Rot)
o Overgrown oral microflora – Aeromonas, Pseudomonas
- Cryptosporidiosis – Cryptosporidium serpentes
o ↓ segment motility, significant thickening of gastric rugae, abdominal distension, postprandial regurg, ↓weight
IGUANA DISEASES
- Normally have DARK RED TONGUE – owners shouldn’t be alarmed by this
- Gravid Female – change in behavior from Nov-June (hyperactivity, irritability, stopped eating, enlarged abdomen)
- Cystic calculi
o Straining to urinate, hematuria, rads to show round calculi
o Change diet, surgery to remove if too large to pass
- Gout – primary overproduction of uric acid OR inability to excrete uric acid (renal failure(
- Renal Failure
o HIGH PROTEIN DIET – get hypertension from renal failure
o Episcleral injection, swelling of pharyngeal regions, pain on abdominal palpation
- Tail Trauma
o Remove tail by snapping at place of least resistance (once it’s lost circulation, its more comfy if removed)

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 EXOTIC BIRD DISEASES – 3%
Anatomy & Clinical Info
- 4 chambered heart, heterophils instead of neutrophils, nucleated RBC
- Complete tracheal rings, 9 air sacs (countercurrent airflow exchange at lung level), no diaphragm
o If present w/ swollen distended neck → ruptured cervical air sac
- Ulna bigger than radius, pneumatized bones (humerus, femur) → IO catheter in ULNA/TIBTIOTARSUS
- Uric acid excretion – to excrete nitrogenous waste (same in reptiles)
- Striated mm controls iris
- Fused lumbosacral region = synsacrum
- Rachis – main feather shaft/axis (what you cut when doing wing trim)
- Rhamphotheca – horny keratin sheath that covers beak
- Aptera – featherless tracts (one on neck good place to draw blood from jugular)
- Choana – passage of air from nasal system to oral cavity (slit on roof of mouth)
- Esophagus on R side – tube feed on this side
- Male ZZ, Female ZW (opposite mammals) – sexual dimorphism (green male eclectus, red female eclectus)
- Regurg on owner = normal courtship behavior (can regurg at themselves in a mirror)
- Can safely blood draw 1% of BW in birds – 100mg bird = 1ml blood
- AVOCADOS – myocardial necrosis in parrots
- SQ fluids – skin fold in groin, btw scapula (NOT lateral neck – want to avoid air sacs
- Pull broken blood feather to stop bleeding
- Liver Values in birds: AST, bile acids
o AST also in muscle cells: ↑ AST and ↑ CK w/ muscle disorder)
- Cytology of Feces from Psittacine
o 200 bacteria/HPF (60-80% G+ cocci, 20-40% G+ rods, few normal yeast)
o 2/3 G+ cocci, 1/3 G+ rods
o Signs of immunosuppression/infection: absence of bacteria, WBC, shift from G+ to G-, high number of budding
yeast
Calcium Deficiency
- Ca, P, Vit D3 imbalance → osteoporosis, acute hypocalcemia (weak, tremors, seizures), egg binding, rickets, splayleg (NOT
proventricular dilation)
o Excess Vit D3 – tissue mineralization (esp. kidneys)
o Signs: fluffed at bottom of cage, ↓ appetite, red tissues from vent, hx of laying eggs
- Birds fed ALL SEED DIETS
- Tx: fluids, Ca supplementation
Hypovitaminosis A
- Squamous metaplasia of MM and glands (oral mucosa, conjunctiva, upper airways, nasolacrimal duct, GI tract) → glands
converted to squamous epithelium w/ keratin → can look like abscesses/pustules but are keratin cysts
o Important for epithelial maintenance, vision, skeletal development
o “Bug Eyes”, sublingual abscesses, white plaques
- Birds fed ALL SEED DIETS
- Severe dyspnea, resp signs, white papules in oral cavity, poor feather quality, resp distress, renal dz, blunted choanal
papilla
o AMAZONS very sensitive
- DDx for white plaques in mouth: pox, Candida, Trichomonas, capillaria, papillomatosis
Xanthoma
- Accumulation of yellow friable fatty tissue, benign lipid/cholesterol growths
- COCKATIELS, BUDGES, COCKATOOS – nonaggressive, can become locally invasive and cause irritation/self mutilation
- Yellow mass on tip of wing/breast, FNA – macrophagic inflammation w/ cholesterol clefts
Hepatic Lipidosis
- Baby birds fed high FAT formula (supplemented w/ peanut butter or oil) → resp distress, heavy for their age, dyspneic
- Tx: cooling, O2 therapy

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Cloacal Papilloma
- Common GI tumor of birds (Amazons, Macaws)
- Cloacal prolapse w/ small fleshy proliferations (pink tissues blanch white w/ 5% acetic acid soln)
- Tx: surgical removal, chemical cautery
Renal Adenocarcinoma
- Polydipsia, weight loss, progressive unilateral leg lameness (compression on ischiatic nerve)
- Palpate abdominal mass, take rads to confirm
Goiter – Thyroid Hyperplasia
- Iodine deficiency – voice change, stertor/wheezes (pressure on syrinx), regurg, R jugular engorgement
- Palpate gross enlargement in neck, feels like soft tissue
Proventricular Dilation Disease
- Avian bornavirus (ABV) – aka PDS, PDD, Macaw Wasting Disease
- NEUROTROPIC – affects nerve cells of intestines – chronic weight loss, regurg, passing undigested seeds, CNS signs (ataxia,
abnormal head movement)
- Enlarged proventriculus on rads, Histopath of proventriculus = Lymphoplasmacytic ganglioneuritis
- ISOLATE – need 3 negative cloacal swabs at weekly intervals before reintroducing to aviary
RBC Parasites
- Hemoproteus, plasmodium, leukocytozoon, trypanosoma
- Plasmodium: transmitted by mosquitos, blood smear – see RBC nucleus pushed to periphery
o Common in passerines – often asymptomatic, but may cause hemolytic anemia
- Leukocytozoon: birds of prey – anemia in immunosuppressed birds
o VERY UNCOMMON in household psittacines
Synovial Gout
- Uric acid crystals in synovium → shifting leg lameness, inability to bend toes
- Aspirates: spindle shaped crystals / bloodwork: ↑ renal values (renal disease)
- Tx: allopurinol (↓ uric acid formation), low protein diet, address underlying dz
Hemosiderosis – aka Hemachromatosis
- Too much IRON in liver/other organs
- TOUCANS, MYNAH BIRDS – poor feathering, overgrown beak, lethargy, weight loss
- Bloodwork: ↑ liver enzymes/bile acids, serum iron levels/plasma iron binding are inconclusive
o Need LIVER BIOPSY to confirm
Egg Bound
- Inability to express egg from cloaca
- Contributing factors: obesity, nutrition, hx of prolonged egg laying, hypocalcemia (Ca demand to makes eggs is very high
but also need Ca for muscle contraction of repro tract)
- Abdominal straining, recent egg laying, obese, distended coelomic cavity (see egg on rads)
- Tx: oxytocin, place in warm/dark environment, Ca administration, gentle manipulation w/ lube
o DO NOT jump right to surgery
Egg Yolk Peritonitis
- Can be fatal – recent anorexia/dyspnea, fluffed feathers, coelomic distention
- Bloodwork: heterophilia, ↑ AST/CK/fibrinogen
- Tx: antibiotics, surgery, anti-inflammatories
Capillaria
- Intestinal parasite, may cause diarrhea or weight loss
Aspergillosis – Aspergillus fumigatus
- Raptors, penguins, waterfowl (NOT psittacines except w/ stress or immunosuppression)
Renal Tumors
- Progressive unilateral lameness in budgies, poor prognosis
- Sciatic nerve passes through renal parenchyma
- Budgies – predisposed to neoplasia in general
Pacheco’s Disease
- Sudden death in young birds
Avian Polyomavirus
- YOUNG BIRD – lethargy, crop stasis, death, sometimes SQ hemorrhages after injections

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 CHICKEN DISEASES – 1%
MITES
- Knemidocoptes mutans – SCALY LEG MITE
o Legs, unfeathered parts – irritation leads to feather picking, thickened leg skin
o Round 0.5mm short legged mite
- Dermanyssus gallinae – COMMON RED MITE
o Nocturnal feeders – control through insecticidal treatment of ENVIRONMENT
o Majority of population = OFF the host
o Severe infestations can cause anemia and ↓ repro potential
- Ornithonyssus bursae – NORTHERN FOWL MITE
o Feathered region around vent
o Spend entire life ON the host – apply pesticide to birds!
- Laminosioptes cisticola – SQ MITE
o 1-3mm nodular lesions in SQ
- Trombicula alfreddugesi – COMMON CHIGGER
o Attach to wings, breast, necks – infected birds become weak, stop eating, and die
FUNGAL INFECTIONS
- Candidiasis – Candida albicans (thrush, sour crop, crop mycosis)
o Develops after antibiotic treatment
o White lesions – mouth, crop, esophagus
o Tx: copper sulfate in water, nystatin in feed
- Aspergillosis – brooder pneumonia, mycotic pneumonia, pneumomycosis
o Necropsy: cream colored plaques throughout lungs
o Tx: USELESS – cull affected birds then thoroughly disinfect all facilities
REPRODUCTION
- Egg Drop Syndrome – ADENOVIRUS
o Only seen in small operations – pretty much eradicated
o Poor eggshell quality in healthy birds – ↓ production, dome have no shells at all
- False Layers
o Normal ovulation but yolk dropped into abdominal cavity instead of oviduct
o Usually result of obstruction – E. coli or Mycoplasma gallisepticum
- Egg Binding
o Egg lodges in shell gland or vagina → MEDICAL EMERGENCY (at least in pet birds)
ONCOLOGY
- Reticuloendotheliosis (retrovirus) – CAUSES LYMPHOMA
o Runting, acute neoplasia, chronic B and T cell lymphoma
▪ Runting syndrome: weight loss, abnormal feathering, occasional paralysis, anemia
▪ Thymic/bursal atrophy, enlarged nerves, neoplasia of liver/heart/spleen/intestine
o Similar to Marek’s and lymphoid leukosis – dx w/ virus isolation
- Avian leukosis – lymphoid leukosis (retrovirus)
o Clonal malignancy of bursal lymphoid system – transformation q1-2 months after infection → tumors can take
several more months to develop
o Vertical transmission – congenitally infected chicken
o Tumors – large lymphoid cells, histologically uniform
- Renal Carcinoma
o Unilateral paresis/paralysis
NUTRITION
- Vit E Deficiency – nutritional encephalomalacia & exudative diathesis and nutritional myopathy
o Chicks (15-30 days old) – ataxia, paresis, prostration, death
o Necropsy: ischemic necrosis, demyelination, neuronal degeneration of many parts of brain
- Choline Deficiency – TURKEYS
o Turkeys – high choline requirement, but seen in chickens too
o Stunting, poor feathering, short thick bowed legs
o Chondrodysplasia (Histopath)

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VIRAL DISEASES
- Infectious Bursal Disease – GUMBORO DISEASE – birnavirus
o Watery diarrhea, incoordination, prostration, vent pecking, poor doers (young chicks)
o Necropsy: bursa of fabricius – swollen cloacal bursa that’s edematous, yellow, hemorrhagic
▪ Congestion/hemorrhage of pectoral, thigh, leg muscles
o NO effective tx – prevention is vaccinate breeders and progeny
- Infectious Bronchitis – coronavirus
o HIGH morbidity – resp signs, coughing, sneezing, facial swelling
▪ DDx for these signs = Newcastle, laryngotracheitis, infectious coryza
o Definitive Dx: virus isolation after serial passage of chick embryo
o Necropsy: mucoid exudate in bronchi, thickened air sacs, interstitial nephritis

- Infectious laryngotracheitis – herpesvirus

o Dyspnea w/ extension of neck during inspiration, coughing up mucus and blood, ↓ production, watery eyes, nasal
discharge
o Dx: intranuclear inclusion bodies in tracheal epithelium
▪ Diphtheritic form of fowlpox = intracytoplasmic inclusions
o Necropsy: caseous exudate and blood in trachea
- Hemorrhagic enteritis – adenovirus
o Birds 6-12 weeks old – depression, bloody diarrhea, sudden death
o Necropsy: intraluminal hemorrhage in small intestines, enlarged friable spleen
▪ Inclusion body hepatitis, hydropericardium
o Vaccinate 4-5 week old turkeys
- Marek’s Disease – adenovirus
o Neuro/cutaneous signs, visceral tumors – thickened nerves, paralysis of leg/wing/neck, grey iris/irregular pupils,
raised skin around feather follicles, grey foci of neoplastic tissue in lever/spleen/kidneys/lungs/heart/muscle
o Necropsy: enlarged vagus and sciatic nerves, nodular tumors in many organs, enlarged feather follicles
o NO treatment – prevention = in-ovo vaccinations
- Fowl Plaque – AVIAN INFLUENZA VIRUS
o Is suspect, call authorities!! Concern over mutation and zoonotic potential
o Hx: ↓ egg potential, greenish diarrhea, cyanosis, edema of head/neck/wattle/comb, blood tinged oral and nasal
discharge
- Newcastle Disease - paramyxovirus
o Neuro signs, coughing, death, green diarrhea, swelling of head/neck, gasping, sneezing, dropped wings, dragging
legs, circling, torticollis, paralysis, clonic spasm
o 3 Strains: velogenic (highly pathogenic), mesogenic (intermediate), lentogenic (low pathogenicity)
o Hemagglutinating virus
o ZOONOTIC – conjunctivitis in humans
- Avian encephalomyelitis – picornavirus
o 1-2 week old birds – neuro signs, ataxia, imbalance, head/wing tremors
o Necropsy: neuronal axon-type degeneration (ghost cells) in brainstem
o Prevention: vaccinate breeding animal to prevent vertical transmission
- West Nile Virus – flavivirus
o Chickens/turkey = Don’t usually develop clinical disease – control mosquitoes anyway
o Affects crows, geese, exotic birds (SERIOUS DZ IN CROWS)
BACTERIAL DISEASES
- Infectious Coryza – HAEMOPHILUS PARAGALLINARUM (G-)
o Older chickens – resp disease, nasal discharge, swelling of face under eyes
▪ DDx: fowl cholera
o Tx: antibiotics → GOOD prognosis (vs AI, infectious bursal dz, infectious laryngotracheitis)

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 - Fowl Cholera – PASTEURELLA MULTOCIDA (G-)
o Fever, mucoid discharge from mouth, WHITISH diarrhea, petechia/ecchymoses, ↑ pericardial/peritoneal fluid,
acute death
o Prevention: vaccination / Tx: sulfa antibiotics
o ZOONOTIC
- Salmonella enteritidis
o Food poisoning in people who eat eggs infected with this!
o Is initially only on embryo but if eggs aren’t refrigerated, yolk membrane weakens and Salmonella enters yolk
where it multiplies and can become significant zoonotic problem
- Salmonella typhimurium
o Causes septicemia in young chickens
Control: strict hygiene in hatcheries – prevent exposure to chicks
- Clostridium perfringens (A and C) – NECROTIC ENTERITIS
o AVOID DRASTIC FOOD CHANGES – minimize fishmeal/wheat/barely/rye in diet
▪ Acute enterotoxemia – onset of explosive mortality due to necrosis of small intestines
o Inappetence, ruffled feathers, dark colored diarrhea
o Necropsy: middle and distal intestine has diphtheric membrane w/ dark brown necrotic material
▪ DDx: Eimeria brunetti, ulcerative enteritis (C. colinum)
o Most common cause of LIVER DAMAGE in broiler chickens – cholangiohepatitis
o Tx: penicillin in drinking water
- Erysipelas – G+
o Sudden death after ataxia and weakness
o Dx: G+ slender rod on impression smear of spleen and liver
o Necropsy: darkened skin, enlarged friable liver and spleen
o Tx: IM sodium penicillin, give erysipelas bacterin
- Avian Tuberculosis – MYCOBACTERIUM AVIUM
o Rarely seen in commercial flocks due to short life span – seen in back yard flocks
o Acid fast bacteria in lesion smears
o Necropsy: granulomatous nodules in liver, spleen, bone marrow, intestines
- Trichomonas gallinae
o Protozoa – enteric/oral lesions, weight loss
▪ Caseous exudate – profuse, can obstruct esophagus
o Tx: metronidazole, dimetrazole, bunch of -izoles
- Pullorum Disease – Salmonella enterica
o Very high mortality (like 100%)
o Young chickens and turkeys
o Clinical Signs: huddle near heat source, anorexia, weak, whitish fecal pasting around vent, acute septicemia, death
o Adults: nodular pericarditis, fibrinous peritonitis, hemorrhagic atrophying ovaries w/ caseous contents
o Indistinguishable from Fowl Typhoid
MISCELLANEOUS DISEASES
- Coccidiosis – EIMERIA
o Numerous species specific to certain regions of GI tract (bloody enteritis, intestinal edema, hemorrhagic cheesy
cecal sores) – severe diarrhea, ↓ production, death
o Dx: oocysts in feces
o Tx: anticoccidial drugs – AMPROLIUM (ZERO withdrawal time)
▪ Thiamine analogue that’s coccidiostatic – other drugs have longer withdrawal times
o In otherwise healthy animal, considered incidental finding
- Avian fowl pox – POX VIRUS
o Spread by mosquitoes – control mosquitoes and vaccinate to prevent
o 2 forms:
▪ Dry: whitish wart like lesions on unfeathered areas (head, legs, vent), lesions heal in 2 wks, low mortality
▪ Wet: diphtheric membrane in mouth/pharynx can ulcerate/erode MM, marked resp signs, lead to death
o NO treatment effective

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 - Visceral Gout
o Renal damage, severe dehydration
o Urate crystals accumulate in affected organs – uric acid produced in liver as end-product of nitrogen metabolism –
chalky substance accumulates in liver, myocardium, spleen
o Articular gout = articular urate deposits
- Malabsorption syndrome – runting-stunting syndrome, pale-bird syndrome
o 1-3 week chickens – poor growth and feathering, abnormal/broken feathers, pale feet/skin, ORANGE feces
o Necropsy: orange mucus in intestines, enlarged proventriculus, small gizzard, atrophied pancreas
o CULL affected birds – prevent w/ good hygiene, good nutrition, good egg selection
Anatomy
- Crop (esophagus) → proventriculus (glandular stomach) → ventriculus (gizzard) → bursa of Fabricius (near cloaca)
o Crop = allows bird to swallow food and fly away quickly (temporary food storage)
o Ventriculus = contains grit/small rocks – grinds up hard seeds/other foods → same function as teeth
o Bursa of Fabricius = aka the bone marrow of birds – dorsal diverticulum of cloaca; site of hematopoiesis and B-cell
maturation (immune function)

TURKEY DISEASES – 1%
Reasons not to house turkeys and chickens together
- Mycoplasma gallisepticum
o MILD in chickens, SEVERE in turkeys – turkeys get nasal discharge, swollen paranasal sinuses, ↓ weight and egg
production, severe sinusitis and air sacculitis
- Histomonas melagridis – BLACKHEAD of turkeys
o Affects turkeys when housed with chickens – FATAL to turkeys
o GASTROENTERITIS, NOT resp signs – YELLOW droppings, dull, depressed, ruffled feathers
o Heterakis gallinarum hosts the protozoan (which causes clinical disease)
o Necropsy: ulcerations and thickening of cecal wall, liver w/ ring shaped yellow lesions
▪ EXTENSIVE LIVER/CECUM NECROSIS!!! PATHOGNOMONIC!!!
o Tx: nitrasone added to feed; also use benzimidazoles (to kill Heterakis)
Turkey Coryza – BORDETELLA AVIUM
- HIGH morbidity, LOW mortality – acute resp disease, nasal discharge, foamy eyes, cough
- Dx: MacConkey agar
- Antibiotics NOT effective – sometimes vaccine is helpful in outbreak
Spontaneous Cardiomyopathy – ROUND HEART DISEASE of turkeys
- Acute death in young turkeys after having labored/gasping breathing – other turkeys in flock have unkempt appearance and
ruffled feathers
o Sudden death: cardiac arrest in young turkeys (3-4 weeks old)
- Necropsy: markedly enlarged heart w/ dilation of ventricles, congested lungs, enlarged liver
- Histopath: lymphocytic infiltration and damage to myofibrils in cardiac muscle
Ornithosis – CHLAMYDIA PSITTACI
- Nasal and ocular discharge, weight loss, inappetence, death
- Necropsy: pneumonia, liver/spleen necrosis, severe pericarditis, intracytoplasmic inclusions
Deep Pectoral Myopathy
- Swollen edematous pectoral muscles – vigorously exercised muscle that when handled leads to swelling, ischemia, necrosis
o Thought to be due in part to selection for breast meat – not contagious, no specific etiology
- Necropsy: degeneration, necrosis, fibrosis, green appearance to muscle
- Meat condemned at processing – economic losses – so to ↓ incidence due to selective breeding
Bluecomb – coronavirus (aka transmissible enteritis, coronaviral enteritis)
- Cyanosis and darkening of head, young turkeys die, old turkeys fail to gain weight, depression, anorexia
- Dx: direct fluorescent antibody for viral antigens in intestins
- Tx: supportive care, antibiotics for 2˚ bacterial infection
- NO VACCINE AVAILABLE – prevent w/ good husbandry

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 PIG DISEASES – 6%
VIRAL DISEASES
- Swine Influenza
o HIGH morbidity, LOW mortality – concurrent illness exacerbates disease
▪ Uncomplicated infection: short course, low mortality
o Lethargy, resp illness, high fever, prostration, coughing, anorexia, conjunctivitis, oculonasal discharge
o IMPORTANT: dz in pigs/waterfowl can mutate – be major zoonotic problem
- Porcine Epidemic Diarrhea and Transmissible Gastroenteritis (TGE) – coronavirus
o ALL age groups – nearly 100% mortality in piglets <1wk old
▪ No other dz spreads so rapidly or causes such high mortality – seldom die if >1month
o Watery diarrhea, vomiting, wet/dirty appearance to litter from profuse diarrhea
o Tx: symptomatic
o Prevention: feed feces and intestinal contents from infected piglets to sows who are >14 days from farrowing
- Hemagglutinating Encephalomyelitis Virus (HEV)
o Piglets <4 weeks old
o Vomiting and wasting disease (VWD) and encephalitic forms
- PRRS – Porcine Respiratory and Reproductive Syndrome – arterivirus
o STILLBORN PIGS – most common cause
o 3 overlapping syndromes – affects ALL ages
▪ Repro impairment/failure – abortions, mummies, stillbirths, early embryonic death
▪ Resp Disease – wean pigs get cough (thumps), purple ear tips from vasculitis
• Nursery pigs – interstitial pneumonia
▪ High pre-weaning mortality – diarrhea, recurrent fevers
o Tx: NONE – may have to depopulate or close herd and follow titers
o Prevention: vaccine
- Rotavirus
o 5 days old – often in association w/ E. coli
- Blueye – tublavirus
o Aka blue eye paramyxovirus
- Hog Cholera – togavirus (Classical Swine Fever)
o REPORTABLE – US is currently free of this
o Closely related to pestivirus – BVD, border disease virus
o Virus affects stem cells in bone marrow → neutropenia, thrombocytopenia – become immune suppressed and
susceptible to enteric bacterial infections
o Oral ulceration, vomit, diarrhea, oral petechiation, paresis/paralysis, fever, shivering, conjunctivitis
o Can cross placenta – repro failure – severe systemic infection and abortion
- African Swine Fever
o Fever, inappetence, hemorrhage of ear skin, acute death
▪ DDx: classical swine fever, erysipelas
o AFRICA – carried by warthogs, transmitted by soft ticks
o Necropsy: petechial hemorrhages on internal organs

- Vesicular Exanthema – calicivirus (aka San Miguel Sea Lion Disease in sea lions)
o Swine and sea lions/seals/marine mammals
o Sea lions off coast of CA – not present in US pigs
o REPORTABLE
- Pseudorabies – herpesvirus (Aujesky’s Disease)
o PIG – primary host
▪ Erradicated from pigs in US, can devastate non-immune herd
▪ Resp, repro, CNS (not GI) – clinical signs depend on age group
• Young neonates <3wks: NEURO, CNS signs, tremors, incoordination, blindness, opisthotonos,
hypersalivation, ataxia, nystagmus, paddling, DEATH → 100% mortality
o DDx for tremors: organophosphates, circovirus, hog cholera, NOT PRRS
o Some are born mummified

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 • Wean pigs: NEURO and RESP – similar signs as young neonates + resp signs, lower mortality
• Grower/Finisher pigs: RESP – cough, sneezing, nasal discharge
• Older pigs at breeding age: resp signs, REPRO FAILURE (abortion, resorption, mummification)
o Ruminants
▪ 1st sign = paresthesia (MAD ITCH) at inoculation site, ataxia, proprioceptive deficits, circling, nystagmus,
strabismus – sometimes see aggression, depression → death in 2 days
• Often have pigs housed nearby – pigs are 1˚ host!
• NO TREATMENT – animals die, prevention = remove the pigs
• DDx for clinical signs: rabies (Negri bodies), Polioencephalomalacia, salt poisoning, lead
poisoning, hypomagnesemia, meningitis
o Horses
▪ VERY RARE – depression, inability to swallow
o NO TREATMENT – older pigs recover on their own → prevent w/ vaccination
- Parvovirus
o BRED SOW RETURNS TO HEAT – embryo resorption, unapparent infection in sow
▪ Mummified fetus, weak piglets, small litters, stillbirths
▪ Abortions – RARE – endometrium is not affected so no PGF2a released
o VACCINATE
o DDx for fetal loss: parvo, toxoplasma, brucella, pseudorabies, PRRS, eperythrozoonosis, erysipelas, lepto
BACTERIAL DISEASES
- Lawsonia intracellularis
o G-, curved bacteria in enterocytes – proliferative enteropathies
▪ Aka Porcine Proliferative Enteritis – FINISHING PIGS (40-80lb)
o Soft buttery (yellow) stool, sometimes acute hemorrhagic diarrhea, gradual wasting, lethargy
o Common – weaned and older pigs – persistent diarrhea, weight loss (similar to Johne’s in cows)
o Necropsy: thickened inflamed ileum – proliferative ileitis w/ edematous mesentery
- Serpulina/Brachyspira hyodysenteriae – SWINE DYSENTERY
o Mucohemorrhagic diarrhea – large bowel diarrhea, fibrinonecrotic typhlitis and colitis
▪ Small intestine unaffected
o Bloody diarrhea and death – grower/finisher pigs
- Salmonella
o RECTAL STRICTURES w/ chronic infection, “button” ulcers in large intestine
o WEANERS and GROWERS – uncommon in piglets (passive immunity from colostrum)
- Erysipelothrix rhusiopathiae – DIAMOND SKIN DISEASE
o 3 Forms – GROWER and FINISHERS pigs
▪ Peracute – pigs found suddenly dead
▪ Acute – pigs are lethargic, painful in joints, anorexia, develop diamond skin lesions
▪ Chronic – arthritis progresses to vertebral joints and limbs joints may fuse – painful swollen joints
o Lesions: red/purple skin lesions in diamond shapes
- Enterotoxigenic E. Coli – Enteric colibacillosis, EDEMA DISEASE
o Lesions: edema, pericardial/pleural effusion (Shiga toxin 2e) – destroys endothelial cells in vessels → blood clots,
hemorrhage, ischemia necrosis, edema of vital organs (including brain)
o Enteric colibacillosis
▪ Most common cause of diarrhea in NURSING piglets (<5 days old) – piglets huddled and shivering
▪ See w/ rotavirus – watery diarrhea, dehydration, acidosis, death
▪ Prevention: vaccinate, NEVER MIX PIGS OF DIFFERENT AGES TOGETHER
o Edema Disease
▪ FATAL dz of rapidly growing WEANED pigs – pigs on high protein, high energy diet
▪ Fever, anorexia, SQ emphysema, dyspnea, open mouth breathing, convulsions, diarrhea, swollen eyelids
(eyelid edema, forehead, lips), circling, acute death
- Brucellosis
o ABORTION – any stage of gestation – placentas and aborted fetuses have NO GROSS LESIONS
o Transmission: venereal, aborted fetuses
o ZOONOTIC – highly pathogenic in humans!!

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 - Mycobacterium avium – swine tuberculosis
- Streptococcus suis
o NURSING and WEANED pigs – polyarthritis, bronchopneumonia, sepsis, meningitis (NOT colitis)
o Varying morbidity/mortality – improved w/ tx
GASTROENTEROLOGY
- Diarrhea in different age groups:
o Unweaned (young) piglets
▪ Clostridium perfringens type C – hemorrhagic/necrotic enteritis
• 1-5 days old
▪ Cryptosporidium parvum – VERY UNCOMMON IN PIGS – no effective drugs
▪ Rotavirus
• 5-21 days old
▪ Isospora suis
▪ Transmissible gastroenteritis virus (TGE) – coronavirus
• Newborn to weanlings
▪ Enteropathogenic E. coli (enteric colibacillosis) – VERY COMMON IN NURSING PIGLETS
o Weaned (older) piglets – Growers and Finishers
▪ Salmonella
▪ Lawsonia intracellularis – infects epithelial cells and causes excessive proliferation
• Thickened hemorrhagic intestines – proliferative enteritis
▪ Trichuris suis – can affect all ages but usually older pigs
▪ Serpulina hyodysenteriae – swine dysentery
- Gastric Ulcers
o Housing stress, type of feed, concurrent disease
o Common in GROWING SWINE – pale MM, dark feces
o Necropsy: clotted blood in stomach (pars esophagea portion) and duodenum
- Intussusception
o OESOPHAGOSTOMUM infection – vomiting w/o diarrhea
▪ Tachycardia, restlessness, colic signs
o Tx: surgery
DEMATOLOGIC DISEASES
- Hernias
o Inguinal → MALES after castration, heritable!
o Umbilical → FEMALES
- Pityriasis rosea
o 12-14 week older pigs – unknown etiology, possibly heritable
o Raised circular lesions on ventral abdomen – NO TREATMENT NEEDED – resolves on its own
- Staphylococcus hyicus
o Exudative epidermatitis – aka GREASY PIG DISEASE (scabs, excoriations)
o Piglets <8wks old – brown exudative spots on skin of head, axillae, groin – brown, crusty
o Morbidity/mortality high in younger pigs, rarely affects adults
- Swine pox - poxvirus
o Transmitted by biting insects (esp. lice!) – control is eliminate hog lice/insect vectors
o 1-2cm round papules, pustules, vesicles, scabs on ventral abdomen
- Aural hematoma
o Caused by bites from pen-mates or from violent head-shaking (from mites/lice in ear)
- Dermatosis vegetans
o Semi-lethal hereditary defect: causes macules and papillomas around coronary band
- Parakeratosis
o Zinc Deficiency! Supplement zinc in diet
▪ Starter diet = 125 ppm zinc + 0.9% Ca
▪ Grower diet = 75 ppm zinc + 0.6% Ca
▪ Finisher diet = 50 ppm zinc + 0.5% Ca
o May resemble “greasy pig disease” (Staph hyicus) which is seen more in younger suckling pigs, tx = abx

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RESPIRATORY DISEASES
- Atrophic Rhinitis – Bordetella bronchisepticum (nonprogressive), Pasteurella multocida (progressive)
o Snorting, sneezing, snuffling, coughing, epistaxis, nasal discharge, turbinate atrophy, facial distortion
o Common in piglets: 3-8 weeks old
o Tx: antibiotics / Prevention: vaccination
- Necrotic Rhinitis – Fusobacterium necrophorum (G+)
o Snout necrosis when it enters nasal/oral mucosa
- Mycoplasma hyopneumoniae – ENZOOTIC PNEUMONIA
o Coughing in feeder pigs (persistent dry cough, fever, inappetence, ↓ weight gain/retarded growth
o Necropsy: purple/grey consolidation in cranioventral lungs with catarrhal exudate in airways
o Prevention: vaccination, address air quality and ventilation
- Pleuropneumonia – ACTINOBACILLUS PLEUROPNEUMONIAE (G-)
o Sudden onset respiratory distress w/ open mouth breathing, frothy pink oral/nasal discharge (blood)
o Pigs <6 months old who commonly have concurrent infections (Mycoplasma, Pasteurella, PRRS, influenza)
▪ DDx – influenza affects ALL ages, no pink discharge
o Necropsy: fibrinonecrotic hemorrhagic lung lesions
▪ Necrohemorrhagic fibrinosuppurative pleuropneumonia
ORTHOPEDIC DISEASES
- DDx for lameness: Strep suis, Erysipelas, Mycoplasma hyorhinis, Haemophilus parasuis
- Osteochondrosis dessicans
o Multiple pigs from herd present lame – usually fast growing well-muscled pigs, lame at 4-8 months old
o Lesion: defects in articular cartilage – medial femoral condyle, humeral condyle, humeral head, glenoid of scapula,
distal ulna, lumbar vertebrae
o Cull affected animals – replace w/ normal animals for breeding - Cross Breeding DOES NOT HELP
o Tx: symptomatic, doesn’t cure dz
- Glaesserella parasuis – GLASSER’S DISEASE
o Painful joints, pneumonia, sometimes neuro – swollen painful joints, shifting leg lameness
o Affects pigs 2-4 months old
o Necropsy: fibrinopurulent pleuritis and peritonitis (polyserositis), sometimes pericarditis/meningitis
o Tx: penicillin
- Mycoplasma hyorhinis
o Presents similar to Glasser’s Disease – polyarthritis, polyserositis, fever, pneumonia, 2-4 month old pigs
o LOW mortality
MISCELLANEOUS
- Eperythrozoonosis – Eperythrozoon suismu
o Vector = biting insects
o YOUNGER pigs affected more severely – anemia, fever, icterus, repro failure, weak, anorexic
o Tx: tetracycline
- Sinus Arrhythmia
o VERY COMMON IN PIG – relatively uncommon in ruminants
o Caused by vagal tone – see ↑ HR on inspiration
- Vit A Deficiency
o Head tilt, incoordination, ↓ weight gains, weak rear limbs w/ NORMAL VITALS
▪ Multiple pigs on same farm
o ↑ middle ear infections; in sows, can cause embryonic mortality/congenital defects
- Failure of Passive Transfer
o Farm w/ ↑ newborn piglet diarrhea – measure IgG in piglets at 24 hours old
- Management
o Weaning @ 16-20 days in North America
o All in/all out – helps synch estrus/breeding in sows → have them all farrow at same time, wean at same time, bred
at same time, vaccinated at same time – clean house in btw groups
▪ Advantages – same schedule, ↓ neonatal mortality, greatest return on pounds of meat at market
▪ Disadvantages – not continuous production of piglets

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 - Xylazine – NOT EFFECTIVE
o Poorly responsive to xylazine alone – have to combo w/ something else
o Have to combo w/ benzos (midazolam) + narcotic (butorphanol) = improved sedation
o Xylazine + Telazol = general anesthesia
- Boars
o Have preputial diverticulum – pouch in dorsolateral aspect of prepuce
o Discharge collects here – source of strong boar smell (attractive to females)
o Removed in pet pigs to reduce odor

CERVID DISEASES – 1%
Chronic Wasting Disease (CWD)
- Transmissible spongiform encephalopathy (prion disease)
o Become thin, PUPD, poor balance/coordination, drooping ears, difficulty swallowing (no body fat, very thin)
o Spread via body fluids – feces, saliva, blood, urine – through direct contact or environmental contamination
- Elk, deer, moose – North America
- Low zoonotic potential
Bovine Tuberculosis
- Contagious, ZOONOTIC
- Mycobacterium bovis – G+, acid-fast
- Transmission: inhalation of aerosols, through breaks in skin
o Progressive wasting, low grade fluctuating fever, weakness, loss of appetite, intermittent diarrhea/constipation
o Pulmonary involvement: moist cough, tachypnea/dyspnea, acute resp distress
o Terminal Stages: emaciation, enlarged/ruptured/draining lymph nodes, lymph node GI obstruction, death
- Dx: culture and isolation = definitive diagnosis
Cervid Brucellosis
- ZOONOTIC – infection via eyes, wounds, genital tracts, contact w/ aborted fetuses
- Abortion in later gestation, babies born immature/weak / uterine inflammation, repro failure
- Chronic infection: lameness, abscesses in bones/joints
Epizootic Hemorrhagic Disease
- Humans can eat deer infected w/ EHD safely
- White tailed deer: swelling of face/neck, inappetence, lethargy, weakness, lameness, resp distress, fever, excess salivation
o Possibly asymptomatic
Foot and Mouth Disease
- Fever, ↑ salivation, lesions on/in mouth and feet (blisters that rupture and cause severe pain when eating/lameness)
- Rarely affects humans, but highly infectious and sometimes fatal for cloven-hoofed animals

RUMINANT DISEASES
Reportable Diseases: Brucellosis, FMD, Vesicular Stomatitis, Bluetongue
Foot and Mouth Disease - picornavirus
- CLOVER HOOFED animals – cattle, sheep, goats, pigs, llamas; also bears, camels, elephants
o NOT HORSES
- Oral and foot lesions – vesicles in mouth, on coronary band, and interdigital space – rupture and result in ulceration and
pain (DDx in cattle: vesicular stomatitis, bovine papular stomatitis, pseudocowpox, bluetongue)
- USA is free of FMD - REPORTABLE
Vesicular Stomatitis
- REPORTABLE – occurs every 7-10 years in western US – reportable bc similar to FMD
- Vector: sand flies, black flies – then spread by direct contact, high morbidity, low mortality
- Can affect HORSES and PIGS – not sheep
o DDx: FMD only affects cloven hoofed animals
- Oral ulcerations (ruptured vesicles on tongue), lesions on feet, teats – salivation, anorexia, depression, fever, drooling,
chomping mouths, ulcerated tongue

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Malignant Catarrhal Fever
- 2 forms:
o African – Alcephaline herpesvirus (AHV-1) – WILDEBEEST reservoir, high mortality
o N. American – Ovine herpesvirus 2 (OvHV-2) – SHEEP reservoir (goats too)
▪ Cattle, water buffalo, deer, pigs, bison (most susceptible) all affected
- Cattle housed near sheep – high fever, resp/GI lesions, lymphadenopathy, corneal opacity, thick white nasal discharge,
thick cracked skin, oral lesions
- Affect lymphocytes – allows animal’s own killer cells to attack blood cells → acute generalized arteritis – involves mucosa of
many systems = lymphocytic vasculitis
- Necropsy: lymphocytic perivasculitis of the brain
Rumen Acidosis – GRAIN OVERLOAD
- Hx: breaking into grain meant for horses – need to SLOWLY introduce ruminants to concentrates
- Pathogenesis – ↑ grain – replication of S. bovis/other G+ bacteria – ↓ rumen pH below 4.5 causing ↑ lactic acid –
lactobacilli multiply due to favorable conditions – crank out a bunch more lactic acid – cannot metabolize D-lactic acid –
causes systemic acidosis
o Osmotic diarrhea – ↑ lactic acid will ↑ osmotic pressure – causes excessive amount of fluid moving into rumen
- Clinical Signs: ↑ HR, depression, anorexia, fluid-filled rumen, scleral injection, diarrhea, staggering
- Dx: rumen fluid pH of <5.5
- Tx: oral antacids (Mg oxide/hydroxide), IV fluids w/ Na bicarb, penicillin, rumenotomy if severe
- Sequelae: liver abscesses, mycotic rumenitis, death from metabolic acidosis, vena caval thrombosis
o Liver abscesses – low rumen pH allows bacteria to translocate – filtered by hepatic circulation
o Vena Caval thrombosis & metastatic pneumonia – bleeding from nose due to liver abscess near caudal vena cava –
thrombosis breaks off and lodges in pulmonary arteries – pulmonary bleeding
o Rumen ulcers – could penetrate mucosa, cause septic abdomen
Polioencephalomalacia – THIAMINE (Vitamin B) DEFICIENCY
- ↑ in grain in diet, hx of being fed horse feed (high in concentrates/molasses)
o Strongest animals get sick first – top of food chain
o ↑ in grain leads to ruminal acidosis, results in thiaminase producing bacteria multiplying in rumen – destroy
thiamine, ↓ population of thiamine producing bacteria
▪ Other causes: bracken fern, amprolium overdose, high dietary sulfate
- Diarrhea, depression, hyperesthesia, head-pressing, stargazing, opisthotonos, dorsomedial strabismus, odontoprisis
blindness (bilarteral) – usually progresses to recumbency
- Necropsy: soft, edematous cerebral cortex w/ grey-yellow discoloration and flattened gyri
o Necrosis of cortical grey matter
- Tx: give thiamine
Dermatophilus congolensis – STRAWBERRY FOOTROT (sheep), RAIN SCALD (ruminants and HORSES)
- Crust lesions at coronary band that are easy to remove – PAINTBRUSH LESIONS; when crusts are peeled off, have pink
granulation tissue
- Cytology: branching RAILROAD TRACKS of cocci bacteria
- Common in animals out in rain/wet conditions
- Tx: remove from rain, 10% zinc sulfate baths, antibiotics
- Rain Scald: crusting lesions on muzzle, ears, face, tail, dorsum – YOUNG animals
o Enters skin damaged by wetness – suppurative casts along dorsum
Corynebacterium pseudotuberculosis – CASEOUS LYMPHADENITIS (aka boils)
- Transmission: injury to skin (i.e. shearing)
- Cattle affected too – large external bleeding sores on skin; not really systemically affected
o Large sore on flank w/ pus and blood – common lateral thorax, neck, flank, head
o Flush wound, let it heal – resolves on its own in 2-4 weeks
- Most Common in sheep/goats – boils and internal abscesses
o Large mandibular/prescapular abscesses – internal lymph nodes too
o Necropsy: mass has “onion ring” appearance w/ concentric layers of fibrous tissue separated by inspissated
caseous exudate – greenish pus
▪ Culture pus: white to opaque colonies that can be pushed across plate like hockey puck

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 - Can also affect mammary gland – CULL or ISOLATE – very hard to treat bc walled off abscess
o If valuable, can do life-saving mastectomy
- ISOLATE AFFECTED ANIMAL – very contagious! Usually just CULL bc is a chronic recurring disease
o If animal is valuable: surgical drainage, abscess removal, antibiotics, isolation
- Prevention: VACCINATE, be careful when shearing – disinfect shears well in btw sheep
Johne’s Disease – Mycobacterium avium ssp paratuberculosis
- >2 years – chronic weight loss, occasionally see green diarrhea, submandibular edema, emaciation, ↓ production, ↓
muscle mass
o Affected when young, don’t show clinical signs until older and STRESSED
o FECAL-ORAL transmission
- Lesion: granulomatous bowel (ileocolic, ILEUM, colitis) – lose albumin into gut, rapid weight loss
o ACID-FAST rods on cytology
- CULL ALL POSITIVE CATTLE – NO TREATMENT
- ZOONOTIC? Crohn’s disease associated w/ this bacteria – ongoing debate
Transmitted in Milk
- Mycobacterium bovis
- Listeria monocytogenes
- Brucella abortus
- Coxiella burnetii

GOAT & SHEEP DISEASES – 3%

GOAT DISEASES
- Caprine Arthritis and Encephalomyelitis Virus (CAEV) – retrovirus – affects MONOCYTES
o HARDBAG – causes fibrosis of udder and results in agalactia
o Transmit to kids via colostrum – arthritis in adults, encephalitis in kids
▪ Leukoencephalomyelitis in kids 2-6 months old
▪ Polysynovitis-arthritis in goats >6 months
o Tx: ineffective → CULL
o Screening test for herd health: ELISA, AGID
- Mycoplasma pneumonia – Mycoplasma mycoides ssp mycoides, M. capricolum
o M. ovipneumoniae causes pneumonia in sheep
o Transmission: transmammary, aerosol – maintained in herd by mammary carrier (subclinical)
o Respiratory disease w/ fibrinous pneumonia on Histopath
o Causes pneumonia, meningitis, mastitis, polyarthritis
▪ Concurrent mastitis in does and polyarthritis and pneumonia in kids (and maybe meningitis)
• Kids 2-4 weeks old – hot swollen joints, respiratory distress
• Does have firm udders w/ brownish watery mild, occasional garget (inflammation)
▪ Dx: milk culture – NON-responsive to antibiotics – CULL all affected animals (even kids)
- Brucella melintensis
o ZOONOTIC – acquired via raw goat milk – severe pathogen in humans!
o B. abortus in cattle, B. suis in pigs, B. canis in dogs – all severe in humans!
o Brucellosis in animals = Contagious abortion! (abortion, stillbirth, infertility)
- Squamous Cell Carcinoma
o Papillomas in Saanen goats tend to transform to SCC – POOR prognosis
o Warts on udder that develop into something more serious
- Sinusitis
o Kids – shortly after dehorning – affects frontal sinus
- Myotonia congenital – FAINTING GOAT SYNDROME
o Autosomal dominant mutation – abnormality in skeletal muscle chloride channel
o Marked general rigidity after visual, tactile, or auditory stimulation

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 - Beta mannosidosis
o Genetic: Anglo-Nubian goats (α mannosidosis in cattle breeds)
o Storage disease – intraneuronal accumulation of mannose-based oligosaccharides
o In kids: inability to stand since birth, short sternum, shortened dome head w/ short curled ears, head tremors,
carpal contractures, no suckle reflex
- Polled Intersex Syndrome
o Hornless goat breeds (esp. Toggenburg, Saanen, Alpine)
o Genetically female – exhibits male, female, or mixed external characteristics (ex. abnormal protruding vulva)
o May see hypospadias = abnormal placement of urethral opening ventral and caudal)
o DON’T BREED
SHEEP DISEASES
- Spider Lamb Syndrome – SUFFOLK SHEEP (aka Ovine Hereditary Chondrodysplasia)
o Carpal valgus – hereditary, caused by semilethal autosomal recessive trait
- Bluetongue – reovirus
o Primarily affects SHEEP – cattle also have reproductive losses (hydrocephalus in calves)
o Vector: CULICOIDES (also sexual spread, transplacentally)
o Causes widespread vasculitis – fever, edema of face/muzzle/lips/ears, respiratory difficulty, mucopurulent nasal
discharge, cyanotic tongue, oral lesions (differentiate from FMD and VSVS)
▪ Teratogenic effects – both sheep and cattle
• Stillborn/weak calf w/ “white eye calf syndrome” – congenital cataracts
• Hydrancephaly in lambs – cerebral hemispheres like swiss cheese
▪ Lameness – Zenker’s degeneration of skeletal muscle – white streaks in muscle
o Necropsy: white streaks in skeletal muscle and endothelial hemorrhage at base of pulmonary artery, ecchymotic
hemorrhages in lymph nodes and spleen = VASCULITIS
- Coxiella burnetti = Q FEVER (G- spore forming intracellular bacteria)
o ZOONOTIC – acquired from sheep – fever, headache, fatigue, premature delivery, abortion
o Uncommonly causes abortion in sheep
- Ulcerative Posthitis – Corynebacterium renale – PIZZLE ROT
o Bacteria contain urease – allows it to thrive in prepuce and converts urea to ammonia which damages mucosal
surfaces – leads to prepuce swelling, stranguria, reluctance to breed, only a few animals affected
▪ More common in castrated sheep and goats
o Lesion: scabs on mucocutaneous junctions of prepuce – painful ulcers, foul smelling scabs
o Sheep on high protein diet – excess protein catabolized to urea
o Tx: ↓ dietary protein, penicillin to control C. renale
- Mycoplasma pneumonia – M. ovipneumoniae – ENZOOTIC PNEUMONIA, ATYPCIAL PNEUMONIA
o Transmission: aerosol (vs. goat – spread by milk)
- Ovine Progressive Pneumonia (OPP) – retrovirus – aka MAEDI-VISNA
o Closely related to CAEV
o Sheep 2-4 years old – emaciation, lag behind flock, expiratory dyspnea, hard udders, open mouth breathing,
occasional NON-productive cough, fever
o Necropsy: grey-blue lungs that don’t collapse, fibrous udder (indurative mastitis) w/ large lymph nodes
- Mannheimia hemolytica – Enzootic Pneumonia < GANGRENOUS MASTITIS (Blue Bag)
o BLUE BAG – Staph aureus also causes blue bag, hard to treat, animals often culled
o ENZOOTIC PNEUMONIA – most common bacterial cause of pneumonia in sheep and goats
▪ Hemorrhagic bronchopneumonia – fever, mucopurulent nasal discharge, coughing, crackles/wheezes
▪ Necrospy: fibrinopurulent pneumonia
- Entropion
o Common in newborn lambs – also common in pigs – usually lower eyelid affected
- Cryptosporidium parvum
o ZOONOTIC – from handling animals or feces
o Acute diarrhea in lambs/calves
o STAINS ACID-FAST

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 - Scrapie – PRION disease (transmissible spongiform encephalopathy)
o Afebrile neuro disease – chronic, progressive, degenerative – clinical signs depend on brain region affected
▪ Aggression, failure to herd, unsteady gait, self-mutilation (pruritis – rub wool off lumbar region),
blindness, seizures, inability to swallow
o Dx: Immunohistochemistry of OBEX
o CULL positives – breed for resistant flock based on pedigree – need to cull to prevent spread of PrP gene
- Meningitis
o Associated w/ tail docking in sheep – progressive ascending paralysis, neck pain
o CSF – xanthochromic, gram stain show many bacteria
- Border Disease Virus – pestivirus – HAIRY SHAKER SYNDROME
o Antigenically related to BVD/hog cholera
o Transmitted from ewe to fetus before 80 days of gestation – macerated/aborted/mummified fetuses
▪ Ones that survive exhibit “hairy shaker” syndrome – infection of hair follicles and cerebellum (domed
heads, short limbs, thick trunks, tremors, fine hairy wool)
- Campylobacter jejuni – VIBRIOSIS
o Most common cause of INFECTIOUS ABORTION – sheep in North America
o DDx for abortion: Toxoplasma, Chlamydia psittici, Bluetongue, Brucella ovis (epididymitis), Akbane virus (dystocia,
arthrogyyposis), Cache Valley Virus (brachygnathia, hydrancephaly, microencephaly)
o Prevention = vaccination! Annually + 2 weeks prior to breeding
▪ If 1st vaccine, give booster mid-pregnancy
- Campylobacter fetus ssp. Fetus
o ABORTION STORMS – late term pregnancy abortion
o Fetal livers: necrotic areas that look like “grey targets”
- Brucella ovis
o Primary lesion = epididymitis
o Orchitis, eventual testicular atrophy, thickening/scarring of tunics, ↓ fertility
o CULL affected rams – persistently infected (if valuable, can try treating w/ chloratetracycline or streptomycin)
o Infection in ewes: late term abortion, stillbirths, weak lambs
- Breeding Ewe Vaccinations
o CCC: Clostridium, Campylobacter, Chlamydophila
- Louping Ill – Flavivirus
o Leaping/bounding gait, tremors, hind-end ataxia, nervous nibbling
o Louping Ill = ovine encephalomyelitis
o Transmission = Ixodes ticks
- Psoroptes ovis = Psoroptic Mange
o Aka Sheep Scab = super itchy, no musculoskeletal issues
GOAT & SHEEP DISEASES
- Contagious Ecthyma (CE) – ORF, SOREMOUTH – parapoxvirus
o ZOONOTIC – along w/ 2 other parapoxviruses – Bovine papular stomatitis, pseudocowpox
o Virus in scabs that fall off lesions – can overwinter in the scabs
o LESIONS IN MOUTH – thick brown crusts – around nose of lambs/kids, sometimes TEATS of mothers
▪ Sore mouths/sore teats = nursing problems
o Lesion: crusting lesions of mucocutaneous junctions of mouth, oral cavity, on feet, eyelids, teats
- Pregnancy Toxemia
o LATE gestation (final stages of pregnancy w/ multiple fetuses)
▪ Multiple fetuses – space-occupying lesion – makes rumen harder to fill just as doe peaks caloric
requirement – tips into negative energy balance – uses fat stores – develops fatty liver – liver can't
produce enough glucose, becomes overwhelmed w/ free fatty acids – ketone production – becomes keto-
acidotic – pregnancy toxemia
• Body can't produce enough OXALOACETATE for citric acid cycle – mobilize fat, produce ketones
o Anorexia, weakness, recumbency, depression, CNS signs (tremors, stargazing, circling, teeth grinding)
o Dx: multiple near term dead fetuses, pale fatty liver on necropsy, ketones in urine, hypoglycemia, neuro signs
(circling, stargazing)

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 o Tx: IV glucose/dextrose and immediate C-section, rumen transfaunation w/ propylene glycol
o Prevention: ↑ energy intake in late gestation – 1 lb/head/day of good quality grain
- Urethral obstruction – calculi
o Most common locations: urethral process, distal sigmoid flexure
o Vocalizing, straining to urinate, kicking at abdomen, dribbling urine, forceful abdominal contractions, teeth
grinding, restlessness, hematuria, dysuria
o Tx: amputating urethral process; if still unable to urinate, do tube cystotomy
▪ Salvage procedure: bladder marsupialization, penectomy, perineal urethrostomy
- Infectious Footrot – Fusobacterium necrophorum & Dichelobacter nodosus
o VERY contagious in sheep; in cattle, also caused by A. pyogenes, Preyotella melaningenicus
o Lesion: interdigital space – lameness and pain, malodorous exudate, separation of horn of hoof
o Dichelobacter nodosus – need the microorganism + wet conditions
▪ Produces proteases – cause horny wall separation; Cytology = BARBELL shaped rods
o Tx: florfenicol SQ (esp. cattle), 10% zinc sulfate bath, remove from wet condition, regular foot trims
▪ CULL SHEEP – so contagious in sheep!
- Systemic Pasteurellosis
o Opportunistic pathogens = Pasteurella and Mannheimia (normal flora of upper resp and oral mucosa)
o Risk factors: stress, viral infection, extreme temps, overcrowding, transportation
o Clinical Signs: sudden death, listless, poor appetite, bilateral purulent nasal discharge, cough, fever
o Tx: oxytetracycline
▪ Others: ampicillin, penicillin, ceftiofur, florfenicol
- Oxalate Urinary Calculi
o Toxic plants = Halogeton, Rumex (dock), sugar beets, greasewood (Sarcobatus vermiculatus)
o If found in 1 male, whole herd at risk
- Ionophore Toxicity
o Lethargy, weakness, stiffness, dyspnea
o Mild tachypnea, tachyarrhythmia, no fever → cardiac muscle damage → congestive heart failure, DCM
- Pseudorabies
o Scratching violently, running aimlessly, no CN deficits
- Bunostomum spp.
o Hookworms: SMALL intestine
- Estrous Cycles
o Goats = 21 days
o Sheep = 17 days

BOVINE DISEASES – 15%

VIRAL DISEASES
- IBR – Infectious Bovine Rhinotracheitis – bovine herpesvirus type 1
o Latent in trigeminal ganglia – loud hacking cough, sneezing, fever, anorexia, open mouth breathing, mucopurulent
nasal discharge, chemosis
▪ UPPER respiratory signs w/ WHITE PLAQUES on conjunctiva/nasal epithelium
▪ Abortions – can kill fetus quickly, show signs of severe inflammation in fetus
- Bovine Papilloma Virus
o Papillomas throughout herd – best treatment is autogenous vaccine – isolate some warts from the herd
(commercial vaccines not effective)
o Common cause of fibropapullomas/wart on tip of penis
▪ Surgically remove – can resume breeding in 90 days
- Bovine Leukosis – lentivirus (aka bovine leukemia virus – BLV, leukosis virus)
o LYMPHOMA – lymphadenopathy, weight loss, ↓ production
▪ Retrobulbar lymphoma: rapid development of bilateral ocular bulging, and discharge
o Biopsy lymph node for Histopath (definitive), positive on ELISA for gp51 antigen (herd test standard)

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 - Bovine Respiratory Syncytial Virus (BRSV) – PARAMYXOVIRUS
o Rapid labored breathing, depression, salivation, nasal/ocular discharge, “honking” cough, tachypnea/dyspnea
o Lesions: pulmonary edema/emphysema - hear crackles throughout lung fields
o Treatment: supportive, antibiotics for 2˚ bacterial infections
- Bovine Viral Diarrhea (BVD) – flavivirus
o Maintained in herd via persistently infected carriers that were infected as fetuses
▪ Passed to fetus when non-immune dame is viremic w/ non-cytopathic BVD – Day 50-150 of gestation
▪ At this time, fetal immune system doesn’t recognize as foreign and becomes persistently infected
o Congenital Disorders: microphthalmia, cerebellar hypoplasia, hydrancephaly
▪ Cerebellar hypoplasia – hypermetria, hyperreflexia, nystagmus, strabismus, opisthotonos
▪ <125 days of gestation – early embryonic death, fetal death, abortion, congenital defects, mummification,
persistent infection
• Persistently infected: most likely w/ noncytopathic before 125 days
▪ Signs of persistent infection: asymptomatic, diarrhea, fever, pneumonia, oral ulceration, abortion,
stillbirths, congenital anomalies
▪ BB’s: Bovine Brain = BVD, Bluetongue
o Thrombocytopenia: BVD adheres to thrombocytes – then removed by RE system
▪ Hemorrhage – when platelets get low enough, hemorrhage from scleral vessels
▪ Dx: thrombocyte count (i.e. 5000) – give blood transfusion w/ fresh whole blood
o Mucosal Disease: chronic and severe BVD
▪ Calf, persistently infected w/ noncytopathic BVD, superinfected w/ cytopathic BVD (rearrangement of
parent non-cytopathic viral RNA)
▪ Diarrhea, acute death, oral ulcerations (on dental pad), occasional corneal opacity
▪ Lesions: severe ulcers in GI tract (ileum, esophagus), dental pad erosions
- Pseudocowpox – parapox virus
o 3 related parapox viruses (ALL ZOONOTIC) – pseudocowpox, contagious ecthyma, bovine papular stomatitis
o Proliferative teat lesions – DDx are pseudocowpox, vesicular stomatitis, bluetongue
- Bovine Papular Stomatitis – parapox virus
o Fever, small raised lesions in mouth around gums/on dental pad
▪ DDx for oral ulceration – vesicular stomatitis, BVD, BPS, FMD
o Usually MILD – “calfhood” disease – if immunosuppressed, can be fatal, but should recover in 3 weeks
o Isolate calf, rule out BVD (BPS has raised lesions, lack of other oral lesions, lack of GI signs)
- Bovine Winter Dysentery – suspect coronavirus
o Explosive outbreak of watery diarrhea, clotted dark blood – in stabled animals in all stages of winter
BACTERIAL DISEASES
- Actinomyces bovis – LUMPY JAW (G+)
o Normal inhabitant of mouth/rumen – can infect injured soft tissued from rough feeds
o ↓ milk production, weight loss, hard non-painful swelling on mandible (productive + destructive lesion)
▪ Rads: show lysis + productive bone lesions w/ distorted teeth in the area
o Sodium iodide (arrests lesions), IV iodine (not recommended due to food safety), usually CULL
- Actinobacillus lignieresii – WOODY TONGUE (G-)
o Normal inhabitant of mouth/rumen - can infect injured soft tissued from rough feeds
▪ Causes granulomatous inflammation of tongue
o Large firm tongue (nodular, painful), ↓ appetite, excessive salivation, weight loss
o Tx: change feed, IV Na iodide and tetracycline
- Fusobacterium necrophorum
o CALF DIPHTHERIA (3-18 months old)
o Will die in a week if not treated – resp distress, moist/painful cough, loud inspiratory stridor, extended head/neck,
swelling around larynx, ozena (wasting away of bony ridges of nose), fever, episcleral injection
▪ Elicit cough on palpation of larynx – also elicit pain and ↑ stridor
▪ Putrid breath, severe inspiratory dyspnea

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 - Salmonellosis
o Salmonella typhimurium
▪ Fever, diarrhea, scleral injection, foul-smelling diarrhea (septic tank odor), watery green diarrhea, ↓
rumen contractions, septicemia, pneumonia, meningitis, death
▪ Pseudo-diphtheritic membrane of intestines
• Foul smell indicates serum proteins in feces, absorbed endotoxins (LPS) cause other clinical signs
▪ Tx: CEFTIOFUR – good against salmonella (unless been used a lot on that dairy)
▪ ZOONOTIC – enteric salmonellosis
o Salmonella Dublin
▪ Carrier cow transmits to neonates at birth/via milk
▪ SEPTICEMIA in dairy calves 4-9 weeks old – ↓ appetite, fever, rapid breathing, death
▪ Histopath: serosal/SQ petechial hemorrhages, heavy wet lungs
▪ CULL carriers, vaccinate calves
- Mycoplasma bovis
o Transmission: MILK
o Respiratory signs (cough, tachypnea, nasal discharge), lameness (swollen joints, tenosynovitis), fever
▪ Otitis media-interna – head tilt, ear droop, unilateral eye ptosis, usually recent resp infection
• DDx for these signs: listeriosis, TEME (thromboembolic meningitis)
o Necropsy: lungs w/ multiple abscesses full of pus/caseous material
o Culture: Hayflick’s agar (microaerophilic environment)
o Tx: tulathromycin (tetracycline, tilmicosin) – approved for M. bovis resp disease (Mycoplasma doesn’t have cell
wall – penicillin/cephalosporin not good choice)
- Campylobacteriosis – Campylobacter fetus ssp veneralis
o Obligate parasite of bovine genital tract – ABORTION, temporary infertility, early embryonic death
ENDOCRINOLOGY/ELECTROLYTE ABNORMALITIES
- Milk Fever – HYPOCALCEMIA in periparturient cows
o Down, recently started lactating, fed TMR, barely responsive, unable to maintain sternal recumbency, tachycardia,
weak HR, no rumen motility, low temp, urine lochia red and mucoid, neck in “S” shaped curve
o Skeletal/cardiac/smooth muscle weakness causes signs – give IV calcium to correct
▪ May cause heart to beat more slowly/strongly – can lead to sinus node arrest – be careful!
o Prevention: DCAD (dietary anion-cation difference) – makes cow more acidic
▪ Enhances PTH, ↓ milk fever incidence, cows absorb Ca more readily
▪ Monitor by checking urine pH (should be acidic – 6.2-6.8) to make sure cows are eating the diet
▪ DCAD = (Na + K) – (Cl – S) – has more anionic salts (Cl, S) and ↓ cations (Na, K)
• Start diet 2-3 weeks prior to calving
o Tx: Calcium gluconate – is a CARDIOTOXIN – expect a tachycardia that slows to bradycardia + strong pulses
- Grass Tetany – HYPOMAGNESEMIA
o Lush pastures ↑ K/nitrogen, ↓ Mg/Na
o Severe beef cattle found dead on pasture, some staggering, down on side, legs paddling, ↑ HR, fever, eyelid
fluttering, nystagmus, jaw champing
- Postparturient hemoglobinuria – HYPOPHOSPHATEMIA
o ↓ erythrocytes ATP which is needed to maintain ATP-dependent membrane pumps – cells lyse
o Lactating cows – pale, icteric, hemoglobinuria – in 1st lactational month
o NO methemoglobinemia or Heinz bodies; Phosphorus <2 mg/dL = hemolysis
GASTROENTEROLOGY
- Calf Diarrhea
o Big 5
▪ Salmonella – 1-7 days old → Yellow-white feces
▪ Coronavirus – 7-10 days old → Watery yellow feces
▪ Rotavirus – 1-6 days old → Watery brown-green feces, blood and mucus
▪ Cryptosporidia – 1-4 weeks old → Watery brown-green feces, blood and mucus
▪ E. coli – 1-10 days old → Yellow-white feces, no straining
o Diarrhea: causes dehydration, hypovolemia, weak, unable to stand, ↑ HR, floppy calf w/ metabolic acidosis
▪ Require Na containing IV fluids + Na bicarb (alkali)

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 ▪ Hypovolemia, severe metabolic acidosis, hyperkalemia, possible sepsis
• Sepsis: bacterial translocation across gut
• Metabolic acidosis causes K to leave cells, causes hyperkalemia
- Abomasal Ulcer – Type 2 are bleeding ulcers
o Melena, anemia, collapse, weak, ↑ HR/RR, heart pounds loudly, pale MM
o Tx: blood transfusion (4-8L fresh whole blood), omeprazole (H2 blocker), ranitidine (↑ abomasal pH), NO NSAIDS –
will promote ulceration & ↓ GI blood flow
- Abomasal Volvulus/Torsion – LESS common than LDA/RDA
o Recently started lactation (freshened), ↓ milk production, anorexia, teeth grinding, episcleral injection, colic
o R flank distension, wide region of R-sided monotone pinging from 9th-13th rib, no rumen contractions
o SOMETIME can palpate (turgid structure to R of midline), fluid on ballottement
o Bloodwork: ↓ Cl, ↓ K, metabolic acidosis
▪ HCl sequestered in abomasum (hypochloremia), become dehydrated to maintain adequate BP by
conserving Na, in the process retain bicarb (alkalosis) which causes H exchange for K – H exits cell to
establish normal pH (hypokalemia)
▪ PARADOXICAL ACIDURIA – ↓ K + need to retain Na due to hypovolemia, kidneys exchange H ions for Na
anions (instead of K) – H excreted in urine
o SURGICAL EMERGENCY – correct before cow goes into shock! – IV saline (NaCl) + K (no more than 0.5mEq/kg/hr)
▪ NO ORAL FLUIDS – will add to fluid filled rumen!
- Left Displaced Abomasum
o Gas filled abomasum moved from normal position (ventral midline) to L of rumen – gets trapped
o Common in 1st 4 weeks postpartum – ↑ metabolic demands for lactation, diet changes drastically, more gas
produced in abomasum
▪ Postpartum hypocalcemia – predisposes to ↓ abomasal motility, may contribute to displacement
o Prominent ping w/ VARIABLE pitch on L side btw 10th-13th rib
o Recently started lactation (freshened), ↓ production, ↓ appetite, normal TPR, gaunt abdomen, scant but normal
feces
o Surgery can be done from either side
- Right Displaced Abomasum
o Much less common than LDA – clinical signs more systemic/distressed – episcleral injection, ↑ HR
- Intussusception
o Colic, scant dark feces (blackberry jam – as bowel mucosa necroses), teeth grinding, restlessness, kicking at
abdomen, no rumen motility, dilated small bowel proximal to lesion, distended abdomen (backed up GI tract)
▪ Fever is leakage occurs – peritonitis!
o Sausage shaped mass palpable per rectum – hard painful mass on R (most common = ileum)
o Hypochloremic, hypokalemic, metabolic acidosis – Cl sequestered in abomasum
o Tx: R flank surgery – remove intussusception, anastomose intestines
- Cecal Dilatation with or w/o Cecal Torsion
o Little feces passed over 24 hours, colic, distended structure palpated just cranial to pelvis (like bread loaf)
o RIGHT sided ping heard from last rib to pelvis (high up)
o Treat w/ RIGHT flank surgery – remove gas/liquid from cecum, replace in normal position (blind end toward pelvis)
▪ Only amputate cecum if necrotic
- Gas in Spiral Colon
o COMMON in any sick cow w/ poor GI motility – 8 inch circular ping high on last rib/just behind
- Frothy Bloat
o LUSH LEGUME consumption – not due to vagal indigestion like free gas bloat is
o Resp distress (↑↑↑ abdominal pressure; pass stomach tube and little/no gas escapes, insert trochar into rumen,
froth escapes
o Tx: poloxalene orally (↓ surface tension, destabilizes froth)

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 - Vagal Indigestion
o Anorexia, ↓ milk production, ↑ temp/HR, no rumen motility, scant feces, PAPPLE shape
▪ “BOINK” hollow sound over left flank – btw ribs 9-13, extending to hip (gas-filled rumen)
▪ PAPPLE – i.e. from hardware disease – local peritonitis leads to poor forestomach motility, rumen fills w/
fluid and develops gas cap, abomasum accumulates fluid
• Pear on Right, Apple on Left
▪ Bradycardia = 25-40% of cows w/ vagal indigestion
o Type 1 = free gas bloat – FAILURE TO ERUCTATE
▪ Swollen mediastinal lymph nodes – signals that detect gas pressure and open the cardia are
compromised; eructation doesn’t occur
▪ Weight loss, enlarged LEFT flank (L abdomen gas filled), rumen has poor motility, bronchopneumonia
▪ Tx the pneumonia – create temporary rumen fistula to allow gas to escape until eructation occurs
o Type 2 = FAILURE OF OMASAL TRANSPORT
▪ Result: fluid filled rumen w/ some dorsal gas – lack of motility, inappetence, depression, ↓ production,
dehydration, variable xiphoid pain
▪ On ballottement: large fluid filled rumen, monotone ping on L side from 11 th ribs to hip, PAPPLE
▪ Hard to differentiate from pyloric outflow failure except is has more profound acid-base/electrolyte
disturbances and cow will appear much sicker
o Type 3 = FAILURE OF PYLORIC OUTFLOW
▪ Cows have internal vomiting and accumulate chloride in rumen – hypochloremic, hypokalemic metabolic
alkalosis – MUCH SICKER
• Result of intestines not being able to resorb chloride into bloodstream after secreted into
abomasum – chloride is strong anion, results in metabolic alkalosis when decreased
o Type 4 = ABOMASAL IMPACTION
▪ Not common in cows – more common in Suffolk sheep
- Bristle Grass Irritation – Sertaria lutescens (yellow bristle grass)
o Grass w/ sharp barbs that stick into mucosa of young cattle/horses – cause oral ulcers, reluctance to eat
o Tx: Remove from diet
MASTITIS
- Lactation – peak at 4-8 weeks postpartum, lasts 305 days, dries off for 60 days
o Oxytocin – responsible for milk letdown
o Prolactin – suckling stimulates this, responsible for all milk production
o Somatic Cell Count – desirable bulk tank levels: <200,000 cells/ml
o Bovine Somatotropin (BST) – approved to be given to promote milk production
- To Prevent:
o Fore strip each quarter, shut off vacuum before removing claw, post dip all teats (↓ CONTAGIOUS causes), pre-dip
all teats (↓ ENVIRONMENTAL causes), replace liner when needed, only milk 5-7 minutes (when they’re milked out)
- CONTAGIOUS MASTITIS
o Staph aureus, Strep agalactiae, Mycoplasma bovis – spread by milker’s hands/equipment
o Streptococcus agalactiae
▪ G+ obligate mammary gland pathogen – usually subclinical but may see ↑ SCC
▪ CAMP reaction – plate S. aureus and S. agalactiae and see them act together to lyse RBC (color clearing)
▪ Tx: intramammary infusion (ONLY organism that responds to this treatment)
o Mycoplasma bovis
▪ Sepsis, joint infections, resp disease, mastitis
• Spread to young calves via milk – ear infections (otitis media)
• Older cows – pneumonia, arthritis, tenosynovitis, mastitis, abortion
▪ Fibrosis of glandular tissue – dx by fibrosis + combo clinical signs
▪ CULL – poor response to tx, very contagious
- ENVIRONMENTAL MASTITIS
o Coliform mastitis (E. coli), Prototheca, Streptococcus, Klebsiella pneumoniae, Pseudomonas aeruginosa,
Enterobacter aeruginosa, Arcanobacterium pyogenes, Proteus

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 ▪ Coliform Mastitis – absorbed endotoxin (LPS) – causes systemic signs
• Cow recently freshened, down and unwilling to rise, scleral injection, empty rumen, poor motility
• Involving uterus on rectal exam – discharges brownish-red, mucoid, non-odorous lochia through
vagina
• Udder is swollen, hot, and painful – serum-like secretions w/ fibrin clumps in it
o Tx: frequent milking, anti-inflammatories, antibiotics, IV fluids
RESPIRATORY
- Shipping Fever (fibrinous pleuropneumonia) – Mannhemia hemolytica - COWS
o Sometimes caused by Haemophilus somnus, Pasteurella hemolytica, viruses, stress
o Depression, off feed, breathing hard, severe fever, ↑ RR/HR, scleral injection dyspnea, cough
▪ Auscultation: crackles, wheezes, pleural rubs (pleural effusion, septic pleuritis), harsh inspiratory and
expiratory sounds w/ expiratory wheezes
o OLDER (>8 months) animals w/ recent hx of being shipping/stressed
o Necropsy: fibrinopurulent bronchopneumonia
o Tx: NO STEROIDS, antibiotics (sulfadimethoxine, ceftiofur, procaine penicillin, tetracycline)
- Enzootic Pneumonia – Pasteurella multocida
o Loud cough, tachypnea, diarrhea, ill thrift for a few days – NO signs of sepsis, depression, anorexia
▪ Usually also have Eimeria bovis (coccidia) – causes diarrhea
▪ Crackles/wheezes, harsh bronchial tone cranioventrally (cranioventral consolidation)
o Common – CALVES 3-8 months old – economically devastating, slow weight gain
o MULTIFACTORIAL – poor housing/environment, many other factors involved (ammonia, CO2, hydrogen sulfide,
Mycoplasma, Corynebacterium, BVD, BRSV, PI3)
- Farmers Lungs – allergies
o Episodic signs – usually housed indoors, exposed to allergens – keeping animal outside will help
- Silo Filler’s Disease – bronchiolitis obliterans
o Animal housed close to silo – inhalation of toxic silo gases
- Pharyngeal Trauma
o Causes: paste/balling gun, foreign body (sticks/wires in feed) – penetrate pharynx
o Mild bloat, inappetence, extended head, drooling, swelling/pain in throat area, fever, coughing, reluctance to
palpate throat area, breath smells necrotic (w/o obvious lesions in mouth)
o Tx: antibiotics, NSAIDs, soft diet – good prognosis w/ conservative therapy
- Laryngeal Papillomatosis – papovirus
o Common in feedlot cattle – stertor, cough – no systemic signs
ORTHOPEDICS
- Lateral Rear Digit – bear most weight here – 80% of foot disease involves this
- Coxofemoral Luxation
o Cranial and dorsal displacement
o Usually cow is down after parturition, doesn’t respond to hypocalcemia therapy
o Dystocia or sciatic/obturator nerve paralysis increased risk of luxation
- Osteochondrosis Dessicans
o Most common site: HOCK (least common: elbow)
- Spread Eagle
o ADDUCTOR muscles injured (gracilis, pectineus, adductor magnus et brevis)
- Ruptured peroneus tertius – extend hock + flex stifle at same time
- Ruptured serratus ventralis – “flying scapula” if it ruptures
- Ruptured cruciate ligament – drawer movement in stifle (hard to do in cattle)
- Flexural Deformities of Distal Limb (in calves)
o Usually from contracted tendons – treat w/ deep digital flexor/superficial digital flexor tenectomy, splinting
▪ NOT external fixator! Still growing!
- Corns – lesion in interdigital area – makes cow lame
o Surgically remove mass w/ sedation – be careful not to invade interdigital fat pad
o Area is bandaged, claws temporarily wired together if necessary

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 - Solar Abscess
o Pare out abscess and drain it
o Apply wooden hoof block to keep in production while it resolves
▪ If lesion is lateral, place block medial
- Pododermatitis circumscripta – lesion at sole/bulb junction
o Usually weight bearing claws affected first (lateral hind digits, medial front digits)
- Septic Arthritis and Osteomyelitis
o Causes: foreign body/puncture wound, hematogenous spread, extension of cellulitis
o Destructive lesions in bone and joint of young animal – dx via culture
o Vigorously lavage/surgically open and flush – aggressive systemic antibiotics based on culture
- Spastic Paresis – Elso Heel
o Hereditary – stiff hocks – see signs at 3 weeks – 1 year
o Combo of genetics + environment – causes overstimulation of gamma motor neurons in spinal cord
o Calf w/ inability to walk, difficulty getting up, no signs of trauma, hocks wont flex due to continuous gastrocnemius
tension – signs progress over a month or two
o Tx: tibial neurectomy or gastrocnemius tenectomy
- Spondylosis
o Degenerative intervertebral joint space disease – OLDER BULLS
▪ Painful osteophytes (enesiophytes) develop across intervertebral space
MUSCULAR DISORDERS
- Periodic Spasticity
o Inherited – DAIRY breeds (rare in beef) – first appears at 3-7 years old, gradually worsens
o Marked muscle spasms of hip/upper leg muscles – episodic spasms/stiffness which can last for minutes
- Myotonia Congenital
o Inherited – disorder in skeletal muscle CHLORIDE channel – confirm via electromyography
o Non-progressive general rigidity, mainly occurs after tactile/auditory/visual stimulation
- Myophosphorylase Deficiency – Glycogen Storage Disorder
o Muscle enzyme – genetic disease in CHAROLAISE cattle
NUTRITIONAL DISORDERS
- Copper Deficiency
o 1˚ – low level of copper in feed
o 2˚ – interference w/ copper absorption due to molybdenum and sulfates
▪ Usually associated w/ low copper and high molybdenum (sagebrush in dry alkaline environment)
▪ Copper in feed should be at least 5x those of molybdenum
o Diarrhea, poor BCS, lameness, anemia, infertility, fever, diarrhea, resp disease nonresponsive to antibiotics
▪ ACROMOTRICHIA – no pigment in hair (around eyes = “spectacles”)
• Dilution of color due to tyrosinase dysfunction (converts L-tyrosine to melanin)
• Demyelination and pathologic fractures of vertebrae
▪ “Peat scours/Teart”
• Severe scours (diarrhea) w/ gas bubbles
o Definitive Dx – LIVER BIOPSY – liver stores have to be depleted before serum copper drops
o Tx: copper supplements (copper oxide orally in molasses or salt), give copper by injection
- Vit C Deficiency – VERY RARE in ruminants – may cause crusting/alopecia/pruritis
- Vit D Deficiency – RICKETS, bone abnormalities
- Vit A Deficiency
o Common in FEEDLOT animals – no access to Vit A rick green plants
o Convulsions/blindness common – stargazing, diarrhea, anisocoria, strabismus
▪ PLR – ABSENT in both eyes – retinal degeneration and CN II constriction
▪ DDx – Polioencephalomalacia, lead poisoning, salt poisoning – but PLRs intact w/ these
- Selenium Deficiency/Vit E Deficiency
o WHITE MUSCLE DISEASE (nutritional myopathy)
o Vit E Deficiency – milk replacers w/ linseed oil, soybean oil, fish oil, corn oil – these are high in polyunsaturated fats
– need to ↑ Vit E to scavenge the resulting free radials

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 o Selenium – needed for glutathione peroxidase which breaks down hydrogen peroxide and lipoperoxide to water
and harmless alcohols (free radical protection)
▪ WMD – excess free radicals – cause intracellular membrane damage – lets excess Ca into cell which
causes ↑ mitochondrial Ca and mitochondrial damage – causes hyper-concentration of muscles and
eventual necrosis/hyalinization
o 2 Forms
▪ Cardiac (acute death), skeletal (show clinical signs)
▪ Severely weak, trouble breathing, frothy nasal discharge, trouble rising, swollen painful muscles
o Necropsy: pale dry skeletal muscle, white streaks running through muscle bundles
o Dx: measure glutathione peroxidase (will be low), ↑ AST/LDH/CK (NOT SDH – others released w/ muscle damage)
- Alpha-mannosidosis
o Genetic defect of enzyme alpha mannosidase
o Breeds: Murray gray, Simmental, Holstein, Galloway, Angus
o Without enzyme alpha mannosidase, cleavage btw N-acetyl glucosamine and mannose will not occur;
oligosaccharide will accumulate in lysosomes of neurons/reticuloendothelial cells/macrophages
o 1st signs at 1-15 months – mild ataxia of pelvic limbs after exercise – lead to hypermetria, aggressiveness, intention
head tremors – eventual diarrhea, recumbency, death
MISCELLANEOUS BOVINE DISEASES
- Mad Cow Disease – Bovine Spongiform Encephalopathy (BSE) – PRION
o Dogs are only species not known to have TSE – cats/sheep/humans/cows all have one
o Neuro signs, hypermetria, ataxia, hyperexcitability, hyperesthesia
o ZOONOTIC – Creutzfeldt-Jakob Disease
▪ Humans have psychiatric symptoms, depression, schizophrenia – neuro signs progress to difficulty
walking, involuntary movements → immobile/mute → death
• Variant Creutzfeldt-Jakob disease – affects young people, linked to exposure to infected meat
- Maple Syrup Urine Disease – Encephalopathy
o Genetic – causes spongiform changes in brain
o Breeds: Hereford, polled Shorthorn calves (2-3 days old)
o Deficiency in branched chain ketoacid decarboxylase
▪ Accumulation of isoleucine, leucine, valine – excreted in urine → BURNT MAPLE URINE SMELL
- Traumatic Reticulopericarditis – HARDWARE DISEASE
o ↓ milk production, fever, ↑ HR, brisket edema, enlarged/distended jugular vein, muffled heart sounds w/
occasional “washing machine” sounds, poor appetite, stiff walk, arched back
o Metallic foreign body (wire, nail) pierces reticulum then pericardium → lots of pericardial fluid and constrictive
heart disease/heart failure
o Dx: clinical signs, scooch/xiphoid test (push down on withers – will grunt in pain)
▪ Palpable linear mass caudal to last rib – enlarged liver from chronic passive congestion
▪ Distended jugular veins
▪ SQ Brisket edema
o Tx: magnet, antibiotics, confinement, surgery if necessary
o Prevention: give all cows a magnet, keep them away from wite
▪ Poor prognosis
- Uroabdomen – usually from urolith
o Not eating well, normal HR/RR, ventral abdominal edema, breath smells like ammonia
o Hyponatremia, hypochloremia, hyperphosphatemia – azotemia and possibly hyperkalemia
- Pyelonephritis – E. coli (and other coliforms), Corynebacterium renale
o Cease lactation, anorexia, ↑ HR/RR, arched back due to pain
o Enlarged painful kidney on rectal, cloudy/bloody urine
- Pinkeye – IBK – Infectious Bovine Keratoconjunctivitis – MORAXELLA BOVIS
o Causes: Mucosa autumnalis (face fly), Moraxella bovis, UV light
o Blepharospasm, chemosis, photophobia, very painful – ↓ production
o Central ulcer in eye – usually resolves in few weeks, may see descemetocele/corneal perforation

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- Fatty Liver Syndrome – HEPATIC LIPIDOSIS
o Usually seen in fat cows – when have negative energy balance (i.e. postpartum when energy needs ↑ for
lactation), they mobilize fat stores in such a way that the liver cannot keep up w/ triglycerides coming in
o Necropsy: enlarged liver, diffusely light yellow color, easily friable, floats in formalin (↓ density of lipid vacuoles)
▪ DDx – lymphoma (but lymphoma liver wont float)
- Lipofuscinosis – storage disease gives liver a dark appearance
- Failure of Passive Transfer
o SEPSIS – in day old calves – ↓ appetite, fever, ↑ HR, scleral injection, cloudy material in anterior chamber
(hypopyon)
o Dx: measure IgG (LOW), protein refractometry (<4.5 g/dL is consistent w/ failure)
o Tx:
▪ <3 days = colostrum
▪ >3 days = transfuse w/ 1-2 L of plasma + antibiotics (after day 3, poor absorption of immunoglobulins
• IgG predominates in bovine colostrum
- Freemartin
o Fusion of fetal membranes btw male and female set of beef cow twins
o Results from exposure of female to Mullerian inhibiting hormone which is being secreted by the male
▪ Exposure via anastomosis btw chorioallantoic vessels
o Usually >90% of cases are Freemartin when it happens
o Clinical Signs: abnormally small ano-genital distance, enlarged clitoris
- Trichomoniasis – Trichomonas foetus
o Usually asymptomatic; in females, causes pyometra post-coital, poor calving percentage, early embryonic death
▪ Usually pyometra is postpartum so if post-coital, consider this + look for reservoir bull
o Maintained by MATURE BULL – ↑ depth of epithelial crypts of bull’s glans penis/prepuce – ↑ niche for organisms
to thrive
▪ Young bulls can usually clear it bc they have SHALLOW crypts
- Uterine Torsion
o If clockwise, push forward on vagina and roll clockwise
- Infectious Pustular Vulvovaginitis – herpesvirus – white plaques on vagina
- Causes of Abortion
o Infectious:
▪ Akbane virus
▪ BVD
▪ IBR (rapid fetal death, focal necrosis of organs)
▪ Brucella abortus (fetal inflammation, placentitis) – eradicated from US – REPORTABLE
▪ Leptospirosis Pomona
o Twinning: see twins on necropsy (about 8 months gestational age), no gross/histopathologic lesions on any organs
- Endometritis
o Ascending infection, usually Arcanobacter pyogenes (also P. multocida, Pseudomonas aeruoginosa, E. coli)
o Normal vitals, normal appetite, normal milk production – mucus and pus running from vulva
o Tx: intrauterine penicillin/tetracycline; povidone iodine + lavage w/ saline if don’t want antibiotic residues in milk
- Dystocia
o Most common cause = fetopelvic disproportion – fetus is too large to pass through maternal pelvic canal
o Significant cause of calf loss, esp. in 1st time heifers
o Standing C-section: paravertebral nerve block (local anesthesia to the flank – flank laparotomy)
o How to check fetal viability:
▪ Gently poke an eye → initial withdrawal reflex (retained the longest)
▪ Palpation of umbilical pulse, stimulation of suckle reflex, pinch a limb to initiate withdrawal, palpate chest
for heartbeat/use ultrasound to check for heartbeat

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 EQUINE DISEASES – 16%
BREED DISPOSITIONS
- Sarcoid: QH
- Melanoma: grey horse
- Cerebellar abiotrophy: Arabian, Oldenburg, Gotland
- Ruptured prepubic tendon: obese draft mares in late pregnancy
- Enteroliths: Arabians
- Hyperkalemic periodic paralysis: QH, Paint, Appaloosa
- Severe combined immunodeficiency (SCID): Arabians
- Exercise induced pulmonary hemorrhage: TB
- Equine recurrent uveitis (Equine Night Blindness): Appaloosa
- Dandy-Walker Syndrome: Arabians, TB
- Small colon impactions: Miniature horse
- Lethal white syndrome: Arabians
VIRAL DISEASES
- Equine Infectious Anemia (EIA) – retrovirus
o Transmission: Tabanidae flies
o Clinical signs: ABORTION, anemia, weight loss, intermittent fever, pale MM
Dx: normocytic normochromic anemia (don’t see other kinds in horses)
▪ COOMB’S TEST – agar immunodiffusion – detect serum antibodies against retrovirus
• Good for chronic, not enough antibodies in acute
• False positives: antibodies from colostrum
• Always confirm ELISA w/ Coggin’s test
▪ COGGINS TEST
o Cause IMHA – don’t treat w/ corticosteroids!! Cause redundance of viremia and worsen the anemia
o Tx: isolation and supportive care
- Equine Herpesvirus 1 (EHV-1) – resp disease in FOALS, abortion in MARES
o Transmission: AEROSOL – rapid spread, also from aborted fetuses/placenta
o Resp Disease in Foals: copious nasal discharge, occasional death from pneumonia
o Abortion: most common INFECTIOUS cause of abortion
▪ Classic Presentation: foals get resp signs several months before abortion storm
▪ Abortion: 7-11 months – LATE TERM ABORTION
• No gross lesions of the fetus or placenta
▪ Do no acquire immunity!! Can be reinfected! → VACCINATE @ 5, 7, 9 months – ↓ risk of abortion
o Myeloencephalitis – rare – causes neuro disease, CNS signs
- Equine Herpesvirus 3 (EHV-3) – COITAL EXANTHEMA
o BALANOPOSTHITIS – papules, pustules, ulcers to vestibular mucosa, vulvar skin, penis, and prepuce
o Tx: not required – spontaneous recovery in 2 weeks after infection
o Transmission: venereal – sexual rest to prevent transmission; can breed once lesions clear
- Equine Viral Arteritis (EVA) – togavirus
o Transmission: venereal – carrier stallion infect mares, also aerosolized
o More mild resp signs than herpes, abortion during various stages of pregnancy (no lag time btw sick mare and
abortion)
▪ Vasculitis leading to edema, conjunctivitis, rhinitis, abortion – edema, oculonasal discharge, petechiae
▪ Foals: severe resp distress, leukopenia, thrombocytopenia, death after 12-24 hours
o VACCINATE – immunity for 1-3 years – can't be differentiated from infected on serology (antibody)
- Equine Adenovirus – UPPER RESPIRATORY TRACT
o Lower resp infection in immunocompromised animal – esp. foals with failure of passive transfer or combined
immunodeficiency
▪ Most common cause of death in foals w/ either condition → FATAL PNEUMONIA

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 - Equine Influenza - ORTHOMYXOVIRUS
o Transmission – AEROSOL – highly contagious
o Rapidly spreading infection w/ high fever and cough
o Dx: nasopharyngeal swab for virus isolation – could dx w/ serology but need paired titers to get dx
BACTERIAL DISEASES
- Endotoxemia
o Fever/hypothermia, leukopenia, tachycardia, obtundation, change in gut motility
o BACTERIAL LIPOPOLYSACCHARIDE – G- bacteria have LPS – monocyte/macrophage receptor reacts to G- LPS to
signal overzealous cascade of physiologic reactions
o Tx: polymyxin B – binds endotoxins at low doses
- Brucella abortus – FISTULOUS WITHERS & POLL EVIL
o Fistulous Withers – open draining lesions over supraspinous bursa btw 2nd-5th thoracic vertebrae
▪ Pain, heat, swelling in this region → eventually ruptures and drains (flush fistula, give antibiotics)
o Poll Evil – inflammation of bursa adjacent to nuchal ligament
- Streptococcus equi ssp equi – STRANGLES (1-5 years old)
o Mandibular/retropharyngeal lymph node abscessation – dx via bacterial culture
o Tx: ISOLATE – highly contagious!!! Lance abscess ventrally, DO NOT GIVE ANTIBIOTICS (prolongs disease, may lead
to internal/bastard strangles that REQUIRES antibiotics)
o Prevention: strangles vaccine – intranasal (IM vaccine caused soft tissue reactions)
o Complications – purpura hemorrhagica/guttural pouch empyema
▪ Purpura Hemorrhagica – Type 3 Hypersensitivity results in immune complex deposition in blood vessel
walls → vasculitis → urticaria, edema in extremities, petechiae and ecchymoses on MM, stiff gait
• Anemia, ↑ TP, ↑ fibrinogen, ↑ globulins, ↑ neutrophils
▪ Guttural Pouch Empyema – purulent material in guttural pouch – chronic nasal discharge, dysphagia,
leukocytosis, swollen/tender throat latch area, food reflux from nose (pharyngeal paresis from damage to
CN 9 and 12)
• Rads: fluid lines in guttural pouches; may need to daily catheterize and lavage pouches (saline),
in inspissated, may need surgical drainage
• CN 7, 9, 10, 11, 12, sympathetic trunk, internal carotid – cross medial pouch
• External carotid – crosses lateral pouch
- Streptococcus equi ssp zooepidemicus
o Most common cause of infertility in US – NOT ABORTION
▪ Most common cause of bacterial endometritis
▪ Also most common cause of Equine Pleuropneumonia (aka equine “Shipping Fever”)
• In cows, Shipping Fever = Mannheimia hemolytica
o Common inhabitant of external genitalia of mares/stallions – opportunistic (immunosuppression, pneumovagina,
damage to endometrium)
o Tx: penicillin
- Taylorella equingenitalis – CONTAGIOUS EQUINE METRITIS
o Rare in US (thought to be eradicated) – NEVER BREED if had previous infection
o No clinically apparent disease – causes infertility
- Rhodococcus (Corynebacterium) equi – FOAL PNEUMONIA (2-6 months)
o BUT – most common cause of foal pneumonia = STREP
o Cough, fever, wheezes, abdominal tucking on inspiration, weight loss, tachypnea, rarely diarrhea
o Dx: transtracheal wash – G+ pleomorphic rods – CHINESE LETTERS
o Rads: abscess in lungs (caudodorsal)
o Tx: erythromycin/azithromycin/clarithromycin (macrolides) (4x/day) & rifampin – tx for 2 months, base on clinical
signs/rads/bloodwork
▪ Newer antibiotics: clarithromycin – 2x/day
- Lawsonia intracellularis
o VERY common in PIGS – also WEANLING horses
o Thick small intestines → hypoproteinemia = ventral edema
o Lethargy, intermittent diarrhea, weight loss

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 - Corynebacterium pseudotuberculosis – PIGEON FEVER
o Ulcerative lymphangitis of limbs, abscess in pectoral region – possible internal abscesses too
o Dx: hemagglutination inhibition test (aka synergistic hemagglutination inhibition test, SHIT)
▪ Shows INTERNAL abscesses – leukocytosis, hyperfibrinogenemia, hyperglobulinemia
o Tx: hot packing, draining abscesses
▪ Antibiotic PROLONG disease – delay abscess formation – only use if horse has systemic signs
- Salmonella typhimurium
o Several different presentations: subclinical, self-limiting diarrhea, acute diarrhea + endotoxemia
o CECUM and proximal COLON – acute onset lethargy, anorexia, explosive watery diarrhea
o Dx: serial cultures of feces for 3-5 days
DERMATOLOGY
- Pemphigus foliaceus
o Autoimmune disease – antibodies against intracellular adhesion proteins
o Result: vesicles, erosions, ulcerations – esp. @ mucocutaneous junctions – crusting on head/limbs/ventrum
o Biopsy of skin = acantholytic cells
o Tx: immunosuppressives (corticosteroids) – juvenile form may have spontaneous regression (good prognosis),
adult form has worse prognosis
- Proud Flesh
o Benign proliferation of exuberant granulation tissue (at PREVIOUS WOUND SITE)
o Etiology = unknown – something to do w/ inhibition of epithelialization
o Tx: excision, skin grafts, irradiation
- Urticaria - HIVES
o Allergies – toxin, plant, insect bite, meds, chemicals, heat, sunlight, stress, abnormal genetics
o Localized edema in dermis – acute cutaneous lesions, restless after coming in from pasture
▪ Elevated, flat-topped, range in size from 2-8cm, scattered multifocally
o Tx: dexamethasone, diphenhydramine (NOT IV – can cause urticaria if given IV)
- Eosinophilic Granuloma – NODULAR NECROBIOSIS OF COLLAGEN / COLLAGENOLYTIC GRANULOMA
o Insect bites, trauma, multifactorial – see nodular mass lesion on lateral neck (no ulceration/pruritis)
o Biopsy: collagen degeneration and granulomatous inflammation w/ eosinophils
o Tx: sublesional steroid injection, surgical excision, systemic antibiotics
CLINICAL PATHOLOGY
- To determine if horse has regenerative or non-regenerative anemia – BONE MARROW ASPIRATE
o No retics in circulation – must look at bone marrow (too invasive to routinely do)
o If regen: hypercellular bone marrow w/ ↓ myeloid/erythroid ratio (<0.5)
o ALWAYS – normocytic, normochromic anemia
- Neutrophils
o Blue aggregates in many neutrophils = SEPSIS; Dohle bodies = toxic change (retained aggregates of round
endoplasmic reticulum)
o Cytoplasmic basophilia, vacuolation, toxic granulation – often seen in septic foals
- Severe Combined Immunodeficiency (SCID) – ARABIANS
o Some Arabian foals are homozygous for SCID gene – now there’s a genetic test for this
o Appear normal at birth, then develop fatal infections – often from unusual organisms (Pneumocystis carnii)
- Failure of Passive Transfer (FPT)
o Foals lack antibodies when born – must ingest maternal antibodies from colostrum (IgG)
▪ Weakness, rapid breathing, fever
o Dx: normal (adequate) >800 mg/dL
▪ ELISA (SNAP) test – rapid detection (takes 5 minutes)
▪ Measure TP (refractometer) – very insensitive but better than nothing
▪ Zinc sulfate turbidity test
▪ RID (radioimmunodiffusion) – most accurate but takes 24 hours to perform
- Neonatal Isoerythrolysis – Aa and Qa (involved antigens)
o Stallions positive for one of these antigens, mare is negative – foal inherits either Qa or Aa from stallion – when
mare is exposed to foal RBC, she makes antibodies against it – which are passed to foal via colostrum → acute
hemolysis occurs

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 o 0-4 day old foals – in utero, foal is protected by placenta; born to multiparous mare
▪ Weak, depressed, ↓ appetites, tachycardia, icterus, anemia, hemolysis, bilirubinemia
▪ Multiparous mares: 1st time, she wont produce sufficient antibodies to cause severe damage to the foal
▪ Mares that got blood transfusion - exposed them to RBC antigens
- Granulocytic Ehrlichiosis – Ehrlichia equi
o NEUTROPHILS and eosinophils – look like intracytoplasmic inclusion bodies, aggregates of purple dots (dots =
morulae)
o Depression, limb edema, petechiation, icterus, ataxia – MILD disease
o Dx: BLOOD SMEAR
- Potomac Horse Fever – Ehrlichia risticii (aka Neorickettsia risticii)
o Transmission: trematodes! (intermediate host = freshwater snails)
o MONOCYTES (macrophages) – obligate intracellular organism – leukopenia, monocytosis
o Anorexia, high fever, lethargy, ileus, colic, watery diarrhea, laminitis
o Dx: NOT blood smear (can't find often) – need paired serum titers (based on 4x ↑ in paired IFA titers or in ↓ titer
btw acute and convalescent samples)
o Tx: TETRACYCLINE – intracellular/rickettsial organisms → rapid response in 24-48 hours
▪ Oxytetracycline = drug of choice – 7-10 days
- Hemochromatosis
o Iron storage disease – hemosiderin deposited excessively in hepatocytes
o Clinical Signs: liver disease (anorexia, weight loss, lethargy)
o Tx: unrewarding
ONCOLOGY
- Seminoma – common TESTICULAR tumor
o Unilaterally enlarged testicle – firm and fibrous – locally invasive, ↓ sperm production
- Granulosa-theca Cell Tumor – common OVARIAN tumor
o Unilateral benign tumors – secrete steroids to prevent cycling (suppress gonadotropins)
o Cause aggression in mares – ↑ testosterone
▪ DDx for aggression = hypothyroidism
- Sarcoids – QUARTER HORSES
o One of most common skin tumors in horses – NON-MALIGNANT, NON-METASTATIC
o Locally aggressive fibroblastic tumor – dermis + subcutis – variable proliferative epithelial component
o Etiology – Bovine Papillomavirus?
o Transmission: direct contact, fomites, arthropod vector
o Types
▪ Flat – slow-growing, can be confused w/ flat warts
▪ Verrucous – warty, look like SCC or papilloma
▪ Fibroblastic – looks like granulation tissue/proud flesh, grows rapidly
o Tx: small lesions = benign neglect (but they don’t regress); bigger lesions = surgical excision (but usually recur even
w/ cryosurgery + radiation therapy)
- Melanoma
o GREY HORSES – seen a lot in Arabians/Percherons due to coat color)
o Common site: perineum, tail base – darkly pigmented, slow growing, locally invasive
o Usually benign w/ various degrees of invasion – have potential to turn malignant
o Tx: surgery/cryosurgery, benign neglect, chemotherapy (systemic, intralesional), immunotherapy (depends on
location/size)
o Prognosis: predisposed to developing others in future
- Mast Cell Tumor
o Often in dermis/subcutis – head/legs – may also invade underlying muscles, often walled off by aggregates of
fibrous stroma
o Excision usually CURATIVE – good prognosis, tumors are benign

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ENDOCRINOLOGY
- Cushing’s/Pars Pituitary Intermedia Dysfunction (PPID)
o PITUITARY TUMOR – pituitary adenoma of pars intermedia – secretes ATCH
o Older horses – avg. age = 20 years
o Stress leukogram (neutrophilia, lymphopenia) from cortisol, hyperglycemia (cortisol has counter-insulin effect), ↓
USG (PUPD), NOT ↑ ALP (only dogs have corticosteroid isoenzyme of ALP)
o Abnormal coat (shaggy appearance), weight loss, pot belly, abnormal sweating
- Equine Metabolic Syndrome
o Gross/severe regional obesity, clinical/subclinical laminitis
o Insulin resistant, often have ↑ insulin levels in blood
o Dx: fasting resting insulin
- Hypothyroidism
o Causes: iodine deficiency (thyroid needs iodine!), iodine excess (damages it – Wolff Chaikoff effect) – can be from
mare or foal’s diet → NOT from pituitary adenoma
o Life threatening in foals, can cause abnormalities (Physeal dysgenesis, incoordination, limb deformities, tendon
ruptures, still births, weakness, death
OPHTHALMOLOGY
- Auriculopalpebral Nerve Block
o CN VII (facial) – disrupts motor to orbicularis oculi (muscle that closes eye)
▪ Very strong in horses – can prevent thorough ocular exam
▪ Lidocaine injection SQ at caudal aspect of zygomatic arch where nerve is palpable
- Infected Corneal Ulcers
o Melting appearance – deepening into corneal stroma from infection
o Dx: cytology – G- rods (Pseudomonas – most common cause of bacterial keratitis)
o Tx: topical (NOT systemic) tobramycin (aminoglycoside) – effective against G-
▪ If G+ (likely Staph) – use Cefazolin topically
- Equine Recurrent Uveitis – APPALOOSA (periodic ophthalmia, recurrent iridocyclitis, moon blindness)
o MOST COMMON CAUSE OF CATARACTS/BLINDNESS
o Cause: infection – Onchocerca, Leptospira, Borrelia, Toxoplasma; immune mediated
o Recurrent bouts of ocular redness, tearing, photophobia, cloudy cornea (“blue-eye”) for years
▪ Recurrent uveitis → cataracts, lens luxation, glaucoma, eventual blindness (damage to optic nerve – can
see pigmented remnants on iris/lens capsule)
o Tx: AGGRESSIVE topical/systemic anti-inflammatories, topical atropine (prevent synechia/ciliary spasm), antibiotics
only if horse is febrile/infectious cause is identified
- Equine Night Blindness – APPALOOSA
o Congenital disease – bilateral, non-progressive, variable degree of ↓ vision on the dark
- Fungal Keratitis
o Tx: topical ocular meds (itraconazole drops) q2 hours; if hard to manage, place subpalpebral lavage system –
allows continuous drop of topical meds without having to handle the horse
- Eyelid Laceration
o Tx: saline lavage (minimal wound debridement), phenylbutazone, 2+ layer closure (make sure edges are opposed,
tetanus toxoid immunization
ORTHOPEDICS
- NERVE BLOCKS
o Palmar Digital – blocks palmar aspect of foot
o Low 4 Point – palmar metacarpal block – blocks foot, pastern, fetlock
o High 4 Point – subcarpal block – blocks leg distal to carpus/tarsus (metacarpals and distal)
o Abaxial Sesamoid – good for problems at pastern joint (proximal interphalangeal joint)
▪ Blocks foot and proximal interphalangeal (pastern) joint
o Suspensory Ligament – blocks deep branch of lateral palmar nerve at level of carpometacarpal joint

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- Laminitis
o P3 rotates w/ inflammation and degeneration of lamina
o Predisposing Factors: systemic disease (i.e. endometritis, salmonellosis), high carb diet, excessive weight bearing
on single limb, corticosteroids
o Dx: palmar digital block, change in P3 angle on rads
o Tx: PHENYLBUTAZONE (α agonist – promotes vasodilation and restoration of blood flow to digits), also
acepromazine, isoxsuprine, hydrochloride, DMSO, heparin, nitroglycerin
▪ NO STERIODS – can induce laminitis!
▪ Deep, soft bedding – more protective to the feet
- Physitis
o Inflammation of GROWTH PLATES – swelling around growth plates of long bones
o Young horses – conformational defects, malnutrition, growth plate compression, abnormal hoof growth
- Sesamoiditis
o Tearing of ligament attachments to sesamoids (during strenuous exercise)
o Same clinical signs as sesamoid fractures – but less severe (lameness, inflammation)
o Rads: new bone formation/osteolytic lesions, radiolucent lines (prominent vascular changes)
o Tx: long term rest + NSAIDs – prognosis is guarded/poor
- Suspensory Ligament Desmitis
o Apical fracture of proximal sesamoid bone, avulsion fracture of palmar aspect of 3rd metacarpal bone, fracture of
distal 1/3 of small metacarpal bones
o Confirm one of these fractures w/ rads, then evaluate with ultrasound
- Splints – INTRAOSSEUS DESMITIS
o Inflammation of intraosseous ligament btw 3rd metacarpal/tarsal bone w/ small metacarpal/tarsal bones
▪ Periostitis occurs w/ new bone formation along splint bones or small metacarpals/tarsals – usually from
repetitive concussion, excessive training, poor conformation, improper shoeing
o Need to take rads to distinguish from splint bone fractures – need REST and NSAIDs
- Carpal Fractures
o Radial = CHIP fracture / 3rd carpal bones = SLAB fracture
o Immediate swelling, severe lameness – arthroscopic surgery to repair
- Fractures
o Tibial → NON-RECONSTRUCTABLE, COMMINUTED fractures – lack of soft tissue covering, highly susceptible to
infection, GRAVE prognosis for return to function
o P3 → as long as articular surface isn’t involved, GOOD prognosis
o P1 → repair w lag screws as long as not comminuted
o Ulnar → tx w/ bone plates, GOOD prognosis, about 70% return to function
- Osteochondrosis
o Defect in endochondral ossification – leads to cartilage flap
o Dietary Ca and Vit D in young horses – dx frequently made in young horses when starting training – severity of
lameness can vary greatly
- Osteochondritis dessicans (OCD)
o Most common sites on hock:
▪ Distal intermediate ridge of tibia (DIRT)
▪ Lateral/medial trochlear ridge of talus
▪ Medial malleolus of tibia
o Significant effusion of tarsus, uncommon to see significant lameness
o Causes: rapid growth rate, ↑ energy diet, mineral imbalances (↓ Cu, ↑ zinc), genetics, large size, articular trauma
o Management:
▪ Mild cases – restrict exercise, ↓ feed intake, correct mineral imbalances
▪ Severe cases – surgical

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- Navicular Syndrome
o Palmar foot pain – problems w/ navicular bone, navicular suspensory, deep digital flexor tendon, navicular bursa),
more painful on hard surfaces than grass
o Dx: hoof tester elicits pain, palmar digital block improves pain
▪ Rads: bone remodeling, enlarges vascular channels, osteophyte formation on navicular bone
• NOT osteolysis – chronic degenerative condition
- Carpal Hygroma – fluid filled carpal swelling
o Usually from repeated trauma leading to local bursitis –usually NOT lame but have ↓ ROM
o Tx: Surgical exploration and drain placement; simply aspirating fluid/injecting steroids is not effective – swelling
will usually recur – may need to excise bursal lining if keeps recurring
- Quittor – chronic infection of P3 CARTILAGE
o Results in draining tract from coronary band due to infection/inflammation of affected cartilage
o Need SURGERY
- Subsolar Abscess
o History of farrier work/penetrating foreign body – acute severe lameness, ↑ heat/pain in foot that progresses to
coronary band, edema over pattern/fetlock
▪ If no tx in 2-3 weeks will see draining lesions on coronary band
o Tx: disinfectants/poultices, ensure adequate drainage, remove FB if present – NO SYSTEMIC ANTIBIOTICS
- Deep Digital Flexor Tendon Contracture – CLUB FOOT
o Distal check ligament controls stretch of long tendon of deep digital flexor – if too short, flexion of interphalangeal
joint occurs → CLUB FOOT (can be caused by rapid bone growth, excessive feeding, faulty nutrition, lack of
exercise)
o Tx: distal check ligament desmotomy and corrective shoeing
▪ Distal check desmotomy: relieves DEEP superficial flexor contracture
▪ Proximal check desmotomy: relieves SUPERFICIAL digital flexor contracture
- Tendonitis – BOWED TENDON
o Intermittent lameness – resolves after working the horse; palmar metacarpal bulge + inflammation
▪ Bulge/bowing of shallow superficial digital flexor tendon
o Ultrasound superficial digital flexor tendon – anechoic regions within tendon (hemorrhage, loss of tendon fibers)
▪ Indicates acute tendonitis
o Tendon healing = take 8-11 months for tendons to heal → eventually newly formed Type 3 collagen is replaced by
Type 1 collagen – process is NEVER complete
o Most commonly injured tendon in horse = superficial digital flexor tendon
- Curb – thickening of TARSAL LIGAMENT from strain
- Sweeny – Supraspinatus Contracture
o Draft horses – damage to suprascapular nerve causes muscle wasting of the supraspinatus muscle
o Typically damaged from pressure from a pulling harness
- Stringhalt
o Myoclonic disease – affects one/both pelvic limbs – may be associated w/ sweet pea poisoning
o HYPERFLEXION OF LEG – when horse lifts hindlimb, it draws foot up sharply until it touches the abdomen and then
strikes it violently at the ground
o Tx: tenectomy of lateral digital extensor tendon – not all cases respond to treatment
- Bone Spavin – osteoarthritis of HOCK
- Bog Spavin – TARSAL HYDRARTHRITIS
o Chronic synovitis of tibiotarsal joint w/ distension of joint capsule from ↑ synovial fluid formation
o Due to poor conformation: affects both hindlimbs, horse usually not lame
o Prognosis: distension may spontaneously appear and reappear in young horses
- Ringbone – osteoarthritis on PHALANGES
o ↓ ROM, may palpate new bone formation in pastern region – see on rads
o Cause: poor conformation, improper shoeing, trauma (wire cuts, repetitive concussion on hard surface)
o Tx: early = cold packing, astringent application, radiation therapy, anti-inflammatories; severe = surgical
arthrodesis of pastern joint – curative and can restore horse to performance status – COMPLETE REST
- Peroneus Tertius Rupture
o Extend the hock + flex the stifle = disrupts STAY APPARATUS of hindlimb

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 - Pedal Osteitis
o Inflammation of structures of feet associated w/ demineralization of P3
o Performance horses: working on hard surfaces
o Tx: prolonged rest, NSAIDs, corrective shoeing
- PREMATURE HORSES – ANGULAR LIMB DEFORMITIES
o Foal born before day 320 of gestation
▪ Take rads of carpal/tarsal bones – if incompletely ossified, indicates prematurity
o As foal ages, carpal bones will ossify but they can collapse w/ weight of foal placing pressure on soft cartilage →
may result in misshapen bones and lameness → angular limb deformities
▪ Carpal valgus = lateral deviation / carpal varus = medial deviation
▪ Result of asynchronous growth of metaphyseal/epiphyseal growth plates
o Tx: periosteal stripping of concave side of growth plate – promotes growth on concave side, has little potential for
overcorrection
o Also: they have short silky haircoat, pliant floppy ears, soft muzzle, laxity in flexor tendons
MUSCLE DISORDERS
- Creatinine Phosphokinase – CPK, Creatinine Kinase (CK)
o Stored in skeletal muscle and cardiac muscle – ↑ w/ muscle damage (i.e. rhabdomyolysis)
- Myoglobinuria vs. Hemoglobinuria
o Myoglobinuria → brownish urine, doesn’t clear w/ centrifuge + NORMAL colored plasma
▪ Doesn’t bind serum proteins, is quickly excreted before reaching levels that would discolor plasma
▪ If animal has painful gait + myoglobinuria = MYOPATHY
o Hemoglobinuria → reddish plasma – hemoglobin is maintained in plasma longer, is lost in urine more slowly
- Hyperkalemic Periodic Paralysis (HKPP) – QUARTER HORSES, Paint, Appaloosa
o Mutation in skeletal muscle SODIUM channel – fail to inactivate, remain open → depolarization of muscle
membrane closer to threshold, hyperexcitability of muscle
▪ Autosomal dominant – discourage breeding – IMPRESSIVE how far the mutation can be tracked back to
▪ Hyperkalemia – movement of K out of cells as myocytes repolarize
o Intermittent muscle fasciculations followed by weakness, well-muscled, muscle stiffness, difficulty walking,
prolapsed 3rd eyelid, recumbency – usually intermittent signs
o Tx: change diet to timothy hay (↓ K) w/ frequent small meals, regular exercise
▪ Acute episodes: 0.9% NaCl + 5% dextrose (drives K+ into cells)
▪ Sometimes diuretics (furosemide) to diurese but don’t give spironolactone bc it’s K-sparing (doesn’t ↓ K)
- Myotonia
o Mild gait abnormality at initiation of exercise, then diminishes – very heavily muscled horses
o EMG (electromyogram) = crescendo-decrescendo signal of high frequency repetitive bursts w/ characteristic
“dive-bomber” sound – repetitive firing after contraction of affected muscles
- Myositis – “TYING UP”
o Overworked racehorse over the past year – stiff gait, lethargy, anorexia, oliguria
o Pigment nephropathy – nephrosis and subsequent renal failure caused by large amounts of myoglobin being
filtered by kidney – animals subjected to extreme conditions that cause animal to break down substantial muscle
NEUROLOGY
- Radial Nerve Paralysis
o Caused by laying in lateral recumbency for long period of time – radial nerve susceptible to damage from pressure
(warm water bed padding has greatly helped ↓ incidence)
o Forelimb: dropped elbow, flexed carpus/fetlock/digits – drags limb when walking, unable to advance leg
o Tx: rapid and aggressive – excellent nursing care
- Fracture to Basilar Bones (Basisphenoid, Basioccipital) – rear up + flip backwards
o Head tilt, drooping ear, deviation of muzzle – UNILATERAL – damage to CN 7,8
o Common form of traumatic nerve injury in foals
- Equine Protozoal Myeloencephalitis (EPM) – SARCOCYSTIC NEURONA
o Sarcocystic neurona – migrates through spinal cord/brain – damage to white and grey matter
o OPPOSUM

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 o Horses 1-6 years old → progressive ATAXIA (CP deficits), focal muscle loss noted around gluteal/quadriceps region,
incoordination of all 4 limbs (or just 1 limb)
▪ Vague ASYMMETRIC/multifocal neurologic signs w/ MUSCLE ATROPHY
▪ Hyporeflexia, spasticity, cerebellar signs, head tilt, facial paralysis, circling, dysphagia, blindness, acute
recumbency – see these signs if there’s brainstem involvement
o Dx: serum and CSF immunoblotting
o Tx: PONZURIL (Marquis); previously used TMS + pyrimethamine
▪ If need cheaper tx: sulfadiazine/pyrimethamine combo – 6 month treatment
- Cauda Equina Neuritis – inflammation of nerve roots
o Usually inflammation of caudal equina, sometimes CNs too – LMN signs
o Paresis/paralysis, chewing of tail head, hypotonic anus, fecal retention, urinary incontinence (urine scalding of
thighs), hindlimb ataxia
o NO TREATMENT OPTIONS
- Cervical Vertebral Stenotic Myelopathy – WOBBLER SYNDROME
o 1st Form: cervical vertebral instability – ventroflexion of neck causes spinal cord compression at C3-4 or C4-5
o 2nd Form: cervical static stenosis – compression of spinal cord regardless of neck position
o UNDER 1 YEAR OLD → wide based stance, CP deficits, ataxia, paresis, spasticity (worse in hind) – SYMMETRICAL
o Tx: surgery to stabilize cervical vertebrae and decompress spinal cord
▪ Anti-inflammatories + stall rest to ↓ clinical signs short term
- Equine Degenerative Myeloencephalopathy (EDM)
o UNDER 1 YEAR OLD – Vit E deficiency
o Ataxia, hypometria, CP deficits, generalized weakness, normal mentation, wide base stance, paresis, spasticity →
SYMMETRICAL ATAXIA (worse in hind)
o Dx: find lesion in caudal brainstem nuclei and spinal cord - histopath
- Equine Herpes Myeloencephalopathy (EHM)
o CNS vasculitis – hindlimb ataxia, dog sitting, intermittent urine dribbling, hypotonia (tail/anus)
o Usually see MULTIPLE horses in same barn affected – generally acute signs
- Equine Encephalomyelitis – WEE (50% mortality), VEE (75%), EEE (90%)
o Prevention: vaccination → ZOONOTIC
o EEE (all 3 are similar)
▪ Transmission: MOSQUITO – spreads via lymphatics, don’t see neuro signs until 5 days later
▪ Cortical and thalamic lesions – ASYMMETRICAL – progressive CNS signs over several days – depressed,
anorexic, progresses to head-pressing and circling, death 2-3 days after onset of clinical signs
▪ CSF tap: protein of 80 mg/dL + primarily mononuclear pleocytosis
- Verminous Myelitis – aberrant migration of parasites through CNS
o Similar to EPM – focal/multifocal/diffuse – muscle atrophy, ataxia, incoordination x4
o Parasites: Strongylus vulgaris, Micronema deletrix, Draschia megastoma, Setaria
o Tx (strongyles): ivermectin, fenbendazole, thiabendazole
- Cerebellar Abiotrophy – ARABIANS
o Young foals (around 6 months) – unknown etiology (genetic? Toxic? infectious?)
o Cerebellum – responsible for coordination, regulation of movement range/rate/strength, balance, posture
▪ Ataxia, intention tremor, NORMAL mentation, dysmetria, hyperreflexia, spasticity, no menace
o NO TREATMENT
- Dandy-Walker Syndrome – ARABIANS, THOROUGHBREDS – rare in both
o Midline defect of cerebellum and cystic dilation of 4th ventricle
GASTROENTEROLOGY
- Colic Sedation w/ Xylazine
o Causes inhibition of intestinal motility, could transiently ↓ CO in potentially hypovolemic horse w/ colic → BUT,
potent analgesic that provides rapid relief from abdominal pain
- Abdominocentesis
o RIGHT of midline – avoid hitting many organs
o Normal: yellow, nucleated cells <5,000/uL, TP <2.5 m/dL
o Septic peritonitis:
▪ pH < 7.2, glucose <30, serum-peritoneal glucose difference >50

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- Anaphylaxis
o Horse shock organ = LUNGS & COLON
o Resp/GI signs = dyspnea, resp distress, diarrhea, anxiety, tachycardia, piloerection, sweating
o Tx: epinephrine, corticosteroids, antihistamine
- Regurgitation
o If horse w/ colic regurges = guarded/poor prognosis
▪ Horses have extremely tight esophageal sphincter tone; regurg only happens when very great pressure is
exceeded (may also have gastric rupture at this pressure)
o Regurg in foals: gastric ulcers, cleft palate, incoordination of swallow reflex
- Small Colon Impaction – colic in MINIATURE HORSE
- Small Intestinal Obstruction
o Acute onset colic, gastric reflux (brown/yellow fluid), CRT 3 sec, red MM, absent GI sounds, peritoneal fluid (cloudy
yellow w/ TP = 3, WBC = 11,000)
▪ pH >5 gastric reflux = small intestinal contents are refluxing into stomach
o Tx: SURGERY – stabilize w/ NG tube first (horses can't vomit – will relieve life-threatening pressure)
o Causes: strangulating lipoma, mesenteric rent, intussusception, hernia, epiploic foramen, incarceration, volvulus
▪ Lipomas = OLD horses / rest of causes = YOUNG horses
- Duodenal-Proximal Jejunitis (DPJ) – ANTERIOR/PROXIMAL ENTERITIS
o Related to Clostridium dificile
o Clinical signs – resemble small intestinal obstruction – acute colic, ↑ RR/HR, pain (↓ than obstruction), gastric
reflux, depression, ↓ gut sounds, injected MM
▪ Small intestinal obstruction = surgical / DPJ responds better to medical management
• Gastric reflux w/ DPJ = orange brown color, foul smelling; feel multiple dilated fluid-filled loops of
bowel, peritoneal fluid is serosanguineous w/ TP = 3.5, WBC = 7,000
o Tx: decompress stomach w/ NG tube, remove excess GI fluid, IV fluids, replace electrolyte deficits, analgesia,
correct acid/base abnormalities
- Nephrosplenic Entrapment = LEFT DORSAL COLON DISPLACEMENT
o Left dorsal colon – displaced over Nephrosplenic ligament (btw spleen and left body wall) – renosplenic space
o Larger horses predisposed! Colic, ↑ HR/RR, pacing, staring at abdomen, no gastric reflux
▪ Milder clinical signs than obstruction – distended large colon on palpation
o Ultrasound: can't see L kidney, do see large colon predominantly on L side
o Tx: surgical correction, can try rolling horse 360˚
- Right Dorsal Colon Displacement
o Colic, ↑ HR/RR, no gastric reflux, on rectal palpation can feel colon palpable btw cecum and body wall (cecum =
RIGHT side – something wrong on the right side)
- Right Dorsal Colitis
o Chronic NSAID use
o Inappetence, intermittent colic, hypoproteinemia
o May see concurrent RENAL MEDULLARY CREST NECROSIS w/ NSAID used
▪ Aka RENAL PAPILLARY NECROSIS – limited blood flow to an area of the kidney
- Cecal Volvulus
o RARE in horses
o Usually 2˚ to large colon volvulus – horse pings similar to cow, presents with acute colic
- Strongylus vulgaris (GI parasite) – thrombosis/arteritis of CRANIAL MESENTERIC ARTERY
o Migration → cranial mesenteric artery – immune response can cause thrombosis of cranial mesenteric → colic!
(cuts off blood supply) and infarction of bowel
o Strongylus edentates and Strongylus equinus (GI parasites)
▪ Migrate through portal vein into liver, through peritoneal and retroperitoneal space, then after a few
months returns to gut – could be found in liver, pancreas, perirenal
o Tx: ivermectin, fenbendazole, oxibendazole
- Enteroliths – ARABIANS in California and Florida
o Alfalfa hay considered to play a role – common in CA bc alfalfa hay in is high in Mg there
▪ Result: Magnesium ammonium phosphate enteroliths

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 - Sand Enteropathy
o Common in Ca and Fl – sandy regions – tx w/ psyllium (hemicellulose laxative that can bind sand & remove it from
GI tract) – in future, feed horse in stall w/ hay racks to prevent horse from eating off of sandy ground
- Meconium Impaction
o Meconium = 1st intestinal discharge of newborn foal – impaction usually is within 24 hours of birth
o Tenesmus, variable degree of colic, straining, swishing of tail, restlessness – most common cause of colic in foal
o May feed numerous hard fecal balls on palpation – tx w/ acetylcysteine enema (cleave disulfide bonds in
mucoproteins of meconium – help break it down), warm water and soap enema
- Gastric Ulcers
o SQUAMOUS region of stomach – non-glandular, unable to resist injury from acid like glandular region (secretes
mucus to protect itself)
o Horses predisposed to gastric ulcers = constantly secrete gastric fluid (others only secrete in response to food)
o Predisposing Factors: giving 2 NSAIDs together
o Tx: OMEPRAZOLE (H-K ATPase blocker), Cimetidine (ranitidine, famotidine – H2 blocker), sucralfate (protects
mucosa), Misoprostol (PGE1 analogue – ↑ GI blood flow, ↓ secretion of acid, ↑ mucus and bicarb secretion)
- Protein Losing Enteropathy
o Damaged bowel leaking protein into gut
o Edema, hx of severe diarrhea, fever, dehydration, weak, anorexic, purple MM, small amount of concentrated urine
▪ NORMAL PCV with LOW TP/albumin
o Tx: IV plasma (raise protein without raising PCV too much)
- Choke – obstruction in esophagus
o Predisposing factors: poor mastication, rapid eating, esophageal stricture, grass clippings/beet pulp/pellets/cubes
o Salivation, food coming out of nose – with choke, have time to resolve it without drastic action
▪ 1st pass stomach tube, try to gently push bolus aborally, flunixin meglumine (NSAID), lidocaine (relieves
discomfort), xylazine (to sedate), NOT mineral oil – could aspirate which is BAD (lipid pneumonia – BAD!)
▪ If doesn’t resolve on 1st try, give horse 12-24 hours and give IV fluids then try again – usually does the trick
unless dealing w/ anatomic choke (esophageal diverticulum) or very severe choke
o Complications – inhalation (foreign body) pneumonia; if caustic can rupture the esophagus
- Foal Heat Diarrhea – 7-14 day old foals
o Mild diarrhea in foals – unknown etiology, maybe grain/hay consumption – may alter GI flora so diarrhea develops
o Called foal heat diarrhea bc occurs at same time as post-foaling estrus in mare
- Lethal White Syndrome – PAINT mares who give birth to all white foals
o Agangliosis of intestines (missing nerve cells in colon) – lead to constipation, hypomotility, megacolon, colic, and
death
RESPIRATORY
- Recurrent Airway Obstruction (RAO) – chronic obstructive pulmonary disease (COPD), HEAVES
o Bronchoconstriction and accumulation of mucus/neutrophils – thought to be environmental – i.e. winter stabled
horse housed near hay storage
o >6 years old (MATURE horse disease) – ↑ RR/effort, end-expiratory wheezes (↓ airway diameter from
inflammation/exudate/edema/bronchoconstriction) – as lung vol ↓ during expiration, narrowed bronchioles
collapse – trapping air distal to closure and creating wheezes
o Dx: neutrophilic inflammation on BAL (healthy horses = macrophages)
o Tx:
▪ Environmental changes – put horse on pasture, feed hay soaked in water, feed pelleted diet
▪ Beta 2 agonist – stimulate airway dilation – relaxes smooth muscle → Clenbuterol, Terbutaline
▪ Corticosteroids – anti-inflammatory, ↓ mucus/neutrophil accumulation
- Exercise Induced Pulmonary Hemorrhage – BLEEDERS – common in THOROUGHBREDS
o Racehorses – ↓ pulmonary capillary pressure
o Seen w/ short period of strenuous exercise – usually speeds >14 m/sec causes bleeding
o BILATERAL epistaxis (only 10% of time) after training – pulmonary bleeding (caudodorsal lobes)
▪ Other signs: labored breathing, ↓ speed during race, poor performance, after race – excessive
swallowing, sometimes coughing

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 o Dx: bronchoscopy, seeing hemorrhage on cytology of BAL
▪ TTW = macrophages containing hemosiderin (dark granules from phagocytized RBC)
o Tx: FUROSEMIDE – give before next race to ↓ severity
- Pleuropneumonia
o Tx: THORACOCENTESIS – 7th rib space at CC junction
▪ One of the most dependent regions – fluid accumulates; also caudal to heart and cranial to diaphragm
- Ethmoid Hematoma
o Progressive and locally destructive mass – resembles tumor but NOT NEOPLASTIC
▪ Originates from mucosal lining of ethmoid conchae or walls of maxillary/frontal sinus
o See smooth, well-defined mass in sinus region (no osseous changes/fluid lines) – surgically remove!
- Laryngeal Hemiplegia – damaged recurrent laryngeal nerve
o LEFT side almost always affected! – direct trauma, certain toxins, husbandry
o Exercise intolerance, noisy breathing, inspiratory dyspnea w/ audible whistling sound on inspiration
- Pharyngeal Paresis
o Can be caused by guttural pouch infections (damage to CN 9-12 as they run through pouch)
o Paresis:
▪ Arytenoid fails to seal glottis, epiglottis doesn’t close normally against rima glottis (coughing, aspiration)
▪ Soft palate doesn’t seal normally against roof of nasopharynx – food refluxes through nose
▪ Tongue can't engage hard palate – dropped food, hard to move food bolus to pharynx to swallow
▪ Upper esophageal sphincter remains open – no clinical signs
- Guttural Pouch Tympany – pouch distended with AIR
o Due to defect in Eustachian tube or pharyngeal tissues
o NONPAINFUL, air-filled swelling in right parotid region (feels pillowy), BAR, slightly stertorous breathing
o Tx: fenestrate the membrane btw the normal and affected pouch
- Guttural Pouch Mycosis – ASPERGILLUS NIDULANS
o CN 7 + CN 9-12, sympathetic trunk, internal carotid – pass through medial pouch
o External carotid – pass through lateral pouch
o Dysphagia, Horner’s Syndrome, hemorrhage if involves vasculature (epistaxis – fungal plaque erodes through
internal carotid artery), NO vestibular signs (CN 8 not involved)
o Tx (persistent epistaxis): ligate internal carotid via surgical occlusion of artery (embolization coil, balloons)
- Pharyngeal Lymphoid Hyperplasia
o Normal finding in young horses, no clinical signs (normal immunological event)
o Bumpy pharyngeal walls on endoscopy
REPRODUCTION
- Persistent Corpus Luteum – progesterone from CL prevents estrus
o If anestrus during breeding season and non-receptive to stallions for months but has had normal pregnancies in
the past → may find follicle in ovary on rectal palpation
o Tx: PGF2a injection – lyses the CL if >5 days old; if unsure how old the CL is, repeat in 7 days
- Retained Placenta
o Considered retained after 3 hours – usually expelled btw 30 minutes and 3 hours after birth
o Tx: oxytocin + uterine lavage (facilitate removal) – DON’T pull on placenta, broad spectrum antibiotics (↓ metritis)
o Mare DOES NOT eat placenta
- Uterine Artery Hemorrhage Post-Foaling
o Low PCV, tachycardia, foaling a few hours ago
o Tx: aminocaproic acid (facilitate stable clot – blocks activation of plasminogen→plasmin which dissolves clots)
- Twinning – most common non-infectious cause of ABORTION
o VERY RARE that both twins are born alive – placental insufficiency usually aborts both twins
o Abortion @ 6-9 months of gestation – preceded by premature lactation
o Dx: day 13-15 w/ ultrasound – manually crush one twin to allow the other to survive (90% success)
▪ Crushing: transcutaneous, transvaginal ultrasound-guided twin reduction
- Gonadal Dysgenesis – chromosomal abnormality – can NEVER have normal pregnancy
- Pneumovagina – “WINDSUCKER”
o Older thin mares – abnormal perianal conformation – anus is pulled forward – lead to tipping of vulva dorsally,
causing opening of vagina

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 o Surgical repair: dorsal portion of labia that’s tipped cranially is sutured; ↑ weight of the mare tends to realign the
anatomy appropriately = CASLICK procedure
▪ Horizontal sutures at dorsal aspect of labia + ↑ mare’s weight
o Predisposes to vaginitis and endometritis – air aspiration = contamination, leads to infertility
- Ruptured Prepubic Tendon – usually LATE in pregnancy
o Tendon runs along ventrum, provides major support for all structures in abdomen
o Obese DRAFT MARES – last month of pregnancy, develops ventral edema from udder to xiphoid, becomes acutely
painful and tachypneic
o May affect ability to ↑ intra-abdominal pressure during parturition
o Tx: if notice ventral swelling, take action immediately!! Restrict activity, use sling under abdomen for support, do
vet-assisted parturition
- Uterine Torsion
o Last trimester – shows signs of colic – anorexia, frequently attempting to urinate
o On rectal palpation: broad ligament pulled tight over uterus from R → L
o Tx: place mare under short-acting anesthesia and roll her (plank-to-flank), surgery may be needed
- Uterine Infection – ENDOMETRITIS
o Dx: uterine cytology (more reliable than cervical swab) – ↑ neutrophils w/ infection (esp. if see bacteria too)
▪ Culture = worthless – too many commensal organisms – can be helpful in choosing antibiotics
▪ If pre-ejaculate swab for culture from stallion has heavy Pseudomonas or Klebsiella, think twice about
using them for breeding – high association of causing endometritis in mare
o If start leaking milk too early (i.e. 7 months)
▪ Placentitis – usually doesn’t have systemic signs
▪ Ascending infection – most common bacteria is Strep zooepidemicus; also E. coli and Klebsiella
▪ Gross lesions: abnormalities at cervical star, dark/hemorrhagic placenta (diffusely abnormal)
- Mare Reproductive Loss Syndrome (MRLS)
o Abortion storms – Kentucky and Australia
o Transmission: Eastern Tent Caterpillars – hairs penetrate GI tract – leads to septicemia in foals
o Affects horses – can also have pericarditis and uveitis
MISCELLANEOUS EQUINE DISEASES
- Chronic Renal Failure
o Weight loss, inappetence, PUPD, USG = isosthenuria (1.008-1.012)
o Azotemia, hypercalcemia, hypophosphatemia, hyponatremia, hypochloremia
▪ Unique to horses = HYPERCALCEMIA – ↑ Ca in diet, P levels might be low because of ↑ Ca
- Glomerulonephritis – most common form of chronic renal failure
o Results from deposition of immune complexes in glomerular basement membrane
o Bloodwork: persistent proteinuria! (may lead to serum hypoproteinemia)
- Uroperitoneum - FOALS
o Usually ruptures during parturition bc large pressures on urinary bladder as they come out
o HYPERKALMEIA, ↓ Na, ↓ Cl – urine is high in K, low in Na/Cl
o Dx: creatinine in fluid will be 2x serum creatinine
o Tx: fluids (DON’T GIVE POTASSIUM)
- Ectopic Ureter – YOUNG FEMALE HORSES – congenital anomaly
o Urine scalding, hx of urinary incontinence → surgically correct
- Parrot Mouth
o Brachygnathism (mandible is shorter than maxilla
o Malocclusion – require dental care often

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 CANINE AND FELINE DISEASES – 46%
ENDOCRINOLOGY
- Hyperthyroidism – CATS (>8 years old)
o Active form = T3 / T4 = unbound, enters cells, is converted to T3/reverse T3 (during illness)
o Cause: adenomatous hyperplasia; also thyroid adenomas/carcinomas
o Dx: serum T4 – if normal and still suspect hyperthyroidism, do free T4 (equilibrium dialysis)
▪ Scintigraphy – determine gland function, may see excitement leukogram (↑ BUN but not creatinine, ↑
GFR which masks underlying renal disease)
▪ Before treating: look at renal/liver values – renal dz often masked by hyperthyroidism, treatment =
methimazole (hepatotoxic)
o Clinical Signs: Palpable nodule in thyroid area (“thyroid slip”), restlessness, polyphagia + weight loss, ↓ BCS,
vomiting, aggression, dull haircoat, PUPD
▪ HYPERthyroidism = HYPERtension = can cause glaucoma
o Tx:
▪ Methimazole – initially – helps unmask renal disease; Side Effects = extreme facial pruritis (excoriations)
▪ Radioactive Iodide therapy (I131 radiation) – use if animal has bad methimazole side effects once renal
values are stable
▪ Thyroidectomy – if thyroid tissue is left behind, disease reoccurs; may also see Horner’s, hypothyroidism,
hypocalcemia (due to excision of parathyroids), laryngeal paralysis
o Complication – ↑ BP (>180-220) – leads to ocular issues (retinal detachment, hemorrhage leading to blindness)
▪ Tx hypertension w/ atenolol if animal goes acutely blind
- Hypothyroidism – DOGS (older, large breed)
o Causes: immune mediated lymphocytic thyroiditis, idiopathic atrophy, suppression of pituitary gland from
glucocorticoids (2˚ hypothyroidism)
o Weight gain (slow metabolism), skin changes (hyperpigmentation, alopecia/rat tail, pyoderma, seborrhea),
lethargy, cold intolerance
o Dx: free T4 (equilibrium dialysis) – T3 NOT USEFUL
o Tx: Sodium levothyroxine (keep T4 slightly above normal and resolve clinical signs)
- Diabetic Ketoacidosis
o PUPD, weight loss, normal to ↑ food intake, lethargy, vomiting
o UA: KETONES in urine, tons of glucose in urine
o Bloodwork: metabolic acidosis (↓ TCO2 – ketones acts as acids), ↓ Na, ↓ Cl, ↓ K (osmotic diuresis, polyuria),
hyperosmolality (↑ glucose/BUN), pre-renal azotemia (dehydration)
o MONITOR while treating – electrolytes, BG (make sure not hypoglycemic)
o Initial Treatment: correct acidosis (bicarb), electrolyte abnormalities (IV fluids, K, P supplementation),
hypoosmolality
▪ REGULAR insulin (Humulin-R) – potent, short acting insulin – used to treat DKA patients
• Give frequent doses until they are stable – then can switch to longer-acting insulin
o Later Treatment: regulate blood glucose, get animal to eat, control obesity/concurrent disease
o If dx DKA in controlled diabetic – look for underlying cause of sudden poor glycemic control
▪ Pancreatitis, cardiac disease, infection
▪ Hyperthyroidism common in DKA cats / Cushing’s common in DKA dogs
- Diabetes Mellitus
o CATS
▪ Polyphagia, weight loss, dull haircoat, PUPD, pelvic limb weakness, plantigrade stance (dropped hocks),
difficulty jumping – amyloid deposition in cats, transient DM after excision of insulinoma
▪ Cats = Insulin dependent 70% of time, non-insulin dependent 30% of time
o DOGS
▪ Bilateral cataracts + 4 classic signs (PUPD, polyphagia, weight loss)
• Glucosuria → polyuria (glucose spills into urine at 180 in dogs, 200-280 in cats)
▪ Dogs = Almost always insulin dependent

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 o Dx: ↑ fasting BG, glucosuria (not ketones), do URINE CULTURE (prone to UTIs, if have underlying infection, can
lead to insulin resistance)
▪ Glucose Curve – greatly affected by stress; in cats, use fructosamine (shows average BG over 2-3 weeks –
useful in stressed cat)
o Tx: insulin injections (NPH/Lente – intermediate acting – manage diabetics w/o DKA), ultralente (long acting),
glargine (insulin of choice for long term control after DKA is corrected)
▪ ↑ fiber diet – delay glucose absorption, ↑ insulin sensitivity
▪ ↓ calorie diet + regular exercise = treat obesity and ↑ insulin sensitivity
▪ Poor glycemic control: hypoglycemia (owner gave too much insulin or when animal wasn’t eating),
infectious/hormonal disorders (hyperadrenocorticism, pancreatitis), inappropriate insulin storage
o Consequences of Insulin Deficiency
▪ Impaired energy utilization (can't import glucose into cells), ↑ hepatic gluconeogenesis (liver upregulates
in response to ↓ energy, exacerbates hyperglycemia), ↑ fat mobilization (to provide energy source),
hepatic lipidosis and ketosis, weight loss (insulin deficient dog is essentially starving body cells)
- Diabetes Insipidus
o Lack of production/response to VASOPRESSIN
o Central – lack of release of vasopressin by posterior pituitary
▪ Problem w/ hypothalamus function (ADH production) ± posterior pituitary (ADH release) – can't respond
to changes in serum osmolality/blood volume/blood pressure
▪ USG: 1.001-1.007 – kidneys function fine, just not enough ADH
▪ Tx: DDAVP (synthetic ADH, desmopressin) – takes up to 3 days to overcome medullary washout from
being PUPD
o Nephrogenic – adequate release of ADH but kidney ADH receptors don’t function properly
▪ Tx: hydrochlorothiazide – avoid excess salt, give unlimited access to water
- Insulinoma
o Low BG, normal-HIGH insulin in face of low glucose – normal insulin control is gone
o Tx: surgical removal (post-op complications: pancreatitis, recurring hypoglycemia)
- Pheochromocytoma
o Tumor of adrenal medulla – secrete catecholamines – not very common in dogs
o Hypertension, tachyarrhythmias, seizures, collapse
o CORTEX – zona glomerulosa = aldosterone / zona fasciculata = glucocorticoids / zona reticularis = androgen
o MEDULLA – chromaffin cells – catecholamines (epinephrine, norepinephrine)
- Addison's – HYPOADRENOCORTICISM
o Middle aged female dogs
▪ Breeds: Great Danes, Standard Poodles, Rotties, Portuguese Water Dogs, WHWT, Wheaten terriers
o Destruction/atrophy of ALL layers of adrenal cortex – deficiency in glucocorticoids AND mineralocorticoids
▪ Less common form: inadequate ACTH by pituitary = deficiency in glucocorticoids only
o ↑ K, ↓ Na, azotemia, hypoglycemia, acidosis, low resting cortisol or low ACTH stim test (GOLD STANDARD – if
plasma cortisol is low after ACTH administration), absence of stress leukogram, ↓ Na:K ratio (less than 27), ECG =
tall T waves (hyperkalemia)
o Tx: supplement mineralocorticoids
o Monitor: serum Na/K – will be hyponatremia + hyperkalemic if mineralocorticoid deficient
- Cushing's – HYPERADRENOCORTICISM
o Most due to 1˚ pituitary dysfunction (↑ ACTH secretion)
o Breeds: Dachshunds – esp. long haired ones!
o Calcinosis cutis (thinning, ↑ fragility of skin, hyperpigmentation, alopecia, seborrhea, pyoderma), panting, lethargy
(muscle weakness), distended abdomen (redistributes fat to abdomen), ↑ infection (immune suppression), PUPD,
polyphagic
▪ 4 P’s = PU, PD, polyphagia, panting
o Dx:
▪ ACTH Stim – plasma cortisol should increase a certain amount
• Too much ↑ – too much ACTH/cortisol being produced – adrenal/pituitary dependent
• Not enough ↑ – iatrogenic Cushing’s

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 ▪ Endogenous ACTH plasma assay
• Normal: After pred, cortisol is high (from steroid), ACTH is low (bc feedback inhibition of ACTH)
▪ LDDST
• Cushing’s animals have ↑ cortisol at 8 hours post dex (most animals will have suppressed by 8
hours) – look at hour 8 to see if has Cushing’s, look at hour 4 to see what kind
o Pituitary dependent – may or may not suppress a little at 4 hour mark, but rebounds
o Adrenal dependent – will not suppress at all
▪ UCCR (urine cortisol:creatinine ratio)
• Sensitive, not specific – if normal, not Cushing's; if ↑, could be Cushing's or other cause of PUPD
▪ Abdominal Ultrasound – can see enlarged adrenals (unilateral – likely adrenal dependent; other adrenal
may be hypoplastic from disuse / if bilaterally enlarged, likely pituitary dependent – excess ACTH)
▪ Bloodwork
• ↑ ALP, ↑ Cholesterol, ↑ ALT (swelling/death of hepatocytes), ↓ BUN (diuresis from ↑ cortisol)
o Tx:
▪ Adrenalectomy (for adrenal dependent) – NOT NOT NOT pituitary surgery!!
▪ Lysodren/Mitotane – treat PDH – causes selective necrosis of zona fasciculata/reticularis
▪ Trilostane – inhibits enzyme needed for cortisol production
▪ Ketoconazole – inhibits production of steroids – used for functional adrenal tumors
- Primary Hyperparathyroidism
o Adenoma of parathyroid glands
o Hypercalcemia, hypophosphatemia – ↓ P as Ca ↑ (and vice versa)
o Tx: surgical removal
▪ Monitor patient’s serum Ca for a week post-op – make sure they don’t get hypocalcemic
• Then weekly for 4 weeks – ↑ pre-op Ca increases chance of ↓ post-op Ca
▪ Give Vit D + Ca supplements as needed – maintain Ca in normal range to stimulate PTH production by
parathyroid cells
• Don’t over-supplement Vit D – causes ↑ Ca, ↑ P (bone resorption, ↑ Ca/P absorption from GI)
• PTH causes ↑ Ca, unchanged/normal P – enhances renal phosphorus secretion
- Nutritional Secondary Hyperparathyroidism
o Imbalance of Calcium and Phosphorus
▪ ↑ P, ↓ Ca = parathyroid hormone excretion
▪ Boneless raw diets = Ca deficient!
o Lethargy, reluctance to move, loose teeth, stunting, malformed bones, lameness, death
CARDIOLOGY
- Hypertrophic Cardiomyopathy (HCM)
o CONCENTRIC hypertrophy – thick left ventricular wall – impairs diastolic filling, no contractility problems
o CATS – Maine Coons/Ragdolls (<2 years old when diagnosed) – commonly associated w/ hyperthyroidism,
hypertension (i.e. from renal disease)
▪ Aortic Thromboembolism (saddle thrombus) – dilation of L atrium + blood stasis = thrombi form and
lodge at aortic bifurcation → acute paraparesis and pain in hindlimbs
▪ Test for hyperthyroidism / fundic exam for hypertension / blood pressure/US for renal disease
o Rads: cardiomegaly, “valentine” shaped heart
o Echocardiogram: L ventricular concentric hypertrophy, systolic anterior motion of mitral valve (SAM)
▪ SAM – mitral valve leaflet obstructs ventricular outflow tract as chamber contracts
o Tx: ↑ diastolic function by ↓ HR
▪ Beta blockers (atenolol) – ↓ contractility/HR – allows better chamber filling
▪ ACE inhibitors (enalapril, benazepril) – ↓ BP by causing vasodilation
▪ Ca channel blockers (diltiazem)
▪ Left Sided Heart Failure: diuretics (furosemide), nitroglycerin, O2
▪ Cats: prevent thromboembolism (heparin, aspirin, clopidogrel)
• Aspirin prevent cyclooxygenase

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 - Dilated Cardiomyopathy (DCM)
o CATS – Taurine deficiency (rare since commercial diets have enough taurine)
o DOGS – DOBERMAN PINSCHERS, large breed dogs; taurine deficiency in Cocker Spaniels
▪ Poor prognosis in Dobermans – die w/in 2 months of dx
o ECCENTRIC hypertrophy – left ventricle
o Tx: pimobendan (calcium sensitizer – ↑ contractility), diuretics, ACE inhibitors (enalapril), ± digoxin
- Vascular Ring Anomalies – rare in dogs and cats
o Dx after weaning – esophageal constriction doesn’t allow solid food to pass – causes regurg – likely leads to
aspiration pneumonia
▪ Poor BCS w/ voracious appetite
o Left 5th – involutes / Left 6th – becomes pulmonary artery and ligamentum arteriosum
o Right 3rd – becomes right internal carotid / Right 4th – most common cause of constriction = persistent right 4th
aortic arch
o Breeds: German Shepherds, Irish Setters
- Pulmonic Stenosis
o SMALL breeds – English Bulldog, Beagles, Mini Schnauzers, Samoyed, MASTIFFS, Fox Terriers
o Dilation of pulmonary vasculature downstream of stenotic region (turbulent blood flow), ↑ R ventricular/atrial
pressures, CONCENTRIC hypertrophy of right ventricle = ↑ resistance to ejection of blood through stenotic
pulmonary outflow tract
o Systolic murmur @ LEFT HEART BASE
o Tx: balloon dilation valvuloplasty – inflate balloon to stretch stenotic region
- Aortic Stenosis
o LARGE breeds – Boxers, Goldens, Newfoundlands, German Shepherd, Rotties, NOT Mastiffs/Irish Wolfhounds
o Systolic murmur @ LEFT HEART BASE
o CONCENTRIC hypertrophy of L heart (pressure overload), post-stenotic dilation of aorta, ventricular arrhythmia
common (reason for ACUTE DEATH)
o Prognosis: guarded – sudden death can happen at any time; dog has ↑ risk for infective endocarditis
o Tx: prophylactic antibiotics, β blockers (atenolol – ↓ myocardial O2 demand, ↓ frequency of ventricular
arrhythmias), balloon dilation (result not usually good)
- Tricuspid Valve Dysplasia
o LABS, German Shepherds, large breed males
o RIGHT heart failure (ascites, hepatomegaly), systolic RIGHT mid-thorax murmur
o Irregular valve leaflets, chordae tendineae, or papillary muscles of valve – prognosis depends of degree of regurg
o Severe cardiomegaly + marked R atrial/ventricular enlargement on rads
- Mitral Valve Dysplasia vs MYXOMATOUS DEGENERATION OF MITRAL VALVE
o Dysplasia – CONGENITAL – valves are thick, fused, fibrosed, etc.
▪ GERMAN SHEPHERDS, GREAT DANES, other large breeds
o Degeneration – OLDER – most common cardiac disease in vet med
▪ Small breeds
o Murmur @ LEFT HEART APEX – leads to pulmonary hypertension, enlarged L atrium on rads
- Right Ventricular Arrhythmogenic Cardiomyopathy – BOXER CARDIOMYOPATHY
o Syncope in boxers
o Dx: 24 hour Holter monitor – causes VPCs to occur (electrical conduction abnormality)
GASTROENTEROLOGY
- Anatomy & Pharmacology
o Canine esophagus = striated mm / feline esophagus = 2/3 striated, 1/3 smooth
o Parietal cells = HCl, produced in response to gastrin = G cells in antrum
o Emetics: Cats = xylazine / dogs = apomorphine
o Appetite stimulants: cats/dogs = cyproheptadine / dogs = capromorelin
- Intussusception
o Invagination of intestinal segment into lumen of adjacent segment (mechanical obstruction)
o Dogs >>cats / most common site = ILEOCOLIC (2nd = jejuno-jejunal)
o Scant bloody diarrhea, abdominal pain, palpable doughy sausage in abdomen, vomiting
o Common: young animals w/ hx of recent enteritis (chronic diarrhea, treated for Coccidia, etc.)

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 o Rads: obstructive pattern w/ dilated SI loops w/o overt mass effect
▪ Barium study helpful
- Rectal Prolapse vs Colorectal Intussusception
o Tissue protruding from anus – pass blunt probe alongside prolapsed tissue:
▪ If only goes short distance = prolapse / if goes long distance = intussusception
o Prolapse: Kittens w/ GI parasites – severe diarrhea + straining = prolapse
o Tx (prolapse): manually reduce w/ lube, tx parasites, dextrose to ↓ edema
o Tx (intussusception): exploratory surgery
- Gastric Ulcers
o Causes: steroids + NSAIDs (compromises mucus-bicarb protection of stomach), liver failure (↓ mucosal blood flow
2ndary to portal hypertension/thrombosis)
o Tx: omeprazole (proton pump inhibitor)
- Inflammatory Bowel Disease (IBD)
o Chronic anorexia w/ intermittent vomiting, diarrhea, weight loss
o Ultrasound: multifocal to diffuse thickening of muscularis layer of small bower
▪ DDx: GI lymphoma
o Histopath: lymphoplasmacytic infiltration of GI tract
o Tx:
▪ Novel protein – easily digestible w/ new protein source, hypoallergenic diet
▪ Corticosteroids (budesonide – concentrates in GI, less systemic effect; prednisone) = MAINSTAY
▪ Metronidazole – 2˚ bacterial infections, Fortiflora (probiotic), Vitamins (cobalamin)
▪ Pro-motility agent (metoclopramide) – may stop vomiting but may also cause diarrhea
▪ Azathioprine (DOGS ONLY) – immunosuppressive drug for unresponsive IBD
▪ Chlorambucil – immunosuppressive for refractory IBD (AND GI LYMPHOMA!)
- Pancreatitis
o CAT – lethargy, anorexia – feed regular diet (cats don’t need low-fat/NPO period), IV fluids, H2 blocker (ranitidine)
o DOG – vomiting, painful abdomen – fast 24 hours, then LOW-FAT diet, IV fluids, H2 blocker, antibiotics
▪ High fat food ↑ risk / surgical excision of insulinoma can predispose
▪ Mini Schnauzer
▪ Prognosis = worse if severe systemic signs, organ failures, acidosis, hypocalcemic, DIC
o Ultrasound: hypoechoic pancreas (edema) + hyperechoic mesentery (peritonitis), ± enlarged/mottled pancreas
o Dx: PLI
- Exocrine Pancreatic Insufficiency
o YOUNG animals, German Shepherds predisposed – RAVENOUS APPETITE, weight loss, PUPD, voluminous pale
diarrhea, polyphagia, abdominal discomfort, pica, coprophagia
▪ Can't digest fat or protein → emaciation
o Most Common Cause:
▪ DOG – pancreatic acinar atrophy
• Small intestinal bacterial overgrowth (SIBO) – ↓ antibacterial factors in pancreatic fluid
• Cobalamin (Vit B12) = ILEUM / Folate = JEJUNUM → ↑ folate, ↓ cobalamin
• Bacteria synthesize folate → ↓ absorption of cobalamin
▪ CAT – chronic pancreatitis
• Concurrently have diabetes mellitus bc endocrine cells are affected
o Dx: trypsin-like immunoreactivity (low is diagnostic)
o Tx: pancreatic enzyme powder, raw pancreas fed w/ meals, digestible diet (w/ ↑ protein)
- Upper GI Obstruction/Foreign Body
o Lethargy, anorexia, vomiting
o Bloodwork (w/ gastric outflow): hypochloremic metabolic alkalosis (↓ Cl, ↑ TCO2)
o Tx: stabilize w/ fluids (correct electrolyte abnormalities – NaCl), enterotomy/gastrotomy
- SIBO – Small Intestinal Bacterial Overgrowth
o German Shepherds, Shar-Peis
o Weight loss, chronic diarrhea w/ flatulence and foul smelling stool (recurrent watery foul smelling diarrhea)
o Dx: ↑ folate, ↓ cobalamin (bacteria produce folate and bind cobalamin)

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HERNIAS
- Diaphragmatic Hernia
o Rapid shallow breathing, quiet lung sounds, heart sounds normal, no crackles/wheezes
o Cause: TRAUMA – could be months after trauma – take rads so you don’t miss it
o Keep animal upright, try to prevent abdominal organs from invading chest cavity
o Dx: barium study, thoracic rads
o Tx: surgical repair
o Peritoneopericardial Diaphragmatic Hernia – ALWAYS CONGENTIAL – never from trauma
- Perineal Hernia – OLDER INTACT MALE DOGS
o Breeds: Boxer, Collies, Kelpies, Pekingese, Boston
o Weak pelvic diaphragm – maybe hormonal cause that weakens it over time
o Straining to defecate, bulge in perineal region – dx via rectal exam
o Tx: surgery – could lead to fecal incontinence, infection, repair failure (muscles too weak)
- Inguinal Hernia – MALE DOGS, congenital or trauma (acquired)
o Internal inguinal ring = inguinal ligament, rectus abdominis, internal abdominal oblique
o External inguinal ring = external abdominal oblique
- Umbilical Hernia – CONGENITAL (failed/delayed fusion of rectus abdominis muscle(
o Small hernias – schedule surgery after 6 months if still present
o Concurrently cryptorchid: always asses for hernia in these patients
ONCOLOGY
- Primary Lung Tumor
o Tx: lung lobectomy (wide margins), chemo in cases where tumor can't be completely excised
o Prognosis: guarded long term
▪ Lung-digit syndrome: primary lung neoplasia metastasizes to toes (present for swollen, painful toes)
- Osteosarcoma
o Clinical Signs: persistent lameness that progressively worsens, can usually isolate pain to 1 long bone
▪ Pathologic fractures: boney lysis weakens the bone – won’t heal w/ rest or fixation
▪ Large/giant breed dogs
o Rads: lytic bone lesion / Dx: FNA of bone
o Tx: AMPUTATION + CHEMO
▪ Amputation is only palliative (wont ↑ MST); need chemo to increase MST
▪ Cats – much better prognosis – lower rate of metastasis (12+ months)
▪ Dogs – usually only live 3-4 months w/ amputation alone (pulmonary metastasis)
• Chemo can ↑ MST to 10-12 months (6 rounds of carboplatin)
- Cutaneous SCC
o Non-pigmented areas, erythema, ulcerations, hx of being outside often/lots of sunlight
o Cytology: atypical keratinocytes
MISCELLANEOUS
- Doxycycline – safe for patients w/ renal insufficiency compared to tetracycline/oxytetracycline
o Less likely to cause skeletal abnormalities
o Small doses of IV doxy in HORSES = cardiac arrhythmias, collapse, death
o Can cause esophagitis and esophageal stricture in cats – make sure to give lots of oral fluids to wash into stomach

CANINE DISEASES
VIRAL DISEASES
- Distemper – paramyxovirus
o Shed for several weeks after infection – 3-6 months old puppies susceptible (esp. w/ poor vaccine regions)
o Very contagious, AEROSOL spread
o TRIO of signs; GI (diarrhea), Neuro (seizures), Respiratory (pneumonia)
▪ ENAMEL HYPOPLASIA – pathognomonic for dogs infected w/ distemper as puppies (infected before
eruption of permanent teeth)
o Dx: IFA on affected epithelium – tracheal, vaginal, respiratory; serology for distemper IgM, ↑ CSF/serum virus
specific IgG

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 - Parvovirus – canine parvovirus 2
o Starts shedding after 4-5 days and continues until 10 days after resolution of clinical signs; incubation 4-14 days,
fecal-oral transmission (survives well in feces)
o GI tract/bone marrow – damages rapidly dividing tissues – lethargy, anorexia, vomiting, diarrhea, young puppy (6
weeks to 6 months), dehydration, fever
▪ Nonsuppurative myocarditis if infected in-utero
- Parainfluenza virus/adenovirus 2
o Canine tracheobronchitis – leads to pneumonia (esp. in young dogs)
BACTERIAL DISEASES
- Campylobacter jejuni
o Mucus diarrhea; on cytology: motile S-shaped or “gull-shaped” rods
o Culture: streak feces on Campylobacter blood agar plate; grow in ↓ O2 atmosphere for 3-4 days
o Kids w/ puppies are 16x more likely to get this
- Salmonella
o Common in dogs fed BARF diet (bones and raw food/biologically appropriate raw food)
o Acute bloody watery/mucoid diarrhea, depressed, weak, slightly pale MM, dehydrated
o DON’T FEED RAW – zoonotic issue too – will transmit salmonella to humans
- Clostridium difficile – hemorrhagic gastroenteritis (HGE)
o Acute onset hemorrhagic diarrhea w/ marked hemoconcentration, raspberry-jam like diarrhea, vomiting,
abdominal pain
▪ Common in mini poodles, mini schnauzers
o Dx: positive fecal test for Clostridium enterotoxin, HIGH PVC, NORMAL TS (protein loss into intestines)
o Tx: bismuth subsalicylate (Pepto Bismol) – causes feces to be black (causes misdiagnosis of melena)
- Actinomyces – filamentous and branching
o Normal inhabitant of oropharynx – common association w/ grass awn migration (gets in oropharynx, migrates
through body from resp/GI tract – could take years to diagnose
o Acute onset of sneezing after running through field, remove grass awn from nasal passage
- Nocardia
o Ubiquitous soil saprophyte, usually introduced via respiratory tract
- Bordetella bronchiseptica – Canine Infectious Tracheobronchitis = KENNEL COUGH
o Primary bacterial pneumonia (Pseudomonas, Pasteurella, E. coli all require underlying problem to cause
pneumonia – aspiration, FB, viral infection, neoplasia)
▪ Other causes of kennel cough = parainfluenza, influenza, adenovirus 2, mycoplasma, distemper
o Tx (if 2˚ bronchopneumonia): coupage, systemic antibiotics, O2 therapy, nebulization
▪ Cough suppressants (hydrocodone, butorphanol)
- Neorickettsia helminothoeca = SALMON POISONING DISEASE
o Severe hemorrhagic enteritis, lethargy, anorexia, hx of going fishing, lymphadenopathy, depression, vomiting
o Vector: intestinal fluke (Nanophyetus salmincola) – dogs eat the salmon fish infected w/ fluke that harbors the
rickettsia – spread through lymphatics – causes ulcerative and hemorrhagic enterocolitis
o Tx: oxytetracyclines (rickettsia), praziquantel (flukes)
OPHTHALMOLOGY
- Collie Eye Anomaly
o Congenital in Collies – seen in 80% of breed
o Choroidal hypoplasia w/ varying degrees of visual dysfunction and bizarre choroidal vessels on fundic exam
o Some are completely blind, some show no visual deficits
o Other signs: optic disc coloboma, retinal hemorrhage, retinal separation
- Extraocular Polymyositis – GOLDEN RETRIEVERS
o Acute onset bilateral exophthalmos, no pain or swelling noted
o Similar to MMM – autoimmune reaction against muscle antigens
o Tx: prednisone ± azathioprine
- Sudden Acquired Retinal Degeneration Syndrome (ARDS)
o Middle aged obese female spayed dogs w/ Cushing's
o PUPD, polyphagia, ↑ liver enzymes/cholesterol, acute blindness

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 o Acute blindness w/o optic or fundic lesions – in 1-2 months, they develop vascular attenuation and tapetal
hyperreflectivity
- Progressive Retinal Atrophy/Degeneration
o Inherited – TOY/MINI POODLES – night blindness, progresses to complete blindness from loss of rods then cones
o Fundic exam – tapetal hyperreflectivity, grey fundic vermiform lines, retinal vascular attenuation, pale optic disc
- Iris Atrophy
o Normal aging change – seen in almost all dogs >10 years
o Normal fundus, somewhat irregular iris-pupil margin (scalloped iris margin), moth eaten stroma, slow/incomplete
PLR, normal menace/palpebral, dyscoria, anisocoria
- Chronic Superficial Keratitis – PANNUS – common in GERMAN SHEPHERDS
o Corneal melanosis/vascularization along the lateral aspect of limbus bilaterally
o Cause: UV light exposure – alters corneal proteins – leads to immune reaction
o Dx: normal Schirmer tear test, negative fluorescein dye
o Tx: topical steroids, cyclosporine (lifelong therapy)
- Horner’s = IDIOPATHIC (50% in dogs, 45% in cat)
o Miosis, 3rd Eyelid Prolapse, Enophthalmos (sunken eye), Ptosis (drooped eyelid)
RESPIRATORY
- Cricopharyngeal Achalasia
o Pharyngoesophageal sphincter wont relax
o Rare congenital condition – diagnosed at weaning; treated w/ cricopharyngeal myectomy
- Cricopharyngeal dysphagia
o Incoordination in swallowing reflex – congenital disorder
o Regurg after eating, repeatedly swallowing & regurgitating, sometimes coughs/sneezes concurrently
- Upper Airway Disease, Brachycephalic Airway Syndrome (BAS)
o Common – young brachycephalics – difficultly breathing, stertor, cough
o Tracheal hypoplasia, stenotic nares, elongated soft palate, everted laryngeal saccules, laryngeal collapse
o Tx: soft palate resection (if elongated), everted laryngeal saccule resection, surgically widening nares
- Tracheal Collapse
o Common – older toy/mini dogs – Chihuahua, Pomeranian, Toy Poodle, Shih Tzu, Lhasa Apso, Yorkie
o Weak tracheal rings – hypocellularity, deficient glycoproteins/glycosaminoglycans in tracheal rings (↓ strength,
loss of ability to remain firm)
o Important to take respiratory rads – end inspiratory + end expiratory – demonstrate tracheal narrowing
- Laryngeal Paralysis
o Progressive exercise intolerance, voice change, stridorous breathing in inspiration
o Dx: sedated laryngeal exam (DOXAPRAM) – giving thiopental/propofol for sedation can cause false dx of laryngeal
paralysis → add Doxapram to stimulate respiration
o Tx: unilateral arytenoid lateralization
- Pulmonary Thromboembolism (PTE)
o Acute resp distress, unremarkable rads, split second heart sound (due to pulmonary hypertension)
o Dx: contrast rads (angiography – see sudden interruptions in blood flow)
DERMATOLOGY
- Acanthosis nigricans – DACHSHUNDS (inherited), others (2˚ to skin diseases)
o Hyperpigmentation of axillary/groin regions
o 2˚ bacterial infections, yeast infections, seborrhea common in affected areas
- Color Dilution Alopecia – FAWN COLORED DOBERMANS, YORKIES
o Hereditary alopecia – affects color-diluted areas (less melanin that normal in hair shafts)
o Tx: NONE
- Zinc Responsive Dermatitis – SIBERIAN HUSKY
o Scaling, crusting, alopecic dermatitis – around eyes, ears, footpads, prepuce, scrotum, vulva
▪ Crusting/hyperkeratosis at mucocutaneous junctions and extremities
o Tx: zinc supplementation
- Canine Familial Dermatomyositis – COLLIES, SHETLAND SHEEPDOGS
o Atrophy of muscles, erosion/crusting/alopecia of skin – exacerbated by heat, sun exposure
o Tx: UNREWARDING – high dose steroids, Vit E, Omega 3 fatty acids

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 - Discoid Lupus Erythematosus
o Depigmentation/ulceration of nasal planum, erythema, alopecia, crusting around muzzle/lips/eyes, loss of
cobblestone appearance of nasal planum
- Lupoid Dermatosis – only GERMAN SHORTHAIRED POINTERS
o Fatal disease – initially causes crusting/scaling of dorsum and head – very itchy and miserable
o Attacks lymph nodes, causes inflammation of tonsils and spleen, swollen joints
o 1-2 years old: die from renal failure / euthanized because terrible quality of life
- Pemphigus Foliaceus
o Depigmentation, erythema, ulceration of nasal planum
- Atopy – atopic dermatitis
o Pruritis and erythema of face, ears, feet – SEASONALLY (high pollen in environment)
o Dx: intradermal skin testing (IDST), serum ELISA (measure antigen specific IgE)
o Tx: hypo-sensitization (inject allergen into pt – ↑ tolerance), cyclosporine, antihistamines, corticosteroids
- Food Allergy
o Pruritis and erythema of face, ears, feet, ventrum, GI signs (less common)
o Dx/Tx: trial diet w/ restricted allergens (novel protein, ultra-hydrolyzed protein)
- Pyoderma – Staph pseudointermedius
o Common in dogs – canine stratum corneum is less efficient barrier than in other species – dogs last ostial plug in
follicles – allows bacteria to invade and colonize more readily
o Tx: antibiotics
- Malassezia Dermatitis – yeast
o Wood’s lamp – SHAFT of hair glows GREEN (glowing skin isn’t diagnostic)
o Cytology: “footprints”
o Tx: systemic antifungals, antifungal shampoos
- Sebaceous Gland Tumor – most common skin tumor in dogs
o Older dogs – Cockers, Beagles, Poodles, Mini Schnauzers
o Multiple small (3-6mm) skin masses – wart/cauliflower like, ulcerated – on limbs, trunk, eyelids
- Otitis
o Otitis externa
▪ Causes: atopy, hypothyroidism, foreign body – alters environment in ear canal, allows overgrowth of
bacteria/yeast – see head-shaking, ear itching
o Otitis interna
▪ Head shaking, ear itching, disorientation circling, head tilt (toward affected side), dx w/ otoscopy
▪ Clean ears w/ saline, prescribe aural medications (after checking that tympanic membrane is intact)
- Aural Hematoma
o Tx: drainage (mattress sutures parallel to blood vessels – minimizes possibility of occluding blood vessels)
- Cutaneous Vasculitis
o Multifocal erosive/ulcerated lesions (i.e. footpads)
▪ Breeds: Jack Russell, Scotties, GSD
o Biopsy: sterile cutaneous vasculitis
o Tx: pentoxifylline and prednisone, tacrolimus (if focal), azathioprine, sometimes cyclosporine
GASTROENTEROLOGY
- Familial Hyperlipidemia/Hypertriglyceridemia – MINI SCHNAUZERS
o Predisposed to seizures, pancreatitis, acute blindness, vomiting, corneal opacities
o Management: low fat diets
- Megaesophagus
o Causes: myasthenia gravis, persistent right 4th aortic arch (PRAA), thymomas, congenital, endocrinopathy
(Cushing's, hypothyroidism), 2˚ to esophagitis, systemic lupus, OP toxicity, dysautonomia
o Dx: FNA of mediastinal masses (thymoma), anti-acetylcholine receptor antibodies for myasthenia gravis
(edrophonium test), rads to look for aspiration 2˚ to megaesophagus
o Regurg, choking on saliva, bringing up white foam
o Rads: distended esophagus, ventral depression of trachea, tracheal stripe sign

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 o Tx: small frequent elevated feedings, high calorie diets, treat 2˚ aspiration pneumonia, Bailey chair
▪ Metoclopramide/cisapride – sometimes stimulates esophageal peristalsis
▪ Anti-cholinesterase (pyridostigmine), corticosteroids to ↓ immune attack on ACh receptors
- GDV – Gastric Dilation and Volvulus – LARGE DEEP CHESTED DOGS (Great Danes, Weimaraners, St. Bernard)
o Stomach rotates counter-clockwise (looking at patient’s face) – twist can be 180-360 degrees
o Retching, hypersalivation, abdominal distension, tachycardia, prolonged CRT, pale MM, weak pulses, unproductive
vomiting
o Rads: RIGHT LATERAL – SMURF HEAD – gas fills left displaced pylorus
o To Decompress – pass tube (measure to last rib), trocharize stomach (14g needle)
o Prevention: GASTROPEXY (circumcostal – around rib / belt loop)
▪ Incisional = BEST! – suture to abdominal wall, easy!
▪ Incorporating = BAD – could cut into stomach at next surgery!! Never incorporate into midline incision!!
- Mesenteric Volvulus
o ACUTE life-threatening disease – severe abdominal pain, shock, gas distension, intestines may appear bunched
- Perforated Bowel
o Lethargy, inappetence, diarrhea, vomiting, abdominal pain, dehydration, febrile
o Ascites and gas distension in small intestines, LOW glucose
o Septic abdomen – compare blood glucose to peritoneal fluid glucose (fluid glucose >20 mg/dl LESS than blood
glucose = rapid reliable diagnosis
- Esophagitis
o Tx: sucralfate (coats and protects erosions in esophagus), H2 blocker/proton pump inhibitor (↓ gastric acid), broad
spectrum antibiotics (w/ severe ulceration or aspiration pneumonia)
- Perianal Fistulas – GERMAN SHEPHERDS, Irish Setters, Labs
o Tx: IMMUNOSUPPRESSIVE drugs (immune mediated disease) – cyclosporine
o Antibiotics reduce symptoms / surgery has guarded prognosis bc fecal incontinence
- Perianal Adenoma – hepatoid tumor
o Testosterone dependent – found in intact males or dogs w/ testosterone secreting tumors
o Tx: castration (will shrink/resolve tumor)
- Lymphangiectasia – Protein Losing Enteropathy
o Dilation and dysfunction of intestinal lymphatics; leakage of protein-rich lymph into intestinal lumen – lose protein,
cholesterol, lymphocytes into GI tract
o Bloodwork: PANHYPOPROTEINEMIA, frequently have ↓ Ca
ORTHOPEDICS
- Ruptured CCL
o Progressive rear limb lameness – reaches point of being minimally weight bearing, pain local to stifle
o Rads: joint effusion mild degenerate changes to bones, absence of primary bone lesion
o Cranial drawer ± tibial thrust, may also cause medial buttress/pain on stifle extension
o Medical Management: ↓ weight, strict rest for 6-8 weeks, NSAIDs, chondroprotectives (glucosamine, chondroitin),
NOT steroids (weakens ligaments)
o Surgery
▪ TPLO (tibial plateau leveling osteotomy) = change angle of tibial plateau to slope cranially – converts
cranial tibial thrust into caudal tibial thrust (caudal cruciate becomes primary stabilizer)
▪ Others: Cranial transposition of fibular head, lateral suture repair, tibial tuberosity advancement,
tightrope (synthetic ligament placement)
o Complication: MEDIAL MENISCAL INJURY – medial most closely associated w/ medial collateral ligament – causes
it to slide against femoral condyle bc it’s stuck in place
▪ Either bucket handle tear (caudal longitudinal tear) or “crush” of caudal horn of meniscus (incomplete
bucket handle tear)
- Luxated Patella – small breeds (i.e. Pomeranians)
o Most common = MEDIAL
o Tx: recession trochleoplasty, wedge/block resection of trochlear groove, lateral imbrication of retinaculum, lateral
transposition of tibial tuberosity, medial release of soft tissues

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 - Hip Dysplasia
o Difficulty rising/laying down on pelvic limbs – do Ortolani sign to look for hip laxity
▪ “bunny hopping” gait
o Ortolani Sign = manipulate femur – may feel/hear a “clunk” = subluxation of coxofemoral joint
o Tx: can try medical management w/ NSAIDs but have to go to surgery
▪ Triple Pelvic Ostectomy – YOUNG dog w/ minimal 2˚ degenerative changes and deep acetabulum
▪ Femoral head ostectomy – salvage procedure for dogs where TPO or THR aren’t options
▪ Total Hip Replacement
- Hip Luxation
o Performed closed reduction and place EHMER sling – prevent weight-bearing, aid in some degree of abduction and
internal rotation of affected limb – leave for 7-10 days
- Osteochondrosis dissecans (OCD)
o Shoulder = caudal aspect of humeral head / Elbow = medial aspect of humeral condyles
o Tarsocrural joint = trochlear ridge of talus / Stifle = femoral condyle
- Osteoarthritis
o Lameness, pain on extension/flexion of any joints – dx w/ rads
o Tx: medical management (NSAIDs, glucosamine, opioids)
- Distal Radial Fractures
o Common – small breed dogs – ↓ blood flow to distal aspect of radius
o Best: internal fixation bc ↓ blood supply means slower healing of fractures and ↑ incidence of non-union
- Elbow Dysplasia
o Fragmented medial coronoid process, OCD, elbow incongruency
o Intermittent lameness in forelimb, pain on flexion/extension of elbow joint
o Dx/Tx: arthroscopy (can do CT to evaluate boney structures better)
▪ W/ FCP, can perform sub-total coronoidectomy and remove diseased cartilage if OCD is there
- Panosteitis
o Young medium to giant breeds, acute lameness, fever
o Long bone pain – multiple long bones have ↑ medullary opacity on rads, periosteal new bone formation
o Tx: analgesics, will eventually resolve on its own; excellent prognosis but may have flare ups
- Legge-Perthes Disease – avascular necrosis of femoral head
o 3-12 months old TOY breed – pelvic limb lameness
o Rads: ↓ opacity of femoral epiphysis, moth eaten appearance of femoral neck and head
o Tx: surgical femoral head ostectomy or total hip replacement, analgesics
▪ Prognosis w/ surgery = good/excellent
NEUROLOGY
- Fibrocartilaginous Embolism (FCE)
o Embolus of disc material into spinal vasculature
o ACUTE onset of myelopathy localized to spinal segments T3-L3, still has superficial and deep pain and some motor
function present in limbs, hyperreflexive patellar/gastrocnemius reflexes
▪ “was running in yard and cried out, fell, and couldn’t get up”
o Prognosis: most get better w/ nursing care, loss of motor neuron signs = poor prognostic indicators
- Idiopathic Polyradiculoneuritis – COONHOUND PARALYSIS
o Raccoon exposure – acutely progressive ascending paralysis of pelvic limbs, progresses to forelimbs
▪ Diffusely affects all motor nerves
o Tx: nursing and supportive care – most will recover spontaneously in several weeks
- Canine Degenerative Myelopathy – GERMAN SHEPHERDS (5-9 years old)
o Often confused w/ hip dysplasia – progressive degenerative spinal cord disease – causes random axonal
degeneration in all spinal cord segments (most severe in thoracic segment)
- Myasthenia Gravis
o Progressive tetraparesis, weakly ambulatory, delayed CP in all 4 feet
o Rads: megaesophagus, aspiration pneumonia, mass in cranioventral abdomen (thymoma)
o Tensilon (edrophonium) test – edrophonium (anticholinesterase) reverses signs of MG in minutes

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 - Cervical Spondylopathy - WOBBLERS
o Cervical stenosis/wedging of vertebral canal, vertebral malalignment, vertebral instability
o Slowly progressive ataxia/paresis of all 4 limbs – ataxia is sporadic – UMN signs to all 4 limbs
▪ Hyperreflexive spinal reflexes in all limbs, delayed CP in all 4 limbs, neck pain on ventroflexion
- Degenerative Disc Disease (IVDD)
o Progressive lameness in hind limbs, trouble rising, drunken gait, acute hindlimb ataxia, CP deficits, no panniculus
o Hansen’s Type 1 = CHONDRODYSTROPHICS (Dachshund, Corgi, Shih Tzu) – acute, painful, emergency
o Hansen’s Type 2 = non-chondrodystrophic dogs – chronic, non-painful, NOT emergency
o Dx: MRI (better for soft tissue), CT/contrast myelogram
o Tx: if only pain (no neuro signs) = strict cage rest, NSAIDs/opiates
o Tx: if non-ambulatory or unresponsive to medical management = surgical decompression (hemilaminectomy –
thoracolumbar discs, ventral slot – cervical discs)
- Discopondylitis
o Hematogenous spread of bacteria to spinal cord (from distant infection)
o Occult infection somewhere else, do blood culture, see vertebral endplate lysis on rads
o Tx: antibiotics, surgery if neuro deficits are severe
- Hydrocephalus = TEACUP CHIHUAHUA
- Brachial Plexus Avulsion
o After trauma: thoracic limb monoplegia, Horner’s on the affected side, dragging of limb (no CP/motor/deep pain)
o Tx: leg amputation (if complete nerve root avulsion)
o Prognosis: partial tear better than complete, lots of PT, lack of deep pain/motor is negative prognostic factor
- Trigeminal (CN V) Neuropathy
o Progressive muscle loss on skull, atrophy of masseter/temporalis muscles on the affected side – UNILATERAL
- Masticatory Muscle Myositis (MMM)
o Autoimmune – atrophy of masseter/temporalis muscles – BILATERAL
ONCOLOGY
- Lymphoma
o Lethargy, inappetence, peripheral lymphadenopathy, HYPERCALCEMIA (produces PTHrP)
o Predominantly lymphoblast population (larger than mature lymphocytes)
o Lymphoma vs leukemia: bone marrow affected in leukemia
o Tx: PREDNISONE, doxorubicin, cyclophosphamide, vincristine, L-asparaginase, lomustine (CCNU)
- Chronic Lymphocytic Leukemia
o Peripheral lymphadenopathy, prominent spleen on palpation
o Bone marrow aspirate: 40% small lymphocytes / FNA of lymph node: 90% small lymphocytes
▪ Considered chronic bc made up of well differentiated mature lymphocytes
- Hemangiosarcoma (HSA) – GERMAN SHEPHERDS
o Schistocytes (fragmented RBC – broken due to irregular vessels, fibrin strands as they pass through tumors),
thrombocytopenia, anemia (NOT Heinz body), leukocytosis
o SPLENIC – most common malignant tumor of spleen (2/3 are malignant splenic masses, 90% chance it already
metastasized by time of dx)
o CARDIAC – Right Atrium/Auricle – leads to cardiac tamponade (excessive fluid in pericardium)
- Mast Cell Tumor (MST)
o Symptoms related to histamine/heparin release, other vasoactive amines
▪ Histamine: GI ulcers – activates H2s on gastric parietal cells – cause ↑ gastric acid secretion
▪ Heparin: coagulopathy
▪ May also see hypotension, vasodilation, local inflammation surrounding tumor
o Tx: NOT MORPHINE – causes significant histamine release!
▪ Palladia – toceranib phosphate (tyrosine kinase – RTK – inhibitor – FDA Approved for MCT)
▪ H1/H2 blockers, proton pump inhibitors – diphenhydramine (H1), famotidine (H2)
▪ Vinblastine, prednisone – chemo good for most MCT
- Histiocytic Neoplasm – BERNESE MOUNTAIN DOG
- Cutaneous Histiocytoma
o Usually BENIGN – small raised alopecic mass, ± ulceration (usually on head, front limbs)
o Usually develop in dogs <3 years old – don’t have to treat: will ulcerate and regress on its own

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 - Transmissible Venereal Tumor (TVT)
o VINCRISTINE alone = >90% cure
o Different # of chromosomes than host cells (59 instead of normal 78 in dogs)
▪ Theory: came from 1 original animal (all TVT are identical copies)
- Testicular Tumors
o Sertoli Cell Tumor
▪ CRYPTORCHID testes – often secrete ESTROGEN
▪ Male feminizing syndrome – gynecomastia, sexual attraction of other males, bilaterally symmetric
alopecia (w/ occasional pruritis, papular eruptions, hyperpigmentation), aplastic anemia (bone marrow
dyscrasias), urinating in female position
o Interstitial Cell Tumor
▪ Usually hormonally silent, usually in scrotal testes
o Seminoma
▪ Can secrete androgens/estrogens, can cause feminization
- Apocrine Gland Anal Sac Adenocarcinoma (AGASACA) – SPAYED FEMALES
o Usually VERY SMALL tumors – most clinical signs due to distant metastases/HYPERCALCEMIA due to PTHrP
secretion by tumor cells
o Result: renal damage, metastatic disease, pelvic canal obstructed by lymph nodes (even from small tumors)
- Prostatic Neoplasia
o Sublumbar mass, bony lysis of L6 vertebral body (more lysis than seen w/ IVDD, spondylitis, immune mediated
polyarthritis)
o Castration DOES NOT ↓ risk of prostatic neoplasia (only ↓ risk of prostatitis)
- Transitional Cell Carcinoma (TCC) – TRIGONE OF BLADDER
o Tx: NSAID - piroxicam (palliative); platinum therapy (can extend progression-free interval and survival w/ chemo);
Chemo: carboplatin, cisplatin, mitoxantrone
MISCELLANEOUS CANINE DISEASES
- Nutrition
o Large breed puppies – limit calcium to prevent skeletal abnormalities (OCD, retained cartilage cores)
o MER = 70 x (BW in kgs)0.75
▪ In tiny (overestimates) or giant dogs (underestimates), not as accurate
o Vit A Deficiency – nyctalopia (night blindness) – retina needs Vit A
o Hypoglycemia
▪ Status epilepticus from not eating, lethargy – common in YOUNG TOY breeds
▪ Neoplasia: insulinoma, β cell tumor, hepatocellular carcinoma
▪ Xylitol poisoning
▪ Sepsis
- Ectopic ureter
o Incontinence, unremarkable abdominal rads – need abdominal contrast CT, cystoscopy, abdominal ultrasound,
excretory urogram, vaginourethrography
- Amyloidosis – SHAR PEIS
o Lethargy, PUPD, ↓ appetite, no response to supportive care, proteinuria (suggests glomerular disease)
o Histopath: waxy kidneys, greyish, enlarged
o 4 signs of Nephrotic Syndrome: proteinuria, hypercholesterolemia, edema/ascites, hypoproteinemia
o Tx: (same for glomerulonephritis) – ACE inhibitors, restrict dietary protein (both ↓ proteinuria), aspirin (↓ platelet
function – alleviate hypercoagulable state when antithrombin III is lost)
- Fanconi Syndrome – BASENJIS – proximal renal tubular disease
- Copper Toxicosis – BEDLINGTON TERRIERS – accumulate copper in livers, show signs of liver failure
- Bile Peritonitis
o Dx: compare bilirubin in fluid vs. serum – 2x higher than serum is diagnostic
- Heart base tumors – brachycephalics predisposed

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 - Vaginal Prolapse
o Young bitch, correlates w/ estrous cycle
o 3 Types
▪ 1 = slight/moderate eversion of vaginal floor w/o protrusion from vulva
▪ 2 = cranial floor and lateral walls of vagina protrude through vulva lips (tongue/pear shape)
▪ 3 = entire vaginal circumference prolapses (donut shaped mass protrudes from vulva)

FELINE DISEASES
VIRAL DISEASES
- Feline Infectious Peritonitis (FIP) – CORONAVIRUS
o Transmission: Fecal-oral – NOT CONTAGIOUS; if 1 cat dies of FIP, doesn’t mean others will
▪ Feline enteric coronavirus mutates to FIP – seen in YOUNG IMMUNOSUPPRESSED cats
o Pyogranulomatous vasculitis – Ag-Ab complexes deposited in venous endothelium
▪ Complement mediated inflammation = pleural/peritoneal fluids (WET FORM)
• Dyspnea, fever, weight loss, anorexia, diarrhea, lethargy, abdominal distension (ascites)
• Pericardial effusion – muffled heart sounds, ↑ HR, weak pulses, large globoid heart
• Pleural effusion – ↑ protein (5-12), thick, low cellularity, predominantly neutrophils, clear to
hazy yellow, sometimes has fibrin clots
▪ Partial cell-mediated inflammation = slow viral replication and granuloma formation (DRY FORM)
• Depends on organ affected – hepatomegaly, splenomegaly, renal failure
o Dx: BIOPSY & HISTOPATH – gold standard
▪ Coronavirus titers are USELESS – reacts w/ all coronaviruses
▪ 7B protein ELISA – not helpful bc some FIP viruses have 7B
▪ Histopath: pyogranulomatous and fibrinonecrotic reaction around small veins
o Prognosis = POOR – FATAL DISEASE
- Feline Immunodeficiency Virus (FIV)
o Transmission: SALIVA – bite wounds – males more aggressive so 2-3x more likely to get infected
▪ Not passed by passive contact/litterbox sharing
o Affects B cells, CD4+ T helper cells, macrophages, CD8+ cytotoxic T cells
▪ Replication in lymphoid and salivary tissue – viruses spreads to mononuclear cells (viremia is suppressed
by host immune system for several years in carrier phase)
• Slow ↓ in CD4+ cells results in immune failure
• Cats are 10-15 years old by the time this occurs
▪ Makes animal VERY IMMUNOSUPPRESSED – susceptible to infections
o Dx: ANTIBODY ELISA for FIV – doesn’t produce enough antigen to measure
▪ Test kittens after 6 months (maternal antibodies are gone); vaccination shows positive antibody titers
o Tx: AZT (azidothymidine – aka Retrovir) – ↓ viral load, improve clinical signs in FIV cats
- Feline Leukemia Virus (FeLV)
o Sheds in SALIVA – requires close prolonged contact to transmit
o Active infection in cats >10 years old – infected when have inadequate immune response, persistently shed,
disease occurs in months/years later when stressed/immunosuppressed
▪ Result: leukemia, lymphoma, anemia, myelodysplasia
• Most Common: mediastinal lymphoma (cats <3 years old)
o Dyspnea, regurgitation, Horner’s syndrome
• 2nd Most Common: multicentric lymphoma
o Dx: ANTIGEN ELISA for FeLV
- Panleukopenia Virus (aka Feline Distemper, kitten parvo) = PARVOVIRUS
o Cats shed for 6 weeks after they recover – most common in YOUNG KITTENS
o Damages rapidly dividing tissues – bone marrow, GI tract = anorexia, lethargy, vomiting, diarrhea, dehydration,
fever
o If infected in utero → CEREBELLAR HYPOPLASIA (inability to regulate motor function – ataxia, tremors, hard to
balance, hypermetria, wide based stance, vestibular signs, postural reactions, UMN signs)

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 - Feline Calicivirus
o Lethargy, anorexia, sneezing, conjunctivitis, nasal discharge, COMMONLY oral ulcerations, chemosis, ptyalism
▪ STOMATITIS, gingivitis (bacterial infection)
▪ Lethal feline calicivirus (highly virulent) = ulcerative and edematous skin lesions on head/limbs
• Maybe jaundice (hepatic necrosis), thromboembolism, coagulopathy (DIC) – possible
petechiations, ecchymoses, epistaxis, hematochezia
o Tx: clindamycin (bacterial infection and stomatitis – NOT DOXY – causes esophageal stricture!), sucralfate (coat GI
ulcers), analgesia, esophagostomy tube (if won’t eat voluntarily), L-lysine (anti-viral)
- Feline Herpesvirus = Feline Viral Rhinotracheitis
o 80-100% of cats become carriers w/o clinical signs → flares with STRESS
o Conjunctivitis, coughing, fever, anorexia, dendritic ulcers in eye (LINEAR), rarely oral ulceration
▪ Ocular signs: conjunctivitis, corneal ulcers, eosinophilic keratitis and corneal sequestrum
(pathognomonic for herpes!) – only infectious cause of corneal ulcers in cats
o Tx: L-lysine (anti-viral), ↓ stress
BACTERIAL DISEASES
- Chlamydophila felis
o Upper resp tract infection – acute onset of severe chemosis, conjunctivitis, sneezing, NO oral/skin lesions
o Tx: tetracyclines
- Mycoplasma haemofelis = Feline Infectious Anemia
o Tx: doxycycline (caution bc esophageal strictures)
- Bartonella henselae = CAT SCRATCH FEVER (humans), Bartonellosis (cats – usually asymptomatic)
o RBC infection in cats, transmitted by FLEAS – cat gets flea dirt in claws, scratches human
▪ ZOONOTIC – human gets fever, headache, malaise, lymphadenopathy
o Tx: doxycycline, flea treatment – will always be carriers so only treat actively bacteremic cats
▪ Bartonella = Doxycycline
o Dx: 5 tests (ELISA, IFA, PCR, culture, Western Blot)
- Yersinia pestis = PLAGUE
o Reservoir = RATS – transmitted by fleas or by eating infected rodent
o Lethargy, fever, mandibular lymphadenopathy w/ draining tract under chin, covered in fleas, outdoor/stray cat in
area w/ lots of rodents (prairie dogs, rats)
▪ Also see in dogs – dog ate rat, fever, lymphadenopathy
o Wear PPE, quarantine the animal, call state vet!
o Cytology: bipolar safety pin appearance, definitive dx based on culture
o Tx: lance “buboes” and flush, usually recover on their own
o ZOONOTIC – bubonic, septicemic, pneumonic, meningeal forms
▪ Clinical signs in 1-2 days in cats, incubation in humans = up to 8 days
HEPATOLOGY
- Cholangiohepatitis
o Causes: 2˚ to biliary obstruction (cholelith), ascending infection, immune mediated liver damage
▪ In conjunction w/ IBD and/or pancreatitis
o Inappetence, depression, fever, dehydration, icterus
o Bloodwork: ↑ WBC, ↑ ALP/ALT/GGT, ↑ bilirubin
o Ultrasound: enlarged liver w/ normal echogenicity, hyperechoic wall of common bile duct, distended bile duct,
possible cholelith causing obstruction, enlarged gallbladder w/ thickened wall
o Histopath: neutrophilic infiltration in portal areas
o Tx: supportive care, fluids, ampicillin, metronidazole, ursodeoxycholic acid, Vit E, milk thistle, Denamarin
▪ Antibiotics for 2 MONTHS – use one that’s excreted unchanged in bile (not TMS – hepatic metabolism)
▪ Surgical decompression (cholelith or complete biliary obstruction) – stabilize w/ fluids first
• Biliary-to-intestinal diversion (cholecystoduodenostomy or cholecystojejunostomy)
o Prognosis: FAIR – ½ do poorly (dead/euthanized in 3 months), ½ respond to tx and live

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 - Lymphocytic Portal Hepatitis
o Similar to Cholangiohepatitis in signalment, clinical signs, lab findings – differentiate w/ LIVER BIOPSY
o Anorexia, weight loss, enlarged liver on palpation normal gallbladder), ↑ WBC, ↑ ALT/ALP
o Histopath: lymphocytic and plasmocytic infiltration (NO neutrophils) in portal areas, not bile ducts
o Prognosis: GOOD – MST >2 years w/ tx – disease is SLOW to progress
- Hepatic Lipidosis – FATTY LVIER SYNDROME
o OBESE older cats (8-9 years) – anorexia, lethargy, icterus, enlarged liver on palpation
o Bloodwork: ↑ liver enzymes (NOT GGT), ↑ bilirubin, bilirubinuria
▪ Cholangiohepatitis and neoplasia have ↑ GGT
o Ultrasound: enlarged liver w/ hyperechoic hepatic parenchyma, normal gallbladder
o Cytology: hepatocyte clusters w/ cytoplasmic lipid droplets
o Tx: feeding tube for immediate/ongoing nutritional support (VERY IMPORTANT – ↓ mortality from 90% to 30%)
▪ + neomycin/lactulose (↓ hepatic encephalopathy), Vit K1 (when has coagulopathy), L-carnitine, manage
electrolyte abnormalities (i.e. hypokalemia)
GASTROENTEROLOGY
- Linear Foreign Body
o Acute onset vomiting, anorexia, dehydration, painful abdomen
o Anchors in cranial GI tract (i.e. under tongue) and causes GI to bunch up – bunched/plicated intestines in accordion
fashion on radiographs
o Tx: exploratory surgery to remove foreign body – DO NOT PULL STRING – could perforate intestines!
- Megacolon
o Chronic stretching from fecal impactions – colon can't move feces out of the body anymore
o Chronic constipation, vomiting, straining to defecate, palpate hard feces in colon = OBSTIPATION
o Medical management: adequate hydration, remove impacted feces (enema), laxative therapy (lactulose),
promotility agents (cisapride), dietary fiber (↑ GI transit time – psyllium, canned pumpkin)
o Surgical treatment (when refractory to medical therapy) – SUBTOTAL COLECTOMY
▪ Transect colon distal to cecum and descending colon proximal to pubis – anastomose them together and
preserve ileocolic junction (ileocolic artery limits the amount you can resect)
- Hairballs
o Intermittent vomiting, usually long-haired, chunks of hair in vomit
o Tx: laxatone, high quality diet, frequent brushing, metoclopramide (anti-emetic, promotility)
- IBD vs GI lymphoma
o Vomiting, diarrhea, lethargy, inappetence, low BCS
▪ Always do rads! Check for foreign body/obstruction!!
o Bloodwork: mild ↑ ALT/ALP, moderate ↑ CK (anorexia)
o Abdominal Ultrasound: thickened small intestinal muscular layer (large dark band in middle of intestinal wall)
o Dx: Need full thickness intestinal biopsies to differentiate
▪ PARR (compare DNA – if all from 1 cell, indicates neoplasia)
▪ Lymphocytes:
• IBD – mixed B and T populations
• Small Cell Lymphoma – only T cells (monoclonal)
o Tx: steroids (IBD responds pretty well to steroids alone, chlorambucil (better for lymphoma and refractory IBD)
▪ Supportive care: Vit B12 (cobalamin), maropitant, highly digestible/novel protein diet
- Idiopathic megaesophagus
o Siamese = familial predisposition
o Regurg! Congenital form seen soon after weaning (starting to eat solid food)
▪ Regurging food/water soon after eating, weight loss, poor growth, possible 2˚ aspiration pneumonia
DERMATOLOGY
- Psychogenic Alopecia
o Systemically healthy, alopecia on ventral abdomen
o Microscopically shows short blunted hairs w/ normal underlying skin = excessive grooming

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 - Eosinophilic granuloma = LINEAR GRANULOMA
o Lesion: linear shape, pink/yellow color, no crusting or pruritis, well circumscribed
o Causes: hypersensitivities/allergies to fleas, food, inhalants
o Tx: control hypersensitivity, sometimes antibiotics/corticosteroids
- Feline Acne
o Deep pyoderma condition on chin – crusting, alopecia on ventral mandible
o Clean w/ antiseptic solution daily
- Upper lip erosive lesions
o Skin biopsy – can differentiate btw SCC, malignant melanoma, eosinophilic granuloma complex
RENAL
- Feline Lower Urinary Tract Disease (FLUTD) – aka Feline Urologic Syndrome (FUS), Feline Idiopathic Cystitis (FIC)
o Clinical signs that occur w/ LUT obstructions (uroliths, mucus plugs, infections, TCC)
▪ Feline Idiopathic Cystitis – otherwise healthy cats w/o other problems
o Clinical Signs: dysuria, pollakiuria, hematuria, crystalluria, urolithiasis, stranguria
o Tx: PAIN CONTROL, surgically remove stones/obstructions; likely to recur once a cat has had it
- Urethral Obstruction
o MALE cats, difficulty urinating, lethargic, weak, vocalizing while frequently posturing to urinate, firm bladder
o Hyperkalemia – impaired urinary excretion of K – life threatening arrhythmias
o Tx
▪ Immediately give IV calcium gluconate (or Ca chloride) – counters effect of hyperkalemia-induced
bradycardia/cardiovascular collapse
▪ Relieve urethral obstruction – place urinary catheter
▪ 0.9% NaCl – no K! (may also give dextrose – stimulate insulin secretion to remove K intracellularly; if give
insulin, give dextrose too!
▪ Perineal urethrostomy – preserve pudendal nerves so don’t have urinary incontinence from lost somatic
innervation to urethral sphincter
o After discharge, if still straining frequently and find bladder empty on palpation but with thickened bladder wall:
▪ PHENOXYBENZAMINE – likely have hypertonicity of urethral muscle – this will ↓ internal urethral
sphincter tone so cat can urinate more easily
▪ NO STEROIDS – predisposes them to UTIs
- Polycystic Kidneys
o PERSIANS – bilaterally enlarged kidneys on palpation, multiple large fluid filled structures in kidney parenchyma
RESPIRATORY
- Pleural Effusion
o Rapid shallow breathing, quiet lung sounds, normal heart sounds, no crackles/wheezes, dyspnea, open-mouth
breathing, tachypnea, fever (if from infection – pyothorax, FIP)
▪ Rads: severe loss of detail in thorax, lung lobe retraction, can't visualize heart
▪ Tx: O2, chest tap to evaluate effusion type, thoracocentesis to drain (unless hemothorax!), take rads in DV
for animals in resp distress
o Chylothorax – common in Siamese and Himalayans, also seen in dogs
▪ Fluid: Lymphatic fluid in pleural space, clear to milky, white to pink fluid, opaque, variable protein (2.6-
10.3 g/dL) WBC count can be >7,000 cells/ul
▪ To confirm: compare pleural fluid triglycerides to serum triglyceride levels – effusion triglycerides are ↑
than serum = chylothorax
▪ Cause: ruptured thoracic duct, abnormal flow/pressures in thoracic duct
▪ Medical Management: low fat diet, Rutin, intermittent thoracocentesis
• Somatostatin – useful in resolution of pleural fluid = EXPENSIVE
▪ Surgical Tx: ligation of thoracic duct and pericardiectomy – when medical management fails

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 o Pyothorax – pus in pleural space
▪ Fluid: white w/ yellow tinge, foul odor, bacteria + degenerate neutrophils, fungi + nondegenerate
neutrophils
▪ To Confirm: ↓ glucose in effusion compared to serum – consistent w/ infection
▪ Cause: bite wound (intro bacteria to chest), migrating foreign body, extension of pneumonia into pleural
space
▪ Tx: chest tube w/ continuous suction, drainage/lavage of pleural space (isotonic fluids), antibiotics (based
on C&S – 4-6 weeks), surgical exploratory
o Hemothorax
▪ Fluid = BLOOD (from trauma, coagulopathy)
▪ Tx: DON’T REMOVE IT!
o Other: neoplastic effusion (lymphoma), infectious effusion (FIP), heart failure effusion
- Feline Asthma
o Acute/chronic airway inflammation from various stimuli – i.e. environmental allergens
o Dyspnea, coughing, open-mouth breathing, abdominal effort when breathing, ↑ RR, wheezing
o Rads: diffuse bronchial pattern w/ airway thickening (“tracks and donuts”)
o STABILIZE BEFORE DOING DIAGNOSTICS – put in O2 cage for a while before touching, β2 agonists, ↓ stress
o Tx: Beta 2 agonists (terbutaline, theophylline, albuterol), O2, corticosteroids (↓ inflammation), NOT ATROPINE
(thickens bronchial secretions, encourages mucus plugging of airways)
ONCOLOGY
- Injection Site Sarcoma (previously Vaccine Associated Fibrosarcoma)
o Mass at injection site – tumors are slow to grow/metastasize but are extremely aggressive locally
o Vaccine: thought to be associated w/ adjuvant (i.e. aluminum based adjuvant): 3/10,000 vaccines
o Tx: radical excision of mass
o Vaccine protocols: Rabies = R hind / FeLV = L hind / FVRCP = R front
▪ None in scapular region!!! All below the elbow/knee!!
▪ DO NOT GIVE IM – will take longer to diagnose!
o Can happen w/ any injection though (not just vaccines)
- Cutaneous SCC
o WHITE CATS – solar exposure (caused by UV light)
o ULCERATIVE, appear around NOSE, ears, eyelids – common on nasal planum
o Tx: surgery/radiation – if small enough, use Strontium-90 radiation; if larger, excise it
- Basal Cell Tumor = EPITHELIAL TUMOR
o OLDER cats – most common skin tumor in cats – firm, freely movable, SQ mass, hairless, slightly melanotic, usually
2-4cm, well circumscribed, slow growing – HEAD, NECK, SHOULDERS
o Most (>90%) show benign behavior even when histologically malignant w/ high mitotic rate
o If dx prior to removal, monitor it without removal unless it ulcerates/gets larger; if already removed, monitor for
recurrence
- Feline Traumatic Sarcoma
o Hx of eye trauma, phthisis bulbi (shrunken, non-functional), corneal edema, scarring, no menace/PLR, blindness
▪ If has history of eye trauma and is now blind, highly suspicious! VERY MALIGNANT in cats~
o Tx: ENUCLEATION – if you wait for signs of pain, it has typically metastasized!
MISCELLANEOUS FELINE DISEASES
- Capital Physeal Dysplasia – young male NEUTERED cats, OBESE
o Fracture across femoral head physis
- Hyperextension injuries of carpal joint
o Common since cats jump from high surfaces and always land on feet
o Tx: carpal arthrodesis – conservative therapy has guarded prognosis
▪ Debride articular cartilage, implant cancellous autograft into debrided joint space, fix bone plate across
injured joint
- Central Retinal Degeneration (FCRD) = TAURINE DEFICIENCY
o Rare now since commercial diets are balanced
o Cause: photoreceptors need lots of taurine and cats can't synthesize it
o Elliptical areas of tapetal hyperreflexia starting in area centralis dorsolateral to optic disk that progresses to
horizontal band and eventually can involve the entire fundus

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- Blindness due to Hypertension
o Causes of hypertension: hyperthyroid, renal disease, cardiac disease – treat underlying cause
o ↓ balance, poor depth perception, bumping into things
o Fundic exam: engorged retinal vessels, hazy retina, difficult to see details of optic nerves/vessels, marked
mydriasis, no menace – suspect eyes have detached retinas
o Blood pressure = HIGH (i.e. 260 mmHg)
o Tx: AMLODIPINE (Ca channel blocker) – slows rate at which Ca moves into heart/into vessel walls – relaxes vessels,
allows better blood flow – ↓ BP
- Diet
o Taurine Deficiency – essential amino acid (cats can't synthesize it)
▪ Dilated cardiomyopathy, central retinal degradation
o Arachidonic acid – also required in diet
▪ Poor reproductive function, insufficient platelet aggregation
o Thiamine Deficiency – rare in outdoor cats because they hunt – causes seizures
- Trichobezoar
o Long haired cat w/ allergic dermatitis = at risk
o Cranial abdominal mass, acute vomiting, eating grass, allergies

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