FILARIAE CM:

- Long, threadlike nematodes - S/Sx of infection are variable (dependent on host factors,
- Inhabit portions of the lymphatic system & subcutaneous worm burden and parasite strain)
and deep CT  systemic parasites - A patient can be asymptomatic but heavily microfilaremic
- Eggs  elongate and wormlike in appearance at the same time
- Microfilariae (highly modified eggs) – capable of living for - Some of these cases showed to have microscopic
a long period within the vertebrate host hematuria and/or proteinuria
o Ingested by their intermediate host & vector (insect) - Others manifest hyperactivity to even a small number of
o Molt and grow inside the insect  infective larvae, worms (esp patients who do not live in endemic areas)
which are deposited on the skin when the insect takes - Early manifestations: F. lymphangitis and LAD  “filarial”
blood from a suitable host or “elephantoid” fever
o Insect bite  [1] deposition of eggs or [2] getting eggs - Fever – begins with a chill and the fever remains high for
o Distinguishing feature – nuclei 1–2 days, and gradually declines in the next 2–5 days
- Lymphangitis commonly affects the limbs but may occur
WUCHERERIA BANCROFTI in the breast, scrotum or elsewhere
- Endemic to the tropics & subtropics (South America, o Inflammation spreads centrifugally (extremities first)
Pacific islands, and Asia – PH) o Affected lymphatic vessel – distended and acutely
- Prolly originated from SEA (Indonesian leaf monkey) tender
- Insect vector: mosquito species – Culex sp., Aedes sp., and o Overlying skin – tense, erythematous, hot
Anopheles sp. o Surrounding area – frequently edematous
o Night biting: Culex and Anopheles o Attacks recur periodically
o Day biting: Aedes o Occasionally accompanied by abscess formation, either
- Microfilariae – sheathed (egg shell; very thin & delicate; along the course of the lymphatic or at a lymph node
protects embryo inside) - Lymphadenitis occur alone or in combination with
o Thin sheath is not shed until it is digested in the periodic lymphangitis attacks
mosquito’s stomach o Affect femoral and epitrochlear (early in subperiodic
o Cylindrical body is bluntly rounded anteriorly and filariasis, less common in periodic filariasis), LNs
tapered posteriorly o When LNs enlarge, they remain so
o Numerous distinct nuclei are seen in the body – except o LNs appear firm, discrete and somewhat tender
the terminal portion of the tail - Scrotal lymphatics – preferential site for localization of
- Periodic Filariasis adult worms
o In most endemic areas - FDS – filarial dance sign; random movements of adult
o Microfilariae appear at the greatest density at 10pm– filariae, in the dilated lymphatics, is demonstrated thru UZ
2am/4am and at very small numbers during daytime o Presence is strongly correlated with higher microfilarial
(undetectable) blood vessels
o When undetected in peripheral blood, microfilariae are - Orchitis plus inflammation of the spermatic cord and
found in the capillaries and small vessels of the lungs some permanent thickening of the cord is very common in
o Migration may be d/t high PO2 in lungs and increased symptomatic patients (inflamed testes in males; in labia or
exertion in the other areas of the body (bc of motion) – groin in females)
asymptomatic - Lymphocoele presents when a lymph varix appears and
- Sub-periodic Filariasis ruptures into the scrotal sac; usu develops gradually as a
o In the Pacific islands and some cases in Vietnam result of recurrent attacks of orchitis
o Patients exhibit microfilariae at all times of the day but - Chyluria – passage of lymph in urine; occurs when a lymph
are greatest between 12nn– 8pm varix ruptures into any part of the urinary tract
o Very rare and by Aedes sp o Microfilariae may be found in chylous urine
Dx: - Elephantiasis – enlargement of one or more limbs, the
- Made on strict clinical grounds but demonstration of scrotum, breasts, or vulva with dermal hypertrophy and
microfilariae in the circulating blood is the only means by verrucous changes (warts)
which one may make a certain dx o Late complication of filariasis
- If microfilariae in small numbers (asymptomatic): Treatment:
o Make thick blood film - Antihistamines & Analgesics – for attacks of filarial
o Provocative administration of diethylcarbamazine lymphangitis
(does not apply to the Pacific or sub-periodic variant - Antibiotic therapy – in cases of 2nd microbial infection
strain) - Diethylcarbamazine (DEC) – effective microfilaricidal drug
- Radiographs give evidence of infection as the words die but eliminates the adult worms slower
and become calcified o MOA is unclear; daily for 12 days or once yearly
- Lymphangiography may demonstrate characteristic o In vivo – effect is dependent on the integrity of the
changes in filarial elephantiasis host’s cellular and humoral immune mechanisms
- Ultrasonography may show the movements of adult o Most of the microfilariae are destroyed by the RES cells
worms in the lymphatics (FDS) in the liver
 - DEC + Ivermectin – a better long-term suppression of Dx:
microfilaremia; once-yearly dosage schedule - Examining blood films stained to demonstrate the
- Surgical procedures – for tx of scrotal elephantiasis and morphological features of the microfilariae
hydrocoeles CM:
- Corticosteroids – administered with cautious supervision - Malayan filariasis – similar to bancroftian infections
and should not be given in the presence of o Elephantiasis involves leg below the knee or the arm
bacterial/fungal infection below the elbow (rare)
o Corticosteroids are immunosuppressant drugs o Allergic reactions tend to be severe
- Lymphadenitis are frequent in inguinal areas
- Followed by a retrograde lymphangitis often with
lymphedema of the foot and ankle
o Usu with ulceration of the affected node
- No involvement of genitalia (funiculitis, orchitis,
epididymitis, hydrocele, chyluria)
Tx:
- Similar to Wuchereria
o DEC in smaller doses or antihistamines may be
administered as a routine measure
o DEC found to destroy both adult worms and
microfilariae (more rapidly)
o Ivermectin given as a single dose of 20, 50, 200 or 20
mcg/kg body weight; repeated in 6 months

Wuchereria and Brugia differ in epidemiology:

Wuchereria bancrofti – found predominantly in regions
close to the equator (Africa, SoAm, and tropical and
subtropical areas); responsible for 90% of lymphatic
filariasis and 120M cases worldwide
Brugia malayi – restricted to South and SEA; responsible
for 10% of lymphatic filariasis and 13M cases worldwide
Lymphatic filariasis is considered neglected tropical
disease
Hosts: Both:
Definitive host: humans (preferred and sole choice; they
have become highly adapted to our physiology
Intermediate host: mosquito acts as vector
Life cycle
Mosquito carrying 3rd-stage larvae (L3) bites host 
parasite penetrates skin  infects host
Larvae move to the lymph nodes (WB) and/or blood
BRUGIA MALAYI
channels (BM) and mature into adults over the course of
- Some in South China and India, the rest in Indonesia,
a year
Thailand, Vietnam, Malaysia, PH, SoKor
Mature adults reproduce sexually and females (BM)
o Wider distribution than Wuchereria
produce an average of 10,000 microfilariae (eggs)
- Reservoir are Macaques and leaf monkeys and can be
Mosquito ingests microfilariae in blood meal and lose
transmitted to cats and civet cats
sheaths as they migrate through the cardiac region and
- Female adults (43-55mm x 130-170um) & Male adults (13-
into thoracic muscles
23mm x 70-80um)
Symptoms (Both)
- Insect vector: Mansonia sp. or Anopheles sp.
Asymptomatic Phase: upon initial infection no symptoms
o Zoophilic strain: by Mansonia sp., aperiodic,
may be present as microfilariae mature
nocturnally sub-periodic or nocturnally periodic in man
and nocturnally sub-periodic in animals – found in Lymphadenitis (LAD): causes swelling of the lymph nodes
swampy areas that may occur prior to maturation
o Anthropophilic strain: by Anopheles sp., always exhibit Lymphangitis: inflammation of the lymphatic vessels
nocturnal periodicity, animals infected but won’t retain usually after maturation – abscess formation and
infection – found in rice-growing areas ulceration of lymph nodes may also occur (more
- Microfilariae – sheathed (170-230um x 5-7um; diagnostic) common in BM)
o Nuclei extend almost to the tip of the tail (contrast to Secondary bacteria infections (lymph node failure caused
Wuchereria) with two terminal nuclei (contrast to Loa) by extended overstimulation)
o Adults are smaller than Wuchereria Lymphedema (elephantiasis): enlargement of the limbs,
late onset condition caused by repeated inflammation of
 lymphatic vessels. Consistent irritation of lymphatic - African eye worm is found throught the rain forest areas
vessels leading to blockages caused by dead adult of Sudan, Basin of Congo, and West Africa
worms, inflammatory fibrosis, or granulomatous - From African monkeys
reactions. Lead to scar formation of affected tissues - Adult migrates actively in subcutaneous tissues, deeper
o Brugia malayi: typically affect distal portions of the CT, bloodstream (diurnal periodicity)
body such as arms and legs o Males are smaller than females but both are not wider
o Wuchereria bancrofti: typically affects arms, legs, than 0.5mm
scrotum of men and breasts of women o Migration is rapid, not painful and less noticed unless it
Adults: passes over the nose bridge or conjunctiva tissue
Wuchereria bancrofti - Most conspicuous and irritating when crossing the
- Females: conjunctiva
o 6-10cm - Insect Vector: mango fly or Chrysops (large flies with a
o Vuvla is near the level of the middle of their painful bite) – night biting and arboreal
esophagus - Microfilariae – sheathed
o Ovoviviparous (thousands of microfilariae) o Body nuclei are continuous to the tip of the tail
- Males: (contrast to Brugia and Wuchereria)
o 40mm o Undergo developmental cycle in the thoracic
o Finger-like tail; no nuclei in end of tail musculature of the fly and reach the infective stage
Brugia malayi after 10-12 days
- Females: o Bite  infective larvae migrate out onto skin surface
o 80-100mm  enter thru wound bite
o vuvla is near the level of the middle of their Dx:
esophagus - On the basis of history of Calabar swellings (fugitive
- Males swellings) or the appearance of the worm in the
o 13.5-20.5mm conjunctiva
o Tail: curved ventrally, bears 3-4 pairs of both adanal o Bc microfilariae do not frequently appear in blood
and postanal papillae, spicules are unequal and CM:
dissimilar - African eye worm or Loiasis – edema of conjunctiva & lids
o Left papillae are complex; no nuclei in end of tail - Patches of localized subcutaneous edema or Calabar
Clinical Features: swellings anywhere on the body, often preceded by
- Most people affected with Brugian or Bancroftian filariasis localized pain and pruritus
in endemic areas are asymptomatic since the o Lasts several days or weeks and subside slowly
development of symptoms relates to the cumulative o Swellings – allergic reactions to the metabolic products
acquisition of increasing numbers of worms of the worms or to dead worms
- Includes 3 phases: - Provokes unusual reactions when in ectopic sites
o Asymptomatic microfilaremia - Hydrocele and orchitis in the tunica vaginalis or spermatic
o Acute episodes of adenolymphangitis (ADL) cord
o Chorionic lymphedema disease (irreversible - Colonic lesion causing obstruction in bowel wall
lymphedema), which is often superimposed upon - Membranous glomerulonephritis in patient who
repeated episodes of ADL developed local encephalitis and diffuse vascular
- Tropical pulmonary eosinophilia obstruction in small vessels of all organs
o Characterized by nocturnal wheezing o With fibrin thrombi around degenerating microfilariae
o Caused by an immune hyper-responsiveness to - Fibroblastic endocarditis, retinopathy, arthritis, peripheral
microfilariae trapped in the lungs and is typically seen neuropathy
in young males - Elevated antifilarial antibody (in amicrofilaremic pts) and
Treatment IgE, with eosinophilia when Calabar swellings are present
- Diethylcarbamazine (with/without corticosteroids) - Hypersensitivity reaction
- Ivermectin – studies have established that ivermectin - Lymphadenitis marked by distention of the subcapsular
given as a single dose in Bancroftian filariasis reduces and medullary sinuses by histiocytes and eosinophils and
microfilaremia by approximately 90% even one year after by atrophy of lymphoid follicles or as a local reaction to
tx dead microfilariae
- Albendazole – has also been used in filarial infections. - Does not produce lasting damage in host life
Prolonged courses of high dose albendazole have a Tx:
significant macrofilaricidal effect and result in a gradual - Few drops of 10% cocaine immobilizes migrating filariae
decrease in microfilarial levels - Surgical removal of migrating adult worms
- Doxycycline – initial studies suggested that doxycycline, - DEC – not for patients with blood microfilaria counts of
which has good activity against filarial spp, leads to 500 or more per 20uL
sterility of adult worms o Readily penetrates BBB and may cause fatal
encephalitis in heavily infected patients
LOA LOA o Retinal hemorrhage and exacerbation of renal lesions
 o 2mg/kg body weight, 3x daily for 21 days or 300mg o Subsides slowly and may recur
once a week (in adults) o Result in permanent thickening of skin with a
- Ivermectin – onset of action is slower than of DEC; S/E are violaceous color – due to death of microfilariae in the
mild, commonly with pruritus skin and liberation of antigenic materials from them
o Single dose of 400mcg/kg body weight o May be provoked by administration of drugs known to
kill the microfilariae and prevented by corticosteroids
- Onchodermatitis – patchy purplish or reddish eruption
that characterizes acute attacks (mal morado or erisipela
de la costa)
o Infected skin is atrophic and wrinkled with
subcutaneous thickening and lymphedema,
depigmentation producing “leopard skin” appearance
and presence of popular to pustular nodules
o Caused by inflammatory reaction to localized
collections of microfilariae in the skin
o Lesions are known as craw-craw
- Onchocerciasis – confined to one leg or an arm, rarely in
the trunk, with puritic popular eruption, swollen and dark
sin, enlarged and soft regional lymph nodes
o Commonly known as Sowda – microfilariae scarce in
skin
ONCHOCERCA VOLVOLUS
o Infected skin lose its elasticity and becomes deeply
- In Central Africa, Saudi Arabia, Yemen and in Western
wrinkled and atrophic, usu in skin and neck region
Hemisphere (Mexico, Guatemala, Ecuador, Brazil)
o In the hip region plus “hanging groin” – a sac of tissue
- Prolly introduced into America by slave trade
forms in the inguinal region, may contain inguinal or
- Adult worms are wirelike and whitish coiled within fibrous
femoral lymph nodes and may hang down as far as the
tissue capsules
knees
o Felames are long and less wide while males are shorter
o Complications: lymphedema of external genitalia and
and not more than 5cm in width
scrotal elephantiasis
- Intermediate host & vector: blackfly or buffalo gnat or
Tx:
Simulium sp.
- DEC – but with severe S/E: intense pruritus and localized
o Its vector, larvae and pupae develop in rivers or
edema, chorioretinal damage and keratitis in the eye,
streams
myalgias and athralgias, headache, dizziness, hypotensive
o Bite  simuliid ingests microfilariae
episodes (rare)
- Microfilariae – unsheathed
- Ivermectin – slow, puritic reactions are less evere, ocular
o Developmental cycle in insect and transform into
reactions are minimal, S/E like that of DEC but milder
infective forms that may enter a new host when the
- Suramin – quite toxic and is seldom warranted
simuliid takes a blood meal
- Nodulectomy – surgical removal of palpabke nodules
o In new host  developing worms wander thru
subcutaneous tissues and settle down in groups
o Worms become encapsulated in fibrous tissue tumor-
like mass  nodules
o From nodules  migrate actively through the dermis
and in the CT
o Rarely found in urine, blood or sputum
Dx:
- Identification of the microfilariae in skin snips
- Mazzotti test when skin snips reveal no microfilariae
o S/E: intense pruritus when DEC is taken
- Ultrasonograhy for detection of onchocercal nodules in
deeper tissues
CM:
- Nodules (mm-cm in diameter, numerous) on trunk or
limbs, few on the head or scalp, less often in other body
parts
o May be due to the biting habits of several vectors
o Not painful TRICHINELLA SPIRALIS (nonfilarial; musculature)
- Acute inflammatory reaction involving the face, eyes, ears, - Cosmopolitan in distribution with high pathogenicity – in
neck or shoulders or elsewhere in the body – may occur European countries
spontaneously - Parasite of carnivorous mammals esp in rats and swine fed
o Skin is hot, edematous, often painful, assctd with with uncooked garbage and slaughterhouse scraps; in
pruritus humans who consume uncooked pork
 - Adult male: with caudal appendages and 2 pairs of o 50-500 larvae – symptomatic
papillae o >1000 larvae – severe infection, potentially fatal 
- Adult female: viviparous (lays larvae); lives for 30 days and - Enteric hase – diarrhea or constipation, vomiting,
is capable of producing 1,500 larvae in her lifetime abdominal cramps, malaise and nausea
- Larva: has a spear-like burrowing anterior tip - Invasion phase – sever myalgia, periorbital edema and
- Infection: eosinophilia, high remittent fever, dyspnea, dysphagia 
o Hosts: human, rats, dogs, cats, pigs, or any other congestive heart failure, meningitis may develop
carnivore Tx:
o Serves as the final and intermediate host - Bed rest and supportive tx for the muscle pain
o Consumption of raw or undercooked pork or other - Corticosteroids for severe cases
meat containing the encysted larvae o Prednisone – 20mg 3x daily tapered over a period of 2-
o Larvae excyst after cysts are digested and penetrate 3 weeks
into the intestinal mucosa; adult within 30-40h - Thiabendazole – 25mg/kg BID for 7 days expels worm
- Intestinal infection: adult worms in the mucosa, transitory from the GIT, proven useless bc the parasite has already
and usu asymptomatic; migration and encystment of migrated to muscles
larvae in the muscles is prolonged with serious symptoms - Mebendazole – larvicidal; 20mg/kg 6-hourly for 10-14
o Male worms < females days
o Mate as soon as they mature and larvae are produced
within 3 days after fertilization
o About 5 days – larvae grow to maturity and begin stage Epidemiology:
of larval deposition and continue as long as female - Infections have been reported in the ff countries:
worms are in intestines o Canada, Mexico, Poland, Hungary, Holland, Yugoslavia,
o Duration of intestinal infection – due to number of Spain, Egypt, Lebanon, Brazil, Chile, Ecuador, Malaysia,
worms present and immune status of host Thailand
Dx: - Absent or rare in India, Australia, New Zealand, New
- Muscle biopsy – demonstration of the larvae Guinea, and some islands in the Pacific
o Most definitive diagnostic exam Prevention and control:
o Diaphragm, pectoral, gluteus, deltoid, biceps, and - Meat should be cooked at 77C
gastrocnemius – among the most parasitized muscles - Freezing kills the larvae
- Latex flocculation test, bentonite folucculation and ELIS - Storage at -15C for 20 days or -30C for 6 days is suggested
are now used - Smoking, salting, or drying meat is NOT effective
- Beck’s xenodiagnoses – meat with encysted larvae are fed
to albino rats
o Presence of female worm in the duodenum after 14
days and larvae in the muscles
- Elevated creatinine phosphokinase,
lactatedehydrogenase, myokinase, eosinophilia
CM:
- Trichinellosis – symptoms are minor and may go
unnoticed or moderately severe; vary according to
intensity of infection
- Usu appear suddenly and are those of a nonspecific
gastroenteritis
- Diarrhea with or without abdominal pain may last of
weeks
- Fever and eosinophilia are consistent
- Leukocytosis is common but not always present
- Hyperimmunoglobulinemia E, myositis appears early with Lifecycle:
the classic sign of trichinosis, circumorbital edema Ingestion of raw or inadequately cooked pork with encysted
- Edema of the eyelids (7th day of infection), photophobia, larvae  larvae excyst in the stomach or in the small
diplopia, or other visual disturbance intestine  burrow in the subepithelium of the villi where
- Sever muscle pain (peaks at 12-20th day) and often they mature  adult worms mate  female produce eggs
sensitive to pressure that grow into larvae in its uterus  female deposits larvae
- Splinter hemorrhages beneath nails in the mucosa (after a few days)  larvae penetrate the
- CNS involvement with symptoms suggestive of acute
mucosa  lymphatic system into the circulation  striated
psychosis, meningoencephalitis, cerebrovascular accident
muscles  grow and develop – encyst (3 weeks)
or brain tumor with clinical trichinosis
- In humans, calcification of the cyst may take place  6-12
- Death in 4-6weeks after infection
MORE Dx: months after infection – may lead to destruction or death
- Patients harbouring: of the larvae through an average lifespan of 5-10 years
o 10 larvae – asymptomatic have been observed
- Cause myositis due to “dead end” in the muscles
 SPOROZOAN (Malarial Parasites) cells of mosquito’s stomach wall  oocyst  sporozoites 
Plasmodium falciparum, P. ovale, P. vivax, P. alariae salivary glands  inoculated unto person bitten 
- Originated from SEA, Africa and Europe bloodstream  liver parenchymal cells or RBC in
- Intermediate host: humans (vertebrates) bloodstream hepatic cells or RBCs rupture  merozoite in
- Definitive host: Anopheles mosquito circulation, release products of metabolism  infect new
- Infective stage: sporozoites RBC; gametocytes in RBC continue asexual cycle  M/F
- Development: 8 (P. vivax) to 35 days (P. malariae) gametocytes  Anopheles bites  transformation of
- MOT: gametes (gametogony) – sexual fusion – sporogony
o Bite of female Anopheles flavirostris mosquito (sporozoite development)
o Blood transfusions from infected donors
o By contaminated needles and syringes Asexual multiplication in liver cells – except P. vivax and P.
o Congenital malaria – infected moms transmit parasites ovale: sporozoites enter a hypnozoite or resting stage before
to their child before or during birth (transplacental) undergoing asexual multiplication. After weeks-months,
- Asexual cycle or schizogony in vertebrate host’s liver or hypnozoite is reactivated and initiates asexual division
within RBC if in the bloodstream (erythrocytic schizogony;
44-72h = 4-36 parasites/cell)
- Sexual cycle in an invertebrate host (Anopheles)

P. VIVAX & P. OVALE

- RBCs burst every 48h  chills + fever followed by
drenching sweats (every 48h)  Tertian/Vivax Malaria
- Produce dormant forms in the liver (hypnozoites) which
can grow years later  Relapsing Malaria (deteriorate)
P. MALARIAE
- RBC rupture every 72h  regular 3-day cycle of chills +
fevers followed by sweats  Quartan Malaria or malariae
malaria
P. FALCIPARUM
- Most common and most deadly
- Aestivoautumnal, malignant tertian, subtertian malaria or
falciparum malaria
- RBC lyse irregularly between 36-48h  chills + fever will
either fall within this period or continuous
- Invades 30% of erythrocytes  anemia and sticky RBC 
plug up post capillary venules in the kidneys, lungs and
brain  ischemia, renal failure, lung edema and coma 
DEATH
- Cerebral malaria in children
- Infected individuals will have hepatomegaly and
splenomegaly (hepatosplenomegaly)
- Cause of Black Water Fever aka malarial hemoglubinuria
(renal failure) – RBC lysis  Hg in blood vessels and urine
 kidney failure

Control and Tx
- Prophylaxis: Chloroquine
o If chloroquine-resistant: Mefloquine or Doxycycline
- DOC: Chloroquine
o P. OVALE and P. VIVAX  Primaquine – kills the
dormant stages in the liver, preventing relapse
o P. FALCIPARUM  Chloroquine, Quinine (in
Chloroquine-resistant areas)
- Chloroquine, Primaquine and Quinine cause hemolysis in
patients with G-6-phosphate dehydrogenase deficiency
Life cycle:
Female mosquito bites infected person  draws blood with
M/F gametocytes  in mosquito: blood temp falls,
microgametocyte matures  production of microgametes 
exflagellation (extrusion of gametes); macrogametocyte
becomes a macrogamete and is fertilized with microgamete
 zygote  ookinete (elongated and active)  penetrate
Malaria parasite undergo three developmental stages: P. MALARIAE
Trophozoite – Schizont – Gametocyte - In subtropical and temperate areas but less frequent
- Asexual cycle takes 72h (48h in others)
P. VIVAX - Ring forms (indistinguishable from P. vivax)
- Vivax or vigorous (Latin)  active ameboid motility o Little ameboid activity as it grows
(during growth period) o Elongate (band or stab) form, stretches partway or
- Predominant malarial parasite in most parts of the world; entirely across the RBC
only species that extends into the temperate regions o Infected cell is not enlarged; parasite may fill the RBC
- Infected cells contain trophozoites or “rings” prior to schizogony
o Appear first as crescent masses at the periphery of the o Cell cytoplasm with dust-fine, pale pink dots or
RBC – accolé forms (French for joined together) Ziemann’s stippling
o Then, vacuole in the cytoplasm pushes the nuclear o Pigment is in some quantity and is dark
chromatin to the periphery – signet ring - Schizont: 6-12 merozoites, usu 8 and arranged in rosette,
o Bizarre or irregular forms in RBC symmetrically around a central mass of pigment
- Between 6 and 24h: trophozoites grow half the size of the o Pigment usu irregularly displaced within the mature
infected cell and brownish pigment appear; infected cell is schizont
enlarged and pale with very fine reddish granules or o Fully-developed schizont usu with 8 merozoites
Schuffner’s dots - Gametocytes are indistinguishable from growing
o Schuffner’s dots in RBC infected in 15-20h or longer trophozoites
o Presence is diagnostic for P. vivax and P. ovale o When mature: slightly larger, ovoid with more pigment
- At 40h: mature trophozoite ceases its ameboid activity & than mature trophozoites
become compact, appear smaller than when active; single - In thick film – trophozoites do not assume ameboid
nuclei divide rapidly comma or swallow forms (like in other sp); compact
- Enters the “Schizont” stage nature, appear as small dots of nuclear material with
o If mature – refer to number of merozoites rounded or slightly elongate masses of cytoplasm
o Cytoplasm segments  form separate small masses - Older Trophozoite are compact with abundant pigment
around each nucleus  individual parasites or
merozoites P. FALCIPARUM
o Infected cell ruptures at 44-48h and infects new RBCs - Almost entirely confined to the tropics and subtropics
- Cycle is never entirely synchronous; after first few - Sharply differentiated from the others
paroxysms, gametocytes are seen: - Trophozoites (young) are minute rings with 2 small
o Mature slower than asexual forms, not much ameboid chromatin dots
activity, more pigment o Earliest stages do not assume a ring form – lie spread
o When fully mature, fills cell more completely and out in accolé form (periphery)
contain more pigment o Parasite grows in size, irregular in outline, pigments are
o Macro nucleus is dense, micro nucleus forms a pale rare but still retain the ring form while in circulation
and loose network o Infected RBC retain original size, with few irregular
- Gametocytes of Vivax, Ovale and Malariae are similar in dark red, rod/wedge-shaped markings or Maurer’s
appearance – Malariae are smaller, darker and w/o dots or clefts
Schuffner’s dots - Schizont: (mature) 8-36 merozoites, usu 24 or 12-28
o Rely on asexual stages of the parasite to identify sp. merozoites
- Distorted early trophozoites are known as comma and o Thus, parasite is only seen as young trophozoites
swallow forms (“rings”) and gametocytes
- In thick film – as parasite become older: ameboid activity o Usu does not take place in the peripheral blood – only
is reflected by irregular shapes, ghostlike shadows of lysed during in heavy infections, only in moribund patients
infected cells around the parasite with Schuffner’s dots - Parasite attacks all stages of RBC and cause double or
triple infections of RBC
P. OVALE - Presence in non-native patients is a medical emergency
- Wide distribution in tropical Africa, displaces P. vivax on - Gametocytes are characteristic – elongate or sausage
the West African coast, South America and Asia shaped (not spherical/ovoid)
- Ovoid shape of infected RBCs o Crescent in outline, ends are pointed or bluntly
- Not as ameboid (as P. vivax), nuclei is larger in all stages, rounded, remains of RBC are seen in the concavity
scanty pigment formed by the arched body of the parasite
- Schizont: 4-12 merozoites, usu 8 (like in P. malariae); o No clinical significance if found w/o other stages but
rarely 12-18, usu 14-16 are easily recognized in thin film
o Infected cells are enlarged and pale, exhibit larger and - In thick film – usu with large number of early trophozoites,
more distinctly red Schuffner’s dots (than P. vivax) frequently collapse and assume comma or swallow form
o Margins are often ragged (delicate)
o Cells are elongate, ovoid or irregularly shaped Dx:
- In thick film – larger schizonts with no more than 12 - Thick and thin blood films
merozoites with distinct Schuffner’s dots
 o Additional thick and thin films every 6-12h as long as Complications:
48h (if first blood films are scanty) - Vivax, ovale and quartan malaria are relatively benign;
o Thick films best used as a screening procedure complications arise during the course of infection due to
o Thin films used for specific diagnosis and examiner is preexisting debility or intercurrent disease
experienced - Infection with P. falciparum: rapidly build up levels due to
- Immediately after paroxysm – merozoite-filled RBC have physiologic characteristics of infected RBCs, may lead to:
ruptured and free merozoites are in bloodstream o Localized capillary obstruction, decreased blood flow,
o Difficult to late and virtually impossible to identify by tissue hypoxia, infarction, death
species - Chronic infection with P. malariae: in children, immune-
o Gametocyte are present and readily identifiable complex deposition on glomerular walls  nephrotic
- Finding ring forms with or without characteristic syndrome
gametocytes in blood film - Tx depend on vigorous tx of that infection and follows the
- The use of recombinant DNA probes and ribosomal RNA usual procedures for handling the particular problem
probes
- Rapid tests rely on detection of plasmodial antigens or [1] Cerebral Malaria
enzymes - Most serious complication of falciparum infection and a
CM: frequent cause of death
- Incubation period is longest in Quartan and shortest in - Sudden onset (a first sign of infection)
falciparum malaria - Severe headache, drowsiness, confusion, coma, cerebellar
o Prodromal symptoms in the last few days of IP: H, A, N, ataxia (neuro)
V, photophobia, muscle aches & pains - Signs of CNS involvement are variable or absent
o May be seen in all types of malaria; at times entirely - Cerebral malaria  cortical blindness, hemiparesis,
absent in vivax infections; mild in ovale malaria generalized spasticity, cerebellar ataxia, sever hypotonia
- Malarial paroxysm with sudden shaking chill or rigor o Tx with quinine or quinidine
lasting for 10-15 minutes or longer [2] Anemia
o Pt experience extreme cold (temperature is elevated at - Due to heavy parasite load
onset and rises as chill occurs), agitated and may be o Treated with due care to prevent fluid overload and
restless, disoriented or delirious, severe frontal overt pulmonary edema
headache and pains in the limbs and back o Treated when hematocrit falls below 20% or if there’s
- Hot stage follows cold – skin is pale and cyanotic then parasitemia of 5% or greater
becomes flushed [3] Renal disease
o Hot stage lasts 2-6h in vivax and ovale malaria, 6h or - Common in severe falciparum malaria
more in Quartan and longer in falciparum - Acute renal failure due to tubular necrosis from red cell
o Hot stage  profuse sweating and feels better  ends sludging and renal anoxia
up weak, exhausted and falls asleep  normal or - Nephrotic syndrome (due to acute glomerulonephritis) is
subnormal temperature upon waking  paroxysm seen in Quartan and falciparum malariae
- Acute splenomegaly is rapid in non-immune patients  - Proteinuria is common during clinical attack of Quartan
tearing of splenic capsule and intra-abd bleeding malariae
o Surgical intervention is required o Assctd with massive edema and other clinical signs of
- Infection follows early primary attack; delayed for months nephrotic syndrome in children
in other species - Renal lesions are secondary to deposition within the
o Variation in onset and relapse are due to strain glomeruli of circulating antigen-antibody complexes
differences [4] Blackwater fever
o Lasts 3 weeks – 2 months or longer, if untreated - Results from massive intravascular hemolysis and
o As attack wanes, paroxysms become les sever and consequent hemoglobinuria
irregular in periodicity - In patients suffering from severe falciparum malaria (also
o Relapses following an asymptomatic period of weeks, in vivax and quartan)
months or years – 5-8 years in vivax malaria; does not - Onset occurs during a paroxysm of falciparum malaria
occur in falciparum malaria - Destruction of RBC may lead to profound anemia
o Early spontaneous recovery in ovale malaria after 6-10 [5] Dysenteric Malaria
paroxysms o Surgical intervention is required
o Quartan attacks terminates at 3 weeks or prolonged as
long as 24 weeks (white) or shorter (black)
 Termination may mean the infection has been
eliminated completely or a series of
recrudescences over a period of years
 Denotes a latent infection and persisting low-
grade parasitemia
- Recrudescences may occur over a period of a year or
slightly longer but usu to first 6 months after infection