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U r i n a r y Tr a c t I n f e c t i o n s
Treatment/Comparative Therapeutics

a, b
Shelly J. Olin, DVM *, Joseph W. Bartges, DVM, PhD

KEYWORDS
 Veterinary medicine  Canine  Feline  Cystitis  Pyelonephritis  Prostatitis
 Urinary tract infection

KEY POINTS
 Determining whether an infection is uncomplicated or complicated is essential to guide
the diagnostic and therapeutic plan.
 Recurrent infections are complicated infections and may be relapsing, refractory/persis-
tent, reinfection, or superinfection.
 Antimicrobials are the cornerstone of treatment of bacterial UTI and, ideally, are selected
based on culture and sensitivity.
 There is limited literature to support preventative therapies; identification and resolution of
underlying causes are essential.

INTRODUCTION

Urinary tract infection (UTI) occurs when there is a compromise of host defense mech-
anisms and a virulent microbe adheres, multiplies, and persists in a portion of the uri-
nary tract. Host defenses include normal micturition, anatomic structures, the mucosal
barrier, properties of urine, and systemic immunocompetence. Most commonly UTIs
are caused by bacteria, but fungi and viruses also may infect the urinary tract. UTIs
may involve more than one anatomic location, and the infection should be categorized
as upper urinary tract (kidneys and ureters) versus lower urinary tract (bladder, urethra,
and vagina). Most bacterial UTI occur as a consequence of ascending migration of
pathogens through the genital tract and urethra to the bladder, ureters, and one or
both kidneys. Rectal, perineal, and genital bacteria serve as the principal reservoirs
for infection.1,2

Disclosure Statement: The authors disclose no commercial or financial conflicts of interest.

a
Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of
Tennessee, 2407 River Drive, Knoxville, TN 37996, USA; b Cornell University Veterinary Special-
ists, 880 Canal Street, Stamford, CT 06902, USA
* Corresponding author.
E-mail address: solin@utk.edu

Vet Clin Small Anim 45 (2015) 721–746

http://dx.doi.org/10.1016/j.cvsm.2015.02.005 vetsmall.theclinics.com
0195-5616/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved.
722 Olin & Bartges

Bacterial Isolates
A single bacterial pathogen is isolated from approximately 75% infections; 20% of UTIs
are caused by 2 coinfecting species, and approximately 5% are caused by 3 species.3–5
The bacteria that most commonly cause UTIs are similar in dogs and cats
(Fig. 1).3,6–8 Escherichia coli is most common, followed by gram-positive cocci, and
then various others, including Proteus, Klebsiella, Pasteurella, Pseudomonas, Coryne-
bacterium, and several other rarely reported genera.3,6 Mycoplasma spp are isolated
from urine of dogs with clinical signs of lower urinary tract in less than 5% of samples;
whether Mycoplasma spp are associated with urinary tract disease in cats is
controversial.3,9–11
Cats may be infected with a unique strain of Staphylococcus, Staphylococcus felis,
and commercial phenotypic identification systems may not differentiate between S
felis and other coagulase-negative Staphylococcus spp.7,8 One study found that S
felis was the third most common isolate based on 16S rDNA sequencing (n 5 25/
106, 19.8% of bacterial isolates cultured), suggesting S felis is the most common
Staphylococcal species causing UTI in cats.7

Pyelonephritis
Pyelonephritis, or infection of the renal pelvis and parenchyma, is most commonly due
to ascending infections from the lower urinary tract in dogs and cats (Fig. 2). In addi-
tion to the components of immunity that protect urinary tract in general, the kidneys
are protected from bacterial infection by vesicoureteral flap valves, relatively long ure-
ters that usually allow only one-way flow of urine via peristalsis, and generally hypoxic
environment of the renal medulla.

Prostatitis
Inherent prostatic defense mechanisms against infection include local immune fac-
tors, such as immunoglobulin A and antibacterial proteins, retrograde flow of prostatic

Fig. 1. Prevalence of common urinary pathogens: 33%–50% E coli, 25%–33% gram-positive

cocci (Staphylococcus sp, Streptococcus sp, Enterococcus sp), 25%–33% other gram-negative
(Proteus sp, Klebsiella sp, Pasteurella sp, Pseudomonas sp, Corynebacterium sp), less than 5%
Mycoplasma sp. (Data from Ling GV, Norris CR, Franti CE, et al. Interrelations of organism
prevalence, specimen collection method, and host age, sex, and breed among 8,354 canine
urinary tract infections (1969–1995). J Vet Intern Med 2001;15:341–7; and Barsanti J. Genito-
urinary infections. In: Greene CE, editor. Infectious diseases of the dog and cat. 4th edition.
St Louis (MO): Elsevier Saunders; 2012. p. 1013–31.)
 Urinary Tract Infections 723

Fig. 2. Lateral abdominal excretory urography showing a pelvically displaced urinary

bladder and renal pelvic dilation (pyelonephritis) due to ascending E coli urinary tract in
a 4-year-old spayed female mixed breed dog.

fluid and urine, and urethral peristalsis, and the urethral high pressure zone.12,13 Dogs
with bacterial prostatitis often have alteration of normal defenses, such as underlying
benign prostatic hyperplasia, prostatic cysts, or neoplasia.14 Most commonly prosta-
titis develops from ascending bacterial infection and may result in prostatic abscessa-
tion in addition to prostatic parenchymal infection (Fig. 3). Hematogenous spread and
prostatitis secondary to cystitis are also possible. Bacterial pathogens are similar to
those causing bacterial cystitis with E coli being the most common (see Fig. 1). Bru-
cella canis should also be considered, especially for intact male dogs, as a cause for
both acute and chronic prostatitis.14

Catheter-associated urinary tract infection

Normal host defense mechanisms are effective in preventing bacterial UTIs; however,
they are not impenetrable. Normal host defenses may be overwhelmed if large quan-
tities of a virulent uropathogen are introduced into the urinary tract during diagnostic
and therapeutic procedures. Catheter-associated bacterial UTI is a common compli-
cation of indwelling urinary catheters, especially if an open-ended system is used. In a

Fig. 3. (A) Sagittal ultrasonographic image of the prostate and urinary bladder showing 2
cystic lesions that were abscesses (*) and (B) purulent prostatic wash fluid due to E coli in
a 6-year-old intact male Rhodesian ridgeback.
724 Olin & Bartges

clinical study, infection developed in 30% to 52% of dogs and cats with indwelling uri-
nary catheters; risk of infection increased with duration of catheterization.15,16 The risk
of infection is further compounded if the patient has pre-existing urinary tract disease.
Use of indwelling urinary catheters during diuresis or corticosteroid administration is
particularly dangerous.

Fungal Urinary Tract Infection

Fungal UTI is uncommon. As with bacterial UTI, fungal UTI occurs because of tempo-
rary or permanent breaches in local or systemic immunity of the lower urinary tract.
Funguria may be due to primary infections of the lower urinary tract or secondary to
shedding of fungal elements into the urine in animals with systemic infections. Primary
fungal UTI is most commonly due to Candida spp, a commensal inhabitant of the gen-
ital mucosa, upper respiratory tract, and gastrointestinal tract.17,18 Candida albicans is
the most commonly identified species, followed by Candida glabrata and Candida tro-
picalis; other ubiquitous fungi may also occasionally cause primary fungal UTI,
including Aspergillus spp, Blastomycosis spp (Fig. 4), and Cryptococcus spp.19

Viral Urinary Tract Infection

Viral-induced disease in humans is increasingly recognized, especially of the upper
urinary tract. However, it can be difficult to determine cause-and-effect relationships
because viral-induced disease may occur in the absence of detectable replicating vi-
rus. Several viruses have been implicated in canine and feline disease (Box 1).20

PATIENT EVALUATION OVERVIEW

Clinical Signs
Lower urinary tract infection: bacterial, fungal, viral
Lower UTI may be symptomatic or asymptomatic, and clinical signs are indistinguish-
able from other causes of lower urinary tract disease. Nonspecific clinical signs of
lower urinary tract disease include, but are not limited to, pollakiuria, dysuria, strangu-
ria, hematuria, and inappropriate urination.21

Prostatitis Acute prostatitis is usually associated with systemic illness, including fever,
anorexia, vomiting, and lethargy. Dogs with acute disease may also have caudal
abdominal pain, stiff gait, and preputial discharge and be unwilling to breed.12–14 In
contrast, dogs with chronic prostatitis are usually not systemically ill or febrile.13

Fig. 4. Blastomyces spp organisms observed by microscopic examination of urine sediment

from a 2-year-old castrated male Doberman pinscher.
 Urinary Tract Infections 725

Box 1
Viruses associated with urinary tract disease in dogs and cats

Species Upper Urinary Tract Disease Lower Urinary Tract Disease

Canine Canine adenovirus type I
Canine herpesvirus
Feline Feline coronavirus Feline calicivirus
Feline immunodeficiency virus Bovine herpesvirus-4
Feline leukemia virus
Feline foamy (syncytium-forming) Feline foamy (syncytium-forming)
virus virus

Adapted from Kruger JM, Osborne CA, Wise AG, et al. Viruses and urinary tract disease. In:
Polzin D, Bartges JW, editors. Nephrology and urology of small animals. Chichester (United
Kingdom): Blackwell Publishing Ltd; 2011. p. 725–33.

Commonly, recurrent UTI or preputial bloody discharge is the only clinical sign of
chronic prostatitis.14 Other presentations include stiff gait, discomfort with rising,
infertility, or orchiepididymitis, or dogs may be asymptomatic.13

Upper urinary tract infection

Pyelonephritis Pyelonephritis may have an acute or chronic presentation. Acute
pyelonephritis is usually associated with signs of severe systemic illness (eg, uremia,
fever, painful kidneys, possible nephromegaly, and/or sepsis). In contrast, chronic
pyelonephritis usually has a more insidious presentation: slowly progressive azotemia
that may not be associated with uremia, progressive kidney damage, and ultimately,
renal failure if untreated. Bacterial pyelonephritis may be associated with hematuria
only.

Diagnosis
Bacterial urinary tract infection
In addition to clinical signs, results of a complete urinalysis may provide evidence of a
bacterial UTI. Hematuria, pyuria, and bacteriuria are often present unless there is sup-
pression of immune response because of underlying disease or drugs (Fig. 5).

Fig. 5. Microscopic examination of a modified Wright stain urine sediment from a dog with
E coli bacterial cystitis showing white blood cells and bacteria (400).
726 Olin & Bartges

Microscopic examination of unstained urine sediment is less sensitive and specific

than examining urine sediment stained with a modified Wright stain.22
A positive urine culture is the “gold standard” for diagnosing bacterial UTI. A quan-
titative urine culture includes isolation and identification of the organism and determi-
nation of the number of bacteria (colony-forming units per unit volume). Quantitation of
bacteria enables interpretation as to the significance of bacteria present in a urine
sample. Caution should be exercised when interpreting quantitative urine cultures ob-
tained by midstream voiding or manual expression of urine.21
Determining whether an infection is uncomplicated or complicated is essential to
guide the diagnostic and therapeutic plan. A simple uncomplicated UTI occurs
sporadically in an otherwise healthy animal with a normal structural and functional uri-
nary tract.23 In contrast, infections are complicated if there is (1) involvement of the up-
per urinary tract and/or prostate, (2) an underlying comorbidity that alters the structure
or function of the urinary tract, such as an endocrinopathy or chronic kidney disease
(CKD), or (3) recurrent infection.23,24 Recurrent infections are further categorized as re-
lapsing, refractory/persistent, reinfection, or superinfection (Table 1).23,24 Most cats
with bacterial UTI have complicated infections.21 Additional laboratory testing and im-
aging studies are often required for complicated infections (Box 2).21

Pyelonephritis Pyelonephritis is an example of a complicated UTI. Diagnosis of pyelo-

nephritis is usually presumptive based on positive urine culture, concurrent consistent
renal diagnostic imaging abnormalities (eg, pyelectasia), and possible improvement in
degree of azotemia following antimicrobial therapy. Although a positive culture is help-
ful for the diagnosis, a negative urine culture does not rule out pyelonephritis.

Prostatitis All dogs with suspected prostatic disease should have a complete physical
examination, including rectal examination, and a minimum database with complete
blood count, chemistry panel, urine analysis, and urine culture. Abdominal radio-
graphs and ultrasound are useful to determine the size, shape, location, and architec-
ture of the prostate as well as if any cysts or abscesses are present (see Fig. 3A).14
Prostatic fluid should be evaluated for cytology and bacterial culture and sensitivity
(see Fig. 3B). Options for prostatic fluid sampling are discussed elsewhere, but
include semen evaluation of the third fraction, prostatic wash, fine-needle aspiration,
and prostatic biopsy.14

Catheter-associated urinary tract infection There is no evidence to support routine

urine culture or culture of the urinary catheter tip following removal in asymptomatic
patients; such cultures do not predict the development of catheter-associated infec-
tion.23 In contrast, urine culture is always indicated for a patient with clinical signs of
UTI, fever of undetermined origin, or abnormal urine cytology (ie, hematuria, pyuria). If
the patient develops new clinical signs or fever after a urinary catheter has been
placed, then, ideally, the urine catheter is removed and a cystocentesis is performed
to provide a sample for culture once the bladder fills. Alternatively, the original urinary
catheter is replaced and a urine sample is collected through the second catheter. It is
less ideal to sample the urine through the original catheter, and a sample from the
collection bag should never be used.23

Asymptomatic bacteriuria Asymptomatic bacteriuria (AB) is a common and often

benign finding in healthy women. Risk factors include pregnancy, diabetes mellitus,
spinal cord injury, indwelling urinary catheter, and being an elderly nursing home resi-
dent.25 Women with AB have more frequent symptomatic episodes, but antimicrobial
treatment does not decrease the number of episodes. A benefit to treatment has not
 Urinary Tract Infections 727

Table 1
Uncomplicated and complicated urinary tract infections

Definition Underlying Cause

Uncomplicated UTI  Healthy individual, normal  Sporadic infection
urinary tract anatomy and
function
Complicated UTI
Comorbidity  Disease that alters the  Endocrinopathies
structure or function of the  Diabetes mellitus
urinary tract  Hyperadrenocorticism
 Relevant comorbidity predis-  Hyperthyroidism
poses to persistent infection,  CKD
recurrent infection, or treat-  Urinary or reproductive
ment failure tract anatomic abnormality
 Immunocompromised
 Neurogenic bladder
 Pregnancy
Recurrent infection
Relapsing  Recurrence within weeks to Failure to eradicate pathogen
months of a successfully  Deep-seated niche
treated infection  Pyelonephritis
 Sterile bladder during  Prostatitis
treatment  Bladder submucosa
 Same organism  Stone
 Neoplasia
Refractory/persistent  Persistently positive culture Rare
with original pathogen  Failure of host defenses
despite in vitro antimicrobial  Structural abnormality
susceptibility  Patient/client incompliance
 No elimination of bacteriuria  Abnormal metabolism/
during or after treatment excretion of antimicrobial
Reinfection  Recurrence with different  Poor systemic immune
organism function
 Variable time course after  Endocrinopathy
previous infection  Immunosuppressed
 Loss urine antimicrobial
properties
 Glucosuria
 Dilute urine
 Anatomic abnormality
 Physiologic predisposition
 Neurogenic bladder
 Urinary incontinence
Superinfection  Infection with different path-  Cystotomy tube
ogen during treatment of the  Indwelling urinary catheter
original infection  Neoplasia

Adapted from Weese JS, Blondeau JM, Boothe D, et al. Antimicrobial use guidelines for treatment
of urinary tract disease in dogs and cats: antimicrobial guidelines working group of the interna-
tional society for companion animal infectious diseases. Vet Med Int 2011;2011:1–9; and Barsanti
J. Multidrug-resistant urinary tract infection. In: Bonagura JD, Twedt DC, editors. Current veteri-
nary therapy XIV. St Louis (MO): WB Saunders; 2009. p. 921–5.
728 Olin & Bartges

Box 2
Diagnostic testing for complicated urinary tract infections

Extended diagnostic testing may be required for complicated infections.

 Urine analysis
 Urine culture (ideally, cystocentesis sample)
 Complete blood count
 Chemistry profile with electrolytes
 Digital rectal examination
 Feline leukemia virus/feline immunodeficiency virus (cats)
 Thyroid testing
 Cats: total T4
 Adrenal testing
 Low-dose dexamethasone suppression test
 Adrenocorticotropic hormone stimulation test
 Abdominal radiographs
 Abdominal ultrasound
 Contrast radiology
 Excretory urography
 Contrast cystourethrography
 Double-contrast cystography
 Contrast vaginourethrography
 Prostatic wash
 Cystoscopy with bladder wall culture

Adapted from Bartges JW. Diagnosis of urinary tract infections. Vet Clin North Am Small Anim
Pract 2004;34:927–29; and Weese JS, Blondeau JM, Boothe D, et al. Antimicrobial use guidelines
for treatment of urinary tract disease in dogs and cats: antimicrobial guidelines working group
of the international society for companion animal infectious diseases. Vet Med Int
2011;2011:2,4.

been found with clinical trials in humans, whereas potential complications include
adverse drug reactions and the development of antimicrobial resistance.25
The prevalence of AB in healthy dogs and cats is low (2%–9%).26–29 Animals with
underlying comorbidities, such as hyperthyroidism, diabetes mellitus, or CKD, or
recurrent infection have increased prevalence of AB, up to 30%29–33 and 50%,34
respectively. There are no prospective studies comparing clinical outcome in veteri-
nary patients with or without antimicrobial treatment of AB. In one recent prospective
study of dogs with AB, 50% had transient colonization and 50% had persistent bacte-
riuria over a 3-month time period; no dog developed clinical signs at any time point.27
Similar to general recommendation in humans, treatment is not recommended for AB
unless there is a high risk for ascending or systemic infection (eg, immunocompro-
mised patients, CKD).23
Fungal urinary tract infection
Diagnosis of fungal UTI most commonly occurs by identification of fungal elements
during routine or concentrated urine sediment examination. Fungal culture and
 Urinary Tract Infections 729

sensitivity are ideal before treatment, especially in cases other than C albicans, which
tend to be more resistant.19

Viral urinary tract infection

Routine diagnostic tests, including urine analysis and light microscopy, cannot identify
viruses or viral-induced disease. Virus isolation is the gold standard for diagnosis, but
this technique is expensive and time-consuming and requires live replicating virus.
Diagnostic polymerase chain reaction assays are rapid and sensitive, but methods
to optimize nucleic acid preparation are essential because the nucleic acids are easily
degraded in urine.20

PHARMACOLOGIC TREATMENT OPTIONS

Antimicrobials
Antimicrobial drugs are the cornerstone of treatment of UTI. In most cases the antimi-
crobial agent chosen should be based on susceptibility testing of the uropathogen.
Overuse and misuse of antimicrobial drugs may result in the emergence of resistant
organisms, a situation that has implications for successful treatment of infections in
the patient as well as overall veterinary and human health.
Patients with uncomplicated UTI and those with clinical signs severe enough to
merit therapy before results of urine culture and sensitivity testing should receive a
broad-spectrum antimicrobial that has excellent urine penetration. Suggested “first-
line” antimicrobials for uncomplicated UTIs include amoxicillin, cephalexin, or
trimethoprim-sulfamethoxazole (Table 2). The use of potentiated b-lactams (ie,
amoxicillin-clavulanic acid), fluoroquinolones, or extended-release cephalexin (ie,
cefovecin) is inappropriate for most uncomplicated UTIs and should be reserved for
complicated or resistant infections (Table 3).

Combination therapies
If multiple bacteria are isolated, then the relative importance of each must be assessed
based on quantification and suspected pathogenicity. Ideally, an antimicrobial effec-
tive against all pathogens is selected. If this is not possible, then combination therapy
with multiple antimicrobials may be considered.23 Assuming there is no evidence of
pyelonephritis or increased risk of ascending infection, then targeting antimicrobial
therapy against the pathogen with most clinical relevance is reasonable. For example,

Table 2
Summary of first-line antimicrobial options for urinary tract infections in the dog and cat

Infection First-Line Drug Options

Uncomplicated UTI Amoxicillin, trimethoprim-sulfonamide
Complicated Guided by culture and susceptibility testing, but consider
amoxicillin or trimethoprim-sulfonamide initially
Subclinical bacteriuria Antimicrobial therapy not recommended unless high risk for
ascending infection. If so, treat as per complicated UTI
Pyelonephritis Start with a fluoroquinolone, with reassessment based on culture
and susceptibility testing
Prostatitis Trimethoprim-sulfonamide, enrofloxacin, chloramphenicol

Adapted from Weese JS, Blondeau JM, Boothe D, et al. Antimicrobial use guidelines for treatment
of urinary tract disease in dogs and cats: antimicrobial guidelines working group of the Interna-
tional Society for Companion Animal Infectious Diseases. Vet Med Int 2011;2011:5,6.
 730
Olin & Bartges
Table 3
Antimicrobial treatment options for urinary tract infection in dogs and cats

Drug Dose Comments

Amoxicillin 11–15 mg/kg q8h, PO Good first-line option for UTIs. Excreted in urine predominantly in active form if normal
renal function is present. Ineffective against b-lactamase-producing bacteria.
Amikacin Dogs: 15–30 mg/kg q24h, IV/IM/SC Not recommended for routine use but may be useful for treatment of multidrug-
Cats: 10–14 mg/kg q24h, IV/IM/SC resistant organisms. Potentially nephrotoxic. Avoid in animals with renal
insufficiency.
Amoxicillin/clavulanate 12.5–25 mg/kg q8h, PO (dose Not established whether there is any advantage over amoxicillin alone.
based on combination of
amoxicillin 1 clavulanate)
Ampicillin Not recommended because of poor oral bioavailability. Amoxicillin is preferred.
Cephalexin, Cefadroxil 12–25 mg/kg q12h, PO Enterococci are resistant. Resistance may be common in Enterobacteriaceae in some
regions
Cefovecin 8 mg/kg single SC injection. Can be Should only be used in situations where oral treatment is problematic. Enterococci are
repeated once after 7–14 d resistant. Pharmacokinetic data are available to support the use in dogs and cats,
with a duration of 14 d (dogs) and 21 d (cats). The long duration of excretion in the
urine makes it difficult to interpret posttreatment culture results.
Cefpodoxime proxetil 5 to 10 mg/kg q24h, PO Enterococci are resistant.
Ceftiofur 2 mg/kg q12–24h, SC Approved for treatment of UTIs in dogs in some regions. Enterococci are resistant.
Chloramphenicol Dogs: 40–50 mg/kg q8h, PO Reserved for multidrug-resistant infections with few other options. Myelosuppression
Cats: 12.5–20 mg/kg q12h, PO can occur, particularly with long-term therapy. Avoid contact by humans because of
rare idiosyncratic aplastic anemia.
Ciprofloxacin 30 mg/kg q24h, PO Sometimes used because of lower cost than enrofloxacin. Lower and more variable oral
bioavailability than enrofloxacin, marbofloxacin, and orbifloxacin. Difficult to justify
over approved fluoroquinolones. Dosing recommendations are empirical.
Doxycycline 3–5 mg/kg q12h, PO Highly metabolized and excreted through intestinal tract, so urine levels may be low.
Not recommended for routine uses.
 Enrofloxacin Dogs: 10–20 mg/kg q24h, PO Excreted in urine predominantly in active form. Reserve for documented resistant UTIs
Cats: 5 mg/kg q24h, PO but good first-line choice for pyelonephritis (dogs 20 mg/kg PO q24h). Limited
efficacy against enterococci. Associated with risk of retinopathy in cats. Do not
exceed 5 mg/kg/d of enrofloxacin in cats.
Imipenem-cilastatin 5 mg/kg q6–8h, IV/IM Reserve for treatment of multidrug-resistant infections, particularly those caused by
Enterobacteriaceae or P aeruginosa. Recommend consultation with a urinary or
infectious disease veterinary specialist or veterinary pharmacologist before use.
Marbofloxacin 2.7–5.5 mg/kg q24h, PO Excreted in urine predominantly in active form. Reserve for documented resistant UTIs
but good first-line choice for pyelonephritis. Limited efficacy against enterococci.
Meropenem 8.5 mg/kg q12h, SC or q8h, IV Reserve for treatment of multidrug-resistant infections, particularly those caused by
Enterobacteriaceae or P aeruginosa. Recommend consultation with a urinary or
infectious disease veterinary specialist or veterinary pharmacologist before use.
Nitrofurantoin 4.4–5 mg/kg q8h, PO Good second-line option for simple uncomplicated UTI, particularly when multidrug-
resistant pathogens are involved.
Orbifloxacin Tablets: 2.5–7.5 mg/kg q24h, PO; Excreted in urine predominantly in active form.
oral suspension: 7.5 mg/kg q24h,
PO (cats) or 2.5–7.5 mg/kg q24h,
PO (dogs)
Pradofloxacin Dogs: 3 mg/kg q24h, POa May cause bone marrow suppression resulting in severe thrombocytopenia and
Cats: 5 mg/kg q24h, POa neutropenia in dogs.
Trimethoprim-sulfadiazine 15 mg/kg q12h, PO Good first-line option. Concerns regarding idiosyncratic and immune-mediated
Note: dosing is based on total adverse effects in some patients, especially with prolonged therapy. If prolonged
trimethoprim 1 sulfadiazine (>7 d) therapy is anticipated, baseline Schirmer tear testing is recommended (dogs),
concentration with periodic re-evaluation and owner monitoring for ocular discharge. Avoid in

Urinary Tract Infections

dogs that may be sensitive to potential adverse effects such as keratoconjunctivitis
sicca (KCS), hepatopathy, hypersensitivity, and skin eruptions.
a
Dose extrapolated from previous studies.37
Adapted from Weese JS, Blondeau JM, Boothe D, et al. Antimicrobial use guidelines for treatment of urinary tract disease in dogs and cats: antimicrobial guide-
lines working group of the International Society for Companion Animal Infectious Diseases. Vet Med Int 2011;2011:5,6.

731
732 Olin & Bartges

anecdotally, resolution of Enterococcus sp infection is often possible after treatment

of concurrent infection.23

Fluoroquinolone update
The use of fluoroquinolones for empiric treatment of bacterial UTI is discouraged
because of the inherent resistance of many gram-positive organisms to this class of
antimicrobials, and the developing resistance of many gram-negative organisms,
including E coli, to this class of drugs.35 Studies have found variable cross-
resistance among different generations of fluoroquinolones, except pradofloxacin
(Veraflox), and once fluoroquinolone resistance has developed, a later generation of
drug may not be beneficial.36 In vitro, pradofloxacin, a third-generation fluoroquino-
lone, outperformed other fluoroquinolones in terms of potency and efficacy; enroflox-
acin was the least potent second only to ciprofloxacin. Molecular alterations of
pradofloxacin allow increased bactericidal activity and decreased propensity for anti-
microbial resistance.35–37 These features make pradofloxacin an attractive choice for
a susceptible fluoroquinolone-naı̈ve isolate or pathogens with reduced fluoroquino-
lone susceptibility.36,38 Currently, pradofloxacin is only licensed for feline skin infec-
tions in the United States, whereas the European license includes a wide range of
indications for both dogs and cats. One prospective clinical trial (n 5 78) found prado-
floxacin was effective and well-tolerated for feline bacterial UTI.38 In experimental
studies, cats treated with 6 to 10 times the recommended dose did not experience
retinal toxicity.39

Short-duration antimicrobials
In human medicine, short-duration antimicrobial therapy, commonly, trimethoprim-
sulfamethoxazole or fluoroquinolone, has become the standard treatment of acute
uncomplicated bacterial cystitis in women.40 The recommendations are antimicrobial-
specific because not all antimicrobials have comparable efficacy when given as only
a 3-day treatment. Benefits of shorter therapy include better compliance, lower cost,
and decreased adverse effects.40 The goal of treatment is to decrease the bacterial
load enough to control clinical signs with the immune system eliminating remaining
organisms.
Two recent prospective, randomized studies evaluated short-duration treatment in
dogs with uncomplicated bacterial UTI. The first study compared 3-day high-dose
enrofloxacin (n 5 35, 20 mg/kg orally every 24 hours) to standard doses of
amoxicillin-clavulanic acid (n 5 33, 13.75–20 mg/kg orally every 12 hours).41 Clinical
and microbiological cure was evaluated 7 days after antimicrobial discontinuation
and short-term, high-dose treatment was not inferior to standard treatment. The sec-
ond study was double-blinded and compared 3-day trimethoprim-sulfamethoxazole
(n 5 20, 15 mg/kg orally every 12 hours) plus 7-day placebo to 10 days of cephalexin
(n 5 18, 20 mg/kg orally every 12 hours).42 There was no significant difference in the
short-term (4-day after treatment) and long-term (30-day after treatment) clinical and
microbiological cure rates between treatment groups. Clinical cure at 30 days was
50% to 65% and microbiological cure was 20% to 44%.42 Additional studies are
needed to determine the appropriate treatment duration for uncomplicated bacterial
UTI.

Pyelonephritis
Antimicrobial therapy should be initiated while waiting for the culture and sensitivity
results. Empirical antimicrobials should have efficacy against gram-negative bacteria,
the most common pathogens; fluoroquinolones are a good first choice (see Table 2).
Acute pyelonephritis requires hospitalization for parenteral antimicrobial therapy and
 Urinary Tract Infections 733

intravenous fluids. Parenteral therapy should be continued until patients will eat and
drink normally and azotemia is no longer improving with intensive therapy; infections
should then be treated as complicated UTIs, with a minimum of 6 to 8 weeks of anti-
biotics and regular monitoring for recurrence of infections during and following ther-
apy. Chronic pyelonephritis should be treated as complicated UTIs as well, but
patients do not usually require hospitalization at initial diagnosis.

Prostatitis
The blood-prostate barrier is compromised with acute prostatitis and an appropriate
antimicrobial should be selected based on culture and sensitivity. Treat as a compli-
cated UTI for a minimum of 4 weeks.12–14 Antimicrobials must be selected more
carefully in cases of chronic prostatitis because the blood-prostate barrier is
generally intact (see Table 2). Nonionized, basic, lipid-soluble antimicrobials have
the best penetration into the prostatic tissue.12–14 Drugs such as trimethoprim-
sulfamethoxazole, chloramphenicol, and enrofloxacin (but not ciprofloxacin) are
excellent choices. Examples of drugs with low-lipid solubility and poor diffusion
across the blood-prostate barrier include penicillin and cephalothin.12–14 Antimicro-
bials are given for a minimum of 6 to 8 weeks. Culture of prostatic fluid should be per-
formed before and after discontinuation of antimicrobials.12–14
Castration is recommended as an adjunctive treatment to medical management to
help reduce the prostatic size, speed recovery, and decrease recurrence.12–14 Finas-
teride, 5a-reductase inhibitor, may be considered in valuable breeding animals or for
owners that refuse surgery.43

Catheter-associated urinary tract infection

Although it seems logical to administer antimicrobial agents while an indwelling urinary
catheter is inserted in an effort to decrease iatrogenic infection, the practice is strongly
discouraged. Concomitant oral or parenteral administration of antimicrobial agents
during indwelling urethral catheterization does not prevent development of bacterial
UTI and promotes infection caused by multidrug-resistant bacteria.15

Antifungals
Fluconazole is recommended as initial treatment in most patients because of the high
margin of safety, sensitivity of most strains of Candida spp, and excretion of active
drug into urine in high concentrations (Table 4).19 Candida spp other than C albicans
are more likely to be resistant to fluconazole, and antifungal sensitivity testing is rec-
ommended to determine if a higher dose of fluconazole is appropriate or if another
drug should be used. Although amphotericin B is renally excreted and achieves
high concentration in urine, it is not often used because it is parenterally administered
and nephrotoxic. Other commonly used antifungal drugs, including itraconazole and
ketoconazole, are not renally excreted in active form.19
Secondary fungal UTI occurs because of shedding of organisms into urine in pa-
tients with systemic infections. Organisms most commonly associated with urine
shedding are Aspergillus spp in dogs (particularly German shepherd dogs) and Cryp-
tococcus spp in cats.44–47 These patients should be treated with antifungal agents
standardly recommended for systemic infections.

Antivirals
Antiviral drugs have not been evaluated for animals with viral-induced urinary tract dis-
ease, and management of these patients is limited to supportive care.20
734 Olin & Bartges

Table 4
Treatment of fungal cystitis

For all cases Identify and correct  Breaches in local or systemic immunity
underlying predisposing
factors
If C albicans Fluconazole 5–10 mg/kg  Urine sediment and culture at 2- to
PO q 12h for 4–6 wk 3-wk intervals to confirm resolution
 Urine sediment and culture 1 and 2 mo
after therapy discontinuation
If non-C albicans Therapy based on culture  Monitor as above
and sensitivity  Consider drug penetration into urine
when selecting therapy
If initial treatment Repeat culture and Consider:
fails sensitivity  Intravesicular infusion 1% clotrimazole
or amphotericin B
 IV or SQ amphotericin B
 Combination fluconazaole at
maximum dose plus terbinafine
 Benign neglect, regular monitoring for
disease progression

Adapted from Pressler BM. Urinary tract infections—fungal. In: Polzin D, Bartges JW, editors.
Nephrology and urology of small animals. Ames (IA): Blackwell Publishing; 2011. p. 719–21.

NONPHARMACOLOGIC TREATMENT OPTIONS

Bacterial Interference
Bacterial interference refers to the use of low-virulence, nonpathogenic bacteria to
compete with and decrease the risk of colonization and infection with more patho-
genic organisms.48,49 Commonly used bacteria include E coli (strains 83972 and
HU2117) and Lactobacillus sp. Proposed mechanisms of action include competition
for nutrients and attachment sites, bacteriocidin (antibiotic-protein) production, biofilm
prevention, and host immunomodulation.48
This treatment strategy is in its infancy even in human medicine, but preliminary
studies are promising, especially in patients with spinal cord injury and neurogenic
bladder.48–50 An experimental protocol for colonizing the canine urinary tract with
E coli 83972 has been described.51 Another potential future application is the preven-
tion of catheter-associated UTI.49

Probiotics
Alterations of vaginal microflora, in particular lactic acid–producing bacteria (LAB),
may play a role in the establishment of UTI.52 For example, women with recurrent
UTI often have depletion of vaginal Lactobacillus sp, whereas increased vaginal colo-
nization with Lactobacillus sp is associated with reduced numbers of recurrent UTI.52
In humans, Lactobacillus sp are the most common LAB, whereas Enterococcus can-
intestini is the most common species in dogs.53,54 LAB create an acidic environment
that inhibits uropathogen colonization, modulates host immune function, and may
downregulate virulence factor expression of pathogenic bacteria.48
Probiotics are a form of bacterial interference and recommended as a treatment and
prophylaxis strategy in women. Probiotics restore Lactobacillus sp vaginal flora and
displace potential uropathogens from the vagina.48 Two studies in dogs have evalu-
ated vaginal microflora before and after probiotic administration and found no
 Urinary Tract Infections 735

significant differences.53,54 However, more prospective studies are needed to eval-

uate the role of probiotics for lower urinary tract disease in veterinary species. Probi-
otics on the market vary by bacterial species, potency (number of colony-forming
units), and viability. In addition, the gastrointestinal microbe has immunomodulatory
effects throughout the body, and the impact of gastrointestinal probiotics on local uri-
nary tract immune function has not been evaluated.

EVALUATION OF OUTCOME AND LONG-TERM RECOMMENDATIONS

Treatment Duration and Monitoring
Uncomplicated bacterial urinary tract infection
There is no consensus regarding the appropriate duration of treatment (Table 5).23 Un-
complicated UTIs are usually successfully treated with a standard 7- to 14-day course
of an appropriate antimicrobial agent.23 There is some evidence that shorter treatment
(ie, 3 days) is not inferior to standard durations of therapy, but more research is needed
in this area.23,41,42 If the proper antimicrobial is chosen and administered at the appro-
priate dosage and frequency, clinical signs and results of a complete urine analysis
should resolve within 48 hours. If possible, a urine culture should be performed 5 to
7 days after cessation of antimicrobial therapy. Uncomplicated infections are rare in
cats because of their inherent resistance to bacterial UTIs, and there is typically a pre-
disposing cause.
Complicated bacterial urinary tract infection
Optimal duration of therapy is unknown. Antimicrobials are usually administered for a
minimum of 3 to 6 weeks.24 Urine should be evaluated with culture in the first week of
treatment for response to therapy, before discontinuing therapy, 5 to 7 days and
1 month after therapy discontinuation.
Catheter-associated urinary tract infection
It is not necessary to treat bacteriuria associated with an indwelling catheter if there is
no clinical or cytologic evidence of infection (Fig. 6). For patients that develop a
catheter-associated UTI, treatment is more likely to be successful if the catheter
can be removed. The infection may be treated as uncomplicated if there is not a his-
tory of recurrent infection and no relevant comorbidity. Otherwise, the infection should

Table 5
Treatment duration and monitoring

Treatment Duration Monitoring Urine Culture

Uncomplicated 7–14 d 5–7 d after discontinue
bacterial UTI 3 d? antimicrobials
Complicated Minimum 3–6 wk  1 wk into therapy
bacterial UTI  Before therapy
discontinuation
 5–7 d after discontinue
antimicrobial
 1 mo, 2 mo after treatment
AB Treatment not recommended unless high
risk for ascending or systemic infection
Fungal UTI Minimum 6–8 wk As above for complicated
bacterial UTI

Data from Refs.19,23,24

736 Olin & Bartges

No clinical or cytological evidence Clinical signs, fever, cytologic

for infection abnormalities (hematuria, pyuria)
develop after catheter placement

No treatment required

Urine culture

No history of recurrent History of recurrent

infection or relevant co- infection or relevant
morbidity co-morbidity

Treat as uncomplicated Treat as complicated

Fig. 6. Algorithm for treatment of catheter-associated UTI. (Modified from Weese JS,
Blondeau JM, Boothe D, et al. Antimicrobial use guidelines for treatment of urinary tract
disease in dogs and cats: antimicrobial guidelines working group of the international
society for companion animal infectious diseases. Vet Med Int 2011;2011:1–9.)

be treated as complicated with 4 to 6 weeks of an appropriate antimicrobial based on

the culture and sensitivity.23

Fungal urinary tract infection

Primary fungal UTIs should always be treated as complicated infections, with a mini-
mum of 6 to 8 weeks of antifungal therapy and regular monitoring during and after
cessation of therapy.19

Prevention
Catheter-associated urinary tract infection
There are several strategies to decrease the risk of catheter-associated UTI (Box 3).

Box 3
Strategies to prevent catheter-associated urinary tract infection

 Avoid indiscriminate use of urinary catheters. Carefully assess the need for placing and
retaining catheter
 Always use hand hygiene
 Use a closed collection system for indwelling catheters
 Sterile catheter placement
 Minimize duration of catheterization
 Avoid indiscriminate antimicrobial use
 Try to avoid an indwelling urinary catheter in immunocompromised patients
 Be cautious with indwelling catheter use in patients undergoing diuresis

Adapted from Siddiq DM, Darouiche RO. New strategies to prevent catheter-associated urinary
tract infections. Nat Rev Urol 2012;9:305–14; with permission.
 Urinary Tract Infections 737

Prophylactic antimicrobial therapy for recurrent infection There are no good studies
evaluating pulse (intermittent) or chronic low-dose prophylactic antimicrobial ther-
apy in animals with frequent reinfections, but anecdotally, some animals may
benefit (Box 3). Careful patient selection is required and the impact of promoting
antimicrobial resistance should be considered. Before prophylactic treatment is
undertaken, urine culture and susceptibility testing should be done to ensure that
the bacterial UTI has been eradicated. For long-term prophylaxis, a drug that is
excreted in high concentration in urine and unlikely to cause adverse effects
is selected. Often a fluoroquinolone, cephalosporin, or a b-lactam antimicrobial is
chosen. The antimicrobial agent is administered at approximately one-third of the
therapeutic daily dose immediately after the patient has voided, at a time when
the drug and its metabolites will be retained in the urinary tract for 6 to 8 hours (typi-
cally at night). The drug is given for a minimum of 6 months. Urine samples, pref-
erably collected by cystocentesis (not by catheterization because this may induce
bacterial UTI), are collected every 4 to 8 weeks for urinalysis and quantitative urine
culture. If the sample is free of infection, then prophylactic treatment is continued. If
bacterial UTI is identified, active (breakthrough) infection is treated as a compli-
cated bacterial UTI before returning to a prophylactic strategy. If a breakthrough
bacterial UTI does not occur after 6 months of prophylactic antimicrobial therapy,
then treatment may be discontinued and the patient should be monitored for
reinfection.

Ancillary therapies
D-Mannose D-Mannose is used to prevent recurrent UTI, but there are no studies of
clinical efficacy in veterinary patients. The D-mannose sugar competitively binds to
mannose-fimbriae on certain E coli strains, thereby inhibiting adhesion to the uroepi-
thelium.55 There are little data available for other bacteria that may express mannose
fimbriae. An extrapolated anecdotal dose for dogs is one-quarter teaspoon per 20
pounds 3 times daily.
Methenamine Methenamine salt is a urinary antiseptic that is converted to bacterio-
static formaldehyde in an acidic environment (urine pH <5.5). There is controversy in
human medicine as to whether methenamine prevents UTI, although there is some ev-
idence that it may be effective for short-term prophylaxis.56 It is unknown if the 2 salts
described in the literature, hippurate and mandelate, are equally effective; the mande-
late salt is difficult to find.56 There is limited veterinary literature on the use of methe-
namine in small animals, although there is a theoretic benefit.23,34 Studies of safety,
efficacy, and appropriate dosing are lacking. Commonly recommended doses are
10 to 20 mg/kg orally every 12 hours (dog) and 250 mg per cat orally every 12 hours.57
Gastrointestinal upset and dysuria are the most commonly reported adverse events;
methenamine is poorly tolerated by feline patients. Methenamine should not be
used in cases of renal failure.57 Concurrent use of a urinary acidifier, such as DL-methi-
onine, is usually required for maximal effect.

Cranberry Proanthocyanidin, the “active ingredient” in cranberry, alters the genotypic

or phenotypic expression of fimbriae, which subsequently inhibits E coli adherence to
human bladder and vaginal epithelial cells.58 Studies in humans reveal inconsistent ef-
ficacy for prevention of UTI. However, in meta-analysis (n 5 1049), humans supple-
mented with cranberry products had less UTI over a 12-month period compared
with placebo.59
There are few veterinary studies in healthy dogs and no feline studies.60,61 In addi-
tion, quality and potency are variable among over-the-counter products; ideally each
738 Olin & Bartges

formulation would be tested in the species of interest. The Consensus of the Antimi-
crobial Guidelines Working Group of the International Society for Companion Animal
Infectious Diseases is that there is insufficient evidence to support use of cranberry
extract to prevent recurrent UTIs in dogs and cats.23
Local therapy Local infusions with antimicrobials, antiseptics, and dimethyl sulfoxide
can be irritating and are not retained within the urinary bladder.23 Anecdotally, instilla-
tion of dilute chlorhexidine (1:100, 0.02%) and/or ethylenediaminetetraacetic acid
(EDTA)-tromethamine (EDTA-Tris)62 via cystotomy tube may decrease the incidence
of bacterial UTI (Bartges JW, personal communication, Knoxville, TN, 2014). In a small
human study, bladder irrigation with dilute 0.02% chlorhexidine significantly
decreased postoperative bacteriuria, although it did not eliminate pre-existing infec-
tion and did not appear to damage the bladder mucosa.63 It has been postulated
that EDTA-Tris has synergistic effects with systemic antimicrobials64 as well as local
chlorhexidine irrigation.63 Proposed mechanisms included divalent ion binding
causing alteration of bacterial DNA synthesis, cell wall permeability, and ribosomal
stability. In additional, in vitro studies suggest that the presence of EDTA-Tris reduces
the minimum inhibitory concentration for various antimicrobial drugs.64 In a small
study (n 517 dogs, n 5 4 with chronic cystitis) daily local infusion via sterile urinary
catheter (25 mL EDTA at 37 C) for 7 days was well tolerated and dogs had negative
urine cultures up to 180 days after treatment.64 Additional studies are needed to deter-
mine the short- and long-term effects of EDTA-Tris therapy.

TREATMENT RESISTANCE/COMPLICATIONS
Treatment Resistance
Bacterial resistance
The emergence of multidrug-resistant bacteria is concerning and has important impli-
cations for both the patient and public health. There are trends toward increasing
resistance in both fecal and environmental reservoirs.65 In addition to acquiring resis-
tance genes via plasmids, there are other bacterial strategies for persistence within
the urinary tract. For example, uropathogenic E coli can invade and persist within
the superficial bladder wall epithelial cells.65 These bacteria may remain dormant for
a period of time followed by recrudescence.

Biofilms Some bacteria have the capacity for biofilm formation, which facilitates
colonization.66–68 A biofilm is composed of organisms adhered together by a self-
produced polysaccharide matrix.66 It has been suggested that the bacteria within
the biofilm become sessile; they are protected from the immune system, are
antimicrobial, and inherently are resistant to shear forces of removal.66 In hu-
mans, bacteria with the capacity to produce biofilms have been associated with
AB.65,66 Biofilms are also implemented in the development of catheter-associated
UTI.69
Strategies to prevent catheter-associated biofilms include using (1) materials that
are less amendable to biofilm formation and (2) coatings or surface modifications
that decrease biofilm formation. For example, silicone catheters are preferred
over latex because scanning electron microscope imaging reveals that latex sur-
faces are more irregular and promote microbial adherence.49 An example of an
agent used for catheter coating is the antiseptic chlorihexidine. In a veterinary pro-
spective study (n 5 26 dogs) evaluating biofilm formation on indwelling urinary
catheters, sustained-release varnish of chlorihexidine-coated urinary catheters sta-
tistically decreased biofilm formation.69 There are an array of other catheter
 Urinary Tract Infections 739

coatings and modifications to decrease bacterial adherence and biofilm formation

that have primarily been studied in a research setting, including silver coating,
nanoparticles, iontophoresis, antimicrobials, urease and other enzyme inhibitors, li-
posomes, and bacteriophages. Other novel strategies include quorum sensing in-
hibitors and vibroacoustic stimulation (Box 4). A detailed discussion of
comparison is beyond the scope of this article and the reader is referred
elsewhere.49
Some oral antimicrobials, in particular combination therapy with clarithromycin,
have shown promise in vitro for antibiofilm activity. For example, Pseudomonas aeru-
ginosa biofilm was eliminated by a synergistic combination of clarithromycin and cip-
rofloxacin.70 Likewise, combination therapy of clarithromycin with fosfomycin was
more effective than either treatment alone to reduce Staphylococcus pseudinterme-
dius biofilm.71 In vivo studies are needed to further evaluate the efficacy of these
therapies.

Fungal resistance
Infections that fail to respond completely to fluconazole should be recultured and anti-
fungal sensitivity testing performed (see Table 4). Some susceptible isolates may

Box 4
Strategies to prevent biofilm formation

Strategy Definition Mechanism of Action

Silver coating Bactericidal activity of silver ion by
inhibiting enzymatic pathways
and disrupting the cell wall
Nanoparticles Nanometer-sized particles that Disrupt cell membranes via lipid
attach to and penetrate peroxidation and interacting
bacterial cells with DNA
Iontophoresis Application of an electrical field Bioelectric effect—enhance
with low intensity direct current antimicrobial efficacy against
bacteria within biofilms
Urease and Eg, acetohydroxamic acid, In vitro, reduce encrustation and
other enzyme fluorofamide, N-acetyl-D- alter biofilm integrity
inhibitors glucosamine-1-phosphate
acetyltransferase inhibitors
Liposomes Act as carriers for hydrophobic and Increase drug half-life, decrease
hydrophilic drugs adverse effects, protect drug
from environment
Bacteriophages A virus that selectively infects Bacteriophage rapidly divides
bacteria within bacteria and lyses.
Bacteria can develop resistance
Quorum sensing Quorum sensing describes a system Eg, Delisea pulchra algae produces
inhibitors of molecular signaling (ie, a molecule that inhibits
autoinducers) that controls autoinducer signaling
population density and gene
expression. Necessary for
bacteria to develop the biofilm
phenotype
Vibroacoustic Low acoustic waves form a Inhibit bacterial adhesion and
stimulation vibrating coat along the catheter quorum-sensing electrical
surface gradients

Adapted from Siddiq DM, Darouiche RO. New strategies to prevent catheter-associated urinary
tract infections. Nat Rev Urol 2012;9:305–14; with permission.
740 Olin & Bartges

respond to intravesicular administration of 1% clotrimazole or amphotericin B.19,72,73

Urinary alkalinization has also been historically proposed as adjunctive therapy in pa-
tients with fungal UTI, because increased urine pH may inhibit fungal growth. Howev-
er, this is not currently favored for treatment of fungal UTI in humans and is of
questionable efficacy in veterinary patients.19

Complications
Magnesium ammonium phosphate (struvite) urolithiasis
Staphylococcus spp and Proteus spp, and more rarely Corynebacterium spp, Klebsi-
ella spp, and Ureaplasma spp, may produce urease (Box 5). This enzyme hydrolyzes
urea to ammonia, which buffers urine hydrogen ions, forming ammonium ions,
increasing urine pH, and increasing dissolved ionic phosphate. In the presence of
magnesium, magnesium ammonium phosphate (struvite) may precipitate around a
nidus to form uroliths (Fig. 7). Bacteria are incorporated into the urolith matrix, and
thus, should be considered complicated UTIs because of poor antimicrobial penetra-
tion. Greater than 90% of struvite uroliths in dogs are induced by urease-producing
bacteria, whereas struvite uroliths in cats are commonly sterile (ie, not associated
with bacterial UTI). Struvite uroliths can be dissolved through a combination of dietary
therapy and appropriate antimicrobial therapy; following dissolution or removal, pre-
venting urolith recurrence requires preventing reinfection. For dogs that are uncom-
fortably symptomatic from urocystolithiasis and/or fail medical management,
minimally invasive procedures, such as laser lithotripsy, laparoscopic-assisted cystot-
omy, or cystotomy, may be considered.

Polypoid cystitis
Chronic bacterial infections may induce microscopic or macroscopic bladder mucosal
proliferation and intramural accumulation of inflammatory cells. Polypoid cystitis oc-
curs when epithelial proliferation is severe, resulting in masslike lesions or diffuse
thickening of the bladder wall (Fig. 8).74,75 Gross differentiation of polypoid cystitis
from bladder wall neoplasms is not reliable; however, polypoid cystitis is more likely
to develop in the bladder apex (vs transitional cell carcinomas, which are more
commonly found in the bladder trigone), is more commonly botryoid in appearance
rather than fimbriated, and is not as grossly vascular as transitional cell carcinomas.
Proteus spp may be more commonly associated with development of these le-
sions.74,75 Polypoid cystitis lesions are niduses of deep-seated bacterial infection
and should be treated as complicated UTIs. In some cases long-term antimicrobial

Box 5
Complications of urinary tract infection

Potential complications of UTI

 Resistant infection
 Polypoid cystitis
 Emphysematous cystitis
 Magnesium ammonium phosphate (struvite) urolithiasis
 Pyelonephritis
 Prostatitis
 Prostatic abscess
 Urinary Tract Infections 741

Fig. 7. Lateral survey abdominal radiograph of infection-induced struvite urocysto-

urethroliths in a 3-year-old spayed female Irish setter.

therapy may result in successful resolution of lesions. However, partial cystectomy re-
sults in more rapid resolution of clinical signs, is likely associated with improved rates
for long-term resolution of infection, and allows shorter antimicrobial treatment
courses.75

Emphysematous cystitis
Emphysematous cystitis refers to accumulation of air within the bladder wall and
lumen secondary to infection with glucose-fermenting bacteria. Most cases are due
to E coli infection, but Proteus spp, Clostridum spp, and Aerobacter aerogenes
have also been reported.76,77 Emphysematous cystitis most commonly develops in
dogs and cats with diabetes mellitus because of the high concentration of fermentable
substrate.77 Treatment of emphysematous cystitis should be as described for compli-
cated UTI; if glucosuria is present, then appropriate treatment should be initiated for
the underlying cause.

Fig. 8. Cystoscopic image of a urinary bladder polyp with cystitis due to E coli in a 6-year-old
spayed female Irish setter.
742 Olin & Bartges

Pyelonephritis
Although no systematic reviews of pyelonephritis in dogs or cats have been per-
formed, animals with systemically compromised immunity (ie, hyperadrenocorticism,
diabetes mellitus), dogs or cats with CKD, and patients with any cause of vesicoure-
teral reflux are likely predisposed to development of pyelonephritis. Chronic pyelone-
phritis is likely underdiagnosed as a cause of renal failure in dogs and cats and should
be especially considered in patients with previously stable CKD that have unexpected
worsening of azotemia (ie, “acute-on-chronic” renal failure).

Prostatic abscessation
Prostatic abscessation is a sequela to prostatitis and is characterized by purulent fluid
accumulations within the prostatic tissue. Clinical signs are variable and dependent on
the size and extent of the abscess as well as systemic involvement. Prostatic ab-
scesses are generally easily identified with ultrasonography and the goal of therapy
is to provide drainage either through ultrasound-guided percutaneous drainage or sur-
gery. Surgical options include partial prostatectomy and prostate omentalization.14

SUMMARY
 Determining whether an infection is uncomplicated or complicated is essential to
guide the diagnostic and therapeutic plan.
 Recurrent infections are complicated infections and may be relapsing, refractory/
persistent, reinfection, or superinfection.
 Antimicrobials are the cornerstone of treatment of bacterial UTI and, ideally,
selected based on culture and sensitivity.
 There is limited literature to support preventative therapies; identification and
resolution of underlying causes are essential.

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