Most bacterial infections of the lower urinary tract respond quickly to antimicrobial treatment; however, urinary tract infections
(UTI) associated with defects in the host immune system (complicated UTI) often fail to respond or recur after antibiotic
withdrawal and can be a therapeutic challenge.
Etiology
The most common bacterial pathogens associated with UTI in the dog include Escherichia coli, Klebsiella, Staphylococcus, Enterococcus,
Proteus, Pseudomonas, Enterobacter, and Streptococcus. These are dermal or intestinal floras that ascend the urethra and
then adhere to the mucosa of the bladder and multiply. Although many enteric organisms are anaerobes, the oxygen tension
in urine probably inhibits growth of strict anaerobic bacteria and therefore, anaerobic UTI is rare. A recent study of recurrent
and persistent UTI in dogs showed that 25% of culture positive urine specimens had two or more bacterial species isolated.
Mycoplasmal infections are relatively rare but have been associated with recurrent or persistent UTI in dogs. Mycoplasma
should be considered in dogs with persistent pyuria and negative urine culture, dogs with persistently alkaline urine and
negative urine cultures, and dogs with persistent or recurrent UTI that don't respond to appropriate conventional antibiotic
treatment.
Normal Host Defense Mechanisms
The status of host defense mechanisms appears to be the most important factor influencing the pathogenesis of UTI. Normal
voiding is an efficient natural defense mechanism against UTI. Mechanical washout as a result of complete voiding is responsible
for removing greater than 95% of non-adherent bacteria that gain entrance into the urinary bladder. Increased urine production
and frequency of voiding enhance washout of bacteria. Disorders that decrease the frequency and/or volume of voided urine,
or that result in an increased urine residual volume may predispose animals to UTI. Normal urine residual volume for dogs
is less than 0.2 to 0.4 ml/kg body weight.
Bacteria are normally present in increasing numbers from the mid to distal urethra, but seldom do these organisms cause UTI
in normal dogs. The high-pressure zone in the mid urethra and spontaneous urethral contractions help prevent ascension of
bacteria. Differences in epithelial morphology (decreased epithelial receptor sites) also help decrease bacterial colonization
in the proximal and mid urethra. The length of the urethra and bactericidal prostatic secretions in male dogs are thought
to decrease the incidence of UTI compared with female dogs, however, nearly equal gender distribution in recurrent/persistent
UTI has recently been reported. In both sexes, the valve-like nature of the vesicoureteral junction helps protect against
bacterial ascension to the upper urinary tract.
Colonization of vulval and preputial luminal mucous membranes by nonpathogenic flora serves to decrease colonization by uropathogens.
Normal flora occupy most of the epithelial receptor sites, produce bacteriocins that interfere with uropathogen metabolism,
and have a high affinity but low requirement for essential nutrients required by uropathogens. Mucosal secretions also help
prevent adherence of uropathogens to epithelium; immunoglobulins coat pathogenic bacteria and glycosaminoglycans form a protective
barrier over the mucosal surface.
The antibacterial property of urine is an additional important host defense mechanism against UTI. Urine is frequently bacteriostatic
and sometimes can be bactericidal depending on its composition. Low pH and high concentrations of urea and weak organic acids
in concentrated urine inhibit bacterial growth. Although polyuric disorders may increase washout of non-adhered bacteria
from the bladder, UTI may occur due to decreased antibacterial properties of urine.
