Problem urinary tract infections (Proceedings)
Ascent of bacteria is the most common origin of bacteria in UTI. Fecal flora from the patient contaminate the perineum, ascend the urethra, and enter the bladder. Organisms that successfully gain entry into the bladder then have the potential to ascend the ureters, cross the renal pelvic epithelium, and enter renal parenchymal tissue. Vaginal, preputial, and distal urethral flora occasionally are the source of ascending bacteria. Ascending organisms can also come from the environment including that from hospital flora. Introduction of normal flora during catheterization and contamination with fecal or hospital flora also is possible. Migration of bacteria around an indwelling urinary catheter or through the catheter lumen occurs at times.
The urinary tract is exquisitely resistant to bacterial colonization during health. The development of a UTI means that the host defenses were overwhelmed at least transiently in order for UTI to develop. Abrogation of some aspect of the normal host defense system is often operative in allowing UTI to be established though we may not be able to identify it. In order for UTI to develop, the animal must be exposed to uropathogenic bacteria in sufficient numbers, the animal must have epithelial receptors for uropathogens, and often suboptimal urinary defenses exist. Failure of normal urinary defenses include the possibilities of reduced anti-adherence properties of the uroepithelium, decreased antibacterial properties of urine, abnormal patterns of voiding, reduced integrity of intrinsic mucosal defenses, and presence of anatomic abnormalities.
Increased risk for the development of UTI occurs in dogs with anatomic abnormalities of the genitourinary system such as urachal remnants, ectopic ureters, excessive perivulvar skin folds/pyoderma (especially in recurrent UTI), or possibly vestibulovaginal stenosis. Exogenous steroid use in dogs, endogenous hyperadrenocorticism, and diabetes mellitus all add risk for development of UTI in dogs. Uroltihiasis can be the result of UTI (struvite stones in dogs) or the stones may compromise the urinary defense systems. Urethrostomy, indwelling urinary catheterization, and single passage of a urinary catheter increase the risk that UTI will be acquired in dogs and cats. UTI occurs in approximately 30% of all cats with chronic renal failure (CRF), many within one year of diagnosis of CRF. Cats over 10 years of age that present for signs of lower urinary tract distress (LUTD) commonly have bacterial urinary infections, unlike young cats presenting with LUTD signs. Dogs with urinary incontinence may be at increased risk for development of UTI possibly due to the "wicking" action of urine that may allow ascent of bacterial organisms.Urinary antibacterials remain the hallmark for treatment of UTI, though correction of predisposing factors is also important. The concentration of antimicrobial that is achieved in the urine (micrograms/mL) is the most important factor in predicting eradication of UTI. Tissue levels of the antimicrobial will be important in those with renal and prostatic infections, as well as those with markedly thickened bladder walls from chronic infection. Antibacterial treatment for UTI is usually given for 10 to 14 days in those with uncomplicated UTI, at least 30 to 60 days for those with upper UTI, and for at least one month to sexually intact males. Antibacterials should be selected after confirmation of UTI by quantitative urinary culture. UTI can be treated on the basis of susceptibility testing, or on the basis of predicted biologic behavior in those with uncomplicated UTI.
Most UTI can be successfully sterilized via the oral route using penicillins (especially those with clavulanate), trimethoprim-potentiated sulfonamides, ormetoprim-potentiated sulfonamides, or first generation cephalosporins such as cephalexin or cefadroxil. Side effects associated with trimethoprim-potentiated sulfonamides include keratoconjunctivitis sicca, cytopenia, hepatopathy, and immune-mediated polyarthritis. Ormetoprim-potentiated sulfonamides are not effective in prostatic UTI. Trimethoprim-potentiated sulfonamides should be used in these cases. Sulfonamides of any kind should not be prescribed for those in which medical calculolytic protocols are in place. Sulfa can precipitate on the surface of the stone and either stop or dramatically decrease the rate of stone dissolution.