URINARY tract infection (UTI) refers to the microbial infection of any normally sterile part of the urinary system. Most UTIs are bacterial in origin, though rarely other organisms such as Mycoplasma spp., Chlamydia spp., viruses and fungi may be implicated.
Whilst UTIs occur mainly in the lower urinary tract (bladder and urethra) from ascending bacterial infections, there is potential for infection to travel further into the ureters and kidneys, leading to pyelonephritis.
The prevalence of UTIs in cats (estimated to be 0.1 to 1%) appears to be much less than in dogs, and females of both species have a higher representation. Further, spayed female cats are more at risk, whilst both male and female intact cats appear to have a decreased risk.
Host defences
Whether or not a UTI becomes established is determined by a complex interaction between organism virulence and number, versus host defences.
Normal local defence mechanisms include frequent, efficient voiding of urine, with near complete emptying of the bladder washing out any non-adherent bacteria.
High pressure in the mid-urethra and urethral contractions help to prevent bacterial ascension in the lower urinary tract while ureteral peristalsis and valve-type junctions between the bladder and ureters help protect the upper tract.
Mucosal strategies such as the incorporation of glycosaminoglycans to formaprotective barrier and secretion of local immunoglobulins with the ability to coat pathogens increase defences further.
Urine itself also plays a role. The high osmolality limits bacterial replication, a property thought to be particularly effective in cats with their very concentrated urine.
The presence of high levels of urea and organic acids together with a low pH also inhibits growth.
Organism virulence
The most common bacteria isolated in UTIs are those which form part of the normal flora of the skin or gastrointestinal tract, from where they are thought to invade through the urethra to the bladder.
In both dogs and cats, E. coli is most frequently isolated and other aerobic bacteria such as Staphylococcus spp., Streptococcus spp. and Proteus spp. are common. Klebsiella spp. and Pseudomonas spp. appear less frequently. Anaerobic infections appear rare.
Viral infections in cats have been suspected to be causative in some cases of lower urinary tract disease (LUTD), and recently two novel strains of feline calicivirus were identified in urine of two cats with naturally occurring LUTD, although the significance of this is not known.
While most infections are the result of a single organism, two may be found on occasion. The culture of three or more organisms should raise a suspicion of contamination.
Whether or not a microbe causes a UTI will depend on virulence factors as well as their absolute numbers. Many Gram-negative bacteria have proteinaceous appendages or components of their cellular surface which help them to adhere to the urinary epithelium (termed adhesins) but other factors can also found in the same organism.
Some possess capsular K-antigens which interfere with phagocytosis and others O-antigens which decrease normally eliminating smooth muscle contractions.
Anything which compromises any of the local defence mechanisms has the potential to allow a more complicated form of UTI to become established: for example, decreased urinary concentration in animals with chronic renal failure, or iatrogenic damage to the intact epithelial lining by catheterisation.
Retention of urine and incomplete voiding due to uroliths or some other mechanical change such as a thickened bladder wall can all lead to recurrent or complicated UTIs. Predisposing systemic conditions include diabetes mellitus, renal failure and hyperadrenocorticism.
Diagnosis
Some UTIs will present with no clinical signs, but more commonly dysuria, haematuria (which may be microscopic only), pollakiuria and stranguria may be seen. Confirmation should be by urinary culture with accompanying bacterial sensitivity to help choose an appropriate antibiotic, particularly in recurrent or relapsing UTIs.
Cystocentesis is the collection method of choice to minimise contamination. Where possible, culture immediately as some bacteria multiply very quickly, whilst others decrease. If this is not possible, then decanting into a boric acid tube will allow preservation for up to 72 hours and these cultures correlate well with freshly cultured samples.
In-house urinary sediment microscopy can help to give some indication of a UTI. Examination of sediments from fresh samples allows the visualisation of bacteria and white blood cells which, if found together, can imply a UTI. More than four white blood cells per high power field (x400), along with identification of bacterial rods or cocci gives some indication.
Rods are only seen in urine when the number exceeds 10,000/ml and cocci may not be seen until they reach 100,000/ml, so care should be taken in interpretation. A negative result for bacterial identification cannot rule out a UTI and shouldn’t preclude culture. Note that some animals with UTIs, particularly pyelonephritis, may not show any white blood cells or bacteria.
Treatment
Most uncomplicated UTIs will respond well to antimicrobial treatment; the choice of agent to use is facilitated by bacterial sensitivity where this is done. In many cases, however, the clinician will often choose to treat straight-forward presentations without doing sensitivity testing (although it is recommended where the UTI is recurrent or relapsing) and choice of antibiotic here can be facilitated by urinary sediment examination.
E. coli may be tentatively diagnosed by the identification of rods in acidic urine, whilst in alkaline urine they may represent Proteus spp. Enterococcus spp. may be represented by cocci in acidic urine, whereas in alkaline urine they may indicate Staphylococcus spp. Treatment in uncomplicated cases should continue for 2-3 weeks and any recurrence or relapse should be investigated for complicating factors.
■ References available on request.
