Treating UTIs with fluoroquinolones: A case study (Sponsored by Pfizer)


Treating UTIs with fluoroquinolones: A case study (Sponsored by Pfizer)

Florie is a 4-year-old, spayed female Labrador-shepherd crossbred dog. Until six months ago, Florie's medical history was unremarkable. At that time, she was diagnosed with a bacterial urinary tract infection (UTI) based on the presence of hematuria and pollakiuria; she received 500 mg cephalexin orally once daily by the referring veterinarian for five days. When the UTI was observed again by the referring veterinarian three months later, Escherichia coli was cultured but sensitivity results were not obtained. Florie was given 50 mg gentamicin subcutaneously three times daily for 10 days.

Three months later, Florie was referred to the University of Georgia Veterinary Medical Teaching Hospital (UGA-VMTH). At this time, she was exhibiting a recurrence of the same clinical signs (i.e., pollakiuria, dysuria, and hematuria). During this exam, the owner reported that Florie had actually experienced pollakiuria and hematuria intermittently for six months and had recently increased her water intake. Florie weighed 44 lbs and her physical examination findings were normal except that she was reluctant to allow caudal abdominal palpation and her urinary bladder appeared small. Because of her size, body conformation, and reluctance for abdominal palpation, Florie's kidneys could not be palpated. Rectal palpation of the distal urethra was normal.

Table 1: Results of Urinalysis at UGA-VMTH
During Florie's exam at UGA-VMTH, a complete blood count (CBC), serum chemistries, urinalysis, urine culture, abdominal radiographs, and ultrasonogram were performed. The results of the CBC and serum chemistries were normal and the urinalysis and urine culture results are listed in Table 1.

The abdominal radiographs revealed normal abdominal viscera. Florie's kidneys were normal-sized but irregularly shaped. The urinary bladder was small. No uroliths were visible. On the ultrasonogram, her kidneys were normal-sized, but medullary echogenicity was irregular and abnormal bilaterally. The renal pelves were mildly dilated bilaterally. A 2-cm polyp was present in the body of the urinary bladder. No uroliths were visible. Based on the physical examination and laboratory test results at UGA-VMTH, the clinical diagnosis was UTI with renal involvement and polypoid cystitis. This clinical course (three successive presentations over six months) is, unfortunately, not uncommon for UTI. This article evaluates these three presentations at zero, three, and six months of Florie's illness.

Initial identification of UTI

Canine UTIs generally involve the lower urinary tract (bladder and urethra), where the inflammation caused by the infection produces obvious clinical signs such as pollakiuria, stranguria, and dysuria. These findings in Florie, typical of lower tract disease in general, led to the initial suspicion of a bacterial UTI. However, other causes of lower urinary tract inflammation, such as cystouroliths or neoplasia, may coexist with a UTI or cause lower tract signs in the absence of bacteria. In this case, the presumptive diagnosis of a bacterial UTI was reasonable because it's a common cause of lower tract signs in dogs, particularly young or middle-aged dogs with no other findings.

Origin of the infection

Most bacterial UTIs are caused by intestinal or cutaneous flora that ascend through the urethra to the bladder. The most common bacterial pathogens associated with UTIs in the dog are E. coli (as later found to be the case in Florie) and Staphylococcus, Streptococcus, Enterococcus, Enterobacter, Proteus, Klebsiella, and Pseudomonas species.

Common contributory causes of UTIs were apparently not factors in Florie, such as urethral catheter use, conditions that would cause local inflammation and prevent efficient urine flow from the bladder (e.g., prostate enlargement in males or uroliths), and urinary tract surgery. Nonetheless, a presumptive diagnosis of a UTI was made. The main reservoir for such a UTI is the bacterial flora of the gastrointestinal tract—this was presumed to be the source in Florie's case.