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EQUINE VETERINARY EDUCATION / AE / MAY 2019


Treatment Based on reports in dogs with polypoid cystitis, a 2-week treatment trial of trimethoprim sulfadimidine (Trimidine2; 30 mg/kg bwt per os q. 12 h) was initiated. The significance of the bacteria observed histologically was unclear; however, based on the clinical course (see below), it was assumed that a bacterial infection was at least a component of the aetiology. The mare was discharged from hospital the same day of examination. Repeat cystoscopy was scheduled for 2 weeks’ time, with a view to perform urine culture if there was no evidence of clinical improvement following empirical antibiotic treatment.


Outcome and follow-up Two weeks after the initial presentation, communication via a telephone conversation with the owners indicated that the haematuria had resolved and that the mare remained otherwise healthy. Cystoscopy was postponed and treatment with the potentiated sulfonamide continued. Repeat cystoscopy was performed approximately 3 weeks after presentation to the VTH to monitor the response to treatment. Subjectively, the appearance of the urine was much improved although there had been little or no change in the appearance of the mucosal polypoid lesions. Urine collected from both ureters was grossly normal in appearance; white cell counts estimated from a haemocytometer were 11 leucocytes/lL from the left ureter and 10 leucocytes/lL from the right. Both samples also had increased red cell counts (19,800–29,621 erythrocytes/lL); this was thought to be a result of trauma associated with sample collection or perhaps vesicoureteral reflux. Renal haemorrhage was considered unlikely based on the overall clinical picture but could not be completely excluded. No bacteria or neoplastic cells were identified in either sample. Due to the clinical improvement, urine culture was not performed and antibiotic treatment was continued for a further 2 weeks. One week after discontinuing antibiotics (6 weeks after


initial evaluation), cystoscopy revealed grossly normal urine and both ureters were observed to expel urine that was grossly normal. There was a marked reduction in the number and size of the polypoid lesions with only a few areas of slightly raised, irregular bladder mucosa and no evidence of haemorrhage. Biopsies were not collected nor were further urinalyses performed due to the clinical improvement. No further treatment was prescribed and the owner was advised to revisit in 4–6 weeks’ time unless the haematuria re- occurred. Prior to the final cystoscopy and 8 weeks after


discontinuing antibiotic therapy, the owners had not observed the pony to urinate. Red-tinged urine was found upon bladder catheterisation and two small, slightly raised areas of mucosa were present on cystoscopy. Another larger, more pedunculated mass was also noted. Urine expelled from both ureters appeared grossly normal. Histopathological evaluation of a pinch biopsy collected from the larger mass confirmed polypoid cystitis. Given the clinical improvement previously achieved with potentiated sulfonamide treatment, a 4-week course of trimethoprim–sulfadimidine (30 mg/kg bwt per os q. 12 h) was re-instigated. Telephone follow-up with the owners one and 5 months after discontinuing medication revealed that the pony’s haematuria had resolved.


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Discussion


Polypoid cystitis is a non-neoplastic condition affecting the bladder mucosa that is associated with gross haematuria in humans and dogs but, as far as the authors are aware, has not previously been reported in horses. A fibromatous polyp characterised by fibrous tissue covered by transitional epithelium has been described in one horse (Fischer et al. 1985). However, that case lacked the histological signs of inflammation of the lesions observed in this case, and did not display the hyperplastic transitional epithelium with associated inflammation and oedema. In this case, a diagnosis of polypoid cystitis was made in an otherwise healthy middle-aged pony based on histological findings. Although surgical removal of polypoid lesions is the recommended treatment in human patients, resolution of haematuria and a marked regression of the lesions were achieved in this case with prolonged, broad-spectrum antimicrobial therapy. Polypoid cystitis is suggested to arise from chronic irritation


of the bladder mucosa. In human patients the condition is most commonly associated with an indwelling urinary catheter, although the condition has been reported in the absence of urinary catheterisation (Young 1988; Kilic


 et al. 2002). In dogs,


polypoid cystitis has been associated with bacterial urinary tract infections and uroliths (Martinez et al. 2003). However, a definitive aetiology has not yet been determined for dogs and it is unclear whether the associated bacterial infection is a cause or a consequence of the polypoid lesions. In the medical literature, the terms polypoid and papillary cystitis have historically been used interchangeably. However, while the two conditions represent a continuum and both are characterised by inflammation and proliferation of the bladder mucosal epithelium, polypoid and papillary cystitis can be distinguished grossly and on their histological appearance. Grossly, polypoid lesions appear as oedematous, broad-based outgrowths of the epithelium while papillary lesions appear as thin frond-like projections (Young 2009). Polypoid cystitis is frequently confused with urinary tract neoplasia based on both gross inspection at cystoscopy and, in some cases, histology. A human study reported that 26% (41/155) of cases of polypoid cystitis were initially incorrectly diagnosed as papillary urothelial neoplasms (Young 1988; Lane and Epstein 2008). The prevalence of haematuria in human patients with polypoid cystitis has not been reported, but 82% of canine cases reportedly present with gross haematuria (Martinez et al. 2003). Simultaneous regression of the polypoid lesions and resolution of the gross haematuria in combination with the overall clinical picture suggests that, in this mare, haematuria resulted from bladder mucosal bleeding. However, it can often be difficult to definitively exclude other sources of haemorrhage. Cystitis is uncommon in horses and not typically


associated with obvious haematuria, although this might depend on the underlying cause and severity of disease. The significance of the proteinuria detected on initial dipstick urine analysis is questionable in this case, as there were no other indicators of renal disease and quantification was not performed. Alkalotic urine or increased haemoglobin concentrations will both result in a positive protein reaction on dipstick analysis; the latter being the most likely explanation in the current case (Wilson 2007). Urinalysis was not consistent with an ascending bacterial infection of the


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