Chronic Prostatitis, Cystitis, Pyelonephritis, and Balanoposthitis in a Cat

Introduction

Feline prostatic disease is rare, with prostatic adenocarcinoma being the most commonly reported disease to date.¹ Nonetheless, other possibilities for feline prostatic abnormalities do exist. A case of chronic active inflammation of the prostate, bladder, kidneys, ureters, penis, and prepuce, most consistent with a chronic infectious process, is described. Clinicians should consider the possibility of chronic prostatitis in their differential list when presented with an older, intact male cat with prostatic disease, particularly when concurrent risk factors for urinary tract infection are present. Chronic prostatitis may have a more favorable prognosis than feline prostatic adenocarcinoma.²

Case Report

An adult, intact male domestic shorthair, weighing 3.7 kg, estimated to be >5 yr, presented for a swelling of his prepuce and penis and urinary incontinence. The cat had been taken in as a stray and had been owned for >1 yr. The owner stated that the penile swelling had been present for close to 1 yr, but in the last 1–2 mo, the cat had begun to lose weight and was dribbling urine. The cat was eating and drinking normally and had no gastrointestinal abnormalities.

The cat's temperature at presentation was 39.0°C. Physical examination revealed a small left-sided thyroid nodule, a grade 2/6 systolic heart murmur, and a firm, irregular, caudal abdominal mass. The prepuce was edematous and the penis appeared uniformly thickened, with proliferative, pale pink tissue. Both testicles were descended, smooth, and symmetrical. The bladder was soft and easily expressible. The cat was lean and slightly dehydrated, with a flaky hair coat, but was bright, alert, and responsive.

A complete blood count showed a mature neutrophilia of 10⁹/L (reference range, 2.5–8.5 thsd/cmm). The serum biochemistry panel revealed significant hyperglobulinemia (8.2 g/dL; reference range, 2.3–5.3 g/dL), elevated blood urea nitrogen (45 mg/dL; reference range, 14–26 mg/dL), and a mild increase in amylase (1302 U/L; reference range, 100–1200 U/L). Tests for the feline immunodeficiency and feline leukemia viruses were negative. Urinalysis obtained by cystocentesis showed pyuria, hematuria, proteinuria, and bacteriuria. Urine specific gravity was 1.028. The urine was not cultured. The thyroid level was 1.4 μg/dL (reference range, 0.8–4.0 μg/dL).

Ultrasound of the caudal abdomen revealed a markedly enlarged prostate, with proliferative tissue extending along the urethra into the pelvic canal. A fine-needle aspirate was attempted, but an adequate sample could not be obtained.

Because of the owner's significant financial constraints and the veterinarians' suspected poor long-term prognosis, the cat was humanely euthanized with intravenous propofol^a (13 mg/kg) and pentobarbital sodium^b (316 mg/kg).

Necropsy showed a very small, irregular, right kidney (Figure 1). The right kidney measured 3.3 cm in length, whereas the grossly normal left kidney measured 4.8 cm in length. The prostate was large (2 cm wide and 3 cm long), firm, and irregular (Figure 2). The prostate was asymmetric, with an overall nodular appearance. Some regions were pale with small white nodules, whereas other regions appeared necrotic and hemorrhagic. Abnormal tissue was present along the entire urethra and onto the penis (Figure 3). The bladder was uniformly thickened. Biopsies of all affected tissues were taken and submitted to two board certified pathologists for review.

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Microscopically, the prostate showed marked, diffuse, subacute suppurative to chronic active and fibrosing/abscessing prostatitis with squamous metaplasia and rupture of the prostatic gland (Figure 4). The prostate was massively and diffusely infiltrated and replaced with pools of mixed inflammatory cells, including plasma cells, neutrophils, macrophages, and lymphocytes. There was multifocal hyperplasia and squamous differentiation of ductal epithelial cells.

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The urinary bladder demonstrated mild hypertrophy and multifocal hyperplasia of mucosal epithelial cells, multifocal mucosal erosion, and submucosal fibrosis, with a mild to moderate infiltrate of lymphocytes.

The normal architecture of the kidneys was disrupted by a moderate to marked interstitial infiltrate of lymphocytes and plasma cells, extending from the peripelvic medullary tissue into the cortex. Increased interstitial fibrous connective tissue was present. There were fields of tubular and glomerular loss adjacent to inflamed zones. In addition, the inflammation present in the stroma of the renal crest/pelvis extended into the ureteral lamina propria. Papillary mineralization was also seen. These findings were consistent with severe, bilateral, ascending, lymphoplasmacytic and fibrosing pyelonephritis and ureteritis.

Pathology of the penis demonstrated extensive, diffuse infiltrates and follicular aggregates of neutrophils, macrophages, lymphocytes, and plasma cells in the dermis of the preputial sheath, extending in the mucosa/lamina propria of the penis. These changes were consistent with balanoposthitis.

The testes were normal and no neoplastic cells or infectious organisms were seen in any sample.

The final pathologic diagnoses were as follows: marked, chronic plasmacytic and suppurative prostatic inflammation; moderate, chronic lymphoplasmacytic and fibrosing cystitis; severe, bilateral chronic active lymphoplasmacytic and fibrosing pyelonephritis and ureteritis; and severe, chronic active lymphoplasmacytic balanoposthitis. These changes were suspected to be secondary to a chronic infectious process.

Discussion

Published information about the feline prostate is sparse. Feline prostatic disease is rare compared with canine prostatic disease, although reports of feline prostatic neoplasia, prostatic squamous metaplasia, prostatic abscess, and bacterial prostatitis are present in the veterinary literature.^2–7 The most commonly described feline prostatic disease is adenocarcinoma.¹

Clinical signs associated with prostatic adenocarcinoma most commonly involve the lower urinary tract.^1,3,5,8 Hematuria, dysuria, pollakiuria, and urinary obstruction are most frequently noted. Other signs related to large bowel obstruction, such as constipation, obstipation, and tenesmus, have also been reported.^5,8

Presenting clinical signs in the patients from the few other case reports describing nonneoplastic prostatic diseases have been variable. One patient with bacterial prostatitis presented with intermittent constipation and dyschezia.² Another patient with squamous metaplasia of the prostate presented with chronic dysuria and bladder atony.⁶ A patient with a prostatic abscess presented with vomiting, lethargy, anorexia, and constipation.⁷ Clearly, clinical signs alone cannot differentiate neoplastic from nonneoplastic feline prostatic disease.

The feline prostate has been described as “rudimentary” and thus is not a common source of clinical disease in cats.⁹ Histologically, the feline prostate is a compact, compound tubular gland lined by secretory epithelium, with small lobules extending into the urethral muscle.^1,10 Like the canine prostate, the feline prostate is an androgen-dependent organ that rapidly atrophies after neutering.¹

In intact male dogs, prostatic enlargement occurs secondary to prolonged androgen secretion. Prostatic growth is modulated by a metabolite of testosterone called 5-α-dihydrotestosterone; however, estrogens also play an important role.¹¹ The canine prostate enlarges via an increase in the size and number of prostatic epithelial cells and proliferation of glandular and stromal components.¹

Chronic, bacterial prostatitis is the second most common prostatic disorder of intact male dogs (second only to benign prostatic hyperplasia).¹² Dogs may be predisposed to prostate infection by an increased bacterial numbers in the prostatic urethra, compromised local immunity, urinary tract disease (e.g., calculi, infection, neoplasia), or altered prostatic tissue (most commonly benign prostatic hyperplasia).¹¹

The types of bacteria found in canine prostatic infections are similar to those that cause urinary tract infections. It is likely that most (but not all) cases of canine bacterial prostatitis begin as pathogens in the urinary tract itself.¹¹ The bacteria that cause urinary tract infections in dogs are similar to those that cause urinary tract infections in cats: Escherichia coli; staphylococci; and streptococci.^11,13 It can be reasonably inferred that feline prostatic infections are also likely caused by common urinary tract pathogens.

Bacterial urinary tract infections are not common in young cats, but numerous sources report that incidence increases with age.^13,14 Urinary tract infections are common in older cats, particularly in those with diseases such as hyperthyroidism, chronic renal disease, and diabetes mellitus.¹⁵ It is likely that the increased susceptibility to urinary tract infections in these cats is a combination of the disease processes and impairment of urinary tract defenses that diminish with aging. Defense mechanisms present in the urinary tract include processes such as extensive renal blood supply and flow, antibody production, urethral high pressure zones, urethral peristalsis, and normal micturition.^11,13,16

There are several possible explanations for this cat's clinical presentation. The cat was an older, intact male, possibly with altered prostatic tissue secondary to chronic androgenic stimulation. Definitive evidence of benign prostatic hyperplasia was not evident. One pathologist (Dr. Stephen J. Engler, personal communication) noted that the inflammatory changes in the prostate were severe and may have masked, but also may have induced, the glandular proliferative change.

The cat in this case also had a thyroid nodule and chronic renal changes, all possible predisposing factors for a urinary tract infection and ascending prostatitis.¹⁵ Although the prostate was the most grossly abnormal organ, based on the rareness of isolated feline prostatic disease, it is certainly possible that prostatitis was not the primary problem for the patient. Rather, the prostate may have been secondarily affected as a result of chronic urinary tract disease.

It is unknown whether this cat could have responded favorably to the treatment protocol generally recommended for canine chronic bacterial prostatitis, comprising an extended course of antibiotics able to cross the blood-prostate barrier and castration.

Conclusion

As illustrated by this case, clinical signs for feline prostatic disease can be quite variable. Chronic prostatitis should be on the list of differentials when an older, intact cat presents with prostatic disease. Chronic prostatitis may have a better prognosis than feline prostatic adenocarcinoma, particularly if identified early. Although the overall sample size of cats with prostatic adenocarcinoma is very small, most cats with the disease died within 3 mo of diagnosis in one study.⁸ In contrast, one case report of a cat with bacterial prostatitis stated that the animal was alive and doing well 5 mo after diagnosis and treatment.¹