Prostatitis in Small Animals
Inflammation of the canine prostate gland usually is suppurative, and acute prostatitis may result in abscesses. Chronic prostatitis occurs secondary to benign prostatic hyperplasia (see Benign Prostatic Hyperplasia in Small Animals). Various organisms, including Escherichia coli,Staphylococcus, Streptococcus, and Mycoplasma spp, have been incriminated. Infection may be hematogenous (acute prostatitis) or ascend from the urethra (chronic prostatitis). Because prostatic fluid normally refluxes into the bladder, a secondary urinary tract infection often accompanies prostatic infection. Acute prostatitis and chronic prostatitis vary based on progression and severity of clinical signs.
Acute prostatitis is associated with malaise, pain, and fever. Dehydration, septicemia, and shock may occur in severe cases. Neutrophilia with a left shift, monocytosis, and/or toxic WBCs may be seen. Ultrasonography shows hypoechoic areas consistent with small pockets of fluid. Ideally, prostatic material is obtained by prostatic massage for cytologic examination and for culture and sensitivity testing. Massage of an acutely infected prostate may release organisms into the blood and cause septicemia. Urinalysis shows hematuria, pyuria, and bacteriuria. The urine should be submitted for culture and sensitivity testing. Often, the urine and prostatic material yield the same organisms.
IV fluid therapy is indicated when acute prostatitis is associated with dehydration or shock. Because the prostate-blood barrier is disrupted in acute prostatitis, antibiotics should be selected on the basis of sensitivity testing and given for 3–4 wk. Enrofloxacin at a dosage of 5 mg/kg, bid, orally is a good empiric treatment choice while awaiting results of microbiologic testing. After the infection is controlled, castration should be considered. In some instances, multiple microabscesses within an infected prostate gland may coalesce into a solitary abscess. Large prostatic abscesses are best treated by surgical drainage and intracapsular omentalization. Urine or prostatic fluid (or both) should be cultured again 2-–4 wk after antibiotic therapy to be certain that infection has resolved.
Chronic bacterial prostatitis may cause no clinical signs except recurrent urinary tract infection. Physical abnormalities may be limited to the urinary tract. Rarely, prostatic size and shape may be normal. Microbiologic examination of the third (prostatic) fraction of the ejaculate is more accurate for assessment of chronic bacterial prostatitis than examination of prostatic massage specimens. Dogs with chronic bacterial prostatitis are usually willing to ejaculate. Prostatic fluid and urine should be submitted for cytologic and microbiologic examination.
Chronic bacterial prostatitis will not resolve without also treating for benign prostatic hyperplasia. In fact, most cases of chronic bacterial prostatitis will resolve with only treatment for benign prostatic hyperplasia, whether surgical (castration) or medical (finasteride). Antibiotic therapy alone is unrewarding. Many antibiotics do not diffuse easily into the prostatic parenchyma because of the presence of the blood-prostate barrier. The mild inflammation associated with chronic prostatitis may not impair the blood-prostate barrier, so antibiotics that are non-ionized at neutral pH with high fat solubility (eg, erythromycin, clindamycin, trimethoprim-sulfamethoxazole, or enrofloxacin) are most effective. If antibiotic therapy is implemented, it should be continued for ≥4 wk.