The prostate is the only major accessory sex gland in the dog. It is a bilobed structure that completely encircles the proximal portion of the urethra. In young animals, the prostate lies entirely within the pelvic cavity but with sexual maturity it increases in size and assumes an abdominal position.
Histologically, the prostate has an epithelial and a stromal component. The epithelial cells form tubule-aveoli that drain into the urethra. The prostate is surrounded by a capsule containing smooth muscle fibres that extend into the organ, dividing the alveolar tissue into distinct lobules.
Blood supply to the prostate is supplied by the prostatic artery, which arises from the pudendal or umbilical artery. Anastomoses can be found between the prostatic vessels and the urethral artery, and the cranial and caudal rectal artery. Venous blood returns via the prostatic vein to the internal iliac vein. Lymph drains into the iliac lymph nodes. Sympathetic innervation is provided by the hypogastric nerve, which stimulates the active secretory process and expulsion of secretions by smooth muscle contractions. Parasympathetic innervation with fibers from the pelvic nerve also contributes to smooth muscle contraction.1
Fluid secreted by the prostate forms more than 90% of the total volume of the ejaculate2 and is expulsed in the first and third fractions of the ejaculate. Its main functions are to reduce the viscosity of the ejaculate and to facilitate sperm transport. Prostatic secretions are acidic and have a bactericidal effect, which may prevent ascending urinary tract infections.
With increasing age and under the influence of androgens the prostate undergoes spontaneous enlargement referred to as benign prostatic hyperplasia.
Several different diseases of the prostate occur in middle-aged and older dogs and include benign hyperplasia, prostatitis, prostatic abscess, prostatic and para-prostatic cysts, prostatic metaplasia and prostatic neoplasia. With the exception of prostatic neoplasia, prostatic disease generally affects intact male dogs.
Pathogenesis of prostatic disease
1. Benign prostatic hypertrophy/hyperplasia (BPH) BPH occurs commonly in older dogs. In BPH there is an increase in cell size (hypertrophy) and cell number (hyperplasia). Two forms of BPH may be distinguished: glandular hyperplasia and complex hyperplasia (or cystic hyperplasia).
BPH occurs only in intact male dogs, suggesting hormonal modulation of the disease. The precise pathogenesis is, however, not entirely understood. It is thought that variations in the ratio of circulating androgens (testosterone and di-hydro-testosterone) and oestrogens with increasing age may induce the morphological changes associated with BPH.3
2. Prostatitis Infection of prostate parenchyma occurs through ascending bacterial infection from the urethra. Acute and chronic infections are recognised. It is likely that an underlying parenchymal change is responsible for the establishment of an infection. Cystic BPH is frequently seen in dogs with prostatitis. E. coli followed by S. aureus, Klebsiella spp. and Proteus mirabilis are the pathogens most frequently isolated from infected prostates. Occasionally infections with anaerobic bacteria and fungi are diagnosed.
Prostatitis can be either acute, causing depression, painful rectal palpation, fever, straining to urinate or defaecate and a stiff-legged gait. Or it can be chronic and asymptomatic or causing only sterility in breeding males due to poor semen quality.
3. Prostatic abscess Abscessation of the prostate is caused by a pre-existing parenchymal infection which develops into micro-abscesses that later coalesce into larger abscesses. In severe cases, dogs with prostatic abscess, peritonitis and septicaemia may show signs of septic shock.4
4. Prostatic and para-prostatic cysts Two types of prostatic cysts are recognised: prostatic retention cysts, which are thought to develop by accumulation of fluid after occlusion of parenchymal ducts, and para-prostatic cysts, which only have minimal communication with prostatic parenchyma.
Para-prostatic cysts are thought to be remnants of the uterus masculinus, whereas retention cysts are associated with parenchymal changes such as BPH, metaplasia or neoplasia. Both types of cysts can reach considerable size and may exercise pressure on the colon or the urethra, interfering with defaecation or urination. Alternatively they may become infected and undergo abscessation.
5. Prostatic squamous metaplasia Squamous metaplasia is the transformation of the normally cubic prostatic epithelial cells into squamous epithelium under the influence of oestrogens. The most frequent cause of high serum levels of oestrogens in male dogs is the presence of a testicular Sertoli cell tumor (either in a normally descended or in a cryptorchid testicle).
6. Prostatic neoplasia Tumours of the prostate are not commonly seen in dogs. Usually old dogs are affected with an average age of occurrence of 10 years5,6 and it appears that castrated males have a greater risk of developing prostatic carcinoma than intact male dogs.7 There is no particular breed disposition; however, a recent retrospective study at the University of Utrecht revealed that the Bouvier des Flandres had almost 8.5 times more risk of developing the disease than other breeds.7
All prostatic tumours reported are malignant and the majority are adenocarcinomas. In some cases transitional cell carcinomas from the bladder can extend into the prostate. Prostatic carcinomas (PCA) are very malignant tumours and metastases are usually already present at the time of diagnosis.
The main sites of metatstatic spread are the sublumbar lymph nodes, lungs and skeletal system, particularly the lumbar vertebrae.
Clinical signs of prostatic disease
Prostatic disease can produce a wide variety of different clinical signs ranging from weight loss to septic shock. Dogs showing signs of tenesmus, penile discharge (blood) not associated with micturition, haematuria, pyuria, stranguria, urinary incontinence, caudal abdominal pain, acute abdomen or ambulatory difficulty should be evaluated for prostatic disorders.1
In addition, prostatic disease may be associated with and present as other clinical problems such as perineal hernia.
Diagnosis of prostatic disease
Besides a complete anamnesis including reproductive, urinary and gastrointestinal system questions as well as recording of previous treatment, general examination of the dog is important as bacterial infection of the prostate can cause signs of fever and systemic disease. Weight loss and cachexia may also be associated with neoplasia.
A complete physical exam should include careful abdominal and rectal palpation. Both testicles are palpated to exclude the presence of tumours. In the case of urinary retention, catheterisation of the urethra allows determination of urethral patency.
Imaging techniques used for the diagnosis of prostatic disease include ultrasound and radiographic examination. Ultrasound examination has the advantage of allowing visualisation of the structure of the prostate and the identification of fluidfilled cavities as well as an estimation of prostatic volume.
Ultrasonography is also useful for guiding a biopsy needle into suspicious areas of the prostate. The normal prostatic appearance is slightly hyperechoic compared to splenic parenchyma and has a uniform homogenous pattern (see Figure 1).
With benign hyperplasia the prostate may become more hyperechoic and heterogenous in structure. Cysts and abscesses are seen as fluid-filled cavities. Tumours may appear hypoechoic at an early stage, then become hyperechoic and contain mineralisation later on.
On survey radiographs it may be difficult to localize the prostate. Contrast urethrography may assist in identifying the position of the prostate. Prostatamegaly can cause dorsal dislocation and compression of the colon. In the case of neoplasia, proliferative changes on the dorsal aspect of the lumbar vertebrae and ventral border of the ilium may be seen1 (see Figure 2).
Results of complete blood count and serum chemistry are often unremarkable and not specific for prostatic disease. Changes such as leukocytosis and neutrophilia with leftshift may reflect infection in the case of prostatitis or prostatic abscess. In advanced stages associated with septic shock, changes relative to organ failure may be seen. Urinalysis including bacteriological culture and sensitivity testing are useful in determining the aetiology of prostatic infections and choosing the appropriate antibiotic treatment.
CPSE (canine prostate-specific arginine esterase) is a hormone secreted by prostatic epithelial cells under the control of sex hormones. The protein belongs to the family of kallikreins like PSA (prostate-specific antigen) in man. CPSE is present in sperm (comprising more than 90% of the protein in prostatic fluid) and in blood. When prostatic cells become hyperplastic, the serum concentration of CPSE increases. The serum concentration of CPSE has been shown to be an excellent indicator of BPH (benign prostatic hyperplasia) in the dog.
Other laboratory tests used in the diagnosis of prostatic diseases include analysis of prostatic fluid obtained either by collecting the ejaculate or by prostatic massage. Fluid obtained can be examined cytologically or used for culture and sensitivity testing.
Additionally, samples for cytological examination can be obtained by fine needle aspiration of the prostate gland or by aspiration of prostatic cells into a urinary catheter under ultrasound control of the location of the catheter tip.8 Finally, surgical biopsy of the prostate is a somewhat more invasive technique for the diagnosis of prostatic diseases.
- Basinger, R. R., Robinette, C. L. and Spaulding, K. A. (2003) The Prostate. In: Slatter, D. (ed.) Textbook of Small Animal Surgery. 3rd edition, Philadelphia: WB Saunders, 1,542-1,557.
- Johnston, S. D., Kamolpatana, K., Root-Kustritz, M. V. and Johnston, G. R. (2000) Anim Reprod Sci 60-61: 405415.
- Mahapokai, W. S. (2000) HormonallyInduced Benign Prostatic Hyperplasia in the Dog. Thesis, University of Utrecht.
- White, R. A. S. (2000) Clin Tech in Small An Pract 15 (1): 46-51.
- Dorfmann, M. and Barsanti, J. (1995) Comp Cont Educ 17 (6): 791-810.
- Cooley, D. M. and Waters, D. J. (2001) In: Small Animal Clinical Oncology. Withrow, S. J. and MacEwen, E. G. (eds). Saunders: Philadelphia, 478-489.
- Teske, E., Naan, E. C., van Dijk, E. M., Van Garderen, E. and Schalken, J. A. (2002) Mol Cell Endocrinol 197: 251255.
- Teske, E. and Nickel, R. (1996) Kleintierpraxis 41: 239-247
