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The similarity of the prostate of dogs and its diseases to that of humans has lead to an enormous number of studies into the pathology of the canine prostate. The major diseases will be detailed individually, with this section limited to those studies of a more general or clinical nature.Many authors have given an overview of prostate diseses (O'Shea 1962, Hornbuckle et al 1978, Basanti and Finco 1986, Olson et al 1987, Krawiec and Helfin 1992, 1994, Knecht, Johnston et al 2000).

O'Shea (1962) identified 3 stages in the life of a prostate - normal growth in the young adult, hyperplastic growth during middle age, and senile involution. 63% of 243 adult dogs had glandular hyperplasia. 10 out of 79 dogs over 11 years had senile involution. Castration causes atrophy. 3 dogs with retained testes all had normal prostates. Those dogs with Sertoli cell tumours (3 dogs) all had atrophy. 4 prostates had abscesses, 3 had squamous metaplasia.

Hornbuckle et al (1978) reviewed 140 cases of prostatic disease. 34 had complicated prostatic hyperplasia, 20 had chronic active prostatitis, 26 had acute prostatitis, 23 had a prostatic abscess, 15 had prostatic cysts, and 22 had carcinoma.

Krawiec and Helfin (1992) studies 177 dogs with prostatic disease. 33 had prostatitis, 27 had cysts, 13 had neoplasia, 11 had hyperplasia, 1 had paraprostatic cyst, and 1 had blastomycosis of the prostate. 90 had prostatic enlargement.

Teske et al (2002) found prostatic hyperplasia in 246 dogs (57.1%), prostatitis in 83 dogs (19.3%), and prostatic carcinoma in 56 dogs (13%).

In the Yager-Best Histovet files there are are 131 cases of hyperplasia, 71 carcinomas, 68 cases of prostatitis, 23 prostatic cysts, 14 cases of squamous metaplasia, and 5 prostatic abscesses.

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Basanti JA, Finco DR. (1986) Canine prostatic diseases. Vet Clin North Amer: Small Anim Pract. 16: 587-599.

Hornbuckle WE, MacCoy DM, Allan GS, Gunther R. (1978) Prostatic disease in the dog. Cornell vet. 68 (Suppl 7): 284-305.

Johnston SD, Kamolpatana K, Root-Kustritz MV, Johnston GR (2000) Prostatic disorders in the dog. Anim Reprod Sci. 60-61:405-415

Knecht CD () Diseases of the canine prostae gland (Part 1). Compend Contin Edu :385-391.

Krawiec DR (1994) Canine prostatic disease. J Amer Vet Med Assoc 204: 1561-1564.

Krawiec DR, Helfin D (1992) Study of prostatic disease in dogs: 177 cases (1981-1986). J Amer Vet Med Assoc 200: 1119-1122.

Olson PN, Wrigley RH, Thrall MA, Husted PW, (1987). Disorders of the canine prostate gland: pathogenesis, diagnosis, and medical therapy. Compend Contin Edu - Small Animal 9: 613-623.

O'Shea JD (1962) Studies on the canine prostate gland. 1 factors influencing its size and weight. J Comp Pathol 72: 321-331.

Teske E, Naan EC, van Dijk EM, Van Garderen E, Schalken JA. (2002) Canine prostate carcinoma: epidemiological evidence of an increased risk in castrated dogs. Mol Cell Endocrinol. 197(1-2):251-255

The prostate is under hormonal control with both estrogens and androgens contributing to size. The prostate undergoes atrophy when there is a reduction in hormone concentration. Castration causes atrophy, especially of the epithelial component. Dogs with Sertoli cell tumours develop atrophy, but there is also a risk of development of squamous metaplasia (O'Shea 1962).

Canine prostates go through progressive changes with age. A prepubertal dog has a very small prostate, and with puberty, it increases in size to 'normal'. The size tends to reflect body size although the Scottish terrier is reported to have a prostate that is about 4 times the size of dogs of a similar size (O'Shea 1962). About 63% of dogs develop progressive enlargement of the prostate with age after puberty (O'Shea 1962). The size can become large enough to cause clinical signs or faecal obstruction rather than urinary obstruction (as occurs in humans). The enlarged prostate hangs over the pelvic brim when the dog is in its normal quadrapedal position, but when the position for defaecation is assumed, the prostate is pulled by gravity into the pelvic inlet and with an increase in intraabdominal pressure, forms a 'ball valve' and compresses the colon. Some dogs develop 'senile atrophy' of the prostate (O'Shea 1962)

The increase in size is reported to be the result of increased interstitial tissue with the overall amount of epithelium not increasing in amount. The lumen of glands, however, increase in diameter with age (James and Heywood 1979, Lowseth et al 1990). Shain and Boesel (1978) examined the androgen receptor content of canine prostates and found that hyperplastic glands had a greater receptor content than normal, but there was no difference in the receptor content per cell, and there was no increase in testosterone. Moore et al (1979) found that estradiol enhanced androgen effects on the prostate by enhancing an androgen binding protein in the cytoplasm.

James RW, Heywood R. (1979) Age-related variations in the testes and prostate of beagle dogs. Toxicology. 12(3):273-279.

Lowseth LA, Gerlach RF, Gillett NA, Muggenburg BA. (1990) Age related changes in the prostate and testes of the beagle dog. Vet Pathol 27: 347-353.

Moore RJ, Qazak JM, Wilson JD. (1979) Regulation of cytoplasmic dihydrotestosterone binding in dog prostate by estradiol. J Clin Invest 63: 351-357.

O'Shea JD (1962) Studies on the canine prostate gland. 1 factors influencing its size and weight. J Comp Pathol 72: 321-331.

Shain SA, Boesel RW (1978) Androgen receptor content of the normal and hyperplastic canine prostate. J Clin Invest 61: 654-660.

The hyperplastic prostate is uniformly enlarged. It typically has a smooth capsular surface and the parenchyma is uniform. While it initially will be a round bilobed structure, as it attains a greater size, it will become elongate. It retains its bilateral uniformity, although as the hyperplasia becomes advanced this is less so.. It is usual for the glands to have an increased luminal diameter and this is variable from gland to gland. Many will become cystically distended to the extent that multiple 'cysts' will be visible on cut section.

Figure : Prostatic hyperplasia (right) compared to a 'normal' prostate of a pubertal dog. The bladder is ventral in each example.

Figure : Advanced prostatic hyperplasia in a dog.

Prostates from entire dogs have a characteristic appearance to the epithelium. The acini are small and are lined by a single layer of columnar epithelial cells that have prominent granules in the apical cytoplasm. The nuclei are basally located .With hyperplasia in some dogs or in some parts of the prostate, there is an increase in the diameter of the lumen of the acini. This increase is variable with some being very large and others normal. The epithelial cells are prominent and are large columnar cells with a prominent apical cytoplasm filled with eosinophilic globules. The interstitium is inapparent. In other areas there is a prominent interstitium that widely separates the acini. Even these acini will be distended. The smooth muscle of the capsule and trabeculae is often prominent and the cells hypertrophied. Inflammation is absent.

Figure : Prostatic hyperplasia, with acinar dilation and prominent epithelial cells.

Figure : Prostatic hyperplasia with an increase in interstitium. Acini are distended.

Gilson et al (1992) report on a dog that had a large prostatic mass that was resected. Histologically it was a combination of glandular tissue and stroma, that was initially called an adenoma, but was then regarded as nodular hyperplasia.

Gilson SD, Miller RT, Hardie EM, Spaulding KA (1992) Unusual prostatic mass in a dog. J Amer Vet Med Assoc 200: 702-707.

Squamous metaplasia occurs when the glandular epithelium of the prostate becomes stratified squamous in type instead of the columnar epithelium normally present. The mechanism for the development of squamous epithelium involves the production of keratins by the basal cells. The most dramatic forms of squamous metaplasia occur with exposure to estrogens or in feminizing syndromes. Irritation (from inflammaton) will also result in squamous metaplasia, but this is a subtle change and not as dramatic as with exposure to estrogens.Administration of estrogens (for prostatic disease!) or in dogs with testicular tumours and a feminisation syndrome is where it is mostly seen (O'Shea 1963).

Pathogenesis

Squamous metaplasia can be readily induced by administering estrogens to male dogs. In all animals, paracrine signals from the stroma define the epithelial type that will develop. It will also define the arrangement of the epithelium, including whether the epithelium will form a gland or a cavity. The mesenchyme also defines the function of the epithelium such as what proteins will be produced. This whole interaction involves epithelial feedback and regulation (reviewed by Cunha et al 2004). Steroid hormones regulate this interaction and in the the normal prostate, androgen receptor (AR) is an important factor. In estrogen induced squamous metaplasia, estrogen stimulates the ERalpha receptor, which is especially important in the stroma (the main ER of the epithelium is ERbeta). Using ERknockout mice, both stromal ERalpha and epithelial ERalpha must be present and stimulated to induce both proliferation and metaplasia. The stratified squamous cells acquire cyclooxygenase 2 activity as as result of estrogen stimulation.

Macroscopic findings.

The prostate can be variably affected so that no abnormalities may be detected grossly. The most severely affected though will be larger and have mulifocal pinpoint to miliary foci of white pasty material. Fibrosis can be dramatic also.

Microscopic findings

The histological changes of squamous metaplasia are those of dramatic replacement of the glandular epithelium with stratified squamous epithelium. The center of the acini are filled with laminations of keratin. The amount of keratin can be so great to cause enlargement of the acinus. The epithelium is well diffferentiated stratified squamous, with a basal layer, stratum spinosum and keratinization. Some acini will also have granulomatous and neutrophilic inflammation.

The squamous metaplasia that occurs secondary to prostatitis is subtle and there is marked accumulation of neutrophils and macrophages in the lumens, and some of the epidthelium is a thin layer of stratified squamous epithelium. Keratinization is unusual.

Cunha GR, Cooke PS, Kurita T (2004). Role of stromal-epithelial interactions in hormonal responses. Arch Histol Cytol 67(5):417-434.

Dore M, Chevalier S, Sirois J. (2005) Estrogen dependent induction of cyclooxygenase-2 in the canine prostate in vivo. Vet Pathol 42: 100-103.

O'Shea JD (1963) Squamous metaplasia of the canine prostate gland. Res Vet Sci 4: 431-434.

It is believed (dogma) that prostatic neoplasia in dogs has no precancerous lesion. There does not appear to be a progression from nodular hyperplasia to adenoma to carinoma in situ to invasive carcinoma. As such, the precancerous lesions are rare if they exist.

The only lesion reported that could be adenoma was considered by the authors to be nodular hyperplasia (see above)

Classification

Prostatic carcinoma is a term with several meanings. The convention is that carcinomas of the prostate are actually adenocarcinoma (from the prostate glandular tissue), and although this is reasonable in humans, it is not necessarily the case in dogs. There are several types of carcinoma in dogs, including adenocarcinoma (presumably from the glands), transitional cell carcinoma (from the prostatic ducts) and mixed carcinomas and squamous cell carcinomas. There is disagreement as to which is the most common and this is because subclassifying carcinomas is subjective . Prognostically, there may be little difference. Virutally every dog develops metastasis (Leav and Ling 1968).

Prostatic carcinomas occur in sexually intact and neutered dogs and there is little difference between them (Bell et al 1991), although Teske et al (2002) found an increase risk in castrated dogs. Tumours in castrated dogs tend to have pulmonary metastasis when diagnosed. O'Shea (1968) classified 6 of 7 to be adenocarcinoma, while 1 was classified as a transitional cell carcinoma. Cornell et al (2000) examined 76 cases from multiple institutions and classified 27 as being adenocarcinoma and 40 as mixed adeno- and transitional cell carcinoma. Of 28 dogs known to be intact, 16 had adenocarcinomas, but of the 13 known to be neutered dogs, only 3 were adenocarcinomas. It therefore seems that those carcinomas with transitional cell differentiation tend to occur more commonly in castrated dogs whereas neutered dogs are evenly split between those with and those without transitional differentiation.

Grieco et al (2003) looked at intermediate filament expression of the canine prostate. They used vimentin (3B4, V9) and cytokeratins AE1/AE3, CK18-8, CK5, CK clone 8.12, CK14 (for basal cells). Normal prostatic epithelia does not stain with vimentins. All stain with AE1/AE3, and none with CK14. The others are variable. They looked at 11 carcinomas - one squamous cell carcinoma, 7 adenocarcinomas and 3 undifferentiated. All stained with AE1/AE3 and with vimentin 3B4. 6 stained with CK14 (for basal cells).

The origin of the various carcinomas has been debated for many years. Weaver (1981) indicated that it was impossible to differentiate primary prostatic carcinoma from transitional cell carcinoma. LeRoy et al (2004) attempted to use a less subjective method than morphological features by using techniques to identify cytokeratin 7 and arginine esterase, but could not differentate between the major types. There are no consistent immunohistochemical markers for prostatic carcinomas. As both cell types (glands) arise from a common progenitor, it is not surprising! Normal and hyperplastic prostate stains for Prostatic specific antigen (PSA), PSA protein (PSEP) and for Canine prostatic antigen. In the 31 cases examined by McEntee et al (1987) only 8 stained for canine prostatic antigen, 2 stained form PSA and 3 stained for PSAP. It seems reasonable to call all carcinomas of the prostate 'carcinoma of the prostate' or 'prostatic carcinoma' and not to try to classify them.

LeRoy et al (2007) investigated potential phenotypes of carcinoma of the prostate by comparing protein expression profiling. They examined carcinomas from 3 dogs and compared from789 top 1305 proteins from these and from normal bladder and prostatic epithelia from 6 dogs. There was no clear similarity of protein expression between the neoplasms and normal tissues and it appeared as thought the protein expression of the neoplasms was different and unique to the protein expression of the normal tissues.

Prognosis

A diagnosis of prostatic carcinoma in a dog carries an extremely poor prognosis. Many have metastasis at diagnosis, and most will develop metatasis.Metastasis to the lung is most common but about 14% have metastasis to bone, especialy the lumbar vertebrae and pelvis (Leav and Ling 1968, Durham and Dietze 1986, Cornell et al 2000).

Pathogenesis

There are no known causes, although there is a slightly increased risk in castrated dogs (Teske et al 2002). As already indicated, castration is not protective so the systemic hormonal environment does not appear to be important. Lai et al (2009) looked at this further and found that androgen receptors were less common in neoplastic prostatic tissue than in normal prostate. Postive staining was in the cytoplasm rather than the nucleus and there was no detectable mutations to DNA coding for the androgen receptor.

There are numerous studies outlining the distribution of estrogen receptors in canine prostates, and the intranuclear receptors are found in stromal cells and in the epithelial cells. Hyperplastic prostates have a similar distribution. Grieco et al (2006) found a loss of estrogen receptors in the stromal of all prostates including those with carcinoma. The main ER in the epithelium is ERBeta. In the more 'differentiated' tumours, ER was present but with less intense staining. Staining was reduced with the less differentiated tumours. The significance of this is yet to be established. Gallardo et al (2007) examined androgen receptor, estrogen alpha and beta, and progesterone receptor expression in prostatic specimens from dogs with prostatic hyperplasia, prostatatitis and neoplasia. Expression of these were less common in disease except for progesterone receptor, where more animals had expression in disease conditions.

Prostatic intraepithelial neoplasia. It is widely believed that precursor lesions, such as low grade prostatic intraepithelial neoplasia (PIN), do not occur in dogs. High grade prostatic intraepithelial neoplasia is seen, and often in prostates with neoplasia. Waters and Bostwick (1997) report the presence of high grade prostatic intraepithelial neoplasia in dogs. They examined 35 prostates from dogs without clinical evidence of prostatic disease. They found high grade PIN in 1 of 13 dogs less than 4 years, and 6 of 11 dogs from 7 to 11 years old, and in 1 of 11 dogs that had been castrated. Waters et al (1997) found high grade PIN in19 of 29 prostates with carcinoma. Madewell et al (2004) examined canine prostates for high grade PIN. No examples were seen in 20 normal prostate glands or in 95 glands from dogs with prostatic hyperplasia. High grade PIN was found in 7 of 20 prostates with carcinoma. Matsuzaki et al (2010) claims to have 5 cases of PIN and examined them by immunohistochemistry. They believe these to be low grade PIN, thus drawing a parallel with the human disease. This study is therefore contradictory to the widely held view of the lack of low grade PIN in dogs. The foci in their study had a higher expression of nuclear p63 and a higher proliferation index (PCNA) than normals. These cells had 'heterogenous' staining with androgen receptor. They surmised that basal cells play a role in the development of canine PIN.

Some prostatic carcinomas have cytogenetic abnormalities and of particular interest is one with a similar abnormality to a human prostatic carcinoma. The carcinoma studies had trisomy of chromosome 13, which is similar to chromosome 8 of humans and which also has cytogenetic anomalies in some human prostatic carcinomas (Winkler et al 2006). This is a recent field of investigaton with the first report being by Winkler et al (2005).

Macroscopic changes

Prostates with neoplasia are highly variable in their gross appearance. Some, particularly those in neutered dogs, have very little change. Slight enlargement may be the only change. When sectioned, there is usually a central cavity with a fibrous wall, or focal white areas of necrosis.

Figure : Prostatic carcinoma, neutered dog. Prostate is on the left and has a central cavity of necrosis. The bladder is central right.

At the other extreme is when the prostate is dramatically enlarged and greater than 10 cm in diameter. They tend to be multinodular, asymetrical, and often have adhesions to the surrounding tissues.

Figure :Prostatic carcinoma with marked enlargement and a multinodular appearance. The small structure on the left is a partially hidden bladder.

Microscopic changes

Histological changes in the prostate are typical of carcinoma. The phenotype is quite variable and many are mixtures of the individual types including a glandular phenotype, a more solid and transitional phenotype, and squamous cell carcinoma. Most have a very scirrhous appearance with large amounts of fibrous tissue and some have areas of necrosis. Most are not very challenging, unless there is concurent inflammation.

Normal prostates have a discontinious capsule through which protrudes glands of well differentiated cells. These should not be confused with invasion of a neoplasm. The presence of prostatic ducts with a transitional type of cell should not be mistaken for neoplastic change, and squamous metaplasia should be differentiated from squamous cell carcinoma.

If there is a 'typical' carcinoma, it is an invasive lesion that replaces and obliterates existing parenchyma. The cells are arranged in cords, nests or individuals surrounded my fibrous tissue. Criterial of malignancy including anosocytosis, anisokaryosis, reduced nuclear to cytoplasmic ratio and a high mitotic rate are present. In some, the cells are arranged in acinar strutures (adenocarcinoma) whereas in others, the cells form solid nests and have a more squamous appearance (transitional cell phenotype). Squamous cell carcinomas are typical of that phenotype and produce keratin pearls.

 

Figure : Prostatic carcinoma, transitional cell type

Figure : Prostatic carcinoma, adenocarcinoma

Figure : Prostatic carinoma, mixed phenotype.

 

Bell RW, Klausner JS, Hayden DW, Feeney DA, Johnston SD (1991) Clinical and pathologic features of prostatic adenocarcinoma in sexually intact and castrated dogs: 31 cases (1970-1987). J Amer Vet Med Asoc 199: 1623-

Cornell KK, Bostwick DG, Cooley DM, Hall G, Harvey HJ, Hendrick MJ, Pauli BU, Render JA, Stoica G, Sweet DC, Waters DJ. (2000) Clinical and pathologic aspects of spontaneous canine prostatic carcinoma: a retrospective analysis of 76 cases. The Prostate 45: 173-183.

Durham SK, Dietze AE (1986). Prostatic adenocarcinoma with and without metastasis to bones in dogs. J Amer Vet Med Assoc 188: 1432-1436.

Gallardo F, Mogas T, Baró T, Rabanal R, Morote J, Abal M, Reventós J, Lloreta J. (2007) Expression of Androgen, Oestrogen a and ß, and Progesterone Receptors in the Canine Prostate: Differences between Normal, Inflamed, Hyperplastic and Neoplastic Glands J Comp Path 136: 1-8

Grieco V, Patton V, Romussi S, Finazzi M. (2003) Cytokeratin and vimentin expression in normal and neoplastic canine prostate. J Comp Path 129: 78-84.

Grieco V, Riccardi E, Rondena M, Romussi S, Stefanello D, Finazzi M. (2006) The distribution of oestrogen receptors in normal, hyperplastic and neoplastic canine prostate, as demonstrated immunohistochemically. J Comp Pathol. 135(1):11-16.

Lai C-L, van den Ham R, Mol J, Teske E (2009) Immunostaining of the androgen receptor and sequence analysis of its DNA-binding domain in canine prostate cancer. The Vet J 181: 256-260

Leav I, Ling GV. (1968) Adenocarcinoma of the canine prostate. Cancer 22: 1329-1345.

LeRoy BE, Nadella MVP, Toribio RE, Leav I, Rosol TJ. (2004) Canine prostate carcinomas express markers of urothelial and prostatic differentiation. Vet Pathol 41: 131-140.

LeRoy BE, Painter A, Sheppard H. Popiolek L, Samuel-Foo M, Andacht TM. (2007) Protein expression profiling of normal and neoplastic canine prostate and bladder tissue. Vet Comp Oncology 5 (2) 119-130.

Madewell BR, Gandour-Edwards R, DeVere White RW. (2004) Canine prostatic intraepithelial neoplasia: is the comparative model relevant? The Prostate m58: 314-317.

McEntee M, Isaacs W, Smith C. (1987) Adenocarcinoma of the canine prostate: immunohistochemical examination for secretory antigens. The Prostate 11: 163-170.

Matsuzaki P, Cogliati B, Sanches DS, Chaible LM, Kimura KC, Silva TC, Real-Lima MA, Hernandez-Blazquez FJ, Laufer-Amorim R, Dagli MLZ (2010) Immunohistochemical Characterization of Canine Prostatic Intraepithelial Neoplasia. J Comp Path 142: 84-88

O'Shea JD (1963) Studies on the canine prostate gland. II Prostatic neoplasms. J Comp Path 73: 244-252

Taylor PA (1973) Prostatic adenocarcinoma in a adog and a summary of ten cases. Canadian Vet J 14: 162-166.

Teske E, Naan EC, van Dijk EM, Van Garderen E, Schalken JA. (2002) Canine prostate carcinoma: epidemiological evidence of an increased risk in castrated dogs. Mol Cell Endocrinol. 2002 197(1-2):251-255

Waters DJ, Bostwick DG. (1997) Prostatic intraepithelial neoplasia occurs spontaneously in the canine prostate. J Urol 157: 713-716.

Waters DJ, Hayden DW, Bell FW, Klausner JS, Qian J, Bostwick DG. (1997) Prostatic intraepithelial neoplasia in dogs with spontaneouos prostate cancer. (The Prostate 30: 92-97.

Weaver AD (1981) Fifteen cases of prostatic carcinoma in the dog. Vet Rec 109: 71-75.

Winkler S, Murua Escobar H, Eberle N, Reimann-Berg N, Nolte I, Bullerdiek J. (2005) Establishment of a cell line derived from a canine prostate carcinoma with a highly rearranged karyotype. J Hered. 96(7):782-785.

Winkler S, Reimann-Berg N, Escobar HM, Loeschke S, Eberle N, Hoinghaus R, Nolte I, Bullerdiek J. (2006) Polysomy 13 in a canine prostate carcinoma underlining its significance in the development of prostate cancer. Cancer Genet Cytogenet.169(2):154-158

In a multiinstitutional study of prostatic carcinoma, Cornell et al (2000) examined the records of 228 cases of prostatic neoplasia and reported 3 cases of sarcoma, but there are no other details.

Cornell KK, Bostwick DG, Cooley DM, Hall G, Harvey HJ, Hendrick MJ, Pauli BU, Render JA, Stoica G, Sweet DC, Waters DJ. (2000) Clinical and pathologic aspects of spontaneous canine prostatic carcinoma: a retrospective analysis of 76 cases. The Prostate 45: 173-183.

Haemangiosarcoma

Hayden et al (1992) reported on a dog with haemangiosarcoma they suggested arose in the prostate and metastasized to multiple organs. There is one case in the Yager-Best Histovet database (YB54561).

Figure : Hemangiosarcoma of prostate.

Hayden DW, Bartges JW, Bell FW, Klausner JS. (1992). Prostatic hemangiosarcoma in a dog: clinical and pathologic findings. J Vet Diagn Invest 4: 2009-211.

Leiomyosarcoma

Hayden et al (1999) reported a case of leiomyosarcoma in the prostate of a dog.

Hayden DW, Klausner JS, Waters DJ. (1999) Prostatic leiomyosarcoma in a dog. J Vet Diagn Invest. 11(3):283-6.

Osteosarcoma

One case of osteosarcoma of the prostate is mentioned by in a discussion of cases with obstruction of the urethra by Weisse et al (2006). .It had pulmonary metastases.

Weisse C, Berent A, Todd K, Clifford C, Solomon J. (2006) Evaluation of palliative stenting for management of malignant urethral obstructions in dogs. J Amer Vet Med Assoc 229: 226-234.

Lymphoma

Mainwaring (1990) reported a case of lymphoma that only was found in the prostate and adrenal. It was considered a primary prostatic lymphoma. There is one case of lymphoma of the prostate in the Yager-Best Histovet database (YB52270).

Mainwaring CJ (1990) Primary lymphoma of the prostate on a dog.J Small Anim Pract 31: 617-619

There are many cysts that can and do develop within and around the prostate. Those around the prostate are lumped together as paraprostatic cysts. Hoffer et al (1977) classified prostatic cysts into 4 groups, and an additional one is added

• Multiple cysts associated with prostatic hyperplasia (these are small cysts within the prostate)
• Prostatic retention cysts (These are within the prostate and are the result if obstruction of prostatic ducts)
• Paraprostatic cysts (these have no contact with the prostate and arise from a uterus masculinus, hematoma, or a serosal cyst.
• Cystic prostate associate with squamous metaplasia. (these arise secondary to squamous metaplasia)
• Paraprostatic lymphatic cysts

Hoffer RE, Dykes NL, Greiner TP (1977) Marsupialization as a treatment for prostatic disease. J Amer Anim Hosp Assoc 13: 98-104.

Bloom F (1954). "Pathology of the Dog and Cat: The genitourinary system, with clinical considerations" Am. Vet. Publ Evanston, Illinois

The grouping here is based on the basic separation of those cysts within the prostate and those outside it..

Multiple cysts in prostatic hyperplasia

During age associated prostatic hyperplasia in intact male dogs there is variable distension of prostatic acini to form cystic structures. Some of these distended lumens are large enough to be classified as cysts, and grossly some are several centimeters in diameter.Black et al (1998) found that of 85 dogs with no indication of prostatic disease, 12 had prostatic cysts that ranged from 1.5 to 2.4 cm diameter. 5 of the 12 had positive cultures for bacteria or mycoplasma. Some of these prostates have a polycystic gross appearance. Histologically these cysts are lined by normal glandular cells. When there is rapid elargement of the cysts, the epithelium may become attenuated.

.Black GM, ling GV, Nyland TG, Baker T (1998) Prevalence of prostatic cysts in adult large breed dogs. J Amer Anim Hosp Assoc 34: 177-180.

Paraprostatic lymphatic cysts

Multiple thin fluid filled cysts are found in old dogs with prostatic hyperplasia. They are lined by flattened endothelial cells.

Bloom F (1954). "Pathology of the Dog and Cat: The genitourinary system, with clinical considerations" Am. Vet. Publ Evanston, Illinois

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p338.

Paraprostatic cysts and pseudocysts

The most common 'cyst' biopsied and submitted is the paraprostatic pseudocyst, and these can assume enormous proportions. Some can be up to 30cm in diameter (or larger) and form a space occupying mass in the abdomen. It is not known how or from what they arise.

Some cysts, particularly the smaller ones, are lined by epithelium and they may communicate with prostatic cysts and acini. Many prostates have projections of glands from the prostate into and through the capsule - and they are seen to extend between bundles of the discontinuous smooth muscle of the capsule. It is likely that many paraprostatic cysts are an extension of cysts in prostatic hyperplasia.

Other possible origins for paraprostatic cysts are serosal inclusion cyst and hematomas (McEntee 1990).

Those that are in the dorsal midline region of the prostate are assumed to be derived from a cystic uterus masculinus, a remnant of the paramesonephric duct.

The structure of the cysts make determining their origin impossible as the inner lining is seldom lined by epithelium. The term pseudocyst is more precise in this instance. The lining is often either fibrous or granulation tissue with an appearance similar to a 'seroma'. The wall is usually of compressed fibrous tissue and the outer lining is mesothelium (serosa).

It is not unusual for the pseudocysts to have mineralisation of the wall, although the literature is scant on this (Girard and Despots 1995, Head and Francis 2002).

The pseudocysts are readily recognised clinically, but are difficult to manage. Some can become infected and become abscesses. There are 9 paraprostatic cysts diagnosed in the Yager-Best Histovet database - 2 had mineralization/ossification and 1 was abscessed.

Figure : Paraprostatic pseudocyst. Bladder is to the right and prostate is lower left.

Figure : Paraprostatic pseudocyst. The inner lining is granulation tissue with no epithelium.

Figure : Paraprostatic pseudocyst. The inner lining is lower left, the ossified portion is central, the dense fibrous wall and serosa is upper right.

Girard C, Despots J (1995). Mineralized paraprostatic cyst in a dog. Canadian vet J 36: 573-574.

Head LL Francis DA (2002). Mineralized paraprostatic cyst as a potential contributing factor in the development of perineal hernias in a dog. J Am Vet Med Assoc 221(4): 533-535.

Weaver AD (1978). Discrete prostatic (paraprostatic) cysts in the dog. Vet Rec 102: 435-440

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p338

Inflammation of the prostate is called prostatitis. Sequential studies of prostatis are lacking, so much is assumed from studies in other animals. Prostatitis is a common finding, even in asymptomatic dogs (Diniz et al 2005). It is reported to occur in canine brucellosis (Brennan et al 2008)

Many dogs have foci of inflammatory cells in the interstitial tissues (James and Heywood 1979), suggesting that subclinical infection may be common. 10% of dogs had these at 6 months but 45% had them at 7 years.

Pathogenesis

It is assumed that prostatis occurs mostly by ascending infection - organisms travel from the penis and prepuce via the urethra to the prostate. Hematogenous spread and localisation in the prostate is probably the way that infection with Brucella reaches the prostate, but infection from epididymitis is also possible. There is also the theoretical possibility of infection of the prostate from the bladder and urine.

Once bacteria infect the prostate, it is likely they grow within the lumen of the glands, and from there either elicit an inflammatory response or invade. It is therefore likely that ascending infection will have an acute intraacinar or glandular phase and later an interstitial phase. Bacteria within the lumen of the glands will likely not be recognised by the body, at least not initially. Neutrophils and the contents of their granules will contribute to the chemotactic factors of the bacteria to encite an inflammatory response. Bacteria would likely be Gram negative and therefore release endotoxin. With time, the interstitial response will become more obvious, with lymphocytes and plasma cells predominating. This interstitial phase will also be accompanied with fibrosis.

Abscessation of the prostate is one outcome of prostatitis. Prostatic abscesses will be discussed separately.

Macroscopic findings

Acute severe prostatitis is a painfull condition that is usually accompanied by systemic illness. Such cases will have edema and hemorrhage of the prostatic and periprostatic tissues. It is difficult to determine the outline of the prostate because of this acute inflammatory response.

Figure : Severe acute prostatitis. There is marked periprostatic edema and haemorrhage.

When the inflammatory response is suppurative, the prostate will be uniformly enlarged and pus will exude from the cut surface, especially when there is pressure applied to the prostate.

Chronic prostatitis will have a firm white appearance, or have no macroscopic changes visible.

On rare occasions, prostatis can be emphysematous (Rohleder and Jones 2002)

Microscopic findings.

In the most severe forms of prostatitis, there is extensive edema and hemorrhage that separate the interstitial tissues and widely separate acini from each other. Necrosis of portions of the prostate can be expected. Neutrophils will be the predominant inflammatory cell - both in the intersitium and within the acini. In the less severe examples, neutrophils, macrophages and necrotic debris will be in the lumens, and cause them to be distended. The interstitium, initially will contain neutrophils, but with time, lymphocytes and plasma cells will appear around the acini and around vessels. Fibrosis will develop as well. Atrophy of glands in the areas near inflammation may occur.

Figure : Chronic interstitial prostatis.

Figure : Chronic interstitial prostatitis

Figure : Chronic intestitial prostatitis

Bacterial prostatitis

There is surprisingly little infomation about the kinds of bacteria involved in prostatis in dogs. Brucella sp infection of the prostate is a well recognized entity and will be discussed below.

The bacteria isolated from cases of prostatitis include Escherichia coli, Proteus, Klebsiella, Staphylococcus, Streptococcus sp, but there is little information on prevalence.

There is one case report of emphysematous prostatitis from which Escherichia coli was cultured. (Rohleder and Jones 2002).

Brucella prostatitis

Prostatitis is part of canine brucellosis, although it may not be clinically evident. The prostatitis tends to be of the chronic interstitial type, although this probably reflects the fact that the lesions take a long time to develop and the acute phase is over. Brucells canis, Brucella suis and Brucella abortus are all capable of causing prostatitis in dogs (Barr et al 1986)

Brennan et al (2008) wrote about brucellosis in a kennel in Saskatchewan. The lesions they found in 5 male dogs with titres to Brucella sp (presumabley B canis) were epididymitis and prostatitis in one dog, prostatitis and in 4 of the 5. dogs. The lesions were of the interstitial type.

 

Barr SC, Eitis BE, Roy AF, Miller R. (1986). Brucella suis biotype 1 infection in a dog. J Amer Vet Med Assoc 189: 686-687.

Brennan SJ, Ngeleka M, Philibert HM, Forbes LB, Allen AL (2008) Canine brucellosis in a saskatchewan kennel. Canadian Vet J 49: 703-708

Mycotic prostatitis

Granulomatous prostatitis occurs in dogs with infection with Blastomyces dermatiditis, Cryptococcus neoformans and Coccidiodes immitis (Johnston et al 2000).

Mycoplasma

L'Abee-Lund et al (2003) report the recovery by culture of Mycoplasma canis from a dog with prostatitis.

 

 

L'Abee-Lund TM, Heiene R, Friis NF, Ahrens P, Sorum H (2003) Mycoplasma canis and urogenital disease in dogs in Norway. Vet Rec. 2003 153(8):231-235.

Diniz SA, Melo MS, Borges AM, Bueno R, Reis BP, Tafuri WL, Nascimento EF, Santos RL. (2005)

Genital Lesions Associated with Visceral Leishmaniasis and Shedding of Leishmania sp. in the Semen of Naturally Infected Dogs Vet Pathol 42: 650-658.

James RW, Heywood R. (1979) Age-related variations in the testes and prostate of beagle dogs. Toxicology. 12(3):273-279.

Johnston SD, Kamolpatana K, Root-Kustritz MV, Johnston GR (2000) Prostatic disorders in the dog. Anim Reprod Sci. 60-61:405-415

Prostatic abscesses are inflammatory lesions where there is the formation of a cavity filled with pus. The size of the 'normal' prostate is sufficiently small that infection and necrosis with the formation of an abscess is unlikely. It is much easier to imagine an abscess developing in a prostatic cyst, and there is often a background of prostatic hyperplasia to acheive this. Paraprostatic pseudocysts are sites for the development of 'prostatic abscesses' although these should be called paraprostatic abscesses.

Figure : Prostatic abscess. The abscess is opened (upper) and the cut surface of the hyperplastic prostate is visible. Bladder is center right.

 

Rohleder JJ, Jones JC (2002) Emphysematous prostatitis and carcinoma in a dog J Am Anim Hosp Assoc. 38(5): 478-481

Prostatic corpora amylacea

Corpora amylacea are usually incidental histologically apparent concretions in the acini of glands. They are composed of concentrically arranged lines and they stain with PAS. They are seen periodically in older dogs (McEntee 1990).

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p339.

Prostatic calculi

Calculi of the prostate are mineralized concretions that may be found in the prostate. They may be macroscopically visible, but some are microscopic. Lumb (1952) reports one case and McEntee (1990) has seen them in 3 dogs.

Lumb WV. (1952) Prostatic calculi in a dog. J Am Vet Med Assoc. 121:14-16.

McEntee K (1990) Reproductive Pathology of Domestic Mammals, Academic Press p339.

Osseous metaplasia of prostate

One case of mineralisation and osseous metaplasia of the prostate is reported (Aughey and Weaver 1977)

Aughey E, Weaver AD. (1977) Calcification of the prostate gland of the dog. Zentralbl Veterinarmed A. 24(9):772-778.