Canine ReproductionPart 5. Disorders Affecting Fertility in the Male Dog
Disorders affecting male fertility are categorized into two groups: those resulting from genetic disorders and those resulting
from acquired disorders.
Cryptorchidism. Cryptorchidism is a condition in which the testes fail to descend into the scrotum (unilateral
cryptorchidism/monorchidism describes the condition in which only one testis descends). Cryptorchidism may occur in conjunction
with other defects in sexual development or occur as an isolated condition. Isolated cryptorchidism is considered the most
common reproductive disorder in dogs, affecting between 1%-15% of dogs. Of these affected dogs, 75% demonstrate unilateral
Cause: Cryptorchidism is inherited as a sex-limited autosomal recessive trait.
Symptoms: In the normal canine male, during fetal development, the testes are located in
the vicinity of the kidneys and then migrate across the abdominal cavity and eventually descend into the scrotum. The rate
of migration can be variable from individual to individual, however, on the average, the testes are completely descended within
10 to 14 days following birth. In only a minority of dogs does descent occur as late as 6 months, and this variation is considered
suspect of a developmental abnormality.
Diagnosis: Palpation of the scrotum provides evidence of the presence or absence of two
testes. Absence of one or both testes in the scrotum by 8 weeks of age warrants a diagnosis of cryptorchidism. Once cryptorchidism
is diagnosed, ultrasonogram is frequently employed to locate the undescended testes or testis within the abdominal cavity
or tissues adjacent to the scrotum.
Treatment: Because of the genetic basis of this disorder and its counter-productive ramifications
on reproductive soundness in future generations, treatment for cryptorchidism other than surgical sterilization (orchidectomy)
is considered controversial from an ethical standpoint. Despite this, however, in one study hormonal treatment using human
chorionic gonadotropin administered 4 times over a two-week period was reported to induce testes descent in 21 out of 25 dogs.
Treatment was most successful when administered to puppies under the age of 16 weeks.
Prognosis: The specialized physiology of the scrotum is vital for ensuring normal spermatogenesis
(sperm production) occurring in the testes. Therefore, normal spermatogenesis fails to occur in bilateral cryptorchids (in
which both testes fail to descend), and as a result these dogs are sterile. Normal spermatogenesis, however, will occur in
unilateral cryptorchids (in which one testis descends) in the descended testis. Cryptorchid testes have a 6- to 13-fold greater
risk for developing a Sertoli cell tumor (testicular cancer) compared to normal testes. Additionally, they run a higher
risk of testicular torsion. In light of these observations, bilateral castration (orchidectomy) is recommended even in instances
of unilateral cryptorchidism.
Disorders of Sexual Development
Abnormalities of Chromosomal Sex. Abnormalities occurring in the number or structure of sex chromosomes are rare.
In males, conditions that may occur include trisomy (XXY) or chimerism (some cells XX and some XY).
Cause: Chromosomal sex abnormalities occur as random "accidents" during chromosome segregation
or fusion of zygotes. Therefore, there is no inherited predisposition for these genetic abnormalities.
Symptoms: Males with chromosomal sex abnormalities may appear "male", but typically exhibit
underdeveloped genitalia and are sterile.
Diagnosis: Direct examination of chromosomes (karyotyping) from a blood or skin sample of
the male is a method to identify abnormalities of chromosomal sex.
Treatment and Prognosis: Chromosomal sex abnormalities constitute a permanent and irreversible
Abnormalities of Gonadal Sex. When disagreement exists between chromosomal sex and gonadal sex, this constitutes
a condition known as sex reversal. Sex reversal occurs in males that have a 78,XX chromosome compliment but develop testicular
tissue in the gonad. In Sry-negative XX sex reversal, the Sry gene that is responsible for development of the
testes is completely absent from the Y chromosome.
Inherited XX sex reversal
Mode of Inheritance
English Cocker spaniel, Beagle, Weimaraner, Kerry Blue terrier, Chinese Pug, German Short-haired Pointer
American Cocker spaniel
autosomal recessive trait
Sry-negative XX sex reversal
(absence of the Sry gene on the Y chromosome)
Mode of Inheritance
American Cocker spaniel, German Short-haired Pointer
Symptoms: The degree of masculinization in an XX male is dependent upon the
amount of testicular tissue present in the individual. XX males may have bilateral testes, but they are often cryptorchids.
Additionally, abnormalities of the anatomy of the prepuce and penis, with abnormal location of the urinary tract opening (hypospadias), are typically observed.
Diagnosis: To identify XX sex reversal in a male, karyotyping to confirm a 78,XX chromosome
compliment followed by histologic evidence of testicular tissue in at least one gonad provides a definitive diagnosis. An
additional molecular test to determine the presence or absence of the Sry gene will provide additional information.
Treatment and Prognosis: Sex reversal is a permanent condition and XX males are sterile.
Treatment is, therefore, limited to removal of the testicular tissue, especially in cryptorchids where there exists an increased
risk for testicular cancer and/or testicular torsion associated with this condition.
Male Pseudohermaphroditism. When XY males with testes also develop female internal or external genitalia, this
condition is known as male pseudohermaphroditism. This disorder occurs as two distinct types: 1) persistent mullerian duct
syndrome and 2) defects in androgen-dependent masculinization.
Persistent Mullerian Duct Syndrome (PMDS)
Cause: PMDS has been reported in Miniature Schnauzers and Basset Hounds and occurs as a
hereditary disorder. In Miniature Schnauzers, PMDS is attributed to a sex-limited autosomal recessive trait (though both males
and females carry the gene only homozygous recessive males will express the disorder). Because affected dogs produce mullerian-inhibiting
substance (MIS), it is believed that a receptor defect in the mullerian ducts themselves makes this tissue unresponsive to
Symptoms: Males with PMDS may have normal testes development (though about half are cryptorchid) and appear masculine by all outward appearances; however, they also have a female reproductive tract
including a uterus with cervix, oviducts and a portion of the vagina. PMDS is typically not detected by routine physical examination,
but is diagnosed when symptoms related to pyometra (uterine infection), urinary tract infection, or prostate infection arise in the affected male.
Treatment and Prognosis: PMDS males with bilateral or unilateral scrotal testes are fertile,
however, because these males will transmit the gene for PMDS to all offspring, breeding is not recommended.
Defects in Androgen-Dependent Masculinization (Testicular Feminization Syndrome)
Cause: Failure or partial loss of function of the androgen receptor in tissues of the male
reproductive system, caused by a mutation in the X-linked androgen receptor gene, results in absence or reduction, respectively,
Symptoms: Affected males have bilateral testes (usually cryptorchid) but lack the epididymides and vasa differentia. Mutations resulting in complete loss of function of
the androgen receptor lead to males that have external female genitalia (vulva, female urethral orifice, and a blind-ended
vagina) and thus appear as females who fail to have a normal estrus cycle. Upon examination of these "females" it is found
that they completely lack a uterus and other components of the mullerian ductal system. Males with partial loss of function
of the androgen receptor may demonstrate ambiguous genitalia (abnormal scrotum with the testes appearing as swellings on either
side of a vulva leading to a blind-ended vaginal tract) and will often have poorly developed components of the Wolffian ductal
Diagnosis: Diagnosis of TFS is accomplished through identification of an XY chromosome karyotype,
the presence of bilateral testes, and demonstration of abnormal androgen binding in androgen-sensitive tissues of the male.
Treatment and Prognosis: Castration of affected males is the recommended treatment for TFS.
It should be noted that although females are not affected by this disorder, up to 50% of the males produced by female carriers
of TFS will be affected by this disorder. The remaining 50% of the males will receive a normal X-linked androgen receptor
gene and thus not be affected, nor will they carry the gene.
Cause: Hypospadias is a defect in the location of the male urinary orifice that typically
accompanies syndromes associated with incomplete masculinization. As such, this condition has a familial (inherited) preponderance.
Symptoms: The urethral opening may appear anywhere between its normal location at the tip
of the penis to the scrotum.
Diagnosis: Diagnosis of the underlying condition associated with hypospadias consists of
identification of other concurrent symptoms of gender abnormalities.
Treatment and Prognosis: Because hypospadias does not typically inhibit normal urination,
surgery is not usually required. Mildly affected dogs may be able to breed normally, however, if the underlying cause for
this condition has not been determined, recommendations for breeding are guarded.
Sperm Abnormalities Affecting Fertility
The normal sperm is composed of a head, midpiece and tail section. The head of the sperm is divided into 1) an acrosome,
a cap-like structure that covers more than half of the forward part of the head; 2) an elliptical-shaped equatorial region
just behind the acrosome; and 3) a post-equatorial region. The midpiece of the sperm is connected to the post-equatorial region
of the head by the neck. The mitochondria, the energy storehouse of the sperm, are contained in the midpiece section. The
tail continues from the midpiece as a slightly thinner section. Defects that occur in these three regions may be classified
as major defects or minor defects. Typically, major defects occur during spermatogenesis (sperm development) and have more
pronounced effects on sperm function. Minor defects most often occur as a result of secondary conditions like environmental
or infectious factors that may compromise mature sperm. The following table provides some of the defects and causes effecting
the different sections of the sperm.
Table 1. Classification of Abnormal Dog Sperm*
lipped, cysts, abnormal distribution
acrosome reaction, swelling, severe damage, loss
aging, extended epididymal transit time; prolonged post-ejaculation incubation of semen; semen processing
macrocephalic (large-headed); microcephalic (small-headed); pyriform (pear-shaped); diadem (crater) defects;
other nuclear vacuoles; ridged sperm; double-forms; severe pleiomorphism or bizarre forms (multiple heads)
frost-bite; increased testicular temperature; stress; corticosteroid treatment
narrow heads; head-base defects; detached heads; nuclear decondensation
aging sperm; defective testicular thermoregulation; heat-stress
retained cytoplasmic droplets; ruptured midpiece; pseudo-droplet defect; kinked midpiece
failure of sperm maturation (young studs or over-used studs); epididymal malfunction; mitochondrial damage
milder degree of sperm immaturity
"Dag" defect (tight coiling); double tails
epididymal malfunction; defective testicular thermoregulation
simple bent or coiled tail; terminally coiled tail
head to tail adhesion; head to tail to tail or attachment to other cells
Brucella canis infection; possible immunologic causes
* Modified from Oettle EE: Sperm morphology and fertility in the dog. J Reprod Fertil, 47(suppl):257-260,
Diagnosis: Assessment of sperm morphology (spermiogram) is an important component of evaluating
reproductive function of the male because sperm quality is highly indicative of male fertility. Examination of fixed and stained
semen smears with at least 100 sperm must be evaluated to ensure adequate representation of the sperm sample.
Prognosis and Treatment:
Table 2. Sperm Morphological Abnormalities Resulting in Decreased Fertility
total head and midpiece abnormalities in excess of 40% of sampled sperm
20% head, acrosome and retained cytoplasmic droplets
fewer than 60% sperm with normal morphology
Dogs with abnormal spermiograms frequently recover, therefore, repeated testing at suitable time points is
recommended. Intervals of retesting should be based upon the underlying suspected cause of the abnormality. Typically, males
with previous abnormal spermiograms will recover within 3 months. Treatment consists of sexual rest and/or avoidance of conditions
that may compromise normal spermatogenesis or viability of matured sperm. If after 3 months, retesting indicates persistence
of the abnormality, then prognosis for future fertility is guarded. If no improvement is observed by 6 months, prognosis is
poor. Abnormalities that extend for up to 12 months suggest irreversible infertility.
Cause: Concurrent infection of the testes and epididymus (orchiepididymitis) may occur as
a result of microorganisms including Staphylococcus, Streptococcus, coliforms, Mycoplasma, Ureaplasma, or Brucella canis. Localized wounds or spread of infectious organisms from distant sites in the body via the circulatory
or lymphatic systems may lead to testicular infection. Additionally, infections of the urinary tract system or of the prostate
gland may spread to the testes/epididymus through the ductus deferens.
Symptoms: Infections associated with orchiepididymitis present with scrotal swelling, testicular
enlargement, pain, and fever.
Diagnosis: Ultrasound imaging of the testes will confirm inflammation associated with infection
and rule out other potential causes for testicular swelling. Bacterial culture of the semen in Amies medium allows for isolation
of Ureaplasma, Mycoplasma, and aerobic bacteria. Ultrasound imaging indicating that inflammation is localized primarily to the
epididymides is highly suspicious of Brucella canis infection. Accordingly, serological testing for Brucella canis should be performed.
Treatment and Prognosis: Treatment of testicular infections includes administration of antibiotics
and anti-inflammatories. Castration is recommended in males that are not intended to be used for breeding or in those diagnosed
with Brucella canis (since treatment of the latter fails to completely eradicate infection and only reduces infection to
a "carrier state"). In those males whose owners wish to salvage reproductive function, additional treatment with cool compresses
may help in reducing heat in the scrotum associated with inflammation, and may assist in reducing permanent detrimental effects
on spermatogenesis. Chronic or treatment-resistant infections, however, typically result in sterility due to destruction of
the spermatogenetic tissue by the inflammatory process. In those dogs in which infection is eradicated by treatment, permanent
side effects on spermatogenesis have been observed, therefore, prognosis in regard to fertility is guarded.
Cause: Testicular torsion, a twisting of the testis around on its venous vasculature, is
more common in cryptorchid males with a retained abdominal testis but may also occur in normal males with bilateral testes. Twisting
of the venous vessels inhibits blood entering the testis from leaving. As a result, the testis becomes engorged with blood.
Symptoms: Dogs with testicular torsion exhibit pronounced enlargement of the testis. Pain
may be so intense as to elicit a state of shock (rapid heartbeat [tachycardia], delayed capillary refill time, pale or muddy
mucus membranes, weak pulse, vomiting). Torsion of a retained testis presents as abdominal pain.
Diagnosis: Torsion of a scrotal testis is made upon observation of the acute presenting
symptoms and evidence of a firm mass in the scrotum. Torsion of abdominal testis is highly suspect in symptomatic, cryptorchid dogs when abdominal palpation indicates a large, firm mass in the abdomen. Ultrasound imaging is a method
for confirmation of this diagnosis.
Treatment and Prognosis: Castration is the preferred method of treatment, particularly in
cryptorchid males. Treatment of males with reproductive value is limited to removal of the torsed testis while attempting
to spare the remaining healthy testis. Attempts to save the torsed testis by derotation are typically unsuccessful due to
irreparable damage resulting from the compromised vasculature.
Cause: Inguinoscrotal hernias occur when a portion of the intestine loops into the scrotum,
separating the testis from the scrotal wall. This is a rare condition that may occur due to congenital abnormalities or trauma
that cause widening or weakening of the inguinal canal in the male.
Symptoms: Dogs with inguinoscrotal hernias present with sudden (acute) swelling of the scrotum.
Typically, the condition is painless unless the intestinal loop becomes twisted. Twisting of the herniated intestine compromises
blood flow to the tissue and will result in an emergency medical condition presenting with intense pain and symptoms of shock
(rapid heartbeat [tachycardia], delayed capillary refill time, pale or muddy mucus membranes, weak pulse, vomiting).
Diagnosis: Palpation of the scrotum reveals a movable, tubular mass that can be confirmed
as a portion of the intestine by ultrasound imaging.
Treatment and Prognosis: Dogs presenting with a twisted inguinoscrotal hernia should be
treated for shock first. Once the dog is stabilized or for those dogs with simple inguinoscrotal hernias surgery is required
to reduce the hernia. The herniated bowel must be examined for any evidence of tissue compromise prior to repositioning it
back through the inguinal ring into the abdomen. Bowel tissue that appears compromised must be resected to avoid subsequent
problems associated with bowel deterioration and/or infection. Nonabsorbable sutures are typically used to narrow the inguinal
ring to prevent recurrence of hernia, while ensuring normal blood flow to the testes. Effects on male fertility will be dependent
upon whether or not the hernia compromised testicular blood flow.
Cause: Inflammation or trauma may lead to an obstruction of the epididymis that results
in an accumulation of sperm near the site of the injury. This accumulation leads to an immune response directed to the sperm
known as a sperm granuloma and results in inflammation and swelling of the epididymis.
Symptoms: Infertility is the primary symptom associated with sperm granuloma.
Diagnosis: Ultrasound imaging will detect enlargement of the epididymis in the early stage
of this disorder and presence of the granuloma in late stages.
Treatment and Prognosis: Prognosis for fertility in males with sperm granuloma is poor because
surgical correction of this disorder is frequently impossible. In light of this, castration is widely recommended as treatment
for sperm granuloma.
There are three types of testicular tumors that occur with similar rate of incidence within the dog.
Sertoli cell tumor: Sertoli cells are located on the walls of the seminiferous tubules within the testicles and support
the development of the spermatozoa. Tumors that originate from the Sertoli cells occur with less frequency in normal descended
testicles, but have the highest incidence for occurrence in cryptorchid testes. These tumor cells have a high incidence for metastasis (spreading to other parts of the body). Sertoli tumors present
as a firm nodule on the testis, and may reach significant size prior to diagnosis in an abdominal testis. Often males with
Sertoli tumors present other systemic symptoms associated with hyperestrogenism (excess production of estrogen) which include
anemia, hair loss, feminization, and attraction of other male dogs.
Seminomas: Seminomas arise from spermatogenic cells of the seminiferous tubules within the testicles. These tumors
have a low incidence of metastasis (5-10% are metastatic). Seminomas usually are small and present as a soft mass within the
testes. Some, however, particularly those that arise in abdominal testes, may become quite large. Like Sertoli tumors, seminomas
may also secrete estrogen, however, they more commonly are associated with hyperandrogenism (excess production of androgen),
which may lead to prostatic enlargement and/or development of perianal adenomas.
Interstitial cell tumors: Interstitial cell tumors originate from the Leydig cells of the testicle, which are testosterone-secreting
cells. These tumors are usually benign and are found predominantly in descended testes and only rarely in abdominal testes.
Interstitial cell tumors present as a soft mass within the testicles.
Diagnosis: Though ultrasound imaging is capable of detecting testicular tumors, only histopathologic
examination will be able to differentiate between the three types of testicular tumors. Radiographs of the chest and abdomen
are essential for conducting clinical staging of the cancer. When metastases occur, they typically are found in the lumbar
lymph nodes, the spleen, and liver.
Treatment and Prognosis: Castration is frequently curative for testicular tumors, especially
when performed in the early course of the disease. When staging indicates progressed disease as evidenced by distant sites
of metastases, combination chemotherapy with vinblastine, cyclophosphamide and methotrexate has been observed to provide greater
than 50% reduction in metastatic tumors. Seminoma metastases are also responsive to radiation therapy.
Cause: Testicular hypoplasia is a rare condition depicted by complete absence or severe
reduction of spermatic tissue in one or both testes. The cause of this condition is unknown, however, it is suspected that
this may occur as a developmental disorder in which the germinal cells fail to migrate to the fetal testes. An alternative
explanation is that the germinal cells are destroyed during fetal development.
Symptoms: Testicular hypoplasia is suspected in young dogs in which one or both testes appear
Diagnosis: Diminished size can be confirmed by ultrasound imaging. Biopsy of the testes
indicates a decrease or absence of the seminiferous tubules and spermatogonia, which comprise about 50-70% of testicular size.
Because testes of dogs with testicular hypoplasia usually have Leydig cells, testosterone is still produced and sexual drive
(libido) is typically normal in these males.
Prognosis and Treatment: Dogs with bilateral testicular hypoplasia are sterile. Treatment
with gonadotropins to stimulate the proliferation of germinal cells has thus far proven ineffective for treatment of this
Cause: Inflammatory and non-inflammatory conditions can result in loss of seminiferous tubules,
germinal cells, interstitial cells, and spermatogonia within the testes. In addition to traumatic conditions like inguinoscrotal hernia, testicular degeneration also occurs commonly in middle-aged dogs as an idiopathic condition.
Symptoms: In early stages, testicular degeneration may not be apparent by testicular appearance.
As the condition progresses, the testes eventually become small and soft. Libido is typically normal because the testosterone-producing
Leydig cells are not involved in the degenerative process.
Diagnosis: Testicular degeneration is confirmed by testicular biopsy.
Treatment and Prognosis: Treatment of testicular degeneration is dependent upon identification
and prompt treatment of the underlying inflammatory or non-inflammatory condition. Idiopathic testicular degeneration that
occurs in middle-aged dogs is unresponsive to treatment and thus prognosis for fertility is considered poor.
Diseases of the prostate occur commonly in dogs, and Doberman Pinschers reportedly having an increased risk compared to
other breeds. The prostate gland is a solid organ that surrounds the base of the urethra in males and is responsible for producing
some of the fluid found in the semen.
Benign Prostatic Hyperplasia
Cause: Benign prostatic hyperplasia (BPH) occurs as an aging change in intact male dogs.
Studies suggest that increasing levels of estrogen associated with age result in an increase in androgen receptors on the
surface of prostate cells. When these receptors bind to circulating androgen, a hormone produced by the testes, this reaction
stimulates the glandular prostate cells causing them to grow and divide. Glandular hyperplasia may begin as early as 2.5 years
in some dogs and by 6 years of age it is estimated that 60% of intact males have BPH; by 9 years this estimate increases to
Symptoms: Most dogs with BPH will have no symptoms or evidence of systemic illness. Occasionally,
some males may develop difficulty to urinate or defecate if the enlarged prostate places pressure on the urethra or the descending
colon, respectively. In other dogs, blood in the urine or a blood-tinged ejaculate for semen analysis may be the only indication
Diagnosis: Physical examination of the prostate by rectal exam will reveal enlargement of
the prostate gland, though texture and consistency will feel like a normal prostate. Usually the enlarged gland is not painful
unless bacterial infection is also present. Though radiographs and ultrasound will confirm enlargement of the prostate, these
methods do not offer a definitive diagnosis because other prostatic disorders may appear similar by imaging. A definitive
diagnosis is best accomplished through ultrasound-guided needle biopsy to obtain a sample of prostate tissue for histopathologic
analysis. Alternatively, serum analysis for elevated levels of canine prostate specific esterase (CPSE), an enzyme marker
that appears to be specific for BPH over other prostatic disorders, may provide diagnostic information.
Treatment and Prognosis: Asymptomatic dogs with BPH usually do not require treatment. When
symptoms become apparent, castration is the most successful form of treatment and results in rapid regression of the prostate
size. Alternative treatments to surgery include the following:
Effects on Breeding
Reduces androgen concentration by inhibiting gonadotropin secretion by the pituitary gland
Decreases prostate size by decreasing cellular mass
anemia, immunosuppression associated with repeated administration. Long-term use will increase prostate size
and predispose to prostatic cysts, bacterial infections, and abscesses
short-course therapy reduces prostatic secretory capability for 2 months
Dihydrotestosterone (DHT) Receptor blockers (anti-androgen flutamide)
blocks DHT (produced from testosterone) activity by competing for DHT receptors
Decreases prostate size in dogs within 10 days to 6 weeks of treatment
prostatic hyperplasia recurs within 2 months if treatment stopped. Not approved for veterinary use/ expensive.
No effects on libido, sperm production or fertility in dogs.
Progestins (Megestrol acetate)
reduces serum testosterone concentration, inhibit DHT receptor binding, decreases DHT levels, and decreases
the number of androgen receptors
reduces prostate size and eradicates associated symptoms
relapse in 10 to 24 months when treatment discontinued. No long-term studies on side effects on the dog. Not
approved for use in males (approved use in bitches for other conditions restricted to 32 days)
No effects on sperm or fertility. May help to maintain short period of breeding soundness in BPH males prior
5-alpha-reductase inhibitors (Finasteride)
blocks DHT production from testosterone
20-30% reduction in prostate size in men for 6-12 months
potentially teratogenic (biologically hazardous to developing fetuses)
no effects on libido or semen production but can cause fetal genetic anomalies and is present in semen of
treated patients (not recommended for use in breeding males)
antifungal drugs (ketoconazole and gonadotropin releasing hormone analogs
block release of lutenizing hormone
reduces prostate size
known as "chemical castrators"
results similar to surgical castration (not recommended for breeding males)
Cause: When bacterial infection occurs concurrently with benign prostatic hyperplasia (BPH), the condition is known as prostatitis. Prostatitis occurs when bacteria
that normally inhabit the male urethra ascend into the prostate gland. Conditions of BPH predispose the prostate to infection
because this disorder creates an environment suitable for bacterial proliferation. Common organisms identified in causing
prostatitis include: Escherichia coli, Staphylococcus aureus, Klebsiella spp., Proteus mirabilis, Mycoplasma canis, Pseudomonis aeruginosa, Enterobacter spp., Streptococcus spp., Pasteurella spp.,
and Haemophilis spp.. Though Brucella canis may infect the prostate, it more commonly infects testicular tissue. Fungal infections are less common
but occasionally occur. In some instances, testicular infections may spread to the prostate. Prostatitis is the most common
prostatic disorder occurring in intact male dogs. In some dogs, particularly those over 5 years of age, prostatitis leads
to the formation of abscesses within the prostate. Prostatitis is rare in castrated males.
Symptoms: Prostatitis may occur as an acute or chronic condition. In the acute phase, fever
and lethargy are present, the dog may strain when urinating or defecating, and the dog may move with a stiff gait. Swelling
of the scrotum and hindlimbs may also be observed. Dogs that have prostatic abscessation may present with symptoms of shock
(rapid heartbeat [tachycardia], delayed capillary refill time, pale or muddy mucus membranes, weak pulse, vomiting), peritonitis,
and systemic infection (sepsis) if the abscess ruptures. Chronic prostatitis may occur following an acute phase or may develop
without symptoms. Evidence suspicious of chronic prostatitis includes poor semen quality, decreased libido associated with
pain upon prostatic contraction during ejaculation, and blood in the urine or semen sample.
Diagnosis: In acute cases of prostatitis, findings of an enlarged and/or painful prostate
upon examination and evidence of bacteria in the urine of the dog, are highly indicative of this condition. A culture and
sensitivity of urine removed from the bladder by cystocentesis is helpful for identifying the causative bacterial organism.
Pain usually impedes the process of obtaining a prostatic fluid sample from the patient. Additionally, manipulation of the
prostate should be avoided to prevent further spread of bacterial infection. In chronic cases, the prostate gland is typically
painless or not as painful as in acute cases. This allows for collection of prostatic fluid for bacterial analysis since bacteria
are not always found in the urine of dogs suffering from chronic prostatitis. Radiographic and ultrasonographic changes in
the prostate are often apparent in dogs with chronic prostatitis. In cases where prostatic fluid culture does not identify
an infectious organism, but diagnostic imaging is indicative of disease, biopsy of the prostate tissue will confirm a diagnosis
Treatment and Prognosis: Aggressive treatment of acute prostatitis may prevent the infection
from developing into chronic prostatitis. Results from urine culture and sensitivity screening will assist the clinician in
selecting an antimicrobial drug with low potential for microorganism resistance and ability to maintain therapeutic concentrations
in the urine and tissues. The anti-microbial agent is administered for at least 3-4 weeks to ensure complete elimination of
the infection. Additionally, it is recommended that urine cultures and prostatic fluid cultures be analyzed 7-10 days after
completion of drug therapy to ensure eradication of the infectious organisms. When treated aggressively and thoroughly, acute
prostatitis is expected to have a good prognosis for recovery.
Chronic prostatitis is more challenging to treat and treatment difficulties are compounded by the fact that many anti-microbial
drugs cannot efficiently cross the prostatic tissues and enter the prostatic fluid. Some anti-microbial agents are more soluble
than others are and these are most effective for the treatment of chronic prostatitis. Such agents include: chloramphenicol,
erythromycin, trimethoprim, ciprofloxacin, enrofloxacin, and carbenicillin. Therapy is typically continued for 4-6 weeks.
Following completion of drug treatment, urine and prostatic fluid culture is performed at 4-7 days and 30 days following completion
of treatment to ensure elimination of the infection. In many cases, follow-up culture indicates insufficient resolution of
the infection by the first treatment regimen and a 3-month course of antibiotics with adjuvant therapy (hormone therapy or
castration) to reduce concurrent prostatic hyperplasia is prescribed. Should this latter approach fail to eradicate infection,
chronic low-dose antimicrobial therapy or prostatectomy are options to consider. Prognosis for chronic prostatitis is fair
considering the limitations to therapy with antimicrobials against this disease and thus, the high incidence for relapse.
Cancer of the Prostate
Cause: Prostate cancer (prostatic adenocarcinoma [PAC]) is an uncommon disease in dogs but
occurs with highest incidence in 8-10 year old intact and castrated males. In fact, risk of prostate cancer in early castrated
males is equal to if not slightly higher than in intact males. This may be associated with the observation that castrated
males usually do not manifest concurrent hyperplastic changes in the prostate as do intact males and thus maintain smaller tumor masses that may go undetected
for longer periods of time allowing for a more invasive tumor phenotype to develop. Unlike human prostate cancer in which
androgens appear to contribute significantly to neoplastic development, prostate cancer in dogs appears to be androgen independent.
It is speculated, therefore, that early testosterone effects or nontesticular androgens of adrenal origin may play a role
in the development and progression of prostate cancer in dogs.
Symptoms: Dogs with PAC develop symptoms consistent with enlargement
of the prostate: difficulty urinating and/or defecating. Many dogs will also demonstrate anorexia and weight loss. Bone pain,
an indication of tumor cell metastasis (spread) to the bone, may occur predominantly in the lower back and is a sign of late
Diagnosis: In geriatric males, enlargement of the prostate in an intact male or a normal-sized
prostate in a neutered male (since castration leads to complete atrophy of prostatic tissue) are suspicious for and highly
suspected for PAC, respectively. Ultrasound-guided needle-core biopsy provides the best method for acquiring a definitive
diagnosis of PAC and allows for evaluation of tumor grade, a clinical criteria that will assist in determining treatment options
Treatment and Prognosis: Tumors assessed as well-differentiated (closely resembling normal
prostate cells) at the time of biopsy may indicate a better prognosis in terms of survival time. Unfortunately, however, PAC
is often not diagnosed until the dog is in late stage of the disease when therapeutic options are limited and thus prognosis
is considered poor. Surgery to remove the prostate is one possible option for therapeutic management of PAC and if the disease
is detected in an early stage, this option may be curative. However, prostectomy is a difficult surgery and is associated
with a chronic condition of urinary incontinence. Palliative treatment for PAC includes castration or hormonal therapy with
Megestrol acetate or Finasteride to reduce concurrent prostatic hyperplasia and thus alleviate symptoms associated with prostate
enlargement. For both intact and castrated males with PAC, external beam radiation therapy may induce temporary regression
of the tumor and provide relief of symptoms. Administration of stool softeners may also provide some relief for constipation
and because many PAC dogs will have secondary complications associated with bacterial infections, continuous antibiotic therapy
may assist in controlling related symptoms. Despite therapeutic intervention with radiation or combination of radiation and
chemotherapy, once diagnosis is made, survival time for dogs with PAC does not typically extend beyond 5 months.
Cause: Urethral prolapse is a rare condition that occurs in young male dogs with a preponderance
to occur in the brachycephalic breeds (Boston terriers and English bulldogs). Other affected breeds have included Yorkshire
terriers, Cocker spaniels, Alaskan Malamutes, and Springer spaniels. Average age of occurrence is 18 months with ages ranging
from 4 months to 5 years. The condition is indicated by extension and thus appearance of the mucosal lining of the urethra
through the urogenital opening at the tip of the penis. This condition is believed to occur as a result of abnormal development
of the urethra that makes it susceptible to prolapse during activities (i.e. breathing in brachycephalic breeds or sexual
activity) that cause increased intra-abdominal pressure.
Symptoms: Appearance of a red to purple, pea-sized, donut-shaped mass protruding from the
urogenital opening at the tip of the penis. Bleeding may occur from the prolapsed urethra. Some dogs also have concurrent
symptoms of urinary tract infection.
Treatment and Prognosis: Surgery to reduce the prolapse is the usual course of treatment
for urethral prolapse, particularly in cases where bleeding is excessive or ulceration or necrosis of the prolapsed urethra
occurs. In some instances where the prolapse is mild and there is little or no bleeding, surgery may not be necessary. Conservative
approaches to management of this disorder include minimizing secondary problems that arise. Reducing trauma to the prolapsed
urethra in dogs with a tendency to lick at the prolapse is accomplished by using an Elizabethan collar. Prevention of urinary
tract infections requires administration of antibiotics. Dogs with severe cases of urethral prolapse that manifest symptoms
of extensive inflammation, ulceration, necrosis and scarring have a higher risk for recurrence following surgery.
Cause: Bacteria of the Brucella sp. are well known for causing infertility in dogs.
B. canis is the most common of the brucellosis-causing bacterial strains found in dogs and, as such, is routinely screened
for by serological testing as part of the breeding management plan.
Symptoms: Males infected with Brucella canis are sterile and asymptomatic for disease.
Epididymitis (refer to testicular infections) with epididymal swelling occurs 3 to 5 weeks after the dog becomes infected but may only be evident
upon palpation of the scrotum. Morphologic abnormalities of the sperm become detectable by 5 weeks after infection. Eventually,
atrophy of the testicles becomes apparent in chronically affected dogs.
Diagnosis: Diagnosis of B. canis is by serological testing and concurrent blood cultures.
Limitations to serological testing for B. canis, however, do exist and typically occur with use of the rapid slide
agglutination test (RSAT) or the tube agglutination test which may result in false-positives or false-negatives. False-positives
should be suspected if a dog is asymptomatic or concurrent blood cultures drawn at the same time as serological samples are
negative for bacterial growth. Follow-up assessment with the agar-gel immunodiffusion (AGID) test will rule-out the possibility
of false-positive results. False-negatives will occur if serological testing is conducted within a 4 week period after the
dog has initially contracted B.canis. Therefore, all negative tests should be confirmed by repeat testing 30 days from
the first test before considering a dog to be free of infection. Dogs may also become infected with other strains of Brucella
sp. that typically infect livestock. Dogs with symptoms consistent with brucellosis but that have negative serological testing
for B. canis and have a history of exposure to livestock may harbor one of the other strains such as B. abortus,
B. suis, and B. melitensis. Since serological tests for B. canis will not cross-react with these other Brucella
sp., dogs suspected of carrying an alternate strain of Brucella should be tested specifically for these other strains.
Treatment and Prognosis: Though B. canis is most often conceived as being transmitted
from dog to dog during the actual act of copulation, the primary mode of transmission actually occurs via oronasal contact
with infected body fluids. Therefore, spread of infection is not limited to breeding contact and as such, once introduced
into a breeding kennel, the highly infectious B. canis will quickly spread through the population. Long-term, multiple
treatments with antibiotics may assist in controlling symptoms and extent of infection within an individual dog, however,
antibiotic treatment has limited efficacy for cure and the dog will remain potentially infectious to other dogs. As such,
infected dogs should be neutered and removed from the breeding kennel environment to prevent spread to other breeding dogs.
Retesting should be performed 6 months following completion of the antibiotic regimen to assess treatment efficacy. The alternative
for controlling spread of B. canis is euthanasia of all confirmed-infected dogs.
Mycoplasmas and Ureaplasmas
Cause: These organisms are of the Mycoplasmataceae family and normally inhabit the
canine urogenital and nasopharyngeal tracts. If, however, there is an increase in the number of these organisms in comparison
to the other common organisms also inhabiting the male urogenital tract, then there is often an increase in incidence of infertility,
testicular infections and prostatitis.
Symptoms: Males infected with Mycoplasma or Ureaplasma demonstrate fertility
problems with or without evidence of testicular infection, prostatitis, or scrotal swelling. Infection leads to inflammatory
processes that create an abnormal environment for production of spermatozoa. Additional effects on sperm may include alteration
of sperm motility, interference of normal sperm metabolism by which the sperm recognizes the ova, impairment of ova-penetrating
ability, and inducing autoimmune damage to the sperm.
Diagnosis: Culture of semen samples for the purpose of identifying an increased proportion
of Mycoplasma or Ureaplasma growth compared to growth of other microorganisms which normally inhabit the urogenital
tract provides a method of diagnosis for infection.
Treatment and Prognosis: Antibiotic treatment for a minimum of 10 to 14 days is used for
the purpose of eradicating infections with Mycoplasma and Ureaplasma. Some Mycoplasma strains are resistant
to the standard Erythromycin treatment and may require therapy with Tylosin, which offers a broader spectrum for elimination
of the various Mycoplasma strains. Semen cultures are typically repeated after completion of therapy to ensure complete
elimination of the infectious organisms. Dogs infected with Mycoplasma or Ureaplasma should not be used for
breeding until antibiotic treatment is completed and follow-up cultures confirm that the dog is no longer a carrier. Stud
dogs should not be allowed to naturally breed bitches suspected of carrying Mycoplasma or Ureaplasma. When the
bitches' status is unknown, breeding by artificial insemination is the safest procedure.