Male Reproductive Disorders

Juan E. Romano, Sr. • Steven P. Brinsko • Terry L. Blanchard • Dickson D. Varner

Infertility Caused by Diseases of the Penis and Prepuce

Penile Injury

■ Stallion

Definition and Etiology

If the penis is injured while erect, it may swell rapidly and massively from vascular rupture and hemorrhage.

■ Clinical Signs and Differentials Cutaneous abra­sions, lacerations, and visible hemorrhage may be present. Paraphimosis occurs when enlargement is sufficient to prevent retraction of the penis through the preputial ring.¹ Edema may extend to the scrotum and interfere with thermoregulation of the testes.⁴ Venous thrombosis, lymphatic occlusion, excoriation, and swelling accompany chronic inflammation.¹ Hemorrhage from the corpus cavernosum penis (CCP) is uncommon. Rupture of the surrounding tunica albuginea, when healed, may develop fibrous adhesions that lead to penile deviation during erection.

■ Treatment and Prognosis Immediate treatment is directed toward reducing edema and inflammation, as well as controlling infection. Treatment is similar to that described in the Paraphimosis section later in this chapter. Sexual rest is indicated until the lesions have healed.⁵ If treatment is initiated early and paraphimosis does not occur, the prognosis for recovery is good.^1,3

Bull

■ Definition and Etiology The penis of bulls is susceptible to injury during mating.

■ Clinical Signs and Differentials Diagnosis of penile hematoma is made based on the presence of a swelling imme­diately cranial to the scrotum. Initially it is soft, fluctuant, and painful, and it becomes firm as clot organization and fibrin formation progress.² The main differential diagnosis is extensive preputial laceration. If a distance of more than two handbreadths is present between the scrotum and the enlargement, the swelling is more likely to be a preputial laceration.

If penile hematoma has been present for longer than 2 weeks, fibrous adhesions may form that prevent penile exten­sion. Adhesions are frequent sequelae to an abscess and have also been reported to occur secondary to infiltration of local anesthetics to block the dorsal nerves of the penis.² Another sequela is the development of venous shunts that communicate between the CCP and either peripenile vasculature or the corpus spongiosum penis (CSP).^1,7 Such vascular shunts result in rapid drainage of blood from the CCP and impotence caused by failure to achieve or maintain full erection. If the dorsal nerves of the penis are damaged, sensation of the distal penis is lost or deficient and results in failure of the bull to successfully seek out the female's vagina and/or ejaculate. Organization of the portion of the blood clot (thrombosis) within the body of the CCP may result in functional blockage of engorgement of the more distal cavernous spaces, preventing full erection.

■ Treatment and Prognosis Treatment of penile hematomas should be aimed at not only restoring the bull to usefulness but also preventing recurrence. Approximately 50% of bulls with hematomas that are treated conservatively (i.e., nonsurgically) are reported to return successfully to breeding.¹ Some theriogenologists believe that small hematomas (less than football size) do not require surgery.⁸ However, surgical correction has the advantages of (1) removing the blood clot before extensive fibrous adhesions develop; (2) permitting removal of a blood clot from within the body of the CCP itself, thereby reducing the chance of blockage of cavernous filling; and (3) suturing the tunica albuginea, which should reduce the chance of recurrence of the condition after return to service and the likelihood of developing vascular shunts that will prevent complete filling of the CCP.

Additional recommendations before electing surgical intervention include extending the penis manually. Cases in which the penis can be extended from 6 to 8 inches or more beyond the sheath orifice, and in which penile sensation remains, carry a better prognosis.⁹ If engorgement of the distal penis does not occur after careful stimulation with the electroejacula- tor, blockage of the CCP should be suspected and reduces the prognosis. Finally, cases with abscesses are poor risks because severe restrictive adhesions usually develop.¹

Regardless of whether surgical or conservative intervention is selected for a penile hematoma, the bull should be treated with high levels of systemic antibiotics in an attempt to prevent abscess formation. Penicillin is a good choice because abscesses are usually caused by T. pyogenes. Postsurgical complications are much the same as those that may occur without surgery, but these adverse consequences are reported to occur less frequently after surgery. Bulls should not be returned to service for 2 to 3 months after treatment.^1,2

■ Ram and Buck Adhesions of the penis and prepuce caused by trauma are uncommon in adult small ruminants. The penis does not separate from the prepuce until puberty and cannot be extended before this time (4 to 5 months of age in bucks).¹⁰ Most traumatic lesions of the penis or prepuce in sheep and Angora goats are from shearing injuries.¹¹ Blockage of the urethral process by calculi can cause necrosis and sloughing of tissue that may extend into the glans penis.¹¹ Fighting among horned animals may result in injury to the external genitalia, including the penis. In dairy goats the intersex condition can result in congenital malformation of the penis and prepuce (hypospadias).¹²

Phimosis and Injury to the Prepuce

■ Stallion

Definition and Etiology

Stenosis of the preputial orifice can prevent extension of the penis.

■ Clinical Signs and Differentials Acute posthitis often accompanies injuries to the prepuce or infections such as equine coital exanthema and dourine.^1,2 Edema is common with acute posthitis, particularly after trauma. Gravitational effects typically worsen the preputial edema, which may induce prolapse of the external prepuce, trapping the penis in the swollen internal prepuce with a constricting preputial ring.¹ Cicatricial scar formation may follow, narrowing the diameter of the preputial orifice. Transpreputial ultrasound examination may be of benefit in differentiating tumors or abscesses from inflammatory edema or hemorrhage. Containment of the penis within the prepuce causes preputial urine accumulation, worsening balanoposthitis and secondary bacterial infection. The extended chronic inflammation leads to cicatrix formation with phimosis.

■ Treatment and Prognosis Preputial edema can be relieved by administration of diuretics and exercise. Application of crushed ice in plastic bags, or preputial immersion in cold water, may reduce inflammatory edema if applied soon after injury. Subsequently, application of emollient antibiotic prepara­tions and hydrotherapy can be used to massage injured tissues and reduce edema. Systemic antibiotics and nonsteroidal antiinflammatory drugs are indicated to control secondary infection and inflammation. Sexual rest is indicated until the lesions have healed.⁵

A biopsy can be procured from encroaching tumors to identify cell types and improve prognostic capability.⁵ Cicatricial scars can sometimes be successfully removed surgically. Once inflammation and infection are resolved with local or systemic antibiotic and antiinflammatory drug treatment, incision of the ventral aspect of the preputial orifice (preputiotomy) may be necessary to enlarge the opening sufficiently to permit penile extension.

■ Bull

Definition and Etiology

Trauma to the prepuce involving the elastic lamellar layers may prevent the required flexibility of the prepuce to permit penile extension. Breed predisposition to preputial injuries corresponds to genetic differences in pendulousness of the sheath and development of the muscles responsible for retraction of the prepuce. The polled gene is linked to weak or failed development of the preputial muscles, leading to habitual preputial eversion, which predisposes to injury. Brahman- blooded cattle have the added predisposition of a loose, pendulant sheath. With their tendency to partially evert the preputial membrane through the sheath orifice, they are at greater risk of damaging the prepuce accidentally than are those breeds of cattle in which the sheath is held in close apposition to the abdominal wall.^1,2,14

Inability of the bull to extend the penis most commonly follows injury to the penis and prepuce that culminates in strictures or adhesions that restrict normal penile movement.^15,16

Other causes of phimosis include congenital anomalies such as a short penis, a short retractor penis muscle, and develop­mental abnormalities of the reproductive tract such as occurs in pseudohermaphrodites.²

■ Clinical Signs and Differentials The more common preputial injuries are contusions, abrasions, lacerations, and frostbite. When the injured prepuce can be retracted, the injury may not be suspected unless hemorrhage is noted from the sheath or the bull is observed having difficulty during breeding. Although minor injuries may spontaneously resolve, more extensive injuries commonly progress to abscess formation and fibrous stricture formation.^1,8,15,16 Extension and examination of the penis may result in further injury if the case is complicated by phimosis. In such cases an attempt to extend the penis to facilitate examination is contraindicated because forcibly stretching the prepuce will extend the laceration and spread infection to uncontaminated areas.¹

■ Treatment and Prognosis Treatment of preputial injuries in the bull may be either medical or surgical. With few exceptions, such as fresh avulsive lacerations in the fornix area, surgical intervention carries a better prognosis when medical treatment is first carried out to control inflammation and infection.¹⁵ The healing leaves more normal tissue to be identified and salvaged during surgery. In cases in which the injured prepuce is retracted into the preputial cavity, digital, speculum, or endoscopic examination can be done in an attempt to locate lesions and determine the extent and depth of tissue involvement. Systemic administration of antibiotic is necessary to reduce the incidence of abscess formation preoperatively, and antibiotic should be administered through the surgical and postsurgical periods if surgery is elected. When the injured prepuce remains prolapsed in presented bulls, the first consideration is to attempt to return the prepuce to the preputial cavity.^1,15 The exposed epithelial covering of the prepuce is easily injured and becomes quite edematous and friable because of its pendent location. Hydrotherapy for 20 to 30 minutes may be helpful in cleansing the exposed prepuce and reducing edema. After gently cleansing the prepuce and determining the degree of patency of the lumen, a protective emollient preparation is used to massage edematous swelling upward out of the prolapse.¹⁵ Massage for 15 to 30 minutes may be required to reduce swelling sufficiently to permit the prepuce to be returned to the preputial cavity. If the prolapsed prepuce can be returned to the sheath, a retention technique should be used to prevent reprolapse. With the prepuce in place, a tube can be inserted just beyond the swollen internal portion of the prepuce to avoid urine retention. The tube is taped in place at the external preputial orifice. Tape should not extend past the proximal end of the tube or urine retention and migration into peripreputial tissue will occur. If this technique will not retain the prepuce, a purse-string suture in the skin of the sheath orifice can be used.¹ It should be tight enough to retain the prepuce but leave sufficient space for urine to pass freely. To avoid suture abscesses and stricture formation, the sheath should be clipped and prepared aseptically for suture placement, and sutures should be removed as soon as swelling and inflammation subside. If the prolapsed prepuce cannot be returned to the preputial cavity, the prognosis for correction without surgery is guarded. After cleansing as described previ­ously, a portion of stockinette is coated in ointment and applied over the prepuce. A diaper constructed from heavy canvas, netting, or burlap with straps and centrally located perforations for urine drainage is applied under the prepuce and tied up over the back to hold the prepuce gently next to the abdominal wall to decrease gravitational edema. It is changed daily until infection and swelling are controlled and the prepuce is either returned to the sheath or surgery is performed. Alternatively, the prolapsed portion of the prepuce can be wrapped in medicated gauze followed by application of a gentle but firm pressure wrap around a section of tubing. The pressure wrap is left in place temporarily to reduce edema, at which time the wrap is removed and the prepuce is replaced into the sheath.¹⁵

Once sufficient healing has occurred, the need for surgery is determined by extending the penis.¹ Adhesions most com­monly take the form of encircling cicatricial strictures that must be removed surgically. Guidelines suggested for predicting successful outcome of surgery include the following: (1) a minimum of 5 cm of normal prepuce should be present on either side of the surgical site or proper unfolding may not be possible after surgery, and (2) free prepuce remaining after surgery should be at least twice the length of the free portion of the penis or the prepuce may be too short to permit full penile extension. Presurgical and postsurgical considerations, as well as surgical techniques used to correct phimosis, are described by Walker and Vaughan.¹

Congenital anomalies contributing to phimosis are diagnosed based on physical examination of the entire reproductive tract. Abnormal karyotypes may be helpful in determining causes. If the penis cannot be extended using the techniques described and evidence of injury or adhesions is not present, congenitally short penis or retractor penis muscles should be suspected.²

Accompanying history may provide information that the bull could copulate when young, but as he aged his abdomen progressively enlarged, causing the penis to be of relatively insufficient length to effect copulation.²

■ Ram and Buck Phimosis is uncommon in small rumi­nants. It may be congenital or acquired as a result of adhesions or preputial scarring associated with trauma or balanoposthitis.¹1 Acquired phimosis can be the result of ulcerative posthitis due to the presence of Corynebacterium renale, Corynebacterium pilorum, or Corynebacterium cystitidis. These bacteria normally inhabit the prepuce and transform urea to ammonia, which is highly irritating to the prepuce. High urine urea levels, which are noted in animals fed high-protein diets, may increase the risk of ulcerative posthitis.^17,18 This condition is diagnosed during the physical examination and/or by observing the animal during the breeding process. If phimosis is due to acute inflam­mation of the prepuce (posthitis), it may resolve when the preputial swelling reduces. However, the prognosis is guarded until scarring can be evaluated.

Paraphimosis

■ Stallion

Definition and Etiology

When injury of the penis and the laminae of the prepuce is attended by hemorrhage and edema, paraphimosis (the inability to retract the penis into the prepuce) is likely to occur.¹ Pro­longed penile prolapse, caused by debility or paralysis after the use of some tranquilizers, usually culminates in extensive penile irritation.^19,20 Protracted priapism (persistent erection) can lead to penile trauma and complications similar to penile prolapse.²¹ Penile paralysis and priapism are distinctly different conditions. Penile paralysis likely develops secondary to insufficient tone of the retractor penis muscles.²² Motor innervation of the retractor penis muscles in stallions is believed to be solely supplied by α-adrenergic fibers. When α-adrenergic blocking drugs such as phenothiazine-derivative tranquilizers are administered, paralysis of these muscles can cause penile prolapse.²³ The prolapsed penis is flaccid and cannot be maintained in the retracted position.^1,22 Priapism is a persistent erection without sexual arousal and is initially unassociated with penile paralysis. It develops from engorgement of the CCP with blood, and although the horse may not achieve a full erection, its penis is not flaccid.^24,25 When the penis fails to detumesce, CO₂ tension in the CCP increases, resulting in increased blood viscosity and subsequent venous occlusion where collecting veins join the cavernous spaces. Edematous swelling of corporeal trabeculae further reduces venous outflow, thus increasing the likelihood of irreversible venous occlusion, fibrosis of the cavernous trabeculae, and arteriolar occlusion. Disruption of the arteriovenous supply and fibrosis of the CCP prevent subsequent erections.^5,26

■ Clinical Signs and Differentials Penile paralysis has been reported in exhausted or debilitated horses, in horses with myelitis or spinal injury, and in horses with severe injury to the penis.^1,19 Traumatic inflammatory edema often results in severe swelling of preputial membranes that prevent retraction of the penis into the prepuce. The inability to retract the penis results in further gravitationally induced edema, and, as the problem worsens, edematous fluid eventually oozes through the increasingly fragile penile and preputial integument. Cel­lulitis develops, and the integument becomes thickened, inelastic, desiccated, necrotic, and irreversibly damaged.^1,5 In cases of long-standing priapism, the distal end of the penis becomes cool to the touch, and the clot may become palpable in the body of the CCP as fibrin organization occurs. The organized clot may be visible on ultrasound examination.²¹

■ Treatment and Prognosis Prognosis for recovery becomes guarded to grave as the chronicity of the problem increases. Principles of treatment are similar to those described for the bull. The key to success is early aggressive intervention to reduce the edema via compression so that the penis can be placed within the prepuce.²⁷ To maintain the penis within the prepuce, a temporary purse-string suture of heavy nonabsorbable suture can be placed near the preputial orifice; however, dehiscence is common following this procedure. Alternatively, a padded plastic bottle from which the bottom has been removed can be used to support retention of the penis within the sheath. After the injured penis is dressed, the bottle is placed over it and pushed back into the sheath. The bottle is held in place with flexible straps or tubing running over the lumbar area and on either side of the scrotum up over the tailhead. Voiding of urine occurs through the bottle. The apparatus should be cleaned and replaced twice daily until the penis can be self­retained in the retracted position. Another effective method for maintaining the penis within the prepuce is the use of a 2-inch outer-diameter probe made of polyvinyl chloride (PVC) or other plastic tubing that is secured to the stallion’s abdomen using elasticated bandage tape.²⁸ If the penis cannot be returned into the prepuce, an external support for the prolapse should be applied. Prolonged penile prolapse may result in excess gravitational pull that damages smooth muscle cells, the retractor penis muscle, and the pudendal nerves^1,22; such sequelae decrease the prognosis for recovery and return to a successful breeding career. Chronic, refractory penile prolapse results in severe balanoposthitis that may require circumcision or penile amputa­tion. Surgical penile retraction (the Bolz technique) is described by Walker and Vaughan.¹ A simple amputation technique that can be performed in the standing horse, using a modified Vinsot procedure, has also been described.²⁹

Medical treatment of horses with priapism has generally been unsuccessful.^5,24 In cases of drug-induced priapism seen within 2 to 4 hours of occurrence, slow IV injection of 8 mg benzotropine mesylate may cause detumescence and penile retraction to occur.³⁰ If not seen immediately, treatment is the same as for traumatic paraphimosis. Rapid detumescence can be induced by injecting 10 mg of phenylephrine into the CCP, even in long-standing cases. However, the detumescence may be transient, especially in chronically affected cases. Flushing the CCP with heparinized lactated Ringer’s solution through 12-gauge needles to remove sludged blood has been recommended for horses with priapism of 12 to 24 hours’ duration that have not responded to medical treatment.⁵ If a blood clot forms in the CCP, the prognosis is poor, and amputation may even be necessary. Some stallions, if severe nerve damage does not occur, may regain the ability to breed and ejaculate when assisted with placement of the penis into either the vagina of the mare or an artificial vagina. When the stallion does not regain the ability to completely retract the penis into the sheath, continued penile trauma is likely to result in damage to the sensory nerves to the glans penis. Such horses may achieve an erection but may have difficulty in seeking the mare’s vulva for intromission and ejaculation. Ultrasonography of the CCP to detect cavernosal fibrosis may be useful in assessing prognosis for recovery from priapism. Prognosis for recovery is good once penile retraction occurs, but breeding should not be permitted until healing is complete.

■ Bull

Definition and Etiology

Paraphimosis is less common than phimosis in the bull. Causes may be the same for both conditions, but for paraphimosis include penile tumors, parasitic invasion, traumatic or spinal disease affecting innervation of structures responsible for penile retraction, inadvertently severed retractor penis muscles, or physical trapping of the penis by a constricted prepuce after injury. Penile paralysis and paraphimosis sometimes occur as a result of spinal injury or disease and in rabies cases as well.^1,2

■ Clinical Signs and Differentials Persistent exposure of the penis results in congestion, inflammation, and necrosis of the penile integument.²

■ Treatment and Prognosis Management of the prepuce has been discussed. Exposed portions of the penis should be frequently cleansed and protected by a bandage soaked in oily antibiotic preparations. The prolapsed penis should be supported close to the abdomen to reduce edema. The penis should be returned to the sheath as soon as possible and mechanically restrained if necessary. If the ability to retract the penis does not return in a few days, prognosis for recovery is poor.

■ Ram and Buck Paraphimosis is uncommon in small ruminants. The diagnosis is obvious, although the etiology may not be. Treatment involves the same principles as in the bull. Prognosis is guarded and correlates with the degree of injury and necrosis at the time the condition is discovered.

Urethral Injury and Urethritis

■ Stallion

Clinical Signs and Differentials

Traumatic injuries to the urethral process are usually obvious and are characterized by hemorrhage. Habronema granulomas are firm and friable. Ulcers of the urethral process often become secondarily invaded with bacteria such as Pseudomonas spp. Parasitic lesions tend to regress during winter, but if untreated they may mineralize and result in recurrence of hemospermia during the following breeding season.³¹

Lesions can occur throughout the urethra, including the pelvic urethra in the area of the ejaculatory ducts. Diagnosis is based on demonstration of the lesions by fiberoptic examina- tion. Ultrasonography and fractionation of the ejaculate may be helpful in eliminating involvement of the accessory sex glands.³²

Urethral inflammation and lacerations may result in fibrous strictures.³³ Strictures are often painful and may separate and bleed during urination and ejaculation. Bacteriologic culture of the urethra, urine, and semen; fiberoptic examination; and histologic examination of biopsies of lesions are helpful in making a diagnosis.¹ Strictures in the distal urethra may be identified by contrast radiography of the extended penile urethra.^1,33

Clinical signs of uroliths include dribbling of urine with chronic cystitis, dysuria and stranguria, occasional hematuria, recurrent colic, and a stilted, painful gait in the hindquarters. Penile protrusion is frequent or constant in cases of chronic, involuntary escape of urine.¹ Diagnosis is by urinalysis, revealing the characteristic crystals, red and white blood cells, and bacteria. Urethral calculi typically restrict the passage of urethral catheters. Bladder calculi may be palpated per rectum or visualized by ultrasonography.^1,31

■ Treatment and Prognosis Treatment of urethral injuries involves first removing inciting factors such as a tight stallion ring. Sexual rest is indicated while palliative therapy is given. The ability to void urine should also be established. Systemic treatment with antibiotics that are eliminated in the urine may be useful as a prophylactic measure or in cases in which secondary bacterial invasion has occurred. More severe cases of urethritis may be treated locally either by infusion of oily antibiotic preparations through sterile, rubber urethral catheters passed to the area of the seminal colliculus of the pelvic urethra or by inserting soluble suppositories through a perineal urethrostomy. After resolution of the urethritis, the urethrostomy is allowed to heal by granulation.³³ Lacerations or rents of the proximal urethra that result in hemospermia can be treated by perineal incision into the corpus spongiosum and underlying urethra (CSU) or by perineal corpus spongi- otomy where the CSP is incised, but the incision is not extended into the urethral lumen. These surgeries are believed to prevent stretching of the urethra when engorgement of the corpus spongiosum occurs during urination or erection. Repeated tissue stretching and bleeding through the site at the time of urination are thought to prevent urethral lacerations from healing without these forms of surgery.³⁴

Inflammation of the urethral process may respond to local antibiotic salves. Treatment of parasitic granulomas with ivermectin speeds resolution of these cases.^13,35,36 Larger, nonresolving granulomas with mineralization may require surgical removal.³⁷ The skin of the urethral process should be rolled inward when sutured to the mucous membrane to prevent eversion that predisposes it to reinjury after healing. Remaining hemorrhagic or ulcerative lesions can be lightly cauterized with silver nitrate.³¹ More proximally located nonresolving urethral strictures, prolapsed subepithelial vessels, or ulcers can be removed surgically.

Calculi lodged within the lumen of the pelvic urethra can be removed via perineal urethrostomy. Treatment for urethral calculi is described in the discussion of diseases of the urinary system (Chapter 34).

■ Bull

Definition and Etiology

Urolithiasis is the primary problem affecting the urinary system that may interfere with normal function of the reproductive tract of the bull. It is of less importance in bulls than in steers but occasionally occurs and may result in hematuria or urethral obstruction.^1,2 Urolithiasis is thoroughly discussed in Chapter 34.

Balanoposthitis

■ Stallion

Definition and Etiology

Inflammation of the glans penis (balanitis) and prepuce (pos­thitis) often occur together (balanoposthitis). Traumatic injury resulting in inflammation of the penis and prepuce has been discussed. Balanoposthitis may also be caused by dourine, equine herpesvirus 3 (EHV-3), miscellaneous bacteria, and parasites.

Equine Coital Exanthema

from swabs or scrapings taken from the edge of erosions, inclusions in lesion specimens, or confirmed by using an electron microscope to visualize typical herpesvirus particles in fluid or tissue samples. Probably the most sensitive, specific, and accurate tool for the detection of EHV-3 is PCR testing. Demonstration of antibody titers in serum may be useful in establishing time of exposure to the virus.⁴²

Infection with EHV-3 is self-limiting. Local treatment with antibiotic ointments will not speed healing but may minimize secondary bacterial infection and soreness. Care should be taken to avoid iatrogenic transmission of the infection (e.g., through contamination of sleeves, water, and examination or insemination equipment) to susceptible animals. Attending veterinarians may choose to refrain from breeding affected stallions until the lesions heal. One method that may be helpful in circumventing transmission of the infection while still breed­ing the stallion is to collect semen in an open-ended artificial vagina as soon as lesions are no longer painful. Collecting the semen as it directly exits the urethra reduces the chance of viral contamination from the penile and preputial lesions.

Bacterial Infections application of 1% silver sulfadiazine cream. The procedure is repeated daily for 1 to 2 weeks followed by serial cultures to determine if treatment was successful.⁴⁸ The clinician should be cognizant that recolonization with these organisms may occur and that routine scrubbing and disinfection may pre­dispose to infection of the genitals with potential pathogens by displacing commensal organisms.⁴³ While not tested in a research setting, individual clinicians have used a tranfaunation procedure to replace normal flora by rubbing the penis and preputial areas of the affected stallion with smegma of a stallion with normal penile and preputial flora.

■ Bull Balanoposthitis in the bull is caused by traumatic injury and infections. Whereas injury of the prepuce is more common, penile inflammation often accompanies the traumatic posthitis. A multitude of potentially pathogenic organisms inhabit the prepuce, and injuries predispose to infection, particularly when deeper tissues are exposed. Pain and preputial discharge may be evident. Because of the presence of the many organisms in the preputial cavity, culture to identify a specific offending organism is likely to be misleading. When injury results in infection of the penis and prepuce, sexual rest in conjunction with local antibiotic treatment is indicated; systemic antibiotics are indicated if the injury is extensive or involves the full thickness of the prepuce. Treatment should be performed as previously outlined for the penis and prepuce until inflam­mation is corrected.

Balanoposthitis unassociated with trauma has been associated with infections caused by infectious bovine rhinotracheitis- infectious pustular vulvovaginitis (IBR-IPV) caused by bovine herpesvirus 1 (BHV-1), tuberculosis, and screwworm infesta- tion.^2,49 Acute lesions associated with IBR-IPV infections are numerous small pustules that progress to ulcers and erosions in a few days. Purulent preputial discharge is present, and lesions may become confluent. The prepuce and penis may become quite inflamed and swollen. Healing is commonly spontaneous and rapid, beginning in 1 week and usually complete in 2 weeks. Severe cases may take longer to resolve.⁴⁹ Virus is shed from the prepuce for 2 weeks or longer, during which time venereal spread is possible. Sexual rest for 6 to 8 weeks has been recommended to prevent spread and to avoid abrasions that may aggravate inflammation.² Enlargement of the lymphoid follicles may be present along with a seromucoid exudate for several weeks. Histologic changes include the transient appearance of eosinophilic intranuclear inclusions in degenerating epithelial cells. Infusion of the preputial cavity daily may be of benefit in treatment, particularly in more severe cases. Vaccination with attenuated intranasal products has been reported as a method to prevent viral shedding into semen in bulls from AI studs.² Bulls infected with BHV-1 remain infected for life, as the virus remains latent in the sacral ganglia.^50,51 Viral shedding through the ejaculate occurs intermittently. Therefore valuable serologic-positive bulls could be tested for the presence of the virus in semen. Detection of BHV-1 in semen by real-time PCR is more sensitive than virus culture isolation. Two straws of extended processed ejaculate are necessary to detect the presence of the virus.^50,51

■ Ram and Buck

Definition and Etiology

Balanoposthitis (also called “pizzle rot,” “sheath rot,” and “ulcerative posthitis”) commonly affects the penis and prepuce of intact and castrated male small ruminants (see also Chapter 34).^11,12 In sheep, it is important to differentiate pizzle rot from ulcerative dermatosis. Ulcerative dermatoses, caused by a parapoxvirus, also present lesions in lips and legs, as well as in the genital area (see also Chapter 32). In goats, the caprine herpesvirus produces balanoposthitis in males and vulvovaginitis 5253 5455

in females.^52,53 It is also a cause of caprine abortion.^54,55

Persistent Penile Frenulum and Penile Deviations

■ Stallion

Definition and Etiology

Persistent frenulum is rare in the stallion. However, penile deviations can occur in older stallions, particularly those that have been subjected to semen collection through most of their breeding career. In the United States, most of the affected horses have deviations to the right. It is thought that repeated bending of the penis to the left to facilitate entry into the artificial vagina causes damage to the CCP/tunica albuginea on the right side, resulting in filling defects and fibrotic lesions that lead to penile deviation.

■ Treatment and Prognosis For most affected stallions, treatment is unnecessary, and the horse continues to ejaculate normally. Some stallions have such a severe deviation that attempts to collect semen result in pain and lack of ejaculation. For these stallions collecting semen on the side ipsilateral to the direction of deviation often alleviates the problem.

■ Bull

Definition and Etiology

Phallocampsis, or deviation of the erect penis, is a relatively common condition in the bull. The most common cause of penile deviation is persistent penile frenulum.² Other types of penile deviations include spiral, ventral, and S-curved devia­tions.¹ Less commonly, preputial or penile injury may result in scar tissue formation that subsequently leads to deviation of the erect penis.¹

When the penile frenulum persists, it remains connected to the ventral surface of the tip of the penis and the prepuce and causes the penis to bend ventrally during erection by preventing complete extension.⁵⁶ Copulatory ability is interfered with except in some of the Zebu-influenced breeds that are endowed with a plentiful prepuce.¹ Diagnosis is based on physical examination of the extended penis.

Because spiraling of the penis is thought to be a normal physiologic event that occurs in the vagina during ejaculation,⁵⁷ care should be taken in making this diagnosis. Bulls affected with penile deviations often have a history of no problems in mating cows for some time, occasionally for several breeding seasons. If such bulls have been closely observed, it may have been noted that the condition did not occur on every mating attempt, but the frequency of occurrence gradually increased until bulls might require numerous mounts to successfully intromit and breed a cow in estrus.² Penile deviations occur at full erection when the CCP is maximally distended with blood. Caution should be exercised in diagnosing this condition during erection stimulated by electroejaculation. Such erections are not considered to be entirely physiologic and frequently result in penile deviations in bulls that have no deviations under natural mating conditions. The spiral deviations that occur with use of the electroejaculator may be a result of tension exerted by the retractor penis muscles.¹ Diagnosis is best based on observing occurrence of the deviation frequently in natural mating situations.

The ventral or rainbow deviation of the penis is less common than the spiral deviation and is a result of the apical ligament being too thin to support the engorged, stretched distal end of the erect penis.¹ The ventral curvature may be quite pro­nounced, preventing affected bulls from directing and inserting the penis into the vagina of the female.

The least common of the spontaneous penile deviations is the S-shaped curvature. It primarily occurs in older bulls with an apical ligament that is short in relation to an excessively long penis.¹ Penile deviations that result from adhesions that developed from penile or preputial injury are diagnosed by physical examination.

■ Treatment and Prognosis Persistent penile frenulum is easily corrected by severing the persistent band. Owners of affected bulls should be advised of the probable genetic basis and therefore the undesirability of retaining such bulls for breeding.¹ Treatment of spiral and ventral deviations is

₁

surgical.¹

Tumors of the Penis and Prepuce

■ Stallion

Clinical Signs and Differentials

The most common neoplasm of stallion genitalia is squamous cell carcinoma (SCC). Generally, it is of low malignancy.^1,58 The tumor usually involves the glans penis but may also involve the shaft of the penis and prepuce and produce a fetid discharge. Large tumors may ulcerate and bleed, resulting in hemospermia. Carcinomas may resemble Habronema granulomas, which are more common and are diagnosed by histologic examination of affected tissue.^2,5 Carcinomas are usually well differentiated and surrounded by eosinophils. Necrosis and calcification may occur, but parasite larvae are usually not present unless second­ary habronemiasis has occurred from flies feeding on the ulcerated tissue. Carcinomas may extend into the CCP or may metastasize to the inguinal lymph nodes or other abdominal or thoracic organs. The superficial inguinal lymph nodes lie midway between the prepuce and external inguinal ring; second­ary tumors in this region often grow rapidly and develop necrotic centers with purulent sinuses that must be differentiated from bastard strangles.¹

Tumors encountered much less frequently include melanoma, papilloma, angioma, lymphosarcoma, and sarcoid. Melanoma is a common equine tumor, especially of gray horses,¹³ and occasionally involves the penis and prepuce^1,2,59 (see Chapter 40). Genital papillomas are rare in stallions but may occur on the glans or shaft of the penis. The lesions appear as multiple proliferative cutaneous growths and may become friable and result in hemorrhage during erection and ejaculation.⁵ The lesions are generally thought to be caused by a papillomavirus, and papillomavirus antigens have been found in cutaneous and genital papillomas.⁶⁰ Angiomas and lymphosarcomas have occasionally been reported on the genitals of stallions.³ Sarcoids may involve the skin of the prepuce or scrotum.^1,59

■ Treatment and Prognosis When SCCs are relatively small and noninvasively attached to the skin, neoplasms may be successfully treated by cryosurgery or hyperthermia. Hyperthermic treatment (50° C for 1 to 2 minutes) appears to be most successful for SCC when lesions are small (less than ≈2 cm). If the tumor is extensive but superficial, cryo­surgery may be attempted after the tumor is debulked and hemorrhage is controlled. The remaining base of the tumor is then frozen and thawed twice; healing occurs as necrotic tissue is sloughed. Successful treatment of small lesions has been reported with topical application of 5-fluorouracil.⁶¹ If removal of tumors is unsuccessful or if neoplasia is extensive, penile amputation may be necessary.^1,62 If superficial inguinal lymph nodes are involved, euthanasia may be required.¹

In contrast to nongenital squamous papillomas, genital forms are generally quite refractory to treatment.⁵ Surgical removal and autogenous vaccine administration to treat fibropapilloma of the penis of two stallions did not effect a cure.³¹

■ Bull

Definition and Etiology

Fibropapilloma is the only tumor that frequently invades the bovine penis or prepuce. The tumor may be single or multiple and usually affects young bulls. The cause is thought to be a papillomavirus antigenically similar to the virus that causes cutaneous papillomatosis in cattle. Frequent mounting among young bulls is thought to result in damage to epithelial surfaces of the penis and prepuce that serves as a route of entry for the virus.^1,2

■ Clinical Signs Small papillomas may be discovered during routine breeding soundness evaluations, but many become larger before they are discovered. Large Abropapillomas may prevent withdrawal of the penis into the preputial cavity. Fibropapillomas are pedunculated and attached at a narrow base in early cases. The surface becomes cauliflower-like and friable; hemorrhage is easily induced.

■ Treatment and Prognosis Many Abropapillomas regress spontaneously within a few months. Regression may be more likely in bulls approaching 2 years of age and usually occurs within 4 months of the appearance on the penis.^63,64 Several vaccines, including autogenous preparations, have been used for treatment, but vaccines may be more successful for prophylaxis.² Frequently surgical removal is indicated, but the Abropapillomas may recur. If only superficial attachment is present, surgical removal is easily accomplished. Catheterization of the distal urethra before surgery is helpful in identifying its location to avoid injury. If attachment has become extensive and sessile, amputation of a portion of the distal penis may be necessary.¹ Housing of young replacement bulls in individual pens, if possible, is recommended as a method to reduce the incidence of penile fibropapillomas.

Parasitic Infestations of the

Penis and Prepuce

■ Stallion

Definition and Etiology

Habronema muscae, Habronema microstoma, and Draschia mega­stoma larvae commonly invade the urethral process, glans penis, and preputial ring of stallions.^1,13 Other terms for this condition are “genital bursatti” and “summer sores.”

■ Clinical Signs Shallow irritations progress to irregular 1- to 3-cm granulomatous growths that may involve the entire circumference of the urethral process.² Lesions are friable and bleed when manipulated. Stretching of the infected urethral process during penile engorgement and ejaculation may result in hemospermia.⁵ Pruritus associated with the lesions may be intense. Frequent micturition and dysuria may resemble urine spraying that accompanies accumulation of smegma in the urethral diverticulum (“bean”). Lesions subside during the colder months in northern areas but usually reappear and increase in size during subsequent warm weather.² Diagnosis is made by seeing yellowish granules (calcified larvae) in the lesion and by microscopic identification of larvae.¹³

■ Treatment and Prognosis See Chapter 40 for treatment and prognosis information.

Hemospermia (Blood in Semen) artificially inseminated with extended semen containing no blood. However, if the extended semen contained 50% blood, no pregnancies were obtained. It was concluded that the level of blood rather the presence of blood affects the fertility. A disproportionate number of leukocytes to erythrocytes sug­gests infection of the internal genital organs. Specific causes of hemospermia include lacerations of the penis, cutaneous habronemiasis, urethritis, urethral lacerations, and infection or inflammation of the accessory genital glands, which are discussed elsewhere in this chapter.

Urospermia (Urination During Ejaculation)

■ Definition and Etiology Urospermia is an uncommon but perplexing disorder of breeding stallions. Affected stallions generally exhibit normal libido and mating ability, but semen becomes contaminated with urine during the ejaculatory process. The problem may be incessant or unpredictably intermittent; urination can occur at any time or continuously during ejacula­tion. The amount of urine is up to 250 mL or more.⁵

The underlying cause or causes of urospermia are speculative. Closure of the bladder sphincter and seminal emission are controlled by the α-adrenergic sympathetic nervous system, and a disturbance in this pathway might contribute to uro- spermia. Similarly, neuropathies that result in bladder paralysis (e.g., cauda equina neuritis or nerve damage secondary to EHV-3 or sorghum/Sudan grass poisoning) can create urinary incontinence that permits voiding during ejaculation. Most stallions with urospermia do not exhibit signs of a neurologic deficit.⁵ In ruminants, urine can also contaminate semen col­lected by electroejaculation. To reduce this risk, it is recom­mended to avoid water ingestion 12 to 24 hours before semen collection.

■ Clinical Signs and Differentials Gross contamination of ejaculated semen with urine is easily detected by its color and odor. Contamination with significant quantities of urine adversely affects sperm motility and fertilizing capacity. Elevated concentrations (relative to serum levels) of urea nitrogen or creatinine in semen document the presence of urine in the ejaculate.^5,67

■ Treatment and Prognosis Treatment options for urospermia vary, can be arduous, and are often unrewarding. Delay of semen collection (or breeding) until immediately after the stallion has voided urine may be a helpful management policy. Urination can be stimulated by administration of a diuretic drug (e.g., furosemide). Stallions may also void urine when provided access to feces of another stallion. Some stallions can be trained to urinate on command. Alternatively, the bladder can be catheterized to aid evacuation of urine before breeding, but urethritis or cystitis may result from routine use of this procedure. Fractionation of ejaculates using an open-ended artificial vagina can be used alone or in combination with any of the previously mentioned measures. When an open-ended artificial vagina is used, only the first three jets of the ejaculate are collected. These jets contain a majority of the spermatozoa in the ejaculate, and urination may not occur until the end of the ejaculatory process. Dilution of urine-contaminated semen in extender can restore sperm motility. Semen may be centrifuged after initial dilution and the sperm pellet resuspended in extender before insemination⁵; however, centrifugation to remove urine may not provide a significant advantage to dilution in extender.⁶⁸

Pharmacologic agents such as bethanechol chloride or flavoxate hydrochloride have been used in an attempt to correct urospermia, but usually without success.⁵ Oral administration of imipramine (100 to 500 mg twice daily) has reportedly been useful for controlling urospermia in stallions, presumably by enhancing contractility of the bladder neck during emission.⁶⁶

Infertility Caused by Diseases of the Scrotum and Testes

Scrotal Injury, Hydrocele, and Hematocele

■ Definition and Etiology Trauma to the scrotum can result in excoriation, lacerations, hemorrhage, and edema.² Systemic diseases such as hepatic disease and equine infectious anemia may result in scrotal edema.^2,20 Suppurative inflammation may develop as an extension of scrotal injury.² Adhesions often develop between the visceral and parietal tunics when inflam­mation, infection, or hemorrhage occurs. Adhesions are usually thin fibrous strands that become thickened with time. In such cases the testis and its tunics are not freely movable within the scrotum.

Hydrocele is an accumulation of serous fluid within the vaginal tunic. Ascites, anasarca, or local lymphedema may contribute to hydrocele because the vaginal tunic communicates with the peritoneal cavity. Accumulation of a significant volume of fluid around the testis may cause thermal degeneration and a decline in seminal quality.⁶⁹ In Texas, a seasonal hydrocele has been described in bulls submitted to breeding soundness examination during the fall and winter season.^70,71 This type of hydrocele was associated with ascites and intestinal edema and has been attributed to a hypersensitivity reaction to gastrointestinal nematodes.^71,72

Hematocele occurs when trauma to the scrotum results in accumulation of blood within the testicular tunics. Hematoceles can be primary due to a testicular trauma or secondary to hemoperitoneum. Scrotal damage initially accompanies hematocele. Thermal degeneration of the testes follows, and a thick fibrous capsule encompasses the testis after the blood clot organizes.⁷³

■ Clinical Signs and Differentials Diagnosis of scrotal injury, hydrocele, and hematocele is made by physical and ultrasonic examination of the scrotum. Testes remain freely movable within the scrotum if hydrocele is present. Ultraso­nographic examination reveals variable amounts of anechoic fluid present surrounding the testes and epididymides, which are easy to visualize because of their echoic nature against the fluid background. With hematocele, evidence of trauma is often present, with thickening of the scrotal skin. Blood sur­rounding the testis and epididymides becomes progressively more echogenic as the clot organizes.^5,74 Extensive edema of the scrotal fascia next to the tunica dartos may be difficult to differentiate ultrasonographically from hematocele. Abdominal paracentesis is helpful in eliminating ascites or peritonitis as causes of hydrocele. Palpation per rectum of stallions and bulls may occasionally reveal that the internal inguinal rings are enlarged, readily permitting fluid transfer into the vaginal cavity.

An aseptic tap is useful to identify the character of this fluid and must be performed with care not to contaminate or penetrate the testis or its visceral vaginal tunic.⁷³ A modified transudate of low cellularity is typical of fluid drained from a hydrocele.⁷⁵ Fluid usually returns after drainage unless the initiating cause is corrected.⁵ Determining and treating the cause of ascites could provide permanent cure of the ascites and hydrocele.^71,72

■ Treatment and Prognosis Acute scrotal injury is treated with cold water or ice application to reduce edema (see earlier discussion on penile and preputial injuries). Lacerations and abrasions should be treated with topical antibiotic ointments. Systemic antiinflammatory drugs and antibiotics may reduce swelling, control infection, and prevent abscess formation.^5,73

Scrotal thickening usually results in elevation of testicular temperature, causing degeneration and atrophy similar to that seen with experimental scrotal insulation.^76-78 Semen quality quickly deteriorates, and a rapid reduction in number and motility of spermatozoa occurs, with a concurrent increase in morphologic abnormalities of spermatozoa.^2,79 If swelling and edema resolve and adhesions do not develop among the testes, tunics, and scrotum, spermatozoa may gradually reap­pear in the ejaculate by 1 to 2 months after injury, but 4 to 5 months may be required for testes to return to normal size and sperm production.⁴ One or both testes may remain atrophic and become firm because of fibrosis and loss of tubules. If only one testis is atrophied, the normal testis may eventually hypertrophy.

If hemorrhage occurs within the scrotum or testicular tunics, the prognosis for return of testicular function is poor. In unilateral cases, surgical removal of the clot and affected testis may minimize damage and speed recovery of the remaining testis.^80,81 Hydrocele is managed by correcting the underlying cause of fluid accumulation such as peritonitis or ascites.⁷³ Exercise may aid in control of fluid accumulation in some horses. Some stallions and bulls with persistent minor fluid accumulations within the tunics may continue to produce sufficient normal spermatozoa.² Permanent testicular degenera­tion may result in cases with extensive fluid accumulation that are unresponsive to therapy. If the condition is unilateral, removal of the affected testis may permit the animal to remain in service.⁷⁵ Because hydrocele and associated impairment of spermatogenesis may be transient (2 to 6 months),⁷⁰ caution should be exercised in recommending castration or culling of affected animals until demonstration that the disorder is long-standing.

Scrotal Dermatitis or Abscess

The scrotal skin is delicate and vulnerable to dermatitis. Causes include nonspecific environmental contaminants, bacteria, fungi, parasites, and frostbite. Scrotal abscesses are not uncommon in small ruminants and are due to shearing injuries and penetrat­ing wounds.¹¹ Treatment is directed toward removing the affected testis. Bulls affected by frostbite should be provided a warm and dry environment.⁸² Systemic and local antibiotics may be indicated. Abscesses should be drained. Thermal degeneration of the testes may follow dermatitis and may be temporary or permanent.² Semen quality should be evaluated at periodic intervals after skin lesions have resolved to gauge prognosis for improvement and return to fertility.

Testicular Aplasia and Hypoplasia

■ Definition and Etiology Complete absence (aplasia) of one or both testes is rare and usually occurs in conjunction with anomalous development of other organs.^2,83 Testicular hypoplasia may be unilateral or bilateral and affects both scrotal and abdominal testes. Testicular hypoplasia is thought to result from failure of germ cells to multiply in the gonad.² Causes of testicular hypoplasia may include transplacental infections and intoxications, zinc deficiency, hormonal insufficiency, impaired testicular descent, abnormal karyotype, and vascular disturbances.^11,12,'9 Exogenous administration of hormones to prepubertal males can result in testicular hypoplasia. Testicular size of adult stallions is reduced after prolonged administration of exogenous steroids.^84-86 Scrotal circumference is diminished in bulls implanted with zeranol.⁸⁷

■ Clinical Signs and Differentials Hypoplastic testes are usually smaller than normal, but they are occasionally normal in size.^88-90 Stallions 3 years of age should have a scrotal width greater than 8 cm.²⁰ Yearling rams with a scrotal circumference of less than 30 cm and mature rams with a scrotal circumfer­ence of less than 32 cm are not recommended for breeding.⁹¹ The texture of affected testes varies from normal to soft in mild or moderate hypoplasia. Severely affected small testes are firm because of the relatively increased amount of stromal connective tissue. History is an important component in the clinical assessment in order to differentiate hypoplasia from atrophy. If uncertain, reexamination needs to be performed. Factors that influence the scrotal circumference in ruminants are breed, age, body condition score, and season.⁹² In bulls, the minimum recommended scrotal circumference is 30 cm for 15 months old or younger and 34 cm for 2 years old or older according to the criteria established by the Society of Theriogenology.⁹³ Scrotal circumference in bulls is positively correlated with the number of normal functional seminifer­ous tubules and is negatively correlated with pathologic seminiferous tubules in bulls.⁹⁰ In bulls the heritability for scrotal circumference is medium to high.⁹² In addition, scrotal circumference is negatively correlated with age at puberty of the female offspring. Bulls with higher scrotal circumference will produce females that acquire puberty earlier than females produced by contemporaneous bulls with smaller scrotal 92

circumference.⁹²

Depending on the number of seminiferous tubules affected, ejaculates from males with testicular hypoplasia may be azo- ospermic or contain a low concentration of spermatozoa with numerous morphologic defects.²

■ Treatment and Prognosis No successful treatment is available for severe hypoplasia. The useful breeding life of males with testicular hypoplasia may be shortened because affected bulls are thought to be predisposed to early testicular degeneration.⁸⁸ Because of the value of some individuals, particularly stallions, owners may elect to breed males with small testes. Effective management of such stallions is based on breeding a book of mares limited by the number of normal, motile spermatozoa present in ejaculates.

Cryptorchidism

■ Definition and Etiology Incomplete or abnormal testicular descent is thought to be a genetic abnormality. The inheritance pattern in horses is thought to be dominant,¹ although studies of offspring of some cryptorchid stallions suggest that inheritance of the condition may be multifactorial.² The relative risk for equine cryptorchidism also appears to be influenced by breed.³ Other modes of inheritance have been suggested from studies of the offspring of cryptorchid rams, bucks, and bulls. These include a recessive gene with incomplete penetrance in Angora goats,⁴ a dominant gene with variable expressivity in Hereford cattle,⁵ and either an autosomal reces­sive gene or a dominant gene with incomplete penetrance in inbred sheep.⁶

Testes originate near the kidney and migrate to the inguinal rings before descending into the scrotum; the epididymis precedes the testis in descent. Retained testes are located at some point along the path of migration. Ectopic testes not associated with cryptorchidism may be found under the skin of the ventral caudal abdomen or elsewhere in bulls.

■ Clinical Signs and Differentials The majority of cases of cryptorchidism in stallions are unilateral.⁷ Although testicular descent can occur in horses up to 2 years of age, the testes are normally descended at birth in large animals.⁸ Testes are readily palpated in the scrotum of colts at 30 days of age. Spermatogenesis is inhibited in the abdominal testis because of the elevated temperature within the abdomen. The interstitial cells remain active and secrete testosterone, enabling even bilateral cryptorchids to maintain libido and copulatory activity. The descended testis may be hypertrophic; unilateral crypt­orchids are fertile but are not considered sound breeders.⁹

Deep palpation of the superficial inguinal rings may reveal the testis in the canal (“high flankers”). If the testis is not located in the inguinal canal, transrectal palpation or ultraso­nography can be performed in stallions and bulls in an attempt to locate a testis or to detect the vas or epididymis entering the superficial inguinal ring, thereby providing evidence of descent into the inguinal canal.¹⁰

■ Clinical Pathology Equine cryptorchids have high basal concentrations of testosterone (usually >100 pg/mL) and respond to human chorionic gonadotropin (hCG) administration (10,000 to 12,000 IU IV) with a significant elevation of circulat­ing testosterone within 30 to 60 minutes if testicular tissue is present. Geldings and “false rigs” (geldings with malelike behavior) have low basal concentrations of testosterone (400 ng/mL) is reported to be almost as reliable in diagnosing cryptorchidism as hCG stimulation.^11,12 Recent data suggest that anti-mullerian hormone (AMH) serum concentrations may serve as a useful marker for the presence of cryptorchid testes in the horse.¹³ In some ruminants, measurement of testosterone concentrations before and after administration of hCG has also proved helpful in identifying cryptorchidism.

■ Treatment and Prognosis Stimulation of testicular descent with repeated injections of gonadotropin-releasing hormone (GnRH), sometimes combined with hCG or acu­puncture, has been attempted, but the success has not been critically evaluated. Surgical removal of the abdominal and scrotal testes is often prescribed; however, many breed registries allow the breeding of stallions with unilateral cryptorchidism. Bilateral cryptorchidism results in sterility because of disrupted thermoregulation of both testes. Surgical placement of a retained testis into the scrotum is not considered an ethical procedure.

Testicular Degeneration

■ Definition and Etiology Testicular degeneration is an acquired condition with multiple etiologies.¹ Infections or traumatic orchitis may progress to permanent degeneration. Degeneration may be associated with thermal factors after elevation of body temperature by systemic infections; prolonged increase or decrease in ambient temperature; scrotal insulation from edema, dermatitis, scrotal hernias, or hemorrhage; or abnormal conformation resulting in an incompetent heat exchange system.^2-4 Degeneration results when testicular vasculature becomes occluded in torsion of the spermatic cord.⁵ Obstruction of the proximal epididymis and malformation of the efferent tubules results in degeneration caused by pressure within the seminiferous tubules.⁶ A variety of chemicals and ionizing radiation are capable of inducing testicular degenera­tion. Administration of steroid hormones may induce testicular degeneration by inhibiting secretion of gonadotropins.⁷ Gradual degeneration also occurs with increasing age.⁸

■ Clinical Signs and Differentials Diagnosis of tes­ticular degeneration is based on physical examination and semen evaluation. Testes are typically thought to be small, but they may be normal size. The testicular consistency and elasticity of the testes is also decreased. Semen examination reveals a low concentration of spermatozoa, a decreased number of spermatozoa in the ejaculate, and a high percentage of sper­matozoa with morphologic defects, sometimes with premature (round) germ cells.¹ Without a history of normal testis size and function before atrophy, differentiation from testicular hypoplasia is usually not possible. Discrepancies between testicular size (measured by scrotal width in stallions and scrotal circumference in ruminants) and daily sperm output may indicate testicular degeneration.^9,10

■ Clinical Pathology The measurement of plasma hormone concentrations may be helpful in establishing a diagnosis of testicular degeneration in large animals. However, the relation­ship between the concentrations of various hormones and the parameters of testicular function appears to be quite variable. Measurements of hormone concentrations in subfertile stallions have demonstrated that serum gonadotropins can be abnormally low or high.¹¹ Hormonal criteria for confirming testicular degeneration in stallions typically include low concentrations of testosterone, with concurrent low LH concentrations in early cases of degeneration or with high FSH and low estradiol concentrations in cases of chronic (or irreversible) testicular degeneration. Less is known about hormone concentrations in other large animal species with testicular dysfunction. Scrotal insulation of rams resulted in an increase in plasma FSH concentrations and a decrease in plasma testosterone concentra­tions within 1 to 4 weeks.¹²

Testicular biopsy can confirm degeneration.¹³ Excision of an amount of tissue sufficient for evaluation often results in hemorrhage, pressure degeneration, and necrosis.² Therefore testicular biopsy is usually undertaken only as a final recourse. However, testicular biopsy in the stallion appears to be a rela­tively safe procedure.¹⁴

■ Treatment and Prognosis Once testicular degeneration has occurred, treatment is usually of no benefit. However, any factors that might contribute to testicular degeneration (such as febrile conditions or systemic illness) should be corrected. Treatment of injuries of the scrotum and its contents is described earlier in this chapter.

Recent findings regarding variations in serum hormone concentrations in subfertile stallions have stimulated an interest in gonadotropin replacement therapy, including the use of GnRH. Although the hypothalamic-pituitary-testicular (HPT) axis of the stallion is remarkably refractory to GnRH-induced downregulation compared with other domestic species,¹⁵ there are few controlled studies to evaluate the effectiveness of GnRH therapy. In one study, pulsatile or constant administration of GnRH for 20 weeks did not promote testicular growth or alter spermatozoa output in reproductively sound or unsound stal­lions.¹⁶ In some cases, degeneration is temporary and improved semen quality is evident after 2 to 5 months. The prognosis for an animal recovering its fertility and the economic losses the client will sustain from treatment and decreased production must be considered when deciding whether treatment of testicular degeneration is warranted.

Orchitis testicular parenchyma and concurrent presence of periorchitis or epididymitis may be detectable by ultrasound examination. Increased testicular temperature, congestion, and interference with circulation lead to ischemia and infarction. Abscesses sometimes develop, occasionally culminating in purulent liquefaction of testicular parenchyma. Testicular atrophy and fibrosis follow as the condition becomes chronic.

Acutely affected animals may refuse to mate. Ejaculates may contain numerous white blood cells. Variable mineralization of seminiferous tubules can occur as a chronic change. Decreased sperm motility and increased sperm morphologic abnormalities are evident. Standardbreds affected by acute orchitis may switch from a trot to a pace, whereas Thoroughbreds may suddenly develop a hopping gait.

■ Treatment and Prognosis Treatment consists of scrotal cryotherapy and systemic administration of antiinflammatory drugs. Bacterial orchitis is treated with antibiotics chosen by semen culture and in vitro sensitivity. Antibiotic therapy should continue for 1 to 2 weeks beyond resolution of testicular swelling and pain. Testicular atrophy and sterility are common sequelae to orchitis. Changes in the testes, including precise measure­ments of in situ testis size, are followed by sequential ultrasound examinations or caliper measurements. Serial semen analyses over a period of several months allow the clinician to monitor response to treatment and return of testes to normal production of spermatozoa.

■ Prevention and Control Support devices may aid in preventing recurrence of traumatic orchitis in racehorses. With Brucella or Actinobacillus orchitis in sheep, the presence of subclinical carriers in the flock must be considered.

Testicular Neoplasia

■ Definition and Etiology Primary testicular tumors are uncommon in large animals but may be slightly more frequent in older bulls than in stallions or rams. Testicular tumors originate from the interstitial (Leydig) cells, Sertoli cells, and the germinal epithelium. Testicular teratomas and lipomas of the testicular surface and lymphosarcoma also occur.^1-3 Although the incidence of testicular tumors is relatively greater in retained than in scrotal testes in dogs, this predisposition has not been confirmed in large animals, perhaps because most are castrated at an early age before the time of usual onset of testicular neoplasia. Retained testes in the horse, however, are thought to be more prone to neoplasia. Teratomas in particular are found more commonly in cryptorchid than in scrotal testes, probably because they are embryonal in origin and their size prevents migration of the testis into the scrotum.

Seminomas are the most common primary testicular tumor in the descended testes of adult stallions, with the majority occurring in stallions older than 10 years of age.⁴ Seminomas are not hormonally active and are usually benign, but they may be malignant and invade inguinal and abdominal tissues.⁵ Seminomas are rare and benign in bulls and are rarely seen in aged rams, in which they are occasionally highly malignant. The tumor arises from the germinal epithelium, occurs in retained and scrotal testes, and grows rapidly.

Interstitial (Leydig) cell tumors have been reported in stallions and bulls and can have a negative impact on semen quality and fertility.⁶ Most do not produce androgenic hormones. They may be single or multiple in one or both testes and are commonly 1 to 2 cm in diameter.

Sertoli cell tumors are reported in horses, cattle, and sheep, but they are rare. Although metastasis is uncommon, extension of neoplastic tissue into the testicular vein and lymphatics can result in hydrocele. Because of the importance of Sertoli cells in spermatogenesis, these tumors are likely to exert an adverse effect on semen quality and fertility. Tumors in newborn or young calves may be due to impaired embryogenesis.³

Teratomas are usually a benign tumor commonly found in cryptorchid testes of horses.^1,7 They are rare in other large domestic species. The tumors are often cystic and vary in diameter from 10 to 25 cm or more. Structures present in teratomas arise from all three embryonic layers and include hair, nervous tissue, salivary glands, adipose tissue, cartilage, and bone.⁷

■ Clinical Signs and Differentials Neoplastic testes are often larger than normal, with an affected scrotal testis often twice the size of the unaffected testis, especially in cases of seminoma. Abdominally located testicular tumors can be quite large. Neoplastic testes, particularly seminomas, are typically irregular and firm. Swelling may extend into the spermatic cord, and pain that interferes with breeding or is evident on palpation may be present. Ultrasonographic appear­ance of testicular tumors tends to be discrete, well-circumscribed hypoechoic areas within the usually homogeneous testicular parenchyma.⁵ However, seminomas may involve so much of the testis at the time of diagnosis that differentiation between neoplastic and normal tissue can be difficult.

Swelling of the affected testis may interfere with thermo­regulation of the contralateral testis, resulting in decreased sperm production. Semen examination, however, may reveal seminal parameters to be within normal limits, and fertility may be acceptable. A significant amount of normal testicular parenchyma may remain covering the tumor, and living spermatozoa may or may not be present in the epididymis on the same side.⁸

■ Treatment and Prognosis Testicular tumors should be surgically removed. Although metastasis is uncommon, early identification and removal of unilateral tumors prevents spread to other tissues. If semen quality is satisfactory in seasonal breeders, removal may be delayed until the breeding season is completed to avoid the transient decrease in semen quality associated with postsurgical swelling. If neoplasia is bilateral, surgical removal may be delayed until semen quality deteriorates sufficiently to negate the use of the animal for breeding.

Infertility Caused by Diseases of the Spermatic Cord

Torsion of the Spermatic Cord

■ Definition and Etiology Torsion of the spermatic cord occurs more commonly in stallions than in other large animals, possibly because of the horizontal position of the testes within the scrotum. Torsions may be transient or permanent and typically are of 180 to 360 degrees, but rotations may be greater.¹ Abnormal elongation of the caudal ligament of the epididymis (scrotal ligament), the proper ligament of the testis, or an excessively long mesorchium may encourage spermatic cord torsion.^1,2

■ Clinical Signs and Differentials Torsion of the spermatic cord occurs in degrees that vary from those producing no pain or abnormality of semen to those involving vascular obstruction and acute colic. Torsion is often a transient condition that does not interfere with testicular function or cause pain.² In those cases the testis is usually rotated 180 degrees or less. If torsion is of sufficient degree to result in vascular compromise, acute pain results.^2,3 Diagnosis of torsion of the spermatic cord is aided when displacement of the tail of the epididymis and scrotal ligament is evident on palpation. The head of the epididymis is normally located craniodorsal to the testis, and the tail lies caudally, where it is attached to the testis by the proper ligament. The tail of the epididymis is most readily palpable, and its location is helpful in determining the degree of rotation. Torsions of 360 degrees or greater generally cause clinical signs that must be differentiated from strangulation of herniated contents into the scrotum. The primary method used to differentiate between the two conditions is palpation per rectum of the superficial inguinal ring to identify if hernia­tion is present.

Clinical signs of vascular impairment with spermatic cord torsion include abdominal discomfort, elevated heart and respiratory rates, unilateral swelling and edema of the scrotum, and increased testicular temperature.⁴ Affected testes are painful and quickly become soft and friable.^2,3

■ Treatment and Prognosis Manual correction of spermatic cord torsion is sometimes possible, but recurrence is likely. To attempt manual correction, the horse is sedated and the testis is rotated in the direction opposite the torsion. Both hands are used to reposition the scrotum as the testis and its tunics are rotated. Surgical correction is indicated if manual correction is not possible. Nonsteroidal antiinflam­matory drugs and analgesics may be administered to control pain.

The rapidity with which correction must occur is unknown; human testes may be salvageable if torsion is corrected within 6 hours. If hemorrhage or necrosis of the testis is evident, removal is indicated because the contralateral testis may become permanently damaged. The mechanism of the damage is probably immunologic, resulting from antibodies to spermatozoa liberated as a result of ischemia.⁴

Varicocele

■ Definition and Etiology Varicoceles are abnormally distended and tortuous veins of the pampiniform plexus.¹ Varicoceles are most often recognized in rams, where dilations in vessels may reach 15 cm and discourage movement and libido. Data from slaughterhouse necropsies show an increased incidence of varicoceles with age, reaching approximately 2% in rams 3 years and older. Varicoceles have been reported very infrequently in stallions.

Varicoceles may result from insufficiency of veins draining the testis or a deficiency of the fascia and connective tissue surrounding those veins that allows backflow and stasis of blood in the vessels. Infertility associated with varicocele is thought to be due to disturbance of the local thermoregula­tory mechanism, causing increased testicular temperature and subsequent disturbance in spermatogenesis. In addition, the varicose veins could affect the level of oxygenation and normal interchange of hormones between the arteries and veins. In rams, bilateral varicoceles are more common than unilateral varicoceles.^1,2 This is in sharp contrast with men, in which 70% of varicoceles are unilateral and located on the left side.² Concomitant atrophy of the testis is common in rams. Bilateral varicoceles and atrophied testes have been reported in the ram.³

■ Clinical Signs and Differentials Diagnosis of vari­cocele is made by palpating the dilated tortuous veins (“bag of worms”) within the spermatic cord. Confirmation of the varicocele has been accomplished by ultrasonographic examina­tion in stallions. Large echolucent areas in the venous plexus of the spermatic cord, sometimes with concurrent distention of the central vein of the testis, are described as the identifying features. The ultrasonographic appearance of a suspected varicocele can be compared with the structures of a noninvolved contralateral testis and spermatic cord or with those of another nonaffected animal.

Thrombosis of the varicocele can occur. The large, organiz­ing laminated thrombi can be mistaken as Corynebacterium pseudotuberculosis abscesses in the scrotal fascia of rams. Vari­coceles might also be mistaken for sperm granulomas of the caput epididymis. Unless thrombosis has occurred, varicoceles are typically fluctuant and soft and fail to elicit pain when palpated.

■ Treatment and Prognosis Surgical removal of varicocele has improved semen quality and fertility of some human patients but has not been reported in large animals. Thrombosis of a varicocele necessitates unilateral castration, with transection of the spermatic cord proximal to the thrombus. Castration is also recommended for rams because of potential heritability risks.

Infertility Caused by Diseases of the Epididymis and Accessory Sex Glands

Epididymitis

portions of the epididymis to the testis and vaginal tunics; atrophic testes; abscess formation; and draining fistulas to the scrotal surface. Ultrasonographic examination of the epididymis may reveal dilated ducts, fluid accumulation around the tail of the epididymis, and cystic areas within the epididymis that contain purulent material.

■ Clinical Pathology Inflammatory cells may be present along with abnormal sperm in the ejaculate of affected animals. Seminal leukocytes correlate positively with epididymitis lesions and correlate negatively with seminal quality. Bacteriologic culture or PCR analysis of the semen may aid in identifying specific infectious causes. Serologic tests for B. ovis and Helcococ- cus ovis are available and are helpful in determining exposure to the organisms.

■ Treatment and Prognosis Infectious causes of epi­didymitis are treated with systemic antibiotics selected by in vitro sensitivity. The ability of the antibiotic to gain access to the epididymides must be considered. Treatment should continue for 1 to 2 weeks after inflammatory cells disappear from the semen. In unilateral cases, removal of the testis, epididymis, and spermatic cord on the affected side may salvage some valuable animals for breeding. If unilateral castration is elected, sequential postcastration examinations are indicated to ensure that infection has not spread to remaining reproductive organs.

Treatment of ram epididymitis is usually not recommended but might be attempted in valuable animals with minimal clinical signs. Oxytetracycline 10 mg/kg and dihydrostreptomycin 25 mg/kg IM twice daily for 7 days resolved shedding of B. ovis. Because ovine brucellosis is a reportable disease in many states and provinces, treatment of affected rams should be conducted with appropriate regulatory oversight.

In cases of moderate or severe bilateral epididymitis, the prognosis for recovery is poor. Obstructions and granulomas usually develop, resulting in sterility. Testicular atrophy is a common sequela to epididymitis.

Seminal Vesiculitis (Vesicular Adenitis)

■ Definition and Etiology Inflammation of the vesicular glands is uncommon in stallions but more likely in bulls. Bacterial infections including B. abortus and P. aeruginosa are

24

incriminated in stallions.^2-4 In bulls, a variety of microorganisms have been isolated from cases of vesicular adenitis, including Actinobacillus actinoides, Aeromonas hydrophila, T. pyogenes, B. abortus, C. psittaci, C. renale, C. pseudotuberculosis, E. coli, H. somni, M. tuberculosis, Mycobacterium paratuberculosis, Mycoplasmas, P mirabilis, Streptococcus, Staphylococcus, Ureaplasmas, and T. foetus.ⁱ'^¹ In bulls, the most frequent microorganism isolated is T. pyogenes.

Vesicular adenitis may affect bulls of all ages but is most common in young, growing bulls fed high-energy rations and housed together.¹ The prevalence may reach 20% to 30% in small groups of yearling bulls in close confinement.¹⁹ The role of viral pathogens in outbreaks of the disease is not defined. Infec­tions may arise by either ascending or descending routes from other areas of the urogenital tract, or hematogenously. Some bulls with vesicular adenitis submitted to necropsy presented anatomic defects at the level of the seminal colliculus, which could impair its normal opening and closing.¹⁹ In addition, it has been suggested that spermatozoa or urine reflux into the vesicular glands could produce inflammation.²⁰ Frequent homosexual activity among young bulls, high nutrition, and fast growth rates may be involved in spread of the infection.¹

■ Clinical Signs and Differentials The seminal vesicles of affected stallions may be of normal size or enlarged and painful when palpated per rectum.^2,3 Stallions may refuse to cover or may be unable to ejaculate.²¹ Semen contains numerous neutrophils and blood. Fertility of infected semen is reduced. Bacterial pathogens are readily recovered from semen of affected stallions, but special culturing methods may be needed (described below).

Bulls affected with vesicular adenitis may be asymptomatic or exhibit nonspecific clinical signs other than deterioration of semen quality. In severe cases, pelvic inflammation and peritonitis result in pain reflected by reluctance to move, stiff gait, tense abdomen, difficulty on defecation, and refusal to mate. In acute vesicular adenitis the palpation per rectum of the vesicular glands produces pain, and the examination is positive for an enlarged gland with loss of its lobulation and increased consistency. Other reproductive organs, particularly the ampullae, testes, and epididymides, may be inflamed.¹ Necropsy specimens of bulls with vesicular adenitis have shown concomitant inflammation of the prostate and bulbourethral glands (seminal vesicular syndrome)^1,22; however, these changes cannot be detected by palpation per rectum. The vesicular glands may not be significantly increased in size during the acute phase. If inflammation becomes chronic, the glands usually enlarge, eventually losing their lobularity and becoming fibrotic. Abscesses are often caused by T. pyogenes and may rupture into the rectum or urinary bladder. Transrectal ultrasonography can be used to determine the degree and extension of the lesion in the vesicular glands.^23,24

Purulent exudate is present in the ejaculate, sometimes as thick clots. Neutrophils may become less evident in semen as the condition becomes chronic. The ejaculate volume could be reduced. Presence of floccules or flakes in the ejaculate can be observed, and color can vary from normal to yellow-brown. Poor sperm motility, increased morphologic defects, and an elevated pH are characteristics of semen from bulls with vesicular adenitis.

Fertility of mildly affected bulls may remain satisfactory. More extensive involvement in which semen quality is markedly affected results in subfertility or infertility.¹⁸ Semen from bulls with vesicular adenitis freezes poorly, and antibiotics used in extenders usually do not control the high numbers of bacteria present.^18,25,26

■ Clinical Pathology Bacterial pathogens can be recovered from the semen of affected stallions. However, without other evidence of infection of the accessory sex glands, recovery of pathogens from the semen should be interpreted with caution because the bacteria could originate from another location. Repeated samples for culture should be obtained from the sheath, penis, fossa glandis, preejaculatory fluid, urethra (before and after ejaculation), and seminal vesicle effluent manually expressed through a sterile urethral catheter positioned at the colliculus seminalis. Prostatic fluids can be collected through a catheter by massage per rectum. The first jet of a fractionated ejaculate includes the secretions of the ampullae. Alternatively, a suitable fiberoptic endoscope can be passed in the urethra to the level of the seminal colliculus and into the seminal vesicles. Purulent material may then be aspirated for culture.

Vesicular secretions from bulls can be collected either by using a sterile artificial vagina⁹ or by extending and disinfecting the penis followed by irrigation of the distal urethra with sterile saline. A sterile catheter is then passed 30 cm into the urethra, and the accessory sex glands are massaged to stimulate their secretion. Fluid is collected in sterile containers. Recently, a new aseptic technique of semen collection as an alternative of both previous methods was developed. The procedure consists of clipping the preputial hairs, urination, antisepsis of the preputial area, flushing the preputial cavity with antiseptic solution, per rectum massage of accessory sexual glands, and semen collection by electroejaculation. Preliminary studies in healthy bulls using this method showed low contamination of semen samples.²⁷

■ Treatment and Prognosis Accessory sex gland infec­tions are treated with antibiotics selected by culture and in vitro sensitivity. Antibiotics are administered for 2 to 4 weeks, but treatment failures may occur. Properties of antimicrobials suitable for parenteral treatment of accessory sex gland infections include high lipid solubility, a favorable pKa (higher than the pH of the target tissue or fluid), and low or limited protein binding. The antimicrobial should have a pH that is basic relative to the accessory gland fluid into which penetration is desired.²⁸ Vesicular and prostatic fluids have a pH of 7.3 to 7.5. Antimicrobials that may prove suitable for treatment include the newer macrolides, which are fat soluble and have a high pKa. Because of its antimicrobial spectrum and tissue diffusion characteristics, enrofloxacin has been found to be effective for systemic treatment of some cases of seminal vesiculitis in stallions. Treatment of stallions by lavage and instillation of antimicrobials directly into the seminal vesicles via a flexible videoendoscope can be accomplished by skilled operators. Removal of the affected gland has been performed in stallions and bulls.^2,25,29,30 A technique used with fair success in stallions with localized vesicular adenitis is repeated irrigation through a catheter guided into the vesicles by endoscopy. Antibiotics are instilled into the vesicular gland lumen after each irrigation. In bulls, some experts recommend antibiotic treatment, either oral or parenteral, for a minimum of 10 days.^31,32 In bulls, direct injection of different medications into the vesicular glands has been reported, but results are mixed.^32-35 In young bulls with vesicular adenitis, parenteral administration of antibiotics was no different than in the “no-treatment” group,³³ which is in agreement with previous reports describing spontaneous recovery.^18,35 Additional measures to treat inflammation include performing repetitive semen collections, not only for monitoring the ejaculate but to evacuate the inflammatory secretions from the seminal glands as well.¹⁸ Massage of the seminal glands per rectum has also been proposed. The inclusion of nonsteroidal antiinflammatory drugs to reduce inflammation, pain, and fibrosis has also been suggested.¹⁸

Seminal vesiculectomy could be used as an alternative after lack of response to medical treatment. Different techniques have been applied with variable results and complications.^29,30,36 If the bull recovers from surgery, it can exhibit a decrease in seminal parameters such as motility, volume, sperm output, and seminal constituents, which could adversely affect the freezability of the semen.

The prognosis of vesicular adenitis is difficult to determine due to the multiple etiologic organisms. Therefore the prognosis for correction of vesicular adenitis is only fair to poor. Mild cases may recover spontaneously in 2 to 3 months. In chronic cases, glands that do not abscess become fibrotic and destroyed even though purulent material does not persist in the ejaculate. In stallions with vesicular adenitis, immediate filtration of the ejaculate in order to remove cellular debris and mixing of semen in an appropriate antibiotic-containing extender to control bacterial growth may maintain sperm motility and fertility.²¹

Blockage of the Efferent Ducts (Sperm Stasis)

Blockage of the efferent ducts between the testes and penile urethra sometimes occurs in stallions. If the condition is bilateral, azospermia results despite apparent ejaculation. The ampullae are frequently tense, and enlargement may be demonstrated by ultrasonography.¹ Massage of the ampullae per rectum followed by frequent intervals for semen collection may result in ejaculation of a semen sample with a high

concentration of spermatozoa, often present as “strings” or “plugs.” Large numbers of detached sperm heads, often in clumps, are commonly observed. Collection of semen on a regular schedule may aid in preventing recurrence once the blockage is relieved. Some refractory cases have responded to administration of oxytocin or cloprostenol prior to attempt at breeding or semen collection. Empiric treatment by blockade of β-receptors and stimulation of α-receptors has been successful in some stallions that fail to ejaculate.²

Sperm granulomas caused by accumulation of spermatozoa in blind efferent ducts are a common cause of infertility in the buck and ram. Granulomas have also been identified in stallions.³