Infectious and Noninfectious Causes of Infertility in Boars

CHAPTER 95 Infectious and Noninfectious Causes of Infertility in Boars

As in other livestock species, breeding soundness evaluations (BSEs) have value in identifying potentially subfertile or infertile boars. Unfortunately, BSEs have been and still are rarely performed on boars used in natural mating programs. With the recent exponential growth in the use of artificial insemination (AI) in the global swine industry, a more developed approach has evolved in evaluating the reproductive potential of an AI stud boar. Boars standing at an AI stud operation are routinely screened for selected pathogens that can reduce reproductive performance. Additionally, a large percentage of stud operations that collect and process semen from boars for AI routinely evaluate the motility, morphology, concentration, and volume of each ejaculate. The more recent incorporation of such screening protocols into swine breeding programs has greatly aided the industry in reducing the untoward effects of boar infertility or subfertility on herd reproductive performance.

Boar infertility is manifested in a herd as an elevated rate of normal returns to estrus, decreased litter size, increased litter scatter, or insufficient number of mated females per unit time. In retrospect, diagnosis of individual boar infertility is difficult to obtain because of the many confounding variables and management practices that can also influence herd reproduction. Accordingly, it is important that veterinarians and their producer clients take a proactive role in boar and ejaculate selection. One of the strengths of an AI program is the opportunity it provides to continuously monitor the boar’s contribution to herd reproductive performance.


Many of the pathogens that can cause boar infertility also have been found to use semen as a vector in their transmission. Infectious pathogens induce boar infertility through several general pathways. Certain infectious pathogens (e.g., Brucella, Chlamydia, Japanese B encephalitis virus [JEV], rubulavirus) can localize within the testicular parenchyma, with the ensuing inflammatory response disrupting spermatogenesis. Other infectious pathogens (e.g., swine influenza virus [SIV], Mycoplasma, the agent of erysipelas) indirectly disrupt spermatogenesis through the febrile response (with temperatures of greater than 40° F) associated with systemic illness. Finally, select infectious pathogens (e.g., the agent of classical swine fever, Leptospira, pseudorabies virus, parvovirus, porcine reproductive and respiratory syndrome [PRRS] virus) are shed in the semen of infected boars, causing disease in the female bred with the infected semen.

Owing to the devastating nature of infectious pathogens on herd reproductive performance, boar stud operations are constructed as independent facilities that preferably are sited away from any other livestock facility. Stringent biosecurity programs are followed to curtail the potential introduction of pathogens into the enclosed facility. Replacement boars, originating from selected pathogen-free herds, frequently undergo a 45-day (or longer) quarantine period. During quarantine, periodic serologic testing along with daily observation for clinical signs of disease is performed to minimize the introduction of disease to the resident stud group. If an animal exhibits clinical signs or has a positive test result for an unwanted disease, it is not uncommon for the farm to reject the entire group of replacement animals. Boar stud operations shoulder a great responsibility to maintain a disease-free herd so that economically devastating pathogens do not originate from them.

To elucidate the impact of infectious disease on boar stud productivity, a survey was conducted by Althouse in 2000 that encompassed 35 U.S. stud operations that stood 11,927 boars. A total of 25.7% (9 out of 35) of studs surveyed experienced a disease outbreak in the resident stud during 1999. Diagnosed causes included swine influenza [h1n1 or h3n2, or both—in most cases the specific type was not reported] (n = 6), PRRS (n = 2), mycoplasmosis (n = 1), salmonellosis (n = 1), and erysipelas (n = 1). In a typical disease outbreak, clinical signs were first observed approximately 4.6 days after the introduction of replacement boars into the resident stud group (n = 6 studs). Clinical signs usually were expressed by 26.7% of the boars standing at stud, with 89.2% fully recovering from any one incident. A negative effect on stud productivity (e.g., decreased semen quality) was observed an average of 32.4 days after onset of clinical signs.


Porcine brucellosis is an infectious disease that can lead to swine infertility. Regulatory programs have been in place for several decades, effectively eliminating this disease from U.S. commercial herds. Feral hogs are considered a reservoir for this disease. Porcine brucellosis is still prevalent and is considered a major cause of reproductive failure in swine of other countries (e.g., Africa, Asia, South America). In boars, Brucella suis (biovars 1, 2, and 3) initially invades regional lymph nodes, with ensuing bacteremia. This bacteremia leads to localization of B. suis in the genital organs, particularly those containing high levels of erythritol (e.g., the testis). A persistent orchitis or accessory sex gland infection ensues. B. suis is shed in the semen of infected boars, resulting in abortion and infertility storms. Diagnosis is by serologic testing. Depopulation of infected swine herds is recommended.

Leptospirosis is a common bacterial disease of swine that can cause reproductive loss. Multiple serovars of Leptospira interrogans (pomona, canicola, icterohemorrhagiae, grippotyphosa, muenchen, hardjo [sejroe], bratislava, tarassovi, australis) have been found to be involved in causing swine leptospirosis, with each serovar having a potentially different epidemiology. In boars, oftentimes leptospirosis infection is inapparent. Carrier animals or bulls with infected semen are responsible for disease spread. Screening or diagnosis of the disease in boars is by serologic testing. Effective commercial bacterins are available to prevent infection with this disease. These bacterins commonly are administered to all breeding stock according to label instructions. Antibiotics (e.g., tetracyclines, dihydrostreptomycin) can be administered to boars to reduce shedding of leptospires but may not eliminate the carrier state of the disease.

Chlamydial infections in boars have been associated with orchitis, epididymitis, urethritis, and reproductive disturbances. Weakness in newborn piglets and stillbirth can result from venereal transmission of Chlamydia organisms. The prevalence of chlamydial infections in swine herds is unknown, but serologic studies suggest that most herd infections are clinically inapparent. Diagnosis of chlamydial infections in swine herds as a cause of reproductive loss is uncommon.

Numerous viruses can affect boar fertility and may use semen as a transmission vector. Important pathogenic organisms in the global swine industry include pseudorabies virus (PRV), porcine parvovirus (PPV), and porcine reproductive and respiratory virus (PRRSV). Other viral pathogens of regional concern are hog cholera/classical swine fever virus, porcine rubulavirus, and JEV.

Pseudorabies, also known as Aujeszky’s disease, is an important disease of swine worldwide. The disease, caused by a herpesvirus, is spread by contact, by aerosol transmission, transplacentally, or through excretion in the semen. Viral replication occurs in the genital tract. Semen quality in recently infected boars may be reduced indirectly because of fever. As with disease due to other herpesviruses, PRV infection can become latent, with recrudescence of the virus when the animal is under stress. Affected herds may be asymptomatic but often suffer reproductive failure, high neonatal mortality rates, and suboptimal growth performance. Commercially available vaccines control losses due to the clinical disease but do not prevent spread of the virus. Serologic screening of boar and biosecurity are essential to prevent PRV entrance into a swine herd. Economic losses were so great in the US that a national eradication program was justified. This current program involves test and removal, herd depopulation, or offspring segregation within infected herds.

PPV is a highly stable virus that is ubiquitous among swine throughout the world. Before preventive medicine programs, PPV was one of the most common causes of infectious abortion in swine. The most common routes of infection are oronasal and venereal. Naturally infected boars generally fail to show any clinical signs associated with infection but nevertheless can shed the PPV in semen. Embryonic and fetal death (including mummies and stillbirths) are common clinical signs observed in naive animals infected with PPV. Other clinical signs may include elevated rates of normal and delayed returns to service and abortion. Proper acclimatization of replacement animals, through vaccination and cull animal exposure, before introduction to the resident herd, has been quite successful in controlling this disease.

PRRSV, an arterivirus, has come to the forefront as one of the top etiologic agents of reproductive failure in swine today. Direct pig-to-pig contact seems to be a major route of PRRSV disease transmission, with infection also being able to occur by aerosol and through semen. Clinically infected herds experience reduced conception and farrowing rates, elevated neonatal mortality rates, and chronic respiratory disease with poor performance in growing swine. Symptomatic therapy appears to be only palliative. Vaccination appears to offer some control over the disease. In the absence of other significant endemic diseases, boars recently infected with PRRSV exhibit few clinical signs beyond those associated with a mild pyrexia. In the presence of endemic disease, PRRSV-infected boars generally exhibit pronounced clinical signs associated with the endemic disease, with disturbances in semen quality associated with the pyrexia. Excretion of PRRSV through semen appears to occur most frequently during the acute phases of the disease. Duration of excretion in semen appears to vary, with reported cases of prolonged or intermittent excretion well beyond 1 month after infection. Carrier states are believed to occur in some animals. Diagnosis of PRRSV disease in boars is based on serologic testing and screening of semen by polymerase chain reaction (PCR) assay.

The industry still struggles to define a program that provides effective control of PRRSV disease. Because of the inherent difficulties associated with endemic PRRSV infection, most boar stud operations typically strive to achieve a PRRSV-negative or -naive status. Many such operations apply a rigorous serologic and semen testing program during quarantine to minimize the chances of introducing PRRSV into the resident boar group. Accidental introduction of PRRSV into a boar stud group generally leads to its complete depopulation, followed by repopulation with naive animals. Boar vaccination with modified live virus attenuates may lead to shedding of the modified live virus in the semen; use of this semen may lead to seroconversion in the recipient animals, confounding future disease control strategies for the herd.

Hog cholera—classical swine fever—is a highly contagious, reportable disease of swine. Significant economic losses to the swine industry led to institution of a national program that resulted in its eradication in the United States in 1976. Pigs appear to be the only natural host for the virus. Hog cholera virus, a pestivirus, is excreted with oronasal and lacrimal secretions and in urine, semen, and feces. Owing to the hardiness of the virus, mechanical vectors and garbage that contains pork products also appear to contribute to the spread of the disease. Acute infection induces a variety of clinical signs, usually leading to the death of the animal 10 to 20 days later. A 2000 report from Bouma and associates has demonstrated the regional spread of hog cholera through extended semen processed from recently infected hog cholera virus–infected boars. This possibility demonstrates the necessity for prudent quarantine and diagnosis for studs exhibiting clinical signs associated with infectious disease.

Porcine rubulavirus, a paramyxovirus, is the agent of blue eye disease, found in Central America, which can cause infertility in boars and sows. Central nervous system signs, corneal opacity, and high piglet mortality rates also can be observed in infected herds. Infected boars may show severe epididymo-orchitis and reduced semen quality, leading to temporary or permanent infertility. Diagnosis is based on clinical signs or with serologic testing, or both. Seropositive breeding stock should be culled.

Japanese B encephalitis is a mosquito-borne viral disease of swine that causes reproductive failure in several Asian countries. Summer infertility in boars appears to be associated with JEV, a togavirus. Experimental infections resulted in edematous and congested testes, epididymitis, reduced libido, and reduced semen quality. Infection can lead to temporary or permanent infertility. The virus can be shed in semen of infected boars, suggesting that semen can be a vector of disease transmission. Diagnosis of JEV disease in boars is through clinical signs or serologic testing, or both. Seropositive boars should be culled. Live attenuated vaccines have been used successfully to prevent infection in endemic areas.

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Sep 3, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Infectious and Noninfectious Causes of Infertility in Boars

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