Also see Pigs.
Many agents that cause reproductive failure in sows produce a broad spectrum of sequelae, including abortions and weak neonates, as well as stillbirth, mummification, embryonic death, and infertility. Mummification is seen more frequently in swine than in many other species due to the large litter size. If only a few fetuses die, abortion rarely occurs; instead, mummies are delivered at term, along with live piglets or stillbirths.
High ambient temperature (>32°C) is associated with increased returns to estrus, increased embryonic mortality, decreased farrowing rates, and small litters. The effect is greatest if heat stress occurs at the time of breeding or implantation. Increased embryonic mortality and increased irregular return to estrus are seen in pigs bred during the summer. High ambient temperature may play a role, but there is evidence that seasonal low progesterone levels are a major factor.
The estrogenic mycotoxins zearalenone and zearalenol interfere with conception and implantation causing infertility, embryonic death, and reduced litter size, but rarely, if ever, abortion. Another class of mycotoxins, the fumonisins, causes acute pulmonary edema in swine; sows that recover from the acute disease often abort 2–3 days later.
Other toxic causes of abortions or stillborn pigs include cresol sprays (used for mange and louse control), dicumarol, and nitrates. Nutritional causes of reproductive failure are not well defined. Vitamin A deficiency can cause congenital anomalies and possibly abortions. Riboflavin deficiency can cause early premature births (14–16 days), and calcium, iron, manganese, and iodine deficiencies have been associated with stillbirths and weak pigs.
Carbon monoxide toxicity due to faulty propane heaters has been associated with increased numbers of stillbirths and autolyzed full-term fetuses. Fetal tissues are cherry red; the sows do not appear affected.
The major infectious causes of reproductive failure in pigs include porcine reproductive and respiratory syndrome virus, porcine parvovirus, pseudorabies virus, Japanese B encephalitis virus, classical swine fever virus, Leptospira spp, and Brucella suis.
Porcine Reproductive and Respiratory Syndrome (PRRS)
PRRS is caused by an arterivirus. It is the most important disease of pigs in the USA and is of major importance throughout most of the world. Most PRRS strains do not cross the placenta until after 90 days of gestation. Consequently, most abortions are near the end of gestation. Affected litters contain fresh and autolyzed dead pigs, weak infected pigs, and healthy, uninfected pigs that often develop respiratory disease within a few days of birth. The sows are often anorectic and feverish a few days before aborting. Concurrent respiratory disease and increased numbers of bacterial infections in the herd are common. Hemorrhage in the umbilical cord, when present, is the only gross lesion associated with PRRS abortions. Not all fetuses are infected, so multiple fetuses should be sampled. Viral antigen is most consistently present in the fetal thymus and in fluid collected from the fetal thoracic cavity. PCR testing of pooled thoracic fluid from 3–5 fetuses is the most reliable means of diagnosis. Herd management is important in control and prevention. Inactivated and modified live virus vaccines are available. (See also Porcine Reproductive and Respiratory Syndrome.)
Porcine parvovirus is ubiquitous in pigs in the USA and most of the world. Almost all females are naturally infected before their second pregnancy, and immunity is lifelong. Consequently, it is a disease of first parity pigs. Fetal infection before 70 days of gestation can result in death of the fetus. Not all fetuses are infected at the same time, and death at different stages of pregnancy is typical. Some fetuses survive and are born alive but persistently infected. Most fetuses infected after 70 days of gestation mount an immune response, clear the virus, and are healthy at birth. Litters with dead fetuses of varying sizes, including mummified fetuses, along with stillborn and healthy pigs born to first parity gilts are the hallmark of porcine parvovirus. Diagnosis is by fluorescent antibody testing, virus isolation using lung from mummified fetuses, or demonstration of precolostral antibody in stillborn pigs. Boars shed virus by varying routes, including semen, for a couple of weeks after acute infection and can introduce the virus into a herd. Effective inactivated vaccines are available.
Pseudorabies (Aujeszky's Disease, Porcine Herpesvirus 1 Infection)
Pseudorabies is a cause of CNS and respiratory diseases. Infection results in latency, and seropositive animals are considered infected. Infection early in pregnancy can result in embryonic death and resorption of the fetuses. Infection later in pregnancy can result in abortion and birth of stillborn and weak pigs. Mummification can occur but is uncommon. There are no gross lesions in most aborted pigs, but a few have pinpoint white foci of necrosis in the liver and tonsils. Diagnosis is by virus isolation, PCR, or fluorescent antibody staining. Effective gene-deleted vaccines that allow serologic differentiation of vaccinated and naturally infected pigs were developed for the eradication program in the USA, but after eradication from commercial pigs was completed in 2003, vaccination was discontinued. Feral pigs in multiple states harbor the virus, and since 2003 there have been sporadic outbreaks of pseudorabies in herds that have contact with feral pigs. These outbreaks are currently controlled by herd depopulation. (See also Pseudorabies.)
Japanese B Encephalitis Virus Infection
Japanese B encephalitis is an arthropod-borne disease that causes reproductive failure in pigs and encephalitis in humans. Infected litters can contain dead pigs of various sizes (including mummies), stillborn pigs, weak pigs, and pigs with CNS signs. Hydrocephalus and subcutaneous edema are the most common gross lesions. Pigs are the primary amplifying host for the virus and are vaccinated not only to prevent reproductive failure, but also to prevent human infection.
Classical Swine Fever (Hog Cholera)
Classical swine fever is caused by a pestivirus that has been eradicated from the USA but is a serious problem throughout much of the world. With highly virulent strains that cause serious maternal illness, abortion is common. With strains of moderate or low virulence, birth of mummified and stillborn pigs, weak pigs, and persistently infected pigs are more common. Fluorescent antibody staining, virus isolation, and PCR are used for diagnosis. Both killed and modified live vaccines are available, but their use in the USA is prohibited. (See also Classical Swine Fever.)
Porcine Circovirus Infection
Porcine circovirus type 2 (PCV2) occurs worldwide, is ubiquitous in pigs, and is associated with several conditions, including sporadic outbreaks of late-term abortions and term litters with increased numbers of dead piglets. The dead piglets vary from small, mummified fetuses to stillbirths. Nonmummified fetuses typically have a large amount of serosanguinous fluid in their body cavities. Microscopically, there is myocardial necrosis and/or fibrosis, and PCV2 is present in the heart and other tissues. The incidence of PCV2 reproductive failure is very low; when it occurs the problem soon disappears, perhaps because most pigs are naturally exposed and immune prior to being bred. Vaccines are available for grower and finisher pigs, but their efficacy in preventing reproductive failure is unknown.
Leptospira interrogans (especially serovar Pomona) is a major cause of reproductive failure in swine. Although acute leptospirosis occurs in adult swine, most cases are asymptomatic. Pigs infected with serovars Pomona and Bratislava can become chronic renal carriers. Abortion occurs 1–4 wk after infection, so the abortuses are autolyzed. Mummification, maceration, stillbirths, and weak pigs are also seen. Diagnosis is based on demonstration of leptospires in fetal tissues or stomach contents. Vaccination with a multivalent bacterin every 6 mo helps prevent the disease. Streptomycin was formerly used to eliminate the carrier state and to treat pregnant sows during an outbreak, but it is no longer available for use in food animals. Experimentally, high levels of injectable oxytetracycline, tylosin, and erythromycin and high levels of tetracyclines in the feed have eliminated the carrier state. However, field results indicate that Leptospira infection cannot be reliably eliminated with antibiotics. Leptospirosis is zoonotic. (See also Leptospirosis.)
Brucellosis (Brucella suis infection) in commercial swine has become rare in the USA as a result of state and federal control programs. However, it is present in feral pigs in multiple states; these represent a source of infection for commercial pigs and humans. Infected sows can abort at any stage of gestation, and abortions are not always accompanied by illness. Abortion is probably due to endometritis and fetal infection. There are few fetal or placental lesions, although some fetuses may be autolyzed. Diagnosis is by serology and isolation from the placenta and fetal tissues. No treatment has been uniformly effective. Control is based on test and slaughter. Brucellosis is one of the few venereal diseases recognized in swine. B suis causes a serious zoonotic disease. (See also Brucellosis in Large Animals.)
Other Infectious Causes of Abortion
Pigs with foot-and-mouth disease (see Foot-and-Mouth Disease), African swine fever (see African Swine Fever), and swine influenza (see Swine Influenza) often abort, but they and their herdmates also have clinical signs of those diseases. Enteroviruses and encephalomyocarditis virus have been reported to cause fetal losses in pigs, but they are not considered economically important. Blue eye paramyxovirus is an important cause of abortion, stillbirths, and mummified fetuses in parts of Mexico. Bacteria that cause sporadic abortions include Staphylococcus aureus, Streptococcus spp, Erysipelothrix rhusiopathiae, Salmonella spp, Pasteurella multocida, Arcanobacterium pyogenes, Listeria monocytogenes, and Escherichia coli.
Last full review/revision July 2011 by Jerome C. Nietfield, DVM, PhD, DACVP