Abortion in Pigs

In pigs, high ambient temperature (> 32°C [> 89.6°F]) is associated with increased returns to estrus, increased embryonic mortality rates, decreased farrowing rates, and small litters. The effect is greatest if heat stress occurs at the time of breeding or implantation.

Increased embryonic mortality rates and increased irregular return to estrus occur in pigs bred during the summer. High ambient temperature can contribute to seasonal reproductive failure; however, seasonal changes in ovarian function and progesterone secretion have also been implicated in the increased rates of embryonic mortality and pregnancy loss during late summer and autumn (1).

The estrogenic mycotoxin zearalenone interferes with conception and implantation in pigs, causing infertility, embryonic death, and decreased litter size but rarely, if ever, abortion. Other mycotoxins, the fumonisins, cause acute pulmonary edema in swine; sows that recover from the acute disease often abort 2–3 days later.

Other toxic causes of pig 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 toxicosis due to faulty propane heaters has been associated with increased numbers of pig stillbirths and autolyzed full-term pig 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.

Infection with the bacterium Brucella suis in commercial swine has become rare in the US as a result of state and federal control programs. In multiple states, however, B suis is present in feral pigs, which are a source of infection for commercial pigs and humans. The route of infection is oral in most cases, but venereal transmission is not uncommon. Brucellosis is one of the few venereal diseases recognized in swine.

Sows infected with B suis 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, but some fetuses are autolyzed.

Diagnosis: Diagnosis of brucellosis is based on serological testing and isolation of B suis from the placenta and fetal tissues.

Treatment and control:No treatment of brucellosis has been uniformly effective. Control is based on test-and-cull.

B suis causes a serious zoonotic disease.

Classical swine fever is caused by a pestivirus that has been eradicated from the US but is still 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, mummified or stillborn piglets are more common.

Diagnosis: Diagnosis of classical swine fever is based on fluorescent antibody staining, virus isolation, and PCR assay.

Control: Both killed and modified live vaccines against classical swine fever are available; however, their use in the US is prohibited.

Japanese B encephalitis is an arthropod-borne zoonotic viral disease that causes reproductive failure in pigs. The disease is reported primarily in Southeast Asia, the Indian subcontinent, Indonesia, and Australasia.

Litters infected with Japanese encephalitis virus 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.

Diagnosis: Diagnosis of Japanese B encephalitis is confirmed by virus isolation and immunohistochemistry. Viral nucleic acid can be detected in tissue and blood samples via RT-PCR or nested RT-PCR assays.

Control: Pigs are the primary amplifying host for the Japanese encephalitis virus and are vaccinated not only to prevent reproductive failure but also to prevent infection in humans.

Japanese B encephalitis virus is zoonotic and causes and encephalitis in humans.

The bacterium Leptospira interrogans (especially serovar Pomona) is a major cause of reproductive failure in swine (infertility, abortion, stillbirths, and the birth of weak piglets). Although acute leptospirosis occurs in adult swine, most cases are subclinical.

Pigs infected with L interrogans serovars Pomona and Bratislava can become chronic renal carriers. Abortion occurs 1–4 weeks after infection, so the aborted fetuses are autolyzed. Mummification, maceration, stillbirths, and weak pigs also occur.

Diagnosis: Diagnosis of leptospirosis is based on the demonstration of leptospires in fetal tissues or fetal gastric contents. However, severely autolyzed fetuses might yield poor fluorescent antibody and immunohistochemistry results. PCR testing has better sensitivity and specificity.

Prevention and treatment: Vaccination with a multivalent Leptospira bacterin is an important component of prevention of leptospirosis in pigs. Revaccination should follow the manufacturer's recommendations; some products use 6-month intervals.

Historically, streptomycin or dihydrostreptomycin was used to treat leptospirosis and decrease or eliminate renal carrier states and urinary shedding; dihydrostreptomycin has an FDA-approved indication for the treatment of leptospirosis caused by L interrogans serovars Pomona and Grippotyphosa in swine.

Current control programs should combine vaccination with biosecurity measures, rodent control, provision of clean water, and prevention of exposure to contaminated urine and wildlife.

Experimentally, high levels of injectable oxytetracycline, tylosin, and erythromycin and high levels of tetracyclines in feed have eliminated the carrier state in pigs. However, field results indicate that Leptospira infection cannot be reliably eliminated with antimicrobials.

Leptospirosis in pigs is zoonotic.

Porcine circovirus type 2 (PCV2) is found 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 serosanguineous 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 reproductive failure due to PCV2 is very low; when it occurs, the problem soon disappears, perhaps because most pigs are naturally exposed and immune before being bred.

Diagnosis: Diagnosis of porcine circovirus infection is based on the presence of PCV2 DNA or antigen in precolostral serum samples from live-born piglets. Immunohistochemistry and in situ hybridization are considered the gold standard for detecting the agent.

Prevention:Vaccines against porcine circovirus are available for growing and finishing pigs; however, their efficacy in preventing reproductive failure is unknown.

Porcine parvovirus is ubiquitous in pigs in the US 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. Gilts that are immunologically naive or have high passive antibody titers have the highest risk of reproductive disorders caused by the virus.

Infection with porcine parvovirus before day 30 of pregnancy results in early embryonic loss. Fetal infection between 30 and 70 days of gestation can result in death of the fetus and sometimes mummification. Not all fetuses are infected at the same time, and death at different stages of pregnancy is typical.

Some fetuses infected with porcine parvovirus survive and are born alive but become persistently infected piglets. Most fetuses infected after 70 days of gestation mount an immune response, clear the virus, and become healthy piglets 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 infection.

Diagnosis: Diagnosis of porcine parvovirus infection is based on fluorescent antibody testing, virus isolation using lung tissue from mummified fetuses, or demonstration of precolostral antibody in stillborn pigs.

Prevention: Effective inactivated vaccines against porcine parvovirus are available. Boars shed virus by varying routes, including semen, for a couple of weeks after acute infection and can introduce the virus into a herd; biosecurity measures or semen testing are good preventive strategies.

Porcine reproductive and respiratory syndrome (PRRS) is caused by an arterivirus. It is of major importance in the US and throughout most of the world. Most PRRS strains do not cross the placenta until after 90 days of gestation. Consequently, most PRRS-caused abortions occur near the end of gestation.

Litters affected by PRRS contain fresh and autolyzed dead pigs, weak infected pigs, and healthy, uninfected pigs that often develop respiratory disease within a few days after birth. The sows often show anorexia and fever a few days before aborting. Concurrent respiratory disease and increased numbers of bacterial infections in the herd are common.

Diagnosis: Hemorrhage in the umbilical cord, when present, is the only gross lesion associated with PRRS-caused abortions. Not all fetuses are infected, so multiple fetuses should be sampled for diagnosis. 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 taken from three to five fetuses is the most reliable means of diagnosis.

Prevention: Herd management is important for controlling and preventing PRRS. Inactivated and modified live virus vaccines are available.

In April 2025, the FDA approved gene-edited PRRS-resistant pigs generated by CRISPR-Cas9 technology. These pigs have a modified CD163 gene that makes them resistant to PRRS infection. Full commercialization is underway.

Pseudorabies is a cause of CNS and respiratory diseases in pigs. Infection results in latency, and seropositive animals are considered infected. Infection early in pregnancy can result in embryonic death and resorption of fetuses. Infection later in pregnancy can result in abortion and birth of stillborn and weak pigs. Mummification can occur but is uncommon.

Most pigs aborted as a result of pseudorabies have no gross lesions; occasionally, there are pinpoint white foci of necrosis in the liver and tonsils.

Diagnosis: Diagnosis of pseudorabies in pigs is based on virus isolation, PCR assay, or fluorescent antibody staining.

Prevention: Effective gene-deleted vaccines that enable serological differentiation of vaccinated and naturally infected pigs were developed for the US pseudorabies eradication program. After eradication from commercial pigs was completed in 2003, however, vaccination was discontinued.

Feral pigs in multiple US states remain an important reservoir of pseudorabies virus and a continuing source of infection for domestic pigs. Sporadic PRV infections occur primarily in outdoor or noncommercial herds with exposure to feral pigs. Infected herds are subject to regulatory control, which can include whole herd depopulation, cleaning and disinfection, and epidemiological surveillance (2, 3, 4).

Sows with foot-and-mouth disease, African swine fever, or influenza often abort; however, they and their herdmates also have clinical signs of those diseases.

Enteroviruses and encephalomyocarditis virus have been reported to cause fetal losses in pigs; however, they are not considered economically important.

Blue eye paramyxovirus is an important cause of abortion, stillbirths, and mummified pig fetuses in parts of Mexico.

Bacteria that cause sporadic abortions in pigs include the following:

• Erysipelothrix rhusiopathiae

• Escherichia coli

• Listeria monocytogenes

• Pasteurella multocida

• Salmonella spp

• Staphylococcus aureus

• Streptococcus spp

• Trueperella pyogenes

• Maes D, Peltoniemi O, Malik M. Abortion and fetal death in sows. Reprod Domest Anim. 2023;58(suppl 2):125-136.

1. Wrathall AE, Wells DE, Jones PC, Foulkes JA. Seasonal variations in serum progesterone levels in pregnant sows. Vet Rec. 1986;118(25):685-687. doi:10.1136/vr.118.25.685

2. Animal and Plant Health Inspection Service, USDA. Pseudorabies. Last modified June 17, 2026. Accessed August 16, 2026. https://www.aphis.usda.gov/livestock-poultry-disease/swine/pseudorabies

3. Animal and Plant Health Inspection Service, USDA. NVAP reference guide: pseudorabies (control and eradication). Last modified January 13, 2026. Accessed August 16, 2026. https://www.aphis.usda.gov/nvap/reference-guide/control-eradication/prv

4. Zanella E, Lager K, Kehrli M Jr, Miller L, Swenson S, Bigelow T. Pathogenesis and transmission of feral swine pseudorabies virus isolates in domestic pigs. https://www.ars.usda.gov/research/publications/publication/?seqNo115=258172