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Porcine Encephalomyocarditis

Dr Kristi Arnot, District Veterinarian Hunter Local Land Service and Hunter McDougall Monk, final year Veterinary Science Student Charles Sturt University

Posted Flock & Herd May 2021


Encephalomyocarditis (EMC) is a viral disease affecting pigs as well as a wide variety of zoological mammals, caused by a Cardiovirus in the family Picornaviridae. The disease is closely associated with rodents with outbreaks commonly linked to an increased rodent population or poor biosecurity measures. Affected piglets usually present with sudden death due to cardiac insufficiency and secondary cardiogenic pulmonary oedema. Animals may occasionally present with other clinical signs including pyrexia, dyspnoea, depression, anorexia and paresis. In sows, infection may cause abortions. Suckling pigs are generally more susceptible than their mature counterparts. There is no specific treatment for EMC and therefore symptomatic treatment and preventative measures are recommended.

Case report


In February 2021 the District Veterinarian spoke to a pig producer in relation to a number of cases of sudden death in their piglet population. The farmer reported that 17 piglets had died in the previous twenty-four hours with seven additional piglets found dead that morning. All piglets were six weeks of age and in the same batch. There were 100 at-risk piglets of this age on the farm. The producer runs a large free-range farming operation that had recently experienced high rainfall. The piglets were still on the sows and a week off weaning. The sows were up to date with vaccinations. The pigs were fed a commercial feed supplemented with vegan cakes from a bakery. The piglets were not vaccinated for erysipelas. Piglets were reported to become dull and isolate in a corner. These clinical signs were followed by violent seizures approximately 20 minutes later, resulting in death. The owner also reported that the piglets’ skin turned purple as they died.

Clinical examination/necropsy

Necropsy of two of the recently deceased piglets, one male and one female, was undertaken. Both animals were in good body condition with no external abnormalities visible. Upon opening the thoracic cavity mild congestion of the lungs was noted, although this finding could be a post-mortem change. The heart appeared grossly normal. Heart and lung sections were taken for histology and culture. Upon opening the abdominal cavity the liver had multifocal areas of discolouration. The spleen, kidney and gastrointestinal tract appeared grossly normal. The stomach and intestinal contents appeared normal. Samples of the liver, spleen, kidney and gastrointestinal tract were taken for histology and culture. Stomach contents were sampled for potential toxin testing. The skull was opened and the brain examined. There were no gross abnormalities observed. The entire brain was placed in formalin for histology.

Due to the clinical signs described exotic diseases such as African swine fever and classical swine fever were added to the list of differential diagnoses. Therefore, all samples were sent immediately for testing and appropriate biosecurity measures were put in place.

Laboratory findings

Real-time PCR and virology successfully ruled out both African swine fever and classical swine fever. Similarly, pestivirus, erysipelas and porcine circovirus type 2 were excluded via negative PCR results. No pathogens were implicated on culture.

EMC virus was identified via PCR undertaken on a pooled sample of heart tissue from both piglets.

Histological findings were similar between both piglets and consistent with EMC. In the myocardial interstitium there were multifocal but widespread minimal to marked infiltrates of lymphocytes and macrophages with occasional neutrophils and eosinophils. There were areas of disrupted myofibres, with some being hypereosinophilic with dark shrunken nuclei. In multiple areas degenerate or necrotic myocytes contained basophilic stippling of the cytoplasm. There was activation of mesothelial cells and the epicardium had moderate levels of infiltration of lymphocytes, macrophages and the occasional neutrophil and eosinophil. The lungs were congested with the alveoli containing a pale eosinophilic fluid and the occasional macrophage. The liver and spleen samples were congested and showed signs of patchy autolysis, potentially due to post mortem changes. There were no abnormalities detected during histopathological examination of the brain or spinal cord.

The morphological diagnosis made was interstitial, non-suppurative, acute to subacute, multifocal, moderate myocarditis with monocyte degeneration and necrosis, which is consistent with EMC.


Due to the number of dead piglets within this production system notifiable diseases had to be excluded. Both African swine fever and classical swine fever are exotic to Australia and notifiable to the Department of Primary Industries (DPI) and World Organisation for Animal Health (OIE). Disease surveillance can be done via serological testing submitted to Australian Animal Health Laboratory (AAHL). Other differential diagnoses of sudden death included erysipelas, meningitis, toxins and metabolic disease.

Cardioviruses are most commonly associated with rodents. Thus, cases of EMC seen in other mammals are usually linked to increased contact with rodents (Seaman et al., 1986). This circumstance can be due to a breakdown in biosecurity surrounding animal or feed enclosures. Previously reported cases have been linked to a local increase in rodent population size. It is hypothesised that the virus is shed in rodent faeces and urine, but it is also possible in the case of piggeries that animals may become infected by eating rodents infected with EMC. As the virus is unenveloped, it can persist in the environment for an extended period of time. It has been shown experimentally that pigs shed the virus via nasal secretions during the first three days following infection but pig to pig transmission is not common (Maurice et al., 2002).

While there is wide variation in severity of clinical signs seen in pigs infected with EMC virus the infection route remains constant (Carocci & Bakkali-Kassimi, 2012). Infection is via the oro-nasal route through the ingestion of contaminated feed, water or carcases. The virus concentrates in the tonsillar tissue and then disseminates into the target organs via circulating monocytes (Carocci & Bakkali-Kassimi, 2012). In pigs the target organ for the virus is most commonly the heart, however, virus isolation can be achieved in a wide variety of tissues from three days following infection (Carocci & Bakkali-Kassimi, 2012; Papaioannou et al., 2003). The pathogenic effects of EMC virus is caused by its lytic replication method resulting in secondary cell necrosis (Carocci & Bakkali-Kassimi, 2012). Associated secondary inflammation results in many of the changes seen on histology (Carocci & Bakkali-Kassimi, 2012).

The predominate clinical sign associated with EMC infection of piglets is sudden death. It may be preceded by clinical signs associated with pulmonary congestion due to heart failure (Carocci & Bakkali-Kassimi, 2012; Torremorrell, 2007). In adult pigs, infection is often subclinical. However, in sows it can cause abortions, foetal loss and mummification (Brewer et al., 2001; Torremorrell, 2007).

At necropsy the typical lesions of infection are myocardial. The heart is often dilated and, in some cases focal areas of myocardial necrosis are present. Secondary findings consistent with the resulting heart failure include secondary pulmonary oedema, ascites and hydrothorax (Carocci & Bakkali-Kassimi, 2012).

Histological findings of affected cardiac tissue will show myocarditis with infiltration of mononuclear cells, vascular congestion, oedema and areas of myocardial fibre degeneration and necrosis (Carocci & Bakkali-Kassimi, 2012). While not seen in this case, histological changes of the central nervous system can be observed in affected pigs as can abortion and foetal deaths in affected sows (Carocci & Bakkali-Kassimi, 2012).

Making a diagnosis of porcine EMC infection relies on combining history and clinical findings, with histopathology and viral testing. Both viral isolation and ELISA on affected tissues have been proven useful in ruling in or out porcine EMC (Carocci & Bakkali-Kassimi, 2012; Maurice et al., 2002; Vanderhallen & Koenen, 1997).

There is no treatment for EMC in pigs. However, reducing stress factors may improve prognosis. There is currently no commercial vaccine for EMC virus available to pig producers (Carocci & Bakkali-Kassimi, 2012). Prevention of viral spread can be achieved through minimising the exposure of pigs, especially young piglets and pregnant sows, to viral particles. This outcome can be achieved by ensuring there is no contamination of feed or water sources with rodent urine, faeces or carcases as these are the primary source of the virus (Seaman et al., 1986). In times of increased rodent numbers, the risk to pig populations is higher. Therefore it is recommended that extra care be taken during these periods to ensure biosecurity practices prevent contamination of feed and water with rodent urine, faeces or carcases (Seaman et al., 1986). These practices are especially important during a rodent plague, which parts of New South Wales experienced in 2021. The producer had initially not noticed an increase in rodent activity. However, on further investigation of his pastures, after receiving the diagnosis of EMC, he did, in fact, detect a significant increase in rodent numbers. While the risk of pig-to-pig transmission is minimal it is still recommended that animals showing clinical signs be separated to mitigate any potential the risk and allow easier symptomatic treatment of infected animals (Maurice et al., 2002).

EMC virus also infects a number of other species. Outbreaks in zoos in Italy, USA and Australia having been reported (Canelli et al., 2010; Reddacliff et al., 1997). A number of non-human primates, including lemurs, squirrel monkeys and a chimpanzee and other mammals, such as the pygmy hippopotamus and tree kangaroos, are also reported to have been infected. The clinical signs, post-mortem findings and histology findings are similar to those described in pigs (Canelli et al., 2010). In all cases the cause of the outbreak was traced back to contact with infected rodents, which were present in increased numbers (Canelli et al., 2010; Reddacliff et al., 1997).

There is little evidence to suggest that EMC is of zoonotic importance, however, the virus has been detected in febrile human patients in Peru (Czechowicz et al., 2011). This zoonotic transmission is hypothesised to be caused by close contact with infected rodents rather than pigs (Czechowicz et al., 2011). Interestingly as pig-to-human organ transplants have the potential to become more common, it has been observed that the virus can persist in a human host post-transplant (Brewer et al., 2001). Therefore, it is important to minimise contact with infected animals, regardless of species, and wear appropriate personal protective equipment while treating or testing suspected cases. Due to the widespread nature of EMC virus and its endemic reservoir within the rodent population spill-over events are likely to continue into the future (Carocci & Bakkali-Kassimi, 2012; Seaman et al., 1986).


Elizabeth Macarthur Agricultural Institute and Australian Animal Health Laboratory veterinary pathology teams for tissue examination, testing and interpretation of results.


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