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IdentityTop of page
Preferred Scientific Name
International Common Names
- English: encephalomyocarditis virus disease of pigs; encephalomyocarditis virus in pigs
OverviewTop of page
EMC virus infection in pigs was first reported in Panama in 1960, and subsequently in Florida between 1960 and 1966, and in Australia in 1970. The virus is classified as genus Cardiovirus of the family Picornaviridae. It causes high mortality in young pigs and reproductive failures in breeding females. Sudden deaths due to myocardial failure are common, and myocarditis and encephalitis are evident in affected piglets. Clinical problems in swine are mostly limited to tropical areas, and endemic infection with significant economic losses has been identified in certain areas of tropical countries. The disease has been observed in different zoo animals.
Hosts/Species AffectedTop of page
Rodents are the major reservoir of the virus. The most important sources for swine infection appear to be feeds or water that are contaminated with virus by rats, other rodents or diseased carcasses.
DistributionTop of page
Besides the countries listed above, evidence of EMCV infection probably exists in all countries throughout the world.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
PathologyTop of page
Young pigs dying in the acute phase may show no gross lesions, but myocardial lesions are common in infected pigs. The heart is usually enlarged, with visible yellowish or white necrotic foci (2-15 mm in diameter). The lesions are most commonly observed on the epicardium of the right ventricle.
Infected foetuses become mummified in various sizes depending on the stage of infection and may be haemorrhagic, oedematous or apparently normal. The myocardial lesions may be seen in some infected foetuses but it would be difficult to observe under field conditions. The gross abnormalities of the foetuses are not easy to distinguish from those caused by other viral infections.
Histopathologically, the most significant finding in young pigs is myocarditis with focal or diffuse accumulation of mononuclear cells, vascular congestion, oedema and degeneration of the myocardial fibres with necrosis. Mineralization of necrotic heart muscle is common but not always present. Congestion with meningitis, perivascular infiltration with mononuclear cells and some neuronal degeneration may be observed in the brain. Nonsuppurative encephalitis and myocarditis were also observed in swine foetuses with natural EMCV infection (Kim et al., 1989a).
DiagnosisTop of page Clinical diagnosis
High neonatal mortality with or without history of reproductive failure is a useful tip in the diagnosis. Dyspnea manifested as rapid abdominal breathing due to heart failure may be observed in young infected pigs.
Gross lesions of white necrotic areas in the heart muscle are characteristic of EMCV infection, although such lesions resemble those of vitamin E and selenium deficiency.
A definitive diagnosis should be based on virus isolation. Heart is the best tissue for virus isolation. Baby hamster kidney (BHK-21), HeLa or Vero cell lines are commonly used for virus isolation. Virus isolation is usually successful from pigs during the acute phase. Microscopically, myocarditis of varying stages with infiltration of mononuclear cells along with nonsuppurative encephalitis is indicative of EMCV infection. Detection of antibody specific to EMCV from born-dead pigs is particularly significant for foetal infection (Joo et al., 1988; Kim et al., 1991).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Vomiting or regurgitation, emesis||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Pigs:Piglet||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Sudden death, found dead||Pigs:Piglet||Sign|
|General Signs / Tetraparesis, weakness, paralysis all four limbs||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Tremor||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Pigs:Sow||Sign|
|Reproductive Signs / Female infertility, repeat breeder||Sign|
|Reproductive Signs / Mummy, mummified fetus||Pigs:Sow||Sign|
|Reproductive Signs / Small litter size||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Pigs:Piglet||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
Disease CourseTop of page
The natural infection of swine most probably occurs by the oral route. Following experimental oral infection in piglets, viremia was demonstrated as early as 2 days post-inoculation and persisted for 2 to 4 days (Craighead et al., 1963). Virus was present in the faeces for as long as 9 days following oral administration. The highest virus titres were recovered from heart tissue. Of other tissues, liver, pancreas and kidney contained virus, usually at a greater concentration than blood. Animals that survived from the acute disease produced EMCV antibodies. The course of infection in swine appears to be influenced by virus strain, viral dose, history and level of viral passage and the susceptibility of the individual animal.
Following intramuscular infection of pregnant sows, a transplacental infection with foetal deaths was observed (Love and Grewal, 1986). Infected and dead foetuses showed myocardial lesions varying from multiple small foci to large diffuse patches. Some difficulty in producing experimental reproductive disease in pregnant sows was also observed with a US isolate. However, transplacental infection was successful when the virus was passaged in young pigs rather than cell culture before inoculation (Christianson et al., 1992). Foetal deaths following infection in sows appear to occur as early as 2 weeks post-infection. At this time it is not known whether all EMCV strains can cause both the typical myocarditis observed in young pigs and reproductive failure. Pathogenic variability in swine foetuses by different EMCV isolates has been reported (Kim et al., 1989b).
EpidemiologyTop of page
EMCV naturally infects rodents and a wide range of vertebrate species. The host range includes chimpanzees, monkeys, elephants, lions, squirrels, mongooses, racoons and pigs. Swine are the domestic animals most susceptible to clinical disease by EMCV infection. Rats and mice are believed to be the principal reservoir of the virus. Many rodents are susceptible to experimental infection, showing high levels of virus in their tissues and infected rodents excrete virus in their faeces and urine. The virus has been isolated from dried faeces and from the intestines of rats or mice captured on farms where swine disease had previously occurred (Gainer, 1967; Acland and Littlejohns, 1975). Although the virus has been isolated from mosquitoes caught in Africa, Brazil and the USA, and from ticks in India (Tesh and Wallace, 1977), there is no evidence that natural EMCV infection in swine is vector-borne.
The most important sources for swine infection appear to be feeds or water sources that are contaminated with virus by rats, other rodents or diseased carcasses. The mode of virus transmission is not clear but rodent-to-pig transmission is probably common. Several outbreaks in Australia were found to be closely associated with rat and mouse plagues (Acland and Littlejohns, 1975; Seaman et al., 1986). Pig-to-pig transmission has been questioned because sentinel pigs failed to become infected after contact with experimentally infected and sick pigs (Littlejohns and Acland, 1975; Horner and Hunter, 1979). However, the role of the infected pigs in natural transmission, either directly or indirectly, cannot be excluded, because infected pigs have been shown to excrete the virus, at least for a short period.
Impact: EconomicTop of page
No data are available for economic loss.
Zoonoses and Food SafetyTop of page
Evidence for human infection with EMCV was demonstrated by antibody detection in human populations (Tesh, 1978) but there are no reports that the virus causes human heart disease.
Disease TreatmentTop of page
There is no treatment. However, mortality may be reduced by avoiding stress or excitement of the pigs at risk.
Prevention and ControlTop of page Immunization and Vaccines
An inactivated vaccine for EMCV infection in swine (for intramuscular injection) is commercially available in the USA (from Intervet, Inc.). The vaccine appears to be effective, since high humoral immunity is detected in vaccinated pigs.
It is important to control rodents on pig farms or minimize their contact with pigs; contact may occur either directly or indirectly via contamination of feeds or water. Although it is not clear whether pig-to-pig transmission occurs, introduction of pigs from previously infected farms should be avoided. Basic rules of sanitation and hygiene should be applied. The virus can be inactivated in water containing common disinfectants.
ReferencesTop of page
Acland HM; Littlejohns IR, 1975. Encephalomyocarditis virus infection of pigs. I. An outbreak in New South Wales. Australian Veterinary Journal, 51:409-415.
Christianson WT; Kim HS; Yoon IJ; Joo HS, 1992. Transplacental infection of porcine fetuses following experimental challenge inoculation with encephalomyocarditis virus. American Journal of Veterinary Research, 53(1):44-47; 16 ref.
Craighead JE; Peralta PH; Mrurnane TG; Shelokov A, 1963. Oral infection of swine with the encephalomyocarditis virus. Journal of Infectious Disease, 112:205-212.
Gainer JH, 1967. Encephalomyocarditis virus infection in Florida, 1960-1966. Journal of American Veterinary Medical Association, 151:421-425.
Hani H; Zimmermann W; Bestetn GE; Muller HK, 1992. A disease outbreak associated with severe myocarditis resembling encephalomyocarditis virus infection in two Swiss farms: clinical and pathological characterization of the disease and etiological studies. Proceedings 12th International Pig Veterinary Society.
Horner GW; Hunter R, 1979. Experimental infection in pigs with encephalomyocarditis virus. New Zealand Veterinary Journal, 27:202-203.
Kim HS; Joo HS; Bergeland ME, 1989. Serologic, virologic, and histologic observations of encephalomyocarditis virus infection in mummified and stillborn pigs. Journal of Veterinary Diagnostic Investigation, 1(2):101-104; 14 ref.
Kim HS; Joo HS; Christianson WT; Morrison RB, 1991. Evaluation of serologic methods for detection of antibodies to encephalomyocarditis virus in swine fetal thoracic fluids. Journal of Veterinary Diagnostic Investigation, 3(4):283-286; 20 ref.
Koenen F; Clerq Kde; Strobbe R, 1992. Isolation of encephalomyocarditis virus in the offspring of swine with reproductive failure in Belgium. Proceedings 12th International Pig Veterinary Society.
Kudo H; Yoshizawa S; Hiroike T; Hirose O, 1995. A retrospective serological survey of the encephalomyocarditis virus among pigs in Chiba Prefecture, Japan. Journal of Veterinary Medical Science, 57(4):793-795; 74 ref.
Littlejohns IR; Acland HM, 1975. Encephalomyocarditis virus infection in pigs. II. Experimental diseases. Australian Veterinary Journal, 51:416-422.
Lopez N; Palencia L; Rolo M; Peroza L; Martinez J; Carcia E, 1998. First report of encephalomyocarditis in Venezuela. Proceedings International Pig Veterinary Society.
Murnane TG; Craighead JE; Mondrogon H; Shelokov A, 1960. Fatal disease of swine due to encephalomyocarditis virus. Science, 131:498-499.
Par NY; Chung CY; Ri CY; Kee HY; Bae SY; Lee BJ; Jung BT; Kim DS, 1990. Encephalomyocarditis virus infection in pigs associated with reproductive failure. Korean Journal of Veterinary Science, 30:441-446.
Paschaleri-Papadopoulou E; Anastaslidis G; Skoufos J; Kyriakis SC; Papadopoulos O, 1992. Encephalomyocarditis in Greece: A follow up. Proceedings 12th International Pig Veterinary Society.
Ramos JR; Gomez L; Mayo M; Sanchez G, 1983. Infections caused by encephalomyocarditis virus in pigs and other species in Cuba between 1975 and 1981. Revista Cubana de Ciencias Veterinarias, 14(1):71-77; 20 ref.
Roehe PM; Rodrigues NC; Oliveira SJde; Guizzardi II; Barcellos DESNde; Vidor T; Oliveira LG; Bangel EV, 1985. Encephalomyocarditis virus (EMCV) in swine in the State of Rio Grande do Sul, Brazil. Revista de Microbiologia, 16(2):117-120; 9 ref.
Sangar DV; Rowlands DJ; Brown F, 1977. Encephalomyocarditis antibodies in sera from apparently normal pigs. Veterinary Records, 100:240-241.
Sidori L; Barigazzi G; Foni E; Marcato PS; Barbieri G, 1988. Encephalomyocarditis due to cardiovirus in Po Valley swine. Preliminary observations. Proceedings Italian Society Swine Pathology, 249-260.
Sutherland RJ; Horner GW; Hunter R; Fyfe BH, 1977. An outbreak of viral encephalomyocarditis in pigs. New Zealand Veterinary Journal, 25:225.
Tesh RB, 1978. The prevalence of encephalomyocarditis virus neutralizing antibodies among various human populations. American Journal of Tropical Medicine & Hygiene, 27:144-149.
Tesh RB; Wallace GD, 1977. Observations on the natural history of encephalomyocarditis virus. American Journal of Tropical Medicine & Hygiene, 27:133-143.
Williams MC, 1981. Encephalomyocarditis virus infection. Journal of South Africa Veterinary Association, 52:76.
Distribution MapsTop of page
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