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Diseases / List of Viral Diseases / Disease description:

Encephalomyocarditis

INDEX - INFORMATION AVAILABLE

GENERAL INFORMATION

SUSCEPTIBILITY, DISEASE CHARACTERISTICS & DIAGNOSIS

TREATMENT & CONTROL

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THE FOLLOWING INFORMATION IS HELD ON THE INFECTIOUS AGENT INFORMATION PAGE
Picornaviridae: Encephalomyocarditis Virus

  • Virus Structure and Identification
  • Associated Host Species of Virus (Animal Types Affected) and Hazard / Risk
  • Virus Life Cycle, Transmission and Effects of Chemicals
  • Transmission and Biogeographical / Climatic Range for Virus

CLICK THIS LINK FOR Picornaviridae: Encephalomyocarditis Virus

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General and References

Disease Summary

This disease, which affects pigs and a wide variety of wildlife species, causes myocarditis and sudden death. Encephalomyocarditis virus appears to produce asymptomatic infection in wild rodents. (B209.5.w5)

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Alternative Names (Synonyms)

  • Mengovirus infection
  • EMC

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Disease Type

 Viral

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Infectious/Non-Infectious Agent (directly associated with the Disease)

The encephalomyocarditis virus or Columbia SK virus group includes: (B22.12.w10, B209.5.w5)
  • Encephalomyocarditis virus (EMCV). (B22.12.w10, B209.5.w5)
  • Columbia SK virus. (B22.12.w10, B209.5.w5)
  • MM virus. (B22.12.w10, B209.5.w5)
  • Mengo virus. (B22.12.w10, B209.5.w5)

Species/Taxa

Chemical

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Physical

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References

Disease Author

Debra Bourne MA VetMB Phd MRCVS (V.w5)
  • Sections on elephants by Gracia Vila-Garcia DVM, MSc, MRCVS (V.w67)

Referee

Charalambos Billinis DVM DrMedVet (V.w174), George Valikos DVM (V.w175)

References

Detailed references are provided attached to specific sections.

ORGANISATIONS-

  • --

ELECTRONIC LIBRARY
(Further Reading)
Click image for full contents list of ELECTRONIC LIBRARY

 

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Epidemiology and Host Susceptibility Factors

Incubation Period, Time Course and Persistence of Disease

General Editorial Description
1) INCUBATION PERIOD

In elephants

  • A experimental study found that the incubation period after oral infection was nine to 10 days; an incubation period of four to five days was observed in elephants infected parentally. (P9.1.w6)
2) DISEASE DURATION (TO RECOVERY) IN INDIVIDUAL ANIMALS
3) TIME COURSE / PERSISTENCE OF DISEASE IN A SUSCEPTIBLE POPULATION

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Mortality / Morbidity / Susceptibility / Life stage affected

General Editorial Description
1) NUMBER OF DEATHS
  • It is probable that many infections are subclinical (death is not a common outcome of infection in most species). (B209.5.w5, B244.w4))
  • Mortality has been reported in Antelopidae, Camelidae, Cebidae, Cercopithecidae, Lemuridae, Marsupialia, Pongidae, Proboscidae, Rodentia, Suidea and Tapiridae species. (B519.9.w9)
  • High mortality was reported in a encephalomyocarditis outbreak in swine in Florida. Forty-two of 57 pigs died. (J4.151.w1, J351.58.w1)
  • Significant mortality has been documented in swine outbreaks in Panama and New South Wales, Australia. (P1.1980.w2)
  • The presence of antibodies in some animals with no history of clinical disease indicates that infection is sometimes subclinical. (B519.9.w9)
Great apes
  • Several fatal cases have been diagnosed in chimpanzees (J2.28.w7, P1.1980.w2), with two confirmed (J543.40.w1) and one presumptive case in a bonobo (J543.34.w1), while a seropositive orang-utan had dilated cardiomyopathy. (P1.2006.w4)
  • At Lola ya Bonobo, three deaths attributable to EMCV occurred out of 10 deaths from 1995 to the second of two EMCV deaths in 2003, and out of 38 deaths to 2010. (J543.40.w1)
2) NUMBER OF ANIMALS AFFECTED
  • Prevalence of infection is very variable and serological surveys have indicated: (B244.w4)
    • Cattle, 4.3 -20%
    • Cats 0 -2.7%
    • Dogs 0 - 17.1%
    • Horse 2.2 - 10.5%
    • Humans 1 - 50.5%
    • rodents 0 - 87%;
    • Domestic pigs, 1 - 69.1%.
  • In pigs in Europe, 1990-2001, seroprevalence in clinically affected farms varied from 2 - 87%; in farms in affected areas but without any history of illness due to EMCV, seroprevalence was 6 - 62%, and in areas without any affected farms, seroprevalence was still up to 17%. (J19.133.w2)
3) EFFECTS OF AGE, SEX AND REPRODUCTIVE STATUS
  • Males seem to be more susceptible to the infection than females; this may be due to testosterone. (B209.5.w5)
  • The development of clinical disease varies depending on host factors. In mice there is higher susceptibility in males than in females, and in pregnant mice than in non-pregnant females. (B244.w4)
Elephants
  • Males appear to be more susceptible than females; (B209.5.w5) in an outbreak in Kruger National Park, South Africa, 83% of the elephants with deaths attributed to EMCV were adult males. (J62.62.w2)
  • Juveniles seem to be more susceptible. (B209.5.w5, P1.1980.w2) 
  • Males seem to be more susceptible to the infection than females. (B209.5.w5)
4) EFFECTS OF BODY CONDITION AND OTHER DISEASES
  • The development of clinical disease varies depending on host factors. In mice there are host strain differences, plus higher susceptibility in obese mice. (B244.w4)
Elephants
  • Stress caused by procedures such as capture and immobilisation may influence in subclinical cases. (J62.62.w2)

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Clinical & Pathological Characteristics, and Diagnosis

Clinical Signs (by physiological system)

Overall Clinical Presentation
  • The peracute form is characterised by sudden death. (B22.12.w10, B209.5.w5, B519.9.w9, J4.151.w1)
  • The acute form is characterised by signs of congestive heart failure, such as depression, listlessness/lethargy, reluctance to move and moderate to severe dyspnoea. Neurological signs may develop but are less common. (B22.12.w10, B209.5.w5, B519.9.w9, J2.20.w3)
  • It is probable that many infections are subclinical. (B209.5.w5, B244.w4, B519.9.w9)
    • Clinical disease is rare in domestic animals except for pigs. (B244.w4)
    • Rodents (Rodentia - Rodents (Order)) are commonly associated with outbreaks of the disease but rarely develop clinical signs. (B209.5.w5)
    • Among rodents, only multimammate rats, Mastomys sp. (Muridae - Rats, mice, voles, gerbils etc. (Family)), are highly susceptible to the infection. (B209.5.w5)
    • Rats and guinea pigs are less likely to develop severe and fatal disease than are laboratory mice, hamsters or gerbils. (B244.w4)
In pigs
  • Sudden death/found dead. (B244.w4)
  • Lethargy and inappetance, trembling, staggering and paralysis, vomiting, dyspnoea. (B244.w4)
  • Reproductive problems: poor rate of conception, resorption of embryos, increases in mummification, stillbirths, abortions and neonatal deaths. (B244.w4)
In elephants

The clinical forms of the disease range from peracute to acute:

  • Peracute form:
    • Sudden death. (B10.49.w21, P1.1980.w2)
  • Acute form:
    • Depression. (J1.23.w6, P9.1.w6, P505.9.w1)
    • Tremor of the distal trunk. (J1.23.w6)
    • "Sucking tip of the trunk and increased trunk activity" (P9.1.w6)
    • Uncoordinated movements. (P1.1980.w2)
    • Recumbency. (P1.1980.w2)
    • Collapse. (J1.23.w6, P1.1980.w2)
    • Anorexia. (B336.53.w53, J4.171.w6, P1.1980.w2)
    • Frothy trunk discharge. (P1.1980.w2)
    • Dyspnoea. (B336.53.w53, J4.171.w6, P1.1980.w2, P505.9.w1)
    • Signs of colic, such as diarrhoea. (P1.1980.w2, P9.1.w6)
  • A subclinical form of the disease has been reported in an experimentally infected elephant. (P9.1.w6)
In great apes

In Pan troglodytes - Chimpanzee:

  • In three individuals at Lion Country Safari, Florida, USA: (P1.1980.w2)
    • Sudden death; reluctance to rise had been noted earlier in the day (adult female).
    • Lethargy, incoordination, dyspnoea, disorientation and subnormal temperature. Death the following day despite supportive treatment (three-year-old female).
    • Sudden death without preliminary signs (six-year-old male).
  • In two individuals at Taronga Zoo: (J2.28.w7)
    • Sudden death in a two-year-old male (diagnosis confirmed by virus isolation).
    • Signs of progressive heart failure in a 12-year-old male (EMCV suspected but virus negative; probable myocardial infarction).

In Pan paniscus - Bonobo:

  • In a female bonobo at the "Lola ya Bonobo" sanctuary, Kinshasa, DRC: (J543.34.w1)
    • Initially breathlessness cough and wheezing with lethargy; respiratory infection or asthma was suspected, but despite appropriate treatment, signs recurred intermittently over a period of three years.
    • An episode of vomiting and diarrhoea (not uncommon in members of the bonobo colony) was followed by shock with depressed consciousness, shallow respiration, tachycardia, weak pulses and poor peripheral circulation. Condition improved slowly following intravenous rehydration; three days later, with resumption of some physical activity, hemiparesis and partial palsy of the seventh cranial nerve (sensation apparently intact) were noted. Physical condition remained poor; assistance required with feeding.
    • Deterioration over the next month, increasing lethargy and breathlessness, periods of restlessness. Heart failure was diagnosed clinically and treatment initiated with Enalapril and frusemide (Furosamide), without any improvement resulting.
    • Shallow respiration and poor perfusion before death.
    • Clinical pathology: 
      • BUN one month before death 43.5 mg/dL, one week before death 69.6 mg/dL (normal chimpanzee range 4 - 22 mg/dL);
      • Blood creatinine: one month before death 1.80 mg/dL, one week before death 2.26 mg/dL (normal chimpanzee range 0.4 - 1.2 mg/dL);
      • Blood total protein: one month before death 4.8 mg/dL, one week before death 5.0 mg/dL (normal chimpanzee range 6.4 - 8.0 mg/dL;
      • Blood albumin: one month before death 1.7 mg/dL, one week before death 1.8 mg/dL (normal chimpanzee range 2.9 - 3.9 mg/dL);
      • Urine protein: one month before death 2+, one week before death 3+; (normal chimpanzee negative)
      • Urine blood: one month before death, negative, one week before death, 2+ (normal chimpanzee negative).
    • (J543.34.w1)
  • In two bonobos, about two and five years of age, at Lola ya Bonobo, rapidly progressive increased respiratory rate and dyspnoea, death within 24 hours of the onset of clinical signs. (J543.40.w1)

In Pongo pygmaeus - Orang-utan

  • Signs [unspecified] associated with dilated cardiomyopathy in a female orang utan for one year. (P1.2006.w4)
    •  High neutralising titre to EMCV (1:6,240). (P1.2006.w4)

In experimentally infected Microtus arvalis - Common Vole

  • No clinical signs except a transient reduction in bodyweight gain. (J83.29.w3)

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Clinical Pathology (Testing Samples incl. Serology)

Overall Clinical Pathology findings Information on serology is given in Picornaviridae: Encephalomyocarditis Virus (Viral Type) - Virus Detection and Identification Techniques

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Pathological Findings (by anatomical system)

Overview
  • The main lesion of encephalomyocarditis virus infection is myocardial necrosis; other lesions may follow due to heart failure. Additionally, encephalitis, pancreatitis and/or myositis may occur. (B209.5.w5)
GROSS PATHOLOGY
  • Thorax: Hydrothorax and presence of fibrin in the thoracic cavity. (B209.5.w5)
  • Heart: Hydropericardium and pale bands within the myocardium. (B209.5.w5, J2.20.w3, J4.151.w1, P505.9.w1)
    • Either generally pale myocardium or more discrete pale foci may be present. (B209.5.w5) Pale streaking is evident. (B519.9.w9)
    • Subepicardial petechial or ecchymotic haemorrhages may be present. (B209.5.w5, B519.9.w9)
  • Lungs: Pulmonary oedema and congestion (marked). Presence of  froth in the trachea and bronchi. (B22.12.w10, B209.5.w5, B519.9.w9, B519.9.w9, J351.58.w1, P505.9.w1)
    • Lung weight may be 2-3 times normal due to the oedema fluid. (B519.9.w9)
  • Abdomen: Fibrin and haemorrhage in the abdominal cavity. (B209.5.w5, J351.58.w1)
  • Liver: Congestion. (J351.58.w1)
  • Congestion of organs other than the lungs may or may not be present. (B519.9.w9)
In pigs
  • Cardiac: Discrete white myocardial foci. (B244.w4)
In Elephants:
  • Thorax:
    • Blood vessel rupture. (P1.1980.w2)
    • Hydrothorax. (J62.62.w2)
  • Heart: 
    • Pericardial effusion. (J1.23.w6, J62.62.w2, P1.1980.w2)
    • Oedema of the coronary fat. (P1.1980.w2)
    • Enlargement. (P1.1980.w2)
    • Flaccid heart, especially the right ventricle. (J1.23.w6, P1.1980.w2)
    • Pale myocardium. (J1.23.w6, J62.62.w2, P1.1980.w2)
    • Mottled myocardium. (J62.62.w2, P1.1980.w2)
    • Petechiation and/or ecchymoses of the epicardium. (J1.23.w6, J62.62.w2, P1.1980.w2)
  • Lungs:
  • Abdominal cavity: Ascites. (J1.23.w6, J62.62.w2, P1.1980.w2)
  • Gastrointestinal tract: Catarrhal enteritis. (P1.1980.w2)
  • Liver: Hepatomegaly; liver rounded and oedematous. (J1.23.w6, J62.62.w2, P1.1980.w2)
  • Spleen: Congested and enlarged. (P1.1980.w2)
  • Kidneys: 
    • Pale. (P1.1980.w2)
    • Haemorrhagic cortex. (P1.1980.w2)
  • Brain: Oedematous and mildly congested. (J62.62.w2)
In great apes

In Pan troglodytes - Chimpanzee:

  • In three individuals at Lion Country Safari, Florida, USA: (P1.1980.w2)
    • Adult female: Myocardium pale, pulmonary oedema, hepatic swelling.
    • Three-year-old female: Myocardium pale, respiratory system petechiation, hepatomegaly, and around some mesenteric lymph nodes, petechiae.
    • Six-year-old male: myocardium pale, pulmonary oedema.
  • In two individuals at Taronga Zoo: (J2.28.w7)
    • In a two-year-old male (diagnosis confirmed by virus isolation).
      • Multiple pale myocardial streaks.
    • In a 12-year-old male (EMCV suspected but virus negative; probable myocardial infarction).
      • Focal pale areas of myocardium, and haemorrhages.

In Pan paniscus - Bonobo:

  • In a female bonobo at the "Lola ya Bonobo" sanctuary, Kinshasa, DRC: (J543.34.w1)
    • Cardiac: markedly enlarged heart; hypertrophy of the left ventricular wall (28 mm thick) and interventricular septum (27 mm thick).
    • Peritoneal, pleural and pericardial effusions.
    • Pulmonary: lungs congested.
    • Hepatic: hepatomegaly (liver reaching 8 cm below the costal margin); signs of circulatory congestion in the parenchyma.
    • Renal: right kidney 7.9 x 3.8 cm with the upper pole atrophic, surface showing granular change; left kidney 7.9 x 5.3 cm.

    (J543.34.w1)

  • In two bonobos at Lola ya Bonobo in 2003: (J543.40.w1)
    • Respiratory: generalised congestion. (J543.40.w1)

In Pongo pygmaeus - Orang-utan:

  • Severe dilated cardiomyopathy [no other details provided]. (P1.2006.w4)
HISTOPATHOLOGY

Multifocal necrosis and an associated inflammatory response are the main findings. (B209.5.w5)

  • Heart: Lymphocytic plasmacytic nectrotizing myocarditis. (B519.9.w9) Myocardial degeneration and necrosis. Inflammatory infiltrates are typically mononuclear cells: lymphocytes and plasma cells. In some cases, necrotic myocardial fibres may also contain neutrophils and macrophages. (B22.12.w10, B209.5.w5, J2.20.w3, J4.151.w1, J351.58.w1)
  • Brain: Encephalitis. (B209.5.w5)
    • This is noted particularly in rodents, possibly because the CNS from larger animals is not always submitted for histopathology. (B519.9.w9)
  • Pancreas: Pancreatitis. (B209.5.w5)
  • Muscle: Myositis. (B209.5.w5)
In Pigs
  • Cardiac: focal interstitial myocarditis, nonsuppurative, together with myocardial necrosis; small numbers of neutrophils may be seen infiltrating. (B244.w4)
    • In the myocardium, focal mononuclear cell infiltration. (J212.1.w2)
  • CNS: Nonsuppurative meningoencephalitis may be present. (B244.w4)
    • In the brain and meninges, perivascular mononuclear cell accumulations, in one piglet; in another, in the cerebellar white matter and thalamus, nonsuppurative (mononuclear cell) inlammation. (J212.1.w2)
In Elephants:
  • Heart: 
    • Cardiomyopathy. (B10.49.w21)
    • Acute myocarditis characterised by interstitial oedema and a mixed inflammatory infiltrate of polymorphonuclear leucocytes, lymphocytes and histiocytes. Myofibers were swollen and fragmented. Mineralisation of the necrotic areas was observed. (J1.23.w6)
    • Disseminated focal lymphocytic myocarditis and necrosis of myocytes. (J62.62.w2)
    • Foci or locally extensive areas of degeneration characterised by the disorganization and disintegration of myofibrils, the presence of contraction bands and the atrophy or hypertrophy of myocytes with enlarged nuclei. (J62.62.w2)
  • Lungs:
    • Alveolar and interstitial oedema and severe congestion. (J62.62.w2)
  • Liver: Acute hypoxic centrilobular coagulative necrosis and sinusoidal dilatation. (J62.62.w2)
  • Gastrointestinal tract: Marked oedema of the serosa and submucosa in the colon and stomach. (J62.62.w2)
  • Brain: Severe oedema of the meninges. (J62.62.w2)
In Great apes

In Pan troglodytes - Chimpanzee:

  • In three individuals at Lion Country Safari, Florida, USA: (P1.1980.w2)
    • Adult female: 
      • Cardiac: myocarditis.
      • Renal: subcortical renal necrosis.
      • Virus detection: EMCV recovered from heart, lung, liver, spleen, kidney and thymus
    • Three-year-old female: 
      • Virus detection: EMCV recovered from heart, liver, spleen and skeletal muscle
    • Six-year-old male: EMCV recovered from skeletal muscle (but not from heart, liver or spleen)
  • In two individuals at Taronga Zoo: (J2.28.w7)
    • In a two-year-old male (diagnosis confirmed by virus isolation).
      • Cardiac: severe subacute myocardial necrosis and inflammation.
      • Virus detection: EMCV isolated from heart.
    • In a 12-year-old male (EMCV suspected but virus negative; probable myocardial infarction).
      • Cardiac: severe acute/subacute myocardial necrosis, probable infarction.
      • Virus detection: Negative EMCV isolation from heart.
  • Florida: Two chimpanzees:
    • Virus detection: EMCV recovered. (P7.1.w9)

In Pan paniscus - Bonobo:

  • In a female bonobo at the "Lola ya Bonobo" sanctuary, Kinshasa, DRC: (J543.34.w1)
    • Cardiac: hypertrophy of myosites, focal lymphocytic infiltrates and interstitial fibrosis of the left ventricular wall.
    • Hepatic: peri-acinar necrosis suggestive of hypoperfusion.
    • Brain: mild focal gliosis, prominent blood vessels with focal fibrinoid change, proliferation of astrocytes, and perivascular cuffing (mild to moderate). No evidence of a cerebrovascular accident
    • Renal: both kidneys showed end-stage pathology; glomeruli showing encircling fibrosis, tubules atrophied, and in the interstitium, diffuse marked mononuclear infiltrates and fibrosis. Also in the right kidney, triangular areas of necrosis, apices of the triangles being at the corticomedullary junction and the bases at the capsule. 

    (J543.34.w1)

  • In two bonobos at Lola ya Bonobo in 2003: (J543.40.w1)
    • Respiratory: In Bonobo 2, mononuclear cell infiltration. (J543.40.w1)
    • Cardiac: Diffuse interstitial mononuclear lymphocytic cell infiltration of the myocardium. (J543.40.w1)
    • Renal: in Bonobo 2,mononuclear cell infiltration in the kidney, on the epithelial surface of the renal tubules.
    • GIT: mononuclear cell infiltration. Also "voluminous germinal centres in Peyer's patches". (J543.40.w1)
    • Immunohistochemistry: EMCV antigens confirmed in the myocardial cells of both bonobos, and in the epithelial cells of the small intestinal villi and renal tubules of Bonobo 2. (J543.40.w1)

In experimentally infected Microtus arvalis - Common Vole

  • At three days post inoculation: (J83.29.w3)
    • CNS: In the meninges and cerebral cortex, slight endothelial cell hypertophy and mild infiltration of mononuclear cells around capillaries. Also occasional pyknosis of neurons and gliocytes.
    • Thymus: moderate to marked cortical lymphocyte depletion.
    • Spleen: moderate to marked cortical lymphocyte depletion.
    • Cardiac: myocardial necrosis minimal.
    • Hepatic: diffuse vacuolation of hepatocytes.
    • Pancreas: exocrine glands showed prominent inflammatory exudation; acinar cell necrosis. Islets normal except for slight atrophy.
  • At seven days post inoculation: (J83.29.w3)
    • CNS: In two of eight voles, lesions still visible at 7 dpi: in the meninges and cerebral cortex, slight endothelial cell hypertophy and mild infiltration of mononuclear cells around capillaries. Also occasional pyknosis of neurons and gliocytes.
    • Thymus: lesions almost no longer present.
    • Spleen:  lesions almost no longer present.
    • Cardiac: lesions not present.
    • Hepatic: lesions not present.
    • Pancreas: necrotic tissue replaced by mesenchymal cells, acinar cell regeneration, islets nearly normal.
  • Virus isolation: no viraemia detected at 3 dpi or 7 dpi. Virus isolated from pancreas (107 pfu/g), brain (105 pfu/g) and heart (104 pfu) at 3 dpi; at 7 dpi, pancreas titre 103 pfu, other tissues negative except in 2/8 voles brain 104 pfu/g. (J83.29.w3)

    (J83.29.w3)

 

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Diagnostic Criteria

General Indicative Signs
  • Consider EMCV infection in instances of sudeen death, particularly in primates. (B209.5.w5)
  • Clinical signs and post mortem findings consistent with congestive heart failure and viral myocarditis. (B22.12.w10, B209.5.w5)
    • At necropsy, diffuse myocardial pallor, or discrete pale foci. Subepicardial ecchymotic haemorrhages. (B209.5.w5)
    • Histopathological findings of myocardial necrosis plus a mononuclear cell inflammatory infiltrate. (B209.5.w5)

Elephants

Definitive Diagnosis

Definitive diagnosis requires identification of the virus, or detection of seroconversion or increasing antibody titre in paired sera. (B209.5.w5)

  • Antibody detection: In live animals, the presence of EMCV-specific neutralising or haemagglutinating antibodies may help to sustain a tentative diagnosis. (B22.12.w10, J2.20.w3)
    • Serum-virus neutralisation test is the serological test of choice. Latex agglutination and ELISA have been used in research, also the immunofluorescent antibody assay and agar gel immunodiffusion; haemagglutination inhibition can be used but shows differences among EMCV strains. (B244.w4)
      • The neutralisation test is specific for EMCV without any cross-neutralisation with a range of human or porcine enterovirus serotypes. (B244.w4)
      • Neutralising antibodies show prolonged persistence following infection therefore a fourfold increase in titre from acute to convalescent serum is required to confirm recent infection. (B244.w4)
  • Virus culture & identification: In acute cases, the identification of the virus in tissues, usually myocardium, of the affected animals is commonly used. The diagnosis is confirmed by inhibition of infectivity or haemagglutination by antisera specific for EMCV. (J2.20.w3, J351.58.w1, B209.5.w5)
    • Heart and spleen are the usual preferred tissues. (P1.2006.w4)
  • Immunohistochemistry: In more chronic cases, identification of the virus is usually not possible. In these cases, immunohistochemistry may be helpful to demonstrate viral antigen in the affected tissues. (B209.5.w5, P1.2006.w4, P504.2001.w2)

Elephants

  • Neutralisation test for antibody to EMCV in sera. (J4.171.w6, J62.62.w2)
  • Immunostaining for EMCV antigen has been used in fresh elephant carcasses. The antigen was found only in and surrounding foci in the myocardium. (J62.62.w2)
  • Virus isolation from affected tissues. (J4.171.w6, J62.62.w2, P1.1980.w2, P505.9.w1)
  • RT-PCR test has been used on the heart muscle of affected elephants to demonstrate the presence of EMCV nucleic acid. (J62.62.w2)
In Pan paniscus - Bonobo:
  • In a female bonobo at the "Lola ya Bonobo" sanctuary, Kinshasa, DRC, diagnosis was presumptive on the basis of clinical signs and gross and histopathological findings. (J543.34.w1)
  • In two bonobos from Lola ya Bonobo, Kinshasa, DRC, diagnosis was confirmed by immunohistochemistry in two bonobos (heart muscle in both, also kidney tubules and intestinal epithelium in one) and by virus isolation from one of the bonobos, in 2003. (J543.40.w1)

In Pan troglodytes - Chimpanzee:

  • In three Pan troglodytes - Chimpanzee at Lion Country Safari, Florida, USA, infection confirmed virologically. (P1.1980.w2)
  • In a two-year-old male Pan troglodytes - Chimpanzee at Taronga Zoo, Australia, diagnosis confirmed by virus isolation. No virus isolated from a 12-year-old male with signs of heart failure and histopathological findings of probable myocardial infarction. (J2.28.w7)

In Pongo pygmaeus - Orang-utan:

  • A female Pongo pygmaeus - Orang-utan at Taronga Zoo, Australia, which survived for a year with signs associated with severe dilated cardiomyopathy had an EMCV antibody titre of 1:6,240. (P1.2006.w4)
Similar Diseases
  • Any infectious or non-infectious diseases that produce sudden death and/or cardiac lesions. (B209.5.w5)
  • In young animals, FMD may produce similar cardiac lesions.
  • Acute capture myopathy (Capture Myopathy)
  • Infarction due to septic emboli.
  • Cardiac glycoside poisoning.

In Elephants

CLICK THE LINKS FOR OVERVIEWS of management techniques available

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Treatment and Control

Specific Medical Treatment (Antiserum, Antidote, Anti-(viral/bacterial/fungal) etc.)

Specific Medical Treatment
ANTISERUM

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ANTIVIRAL DRUGS

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CLICK THE LINKS FOR OVERVIEWS of management techniques available
  • No specific techniques described

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General Nursing and Surgical Techniques

Nursing and Supportive Care

In Elephants

  • Fluid therapy, steroids, antihistamines, antibiotics and stimulants have been used unsuccessfully. (P1.1980.w2)

In Great Apes

  • In a female Pan paniscus - Bonobo at the "Lola ya Bonobo" sanctuary, Kinshasa, DRC, repeated antibiotics in response to signs indicative of respiratory disease, and treatment for apparent asthma. Later intravenous rehydration for treatment of shock, followed by enalapril (ACE Inhibitor) and furosamide (Diuretic) for treatment of heart failure (treatment was ineffective). (J543.34.w1)
  • In two bonobos from Lola ya Bonobo, Kinshasa, DRC, treatment for dyspnoea and tachypnoea included antibiotics. (J543.40.w1)
Surgical Treatment
  • Not applicable for this disease.

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Vaccination & Prophylactic Treatment

Vaccination
  • An inactivated vaccine for Sus domesticus - Domestic pig has been made available commercially (B209.5.w5, B244.w4), however, its efficacy in wildlife species has not been reported. (B209.5.w5)
  • Various experimental vaccines have been described for use in mice. (B244.w4)
  • An oil-adjuvanted inactivated EMCV vaccine produced high antibody titres in mice and pigs. Protection against challenge was demonstrated in mice but could not be proven in the pigs since disease did not develop in control (unvaccinated) pigs challenged with the same EMCV strain. This vaccine was also tested in elephants [see data below]. (J70.16.w3)
  • An inactive vaccine was develop from a -propiolactone inactivated virus preparation using either aluminum hydroxide, mineral oil and dimethyl dioctadecyl ammonium bromide (DDAB). These preparations produced varying levels haemagglutination- inhibition antibodies in the vaccinated animals. (P7.1.w9)
  • A formalin-inactivated vaccine was develop in a zoo outbreak and safely administered to a variety of species. However, the antibody response was found to be variable. (J2.20.w3)
  • An inactive vaccine derived from a virulent strain of EMCV in a zoo outbreak was efficient to create antibodies in macaques Macaca mulatta - Rhesus macaque). (B209.5.w5)
  • Live vaccines have been experimentally developed to protect primates and other zoological species, and domestic pigs, from lethal doses of EMC virus. (B209.5.w5, P1.1997.w5) 
    • A genetically engineered strain (vMC24) of Mengo virus, inoculated into Papio cynocephalus - Olive baboons, Macaca mulatta - Rhesus macaque and domestic pigs, caused seroconversion in all the animals; it was noted that baboons produced a significantly higher neutralising antibody titre that developed after immunisation with an inactivated EMCV vaccine. Challenge of the pigs and baboons with ECMV showed that the vaccine was protective. (J70.14.w1)
    • Preliminary trials of a modified live virus (genetically engineered Mengovirus with a shortened poly (C) tract) vaccine in Alouatta araya - Black howler monkey, Cercopithecus talapoin - Talapoin monkey, Tapirus terrestris - Brazilian tapir and Babyrousa babyrussa - Babirusa found that at 21 days post-vaccination the talapoin monkeys had increased antibody titres while howler monkeys and tapirs with pre-existing titres showed some increase in titre. No increase in antibody titre was seen in some animals, whether due to lack of response to the vaccine or insufficient time for an immune response to become apparent. (P1.1997.w5)
    • Inoculation of various primates, artiodactylids, tapirs and Hystrix africaeaustralis - African crested porcupine (Hystrix - (Genus)) with a genetically engineered Mengo virus vaccine resulted in no ill effects from the vaccine in any animal. Many primates with a pre-vaccination titre of <1:8 showed a greater than four-fold increase in antibody titre at 21 days post-vaccination. However in some species such as lemurs, marmosets and camels, no or minimal increases were seen. It was not known whether this was due to lack of response to the vaccine or insufficient time for an immune response to become apparent. It is not known whether the positive titres recorded would be protective against challenge with wild-type EMCV; no challenge was carried out. (J1.35.w9)
  • Inoculation of Pan troglodytes - Chimpanzees, Ammotragus lervia - Barbary sheep, Antilope cervicapra - Blackbuck Macropus robustus - Eastern wallaroos with an inactivated vaccine at Taronga Zoo, Australia, resulted in development of significant antibody titres by one month post-vaccination. In Macropus robustus - Eastern wallaroos, raised titres persisted to at least six months post-vaccination. In those of the ungulates (Barbary sheep and antelope) which were boostered four weeks after the initial inoculation, titres at three and six months were significantly higher than those which had received only the initial vaccine dose, although only two of the antelope given a single dose and only three of seven antelope given the booster had detectable antibody titres at six months. At 12 months, titres in the Barbary sheep were higher for those given the booster; only one of the antelope had detectable antibodies at 12 months. (J2.36.w6, P504.2001.w2)
    • This vaccine has since been used on various species. A 2 mL dose of the vaccine is given by deep intramuscular injection in anaesthetised animals. In small individuals it may be divided and given at two sites. If the species is relatively easy to restrain, a booster is given four weeks later, but most are simply vaccinated once initially and then either annually or opportunistically. (P1.2006.w4)
  • Autogenous vaccines have been used successfully. (B519.9.w9)
  • Note: research into experimental vaccines for use in non-domestic animals is ongoing. (B519.9.w9)
In elephants
  • An inactivated vaccine was developed, using the virus isolated from the outbreak of encephalomyocarditis in Loxodonta africana - African Elephant during 1993-1994 in Kruger National Park. All vaccinated elephants were protected from challenge with virulent virus. (P9.1.w6)
  • An oil-adjuvanted inactivated vaccine was develop to protect wild populations of Loxodonta africana - African Elephant against natural outbreaks of encephalomyocarditis. The vaccinated elephants develop a high antibody titers approximately two months post-vaccination. (J70.16.w3)

 

Prophylactic Treatment
Antiviral drugs:

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Passive immunisation:

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Personal protective measures:

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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection
  • Rodent control. (B22.12.w10, B209.5.w5, B244.w4, D301.3.w3)
  • Ensure that food storage is rodent proof. (B22.12.w10, B209.5.w5)
  • Good general hygiene. (B209.5.w5)
  • Effective disposal of garbage. (B209.5.w5)
  • Clean and disinfect contaminated enclosures/areas, as well as e.g. food bowls. (B519.9.w9)
  • Disinfectants effective against other picornaviruses would be expected to be effective against EMCV. (B244.w4)
  • Effective disinfectants with which EMCV contaminated surfaces can be cleaned include (based on effectiveness against Picornaviridae: Foot-and-Mouth Disease Virus): B519.9.w9
    • 5.25% sodium hypochlorite (NaOCl) i.e. household bleach. This is used at a 3% dilution: mix three parts bleach to one part water and mix thoroughly. (B519.9.w9)
    • Acetic acid, at 4-5% dilution: Mix 6.5 oz of glacial acetic acid with 1 gallon (US) water. Note: vinegar is a 4% acetic acid solution. (B519.9.w9)
    • Sodium carbonate (NaCO3, sodium ash) at 4% dilution: mix 5.33 oz with one gallon (US) of hot water. (B519.9.w9)
      • Caution: this solution is mildly caustic. (B519.9.w9)
      • Note: This is NOT effective against swine vesicular disease virus [therefore probably not against EMCV] due to differences in pH stability. (B216.35.w35)
    • Sodium hydroxide (NaOH) or Lye (NaOH plus soda ash) at 2% dilution: add 1/3 cup (2.7 oz) NaOH pellets to one gallon (US) of cold water and mix.
      • CAUTION this solution is highly caustic; protective rubber clothing, gloves and safety glasses should be worn.
      • Always add the NaOH to the water, not the other way around. (B519.9.w9)
    • Formaldehyde: 10-30% dilution. This is not generally used for the disinfection of surfaces. Note: It is highly toxic to tissues. (B519.9.w9)
    • Ethylene oxide gas: this is used for instrument sterilization. Note: the gas is toxic and it is a skin irritant. (B519.9.w9)
CLICK THE LINKS FOR Technique Descriptions, if available
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Population Control Measures
  • Reducing or eliminating rodent populations is recommended for EMCV prevention and control. (B244.w4)
    • Rodent control has been followed by the rapid cessation of an outbreak on at least two occasions. (B209.5.w5)
    • Careful use  of rodenticides should be considered. (B519.9.w9)
CLICK THE LINKS FOR Technique Descriptions, if available
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Isolation and Quarantine
  • --
CLICK THE LINKS FOR Technique Descriptions, if available
  • --
  • -
CLICK THE LINKS FOR OVERVIEWS of management techniques available
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Authors & Referees

Authors Debra Bourne MA VetMB PhD MRCVS (V.w5)
Referee Charalambos Billinis DVM DrMedVet (V.w174), George Valikos DVM (V.w175)

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