JPC SYSTEMIC PATHOLOGY

CARDIOVASCULAR SYSTEM

March 2025

C-V02 (NP)

 

SIGNALMENT (JPC #2133912): A pig

 

History: None

 

HISTOPATHOLOGIC description: Heart, ventricle: Multifocally infiltrating the epicardium, myocardium, and endocardium and surrounding, separating, and replacing cardiomyocytes are numerous lymphocytes, plasma cells, and macrophages, moderate amounts of clear space (edema), eosinophilic fibrillar material (fibrin), and basophilic granular material (mineral). Within affected areas, cardiomyocytes are swollen with vacuolated sarcoplasm (degeneration) or shrunken with hypereosinophilic sarcoplasm, loss of cross striations, and pyknosis (necrosis). There is a mild increase in fibrous connective tissue in affected areas. 

 

Morphologic diagnosis: Heart: Pancarditis, lymphoplasmacytic and histiocytic, chronic, multifocal, severe, with myocardial necrosis, breed unspecified, porcine.

 

cause: Encephalomyocarditis virus (EMCV)

 

Etiologic diagnosis: Picornaviral myocarditis

 

General discussion:

• Family Picornaviridae; genus Cardiovirus, a group of 3 closely related viruses all referred to as EMCV
• Depending on viral strain and host, may result in myocarditis, reproductive failure, diabetes, or nervous disorders 
• Rodents may act as a reservoir host with shedding of virus in urine and feces (clinically inapparent)
• Pigs are the most often and severely affected species (myocarditis and reproductive failure)

 

Pathogenesis:

• Transmission to swine is oral (ingestion of rodent carcasses, or fecal or urine contamination of food or water), and horizontal transmission has been reported in swine 
• Clinical disease due to both viral effect and immune response to virus within the myocardium, including myocytes and endothelium
• Experimentally infected swine may die 2-11 days post-inoculation and virus is present in feces for 7-9 days following oral ingestion.

 

typical Clinical findings:

• Any age of pig can be affected
• Young (pre-weaning) pigs: Sudden death or brief excitation, collapse, then death due to myocardial failure
• Milder cases: Fever, anorexia, listlessness, trembling, staggering, progressive paralysis, or dyspnea 
• Sows: Reproductive failure, mummified fetuses, still birth, early embryonic death, failure of conception 
• Exotic zoo animals (primates, elephants): Sudden death from acute myocarditis

 

typical Gross findings:

• Hydrothorax, hydropericardium, ascites, pulmonary congestion, edema
• Severe cases: extreme pallor of the ventricles, yellow-white 2-10 mm diameter foci throughout myocardium
• Less severe cases: minimal to no findings

 

typical light MICROSCOPIC findings:

• Focal to diffuse myocardial necrosis (predominant lesion) with patchy mineralization and variable amounts of lymphocyte and macrophages, progression to fibrosis with chronicity
• Late-term aborted fetuses: Multifocal myocardial necrosis
• Scant evidence of encephalomyelitis (typically rodents only)

 

ULTRASTRUCTURE:

 

ADDITIONAL DIAGNOSTIC TESTS:

• Virus detection by culture, PCR, or immunohistochemistry (not commercially available)
• Virus can be isolated from all organs of infected swine, but highest titer in myocardium 
• Virus titer decreases quickly and may be negative in cases >11 days long

 

Differential diagnosis:

Myocarditis in pigs:

• Foot and mouth disease (picorna/aphthovirus, D-V17): Gross and microscopic cardiac lesions may be indistinguishable from EMCV
• Porcine parvovirus in pigs can induce a nonsuppurative myocarditis
• Porcine circovirus-2 associated with post-weaning multisystemic wasting syndrome
• Vitamin E/Se deficiency (Mulberry heart disease, C-M06)

 

Edema:

 

Reproductive Failure:

• Porcine reproductive and respiratory syndrome virus (PRRSV, arterivirus, P-V25) - Epidemic disease is characterized by an acute phase of slowly spreading inappetence, fever, and dyspnea lasting 2 weeks (rolling inappetence) followed by a second phase lasting 1-4 months and consisting of late-term reproductive failure
• Porcine circovirus-2 (H-V11)
• Aujeszky's disease (pseudorabies virus, N-V07): Transplacental infections occur in pigs causing abortion in about 50% of sows pregnant in the first month, and the delivery of macerated, mummified, and normal fetuses when infection occurs at later stages of gestation
• Porcine Parvovirus (PPV): Classically considered the cause of SMEDI
• Bacterial infection: E. coli, Streptococcus sp., Staphylococcus sp., Pasteurella sp., Shigella sp., Yersinia sp.

 

Comparative pathology:

• The type B strain of EMCV can affect multiple species including primates (including humans), swine, mice, raccoons, and other mammals
• Nonhuman primates:
  • Many species can affected, both wild and captive, with outbreaks reported
  • In addition to the normal exposure from rodents, horizontal transmission is suspected, and placentitis with increased fetal loss has been reported in baboons
  • The heart is the most significantly affected organ; neurologic lesions are rare, and best described in squirrel monkeys, including cerebral perivascular lymphohistiocytic infiltrates, neuronal necrosis, satellitosis, and meningeal hemorrhage
  • Baboons: There have been several recorded epizootics, suggesting increased susceptibility
  • Differential diagnosis for myocarditis in NHP: coxsackie virus (enterovirus), toxoplasmosis, trypanosomiasis, experimental SIV infection
• Rodents: 
  • May act as a reservoir host, spreading disease to animals via contaminated food, water, or surface from shedding of virus in urine and feces 
  • Infection is usually clinically inapparent
  • Virus is not reported to naturally infect laboratory rodents, although fatal encephalitis and/or myocarditis is common with experimental infection
  • Mice: Natural reservoir host, experimental inoculation routinely results in both encephalitis and myocarditis
  • Rats: Often also implicated in viral transmission, virus can spread between rats
• Zoo/Wildlife:
  • Outbreaks cause sudden death (fatal myocarditis) and tend to occur across mammalian taxa; infection has been reported in carnivores, tapirs, rhinoceros, pygmy hippopotamuses, Thomson’s gazelle, elephants, an oryx-addax cross, and other exotic hoofstock
  • Elephants: Infection occurs in captive and free-ranging African and Asian elephants; virus does not spread between elephants; primary differential diagnosis is elephant endotheliotropic herpesvirus (see C-V05)

 

References:

1. Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents and Rabbits. 4th ed. Ames, IA: Blackwell Publishing; 2016: 35.
2. Duncan M. Perissodactyls. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018:446-447.
3. Gal A, Castilo-Alcala F. Cardiovascular System, Pericardial Cavity, and Lymphatic Vessels. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7^th ed. St. Louis, MO: Mosby Elsevier; 2022: 688-689.
4. Jones MEB, Gasper DJ, Mitchell E. Bovidae, antilocapridae, giraffidae, tragulidae, hippopotamidae. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018:119, 129.
5. Landolfi JA, Terrell SP. Proboscidae. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018:421, 424n.
6. Lowenstine LJ, McManamon R, Terio KA. Apes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018:389.
7. McAloose D, Stalis IH. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018:334.
8. Robinson WF, Robinson NA. Cardiovascular system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 3. 6th ed. Philadelphia, PA: Elsevier; 2016:43.
9. Romey A, Lamglait B, Blanchard Y, et al. Molecular characterization of encephalomyocarditis virus strains isolated from an African elephant and rats in a French zoo. J Vet Diagn Invest. 2020;33: 313-321.
10. Wachtman L, Mansfield K. Viral diseases of nonhuman primates. In: Abee CR, Mansfield K, Tardif S, Morris T, Morris T, eds. Nonhuman Primates in Biomedical Research. London, UK: Academic Press; 2012: 73-74.

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