Experimental Encephalomyocarditis Virus Infection in Mongolian Gerbils (Meriones unguiculatus)

Abstract

Abstract. Two strains of Mongolian gerbils (Meriones unguiculatus), Tumble Brook (TUM) and Japan Medical Science (JMS), were intraperitoneally inoculated with the D variant of encephalomyocarditis virus (EMC-D) and killed 3 days later. Mortality was significantly higher in females than in males. Evidence of viral replication was detected in the heart of both strains and in the pancreas of the TUM strain. Histopathological alterations were found in the heart and pancreas. Heart lesions involved foci of necrosis with inflammatory cell infiltration and calcification in both strains. Pancreatic lesions were restricted to the exocrine glands; islets of Langerhans were rarely and secondarily involved in the extensive destruction of exocrine glands. Severe acinar cell necrosis with marked inflammatory edema was conspicuous in TUM, whereas only slight acinar cell involvement was detected in JMS gerbils. Immunoperoxidase staining showed viral antigens in intracytoplasmic vacuoles in damaged acinar cells.Encephalomyocarditis (EMC) virus was first isolated from pigs with myocarditis in Panama14 and has been known as an important cause of spontaneous porcine myocarditis.'J2 Small rodents are suspected to be reservoir hosts or carriers.2 EMC virus has also been a useful tool for investigations of diabetes mellitus; e.g., the virus induces a diabetes-like syndrome in mice.9 Detailed virologic and histopathologic studies on EMC virus infection have been done in mi~e.~,~JO This paper describes the virology and histopathology of Mongolian gerbils (Meriones unguiculatus) infected with the

Pathogenesis of encephalomyocarditis experimental infection in young piglets: a potential animal model to study viral myocarditis

“…Isolates that have caused myocarditis in pigs have been associated with rodent outbreaks [2,19,30]. In wild rodents, the natural hosts, the virus usually persists without causing disease [32], whereas infection in laboratory rodents commonly [30] produces fatal encephalitis or myocarditis [7,9,23,27,33,38]. In swine, the reported natural infections with EMCV have different epidemiological characteristics, probably depending on different EMCV strains which act with different pathogenicity [1,6].…”

Encephalomyocarditis-virus-induced diabetes model resembles ?fulminant? Type 1 diabetes in humans

“…1), in the EMC-virus-induced diabetes model resembles fulminant Type 1 diabetes (Table 1). Although it has been recognised that the EMC virus diabetic strain does not infect exocrine acinar cells, this virus does infect exocrine glands in Mongolian gerbils [6] and Syrian hamsters, suggesting that it may also cause exocrine damage in mice as we presented here. Moreover, approximately 70% of fulminant Type 1 diabetic patients have a history of flu-like symptoms such as fever, headache, sore throat, coughing, rhinorrhoea and joint pain, suggesting the involvement of viral infection in this type of Type 1 diabetes [3].…”

Encephalomyocarditis (EMC) virus infection in PC12 and C6 cells

“…The virus was first isolated from nonhuman primates and then from pigs and is an important cause of lethal acute myocarditis in piglets and of foetal death or abortion in pregnant sows (Murane et al 1960;Kim et al 1989). In this regard, Matsuzaki et al (1989a) reported that adult rats showed no susceptibility to EMC virus infection, though almost all species of laboratory rodents examined in our laboratory showed susceptibility to EMC virus infection (Matsuzaki et al 1989b;Hirasawa et al 1991;Petruccelli et al 1991;Takeda et al 1995;Doi et al 1995;Ueno et al 1996). In this regard, Matsuzaki et al (1989a) reported that adult rats showed no susceptibility to EMC virus infection, though almost all species of laboratory rodents examined in our laboratory showed susceptibility to EMC virus infection (Matsuzaki et al 1989b;Hirasawa et al 1991;Petruccelli et al 1991;Takeda et al 1995;Doi et al 1995;Ueno et al 1996).…”

“…Anti-EMC-D guinea pig serum prepared in our laboratory (Matsuzaki et al 1989b) was used as the primary antibody and fluorescein-labelled antiguinea pig IgG goat serum as the secondary antibody, respectively. Anti-EMC-D guinea pig serum prepared in our laboratory (Matsuzaki et al 1989b) was used as the primary antibody and fluorescein-labelled antiguinea pig IgG goat serum as the secondary antibody, respectively.…”