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

Abstract

-The pathogenesis of encephalomyocarditis (EMC) due to the EMC virus (EMCV) was studied in 24 piglets oro-nasally infected with the field isolate B279/95. Two pigs were kept as negative controls and were euthanised at hour 0. The remaining 24 were euthanised every 6 h up to 78-h post infection (hpi). Virus isolation, histological examination and EMCV immunodetection were performed on the spleen, intestine, pancreas, liver, kidneys, heart, lungs, lymph nodes, tonsils and brain. EMCV was isolated at 6-hpi from the intestine and lymph nodes and at 12-hpi from the heart. From 6 to 12-hpi, scattered degenerate myocardiocytes were immunolabelled. Subsequently, myocarditis developed and progressively worsened. Immunopositive reaction in tonsil macrophages, observed in the early stage of infection (6-hpi), suggests that tonsils are the portal of entry, and by mean of wandering macrophages the EMC virus is then distributed through the body. Afterwards, EMCV-B279/95 replicates intensively in the cytoplasm of myocardiocytes and the acute myocarditis is strictly related to the tropism of these cells. Four pigs died spontaneously. In three animals no post mortem lesions or virus were isolated/detected, although all of them showed mild myocarditis. The experimental infection with EMCV B279/95 indicates: (i) the experimental protocol mimics the individual variability observed in natural disease, (ii) tonsils are the portal of entry of infection and the heart is the target organ, (iii) EMCV provides a valuable animal model for comparative studies on progressive viral myocarditis. encephalomyocarditis virus-EMCV / swine / myocarditis / immunohistochemistry

Encephalomyocarditis virus in a captive Malayan tapir (<i>Tapirus indicus</i>)

“…In our case that aged 5 months, the animal was clearly much younger and more comparable to the young pigs that die due to EMCV in Belgium. Moreover, the viral sequences of our tapir strain are identical to the porcine isolate, which was collected in the same period, and share a high (> 95%) identity with the typical Belgian porcine myocardial strain (Koenen et al, 1999;Gelmetti et al, 2006). Also the gross and histological lesions are comparable to the lesions described in young piglets with EMCV (Billinis et al, 1999;Psychas et al, 2001).…”

“…Since the toxicology lab did not find any of the ionophores that could be involved in Belgium (maduromicin, narasin, lasalocid, monensin, salinomycin, semduramicin) in the liver tissue, this possibility was also excluded. Outbreaks of encephalomyocarditis virus are notorious for their suddenness and many cases occur as asymptomatic deaths both in zoo mammals and in young domestic pigs (Wells et al, 1989;Reddacliff et al, 1997;Gelmetti et al, 2006;Vogelnest et al, 2006;Canelli et al, 2010;Yeo et al, 2013). In our case, the Malayan tapir died suddenly without any predictive symptoms.…”

Selective inhibitors of picornavirus replication

“…EMCV was isolated from several animals, as well as humans, and was shown to cause lesions in multiple organs, including heart, pancreas and CNS. 6,7 The prototype of the enterovirus genus or of the picornavirus family in general, is poliovirus. This virus, causing amongst others paralytic poliomyelitis, threatened the lives of millions of people worldwide until the introduction of oral polio vaccines in 1960.…”

Sudden infant death syndrome and Ljungan virus

“…This is also concordant with known stress-related risk factors associated with SIDS including sleeping position and environmental tobacco exposure. In addition, a closely related virus, encephalomyocarditis virus, causes sudden death in infant pigs [38,39]. The third line of evidence focuses on the intriguing fact that the incidence of SIDS coincides with the density of an apparently primary rodent reservoir of LV.…”