Gelmetti Daniela, Meroni Alessandra, Brocchi Emiliana, Koenen Frank, Cammarata Giorgio
Istituto Zooprofilattico Sperimentale Lombardia-Emilia Romagna,Via Celoria 12, 20133 Milano, Italy.
Vet Res. 2006 Jan-Feb;37(1):15-23. doi: 10.1051/vetres:2005041.
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.
对24头经口鼻感染野毒株B279/95的仔猪进行了研究，以探讨由脑心肌炎病毒（EMCV）引起的脑心肌炎（EMC）的发病机制。将2头猪作为阴性对照，并在0小时实施安乐死。其余24头猪在感染后（hpi）每6小时实施安乐死，直至78小时。对脾脏、肠道、胰腺、肝脏、肾脏、心脏、肺、淋巴结、扁桃体和大脑进行病毒分离、组织学检查和EMCV免疫检测。在感染后6小时从肠道和淋巴结中分离到EMCV，在12小时从心脏中分离到。在感染后6至12小时，散在的变性心肌细胞被免疫标记。随后，心肌炎发展并逐渐恶化。在感染早期（6小时）观察到扁桃体巨噬细胞中有免疫阳性反应，这表明扁桃体是病毒的侵入门户，EMC病毒随后通过游走的巨噬细胞在体内传播。此后，EMCV - B279/95在心肌细胞的细胞质中大量复制，急性心肌炎与这些细胞的嗜性密切相关。4头猪自然死亡。在3只动物中，尽管它们都表现出轻度心肌炎，但未分离/检测到死后病变或病毒。用EMCV B279/95进行的实验性感染表明：（i）实验方案模拟了自然疾病中观察到的个体变异性，（ii）扁桃体是感染的侵入门户，心脏是靶器官；（iii）EMCV为进行进行性病毒性心肌炎的比较研究提供了有价值的动物模型。
