Особливості епізоотології та патогенезу за африканської чуми свиней

Abstract

В статті описані деякі ланки патогенезу за АЧС, представлені можливі шляхи зараження, видовий склад резервуару збудника – кліща, у різних ареалах, припущена його роль у циклі розвитку хвороби. Обґрунтовано, що вірусна реплікація збудника АЧС призводить до лімфоїдного виснаження в організмі через руйнування і апоптоз моноцитів та неінфікованих лімфоцитів. Доведено, що в основі планування оздоровчих заходів при АЧС лежить не тільки вивчення особливостей збудника та симптомокомплексу хвороби, а чітке розуміння патогенезу захворювання і вивчення механізмів її поширення.

В статье описаны некоторые аспекты патогенеза при АЧС, представлены возможные пути заражения, видовой состав резервуара возбудителя – клеща – в разных ареалах, предположена его роль в цикле развития болезни. Аргументировано, что репликация возбудителя АЧС вызывает лимфоидное истощение организма, вследствии разрушения и апоптоза моноцитов и неинфицированных лимфоцитов. Доказано, что в фундаменте планирования оздоровительных мероприятий при АЧС лежит не только изучение особенностей возбудителя и симптомокомплекса болезни, а четкое понимание патогенеза заболевания и изучение механизмов его распространения.

The article describes some of the pathogenesis' components under ASF. It also presents the possible ways of infection as well as the specific composition of the pathogen reservoir (tick) in different areas. The role of tick in the cycle of the disease development is assumed. Without tick involvement, ASFV enters the body via the tonsils or dorsal pharyngeal mucosa to the mandibular or retropharyngeal lymph nodes, from where the virus spreads systemically through viraemia. Thereafter, the virus is detectable in almost all tissues. Highest titres are observed in tissues containing a large component of the mononuclear phagocyte system (reticuloendothelial cellular elements) like the spleen and lymphnodes. It was observed that different subsets of monocytes and macrophages show a different susceptibility to ASFV, both in vivo and in vitro. Bone marrow derived cells and fresh blood monocytes are less susceptible to in vitro infection than alveolar macrophages. In general, it could be shown that cells of higher maturation stages expressing higher levels of macrophage specific markers and SLA II antigens were most susceptible to ASFV infection. Upon ASFV infection, several macrophage subpopulations show signs of secretory and/or phagocytic activation. Moreover, destruction of monocytes/macrophages leads to release of cellular components. Activated monocytes/macrophages secrete a wide range of mediators including proinflammatory cytokines such as IL-1, IL-6, and TNF. These cytokines can trigger acute phase reactions, inflammation, activation of endothelial cells, and apoptosis. Among these factors, TNF is particularly important. It can induce vascular changes (vasodilatation and increased permeability) and modulates the activation status of the vascular endothelium (procoagulant/anticoagulant). Moreover, TNF is involved in the control of apoptosis. Thus, survival of animals may at least partly depend on the nature of cytokine responses. An interesting finding in line with both above mentioned considerations is that pulmonary intravas- cular macrophages but not alveolar macrophages are infected. Infection of these cells leads to intense activation and consequently expression of IL-1a and TNF. Later on, additional cell types in various organs including megakaryocytes tonsillar epithelial cells, hepatocytes, kidney cells and endothelial cells get infected. In vivo haemadsorption is observed in hepatic sinusoids, lymphsinuses, and red splenicpulp. The kidney is another organ with severe pathomorphological changes including haemorrhages. In acute ASF, proliferative glomerulonephritis including hyperplasia of collecting ducts is seen while in subacute forms immune-mediated, subendothelial and mesangial deposits of immunoglobulins and complement prevail. In addition, virus replication in fibroblasts and smooth muscle cells of small blood vessels is seen in later stages. In case of subacute and chronic forms, immune mediated events including immune-complex deposits are discussed as a cause of interstitial haemorrhages associated with diapedesi. It has been substantiated that viral replication of the ASF causative agent leads to lymphoid depletion in the body due to the destruction and apoptosis of monocytes and uninfected lymphocytes. It is proved that the basis of the health-improving planning measures at ASF is not only the study of the pathogen characteristics and the symptom complex of the disease, but also a clear understanding of the disease’s pathogenesis and the study of its spread mechanisms.