Economically important and world-wide distributed, porcine pleuropneumonia is one of the most important diseases of the respiratory tract of pigs. The pathogenesis of the disease is a very complex process, which has not been fully elucidated as yet. This paper presents data currently available on this subject. Pigs are the main and highly specific reservoir of Actinobacillus pleuropneumoniae (App). It was shown that as little as 10 bacteria can induce the disease. Its spread is facilitated by excessive concentration of animals, increased trade, transport, mixing piglets from different litters and of different immune status, coexisting diseases, and unfavorable environmental conditions. To induce pleuropneumonia, the colonization of the respiratory tract by App is required, which depends on their ability to adhere to epithelial cells. It was demonstrated that App bound very weakly with the cilia and tracheal or bronchial epithelium, but adhered closely to the cilia of bronchioles and alveolar epithelial cells. Virulence factors produced by App, especially Apx toxins, play an important role in the pathogenesis of pleuropneumonia. To induce lesions in tissues, App has to replicate in the host’s organism. Replication efficiency depends on their ability to obtain nutrients, especially iron. App synthesized a large number of factors involved in the acquisition and transport of iron ions (transferrin-binding proteins, hemoglobin-binding proteins, siderophores). If App are capable to replicate and survive in a pig’s tissues, symptoms and lung lesions typical of pleuropneumonia are observed within few hours after infection.
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