Immunopathology of Dirofilaria immitis Infection

Abstract

Heartworm disease caused by Dirofilaria immitis affects canine and feline hosts, with infections occasionally being reported in humans. Studies have shown that both dirofilarial antigens and those derived from its bacterial endosymbiont Wolbachia, interact with the host organism during canine, feline and human infections and participate in the development of the pathology and in the regulation of the host's immune response. Both innate and acquired immune responses are observed and the development of the acquired response may depend on the host and, or on its parasitological status. This review aims at illustrating current research on the role of both D. immitis and Wolbachia, in the immunology and immunopathology of dirofilariosis.

Heartworm (Dirofilaria immitis) disease in a Brazilian oncilla (Leopardus tigrinus)

“…The female heartworms are viviparous, releasing microfilariae into the bloodstream. These are taken up by blood-sucking mosquitoes, where they develop to infective larvae and are inoculated into the dermis of the final host where, after several months of migration and maturation, reach the sites where they will live as adults (Simón et al 2007, Litster & Atwell 2008. Pathological changes induced by heartworms are in part due to physical obstruction of the heart chambers, valves, and vessels.…”

“…Pathological changes induced by heartworms are in part due to physical obstruction of the heart chambers, valves, and vessels. The immunopathology of infection is complex and the clinical manifestations largely depend on the immune response that is stimulated by the parasites (Simón et al 2007). A pulmonary endarteritis develops, characterized by myointimal proliferations and obstructive fibrosis, which leads to pulmonary hypertension and congestive right heart disease (Robinson & Maxie 1993, Nelson et al 2003, Simón et al, 2007.…”

“…The immunopathology of infection is complex and the clinical manifestations largely depend on the immune response that is stimulated by the parasites (Simón et al 2007). A pulmonary endarteritis develops, characterized by myointimal proliferations and obstructive fibrosis, which leads to pulmonary hypertension and congestive right heart disease (Robinson & Maxie 1993, Nelson et al 2003, Simón et al, 2007. Surface proteins of Wolbachia bacterial endosymbiontics of heartworms are released, especially after death of the parasites, stimulating the host immune system and acting as important protagonists in the inflammatory pathology of heartworm disease (Simón et al 2007).…”

“…A pulmonary endarteritis develops, characterized by myointimal proliferations and obstructive fibrosis, which leads to pulmonary hypertension and congestive right heart disease (Robinson & Maxie 1993, Nelson et al 2003, Simón et al, 2007. Surface proteins of Wolbachia bacterial endosymbiontics of heartworms are released, especially after death of the parasites, stimulating the host immune system and acting as important protagonists in the inflammatory pathology of heartworm disease (Simón et al 2007). Dead adult heartworms cause tromboembolism, exacerbating the pulmonary hypertension and initiating a granulomatous reaction in the vessel wall that may extend to the pulmonary parenchyma.…”

“…The death of adult heartworms can be associated with a peracute syndrome consisting of respiratory distress, ataxia, collapse, seizures, hemoptysis, and sudden death of the host (Nelson et al 2005). In cats, severe complications can occur in the presence of even a small number of adult heartworms (Simón et al 2007). Feline heartworm disease is characterized by strong vascular inflamatory reactions, frequent tromboembolisms, central nervous system and gastrointestinal involvement (Lister & Atwell 2008).…”