Yeast cells of Histoplasma capsulatum var. Capsulatum are able to attach and agglutinate human and other mammalian erythrocytes. This hemagglutination favors the fungal dissemination in the host and could be a cofactor to clot formation. Yeast cell-erythrocyte clusters formed during massive fungemia could function as emboli, leading to ischemia and multiple-organ dysfunctions. Besides macrophage and neutrophil activation, disseminated histoplasmosis triggers extensive innate immune mechanisms that produce a systemic inflammatory response associated with microvascular injury and/or changes in the endothelial lining from an anti-coagulant to a procoagulant surface. Thus, disseminated histoplasmosis, particularly in immunocompromised patients, must be better understood not only as just an infection, but also including the mechanisms of the pathogenesis of septic shock. The hemagglutination of H. Capsulatum observed in vitro is dependent on yeast cell-density. Massive fungemia may lead to a similar situation in vivo, resulting in emboli with dangerous consequences for the infected host.
2010-12-22 | 818 visitas | Evalua este artículo 0 valoraciones
Vol. 22 Núm.1. Enero-Marzo 2010 Pags. 5-8 Lab acta 2010; 22(1)