PubMedDate not supplied
The purpose of this review is to assist mycologists in having a better understanding of Pneumocystis carinii and the disease that it causes. Now considered to be a fungus, P. carinii is unusual in its life cycle and relationship with the host. P. carinii pneumonia (PCP) pathogenesis, immunology and host defence mechanisms are examined, as well as epidemiological and control strategies. Most pneumocystosis pathophysiological changes result from the parasite's attachment and proliferation in the lungs, resulting in a filling of the alveoli with masses of the micro-organism. Pathological changes include an increase in alveolar capillary membrane permeability and injury to the alveolar epithelium, which may be mediated by the release of degradative enzymes from the pathogen. A host response takes place by hypertrophy, and hyperplasia involving type II epithelial alveolar cells. P carinii interacts with pulmonary surfactants by binding to the hydrophilic proteins A and D, and by modifying their phospholipid composition. Alveolar macrophages and CD4+ T cells play a key role in the host's defence against Pneumocystis. The epidemiology of PCP remains poorly understood. Airborne transmission has been established, but the actual infective form and its source remains unknown. Studies concerning P. carinii genetic diversity have shown that the parasite polymorphism is related, at least partially, to the host species. A strong host-species specificity in P. carinii has been found. From an epidemiological perspective, there appears to be no animal reservoir for the agent of human PCP. Thus, this disease should not be considered to be zoonotic. Although a significant decrease in the incidence of pneumocystosis has been obtained when employing chemoprophylaxis, anti-P. carinii drugs are not completely successful, often inducing deleterious side-effects. For these reasons, new prophylactic and therapeutic strategies need to be developed. One approach could be based on the anti-P. carinii effect of yeast killer toxins and antibiotic anti-idiotypic antibodies.