PNEUMOCYSTIS-CARINII - AN ATYPICAL FUNGAL MICROORGANISM

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 cycl e and relationship with the host. P. carinii pneumonia (PCP) pathogene sis, immunology and host defence mechanisms are examined, as well as e pidemiological and control strategies. Most pneumocystosis pathophysio logical changes result from the parasite's attachment and proliferatio n in the lungs, resulting in a filling of the alveoli with masses of t he micro-organism. Pathological changes include an increase in alveola r capillary membrane permeability and injury to the alveolar epitheliu m, which may be mediated by the release of degradative enzymes from th e pathogen. A host response takes place by hypertrophy, and hyperplasi a involving type II epithelial alveolar cells. P. carinii interacts wi th pulmonary surfactants by binding to the hydrophilic proteins A and D, and by modifying their phospholipid composition. Alveolar macrophag es and CD4(+) T cells play a key role in the host's defence against Pn eumocystis. The epidemiology of PCP remains poorly understood. Airborn e transmission has been established, but the actual infective form and its source remains unknown. Studies concerning P. carinii genetic div ersity 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 a ppears to be no animal reservoir for the agent of human PCP. Thus, thi s disease should not be considered to be zoonotic. Although a signific ant 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. On e approach could be based on the anti-P. carinii effect of yeast kille r toxins and antibiotic anti-idiotypic antibodies.