This study was undertaken to assess whether glycolipid antigens (particularly gangliosides) are associated with Pneumocystis carinii obtained from human lungs. Gangliosides were extracted, purified in high performance thin-layer chromatography and stained with resorcinol. Two resorcinol-positive bands, co-migrating with GM1 and GD1a were demonstrated, suggesting the existence of ganglioside molecules on P. carinii. No resorcinol-positive bands were revealed in the pulmonary control tissue. In addition, an antiserum obtained from rabbits immunized with P. carinii antigen reacted with gangliosides GM1, and GD1a, as revealed by a dot immunobinding assay. This reactivity was inhibited by first incubating the antiserum with ganglioside micelles. Furthermore, anti-glycosphingolipid antibodies (aGM1) reacted with the bands of 200 and 55 kDa of P. carinii antigen. These results suggest that ganglioside antigens expressed on P. carinii can trigger specific immune responses.

Pneumocystis carinii pneumonia (PCP) is a life-threatening infection that occurs in immunocompromised individuals, particularly those with advanced human immunodeficiency virus (HIV) infection. Interestingly, morbidity and mortality is related to the underlying cause of immunosuppression, with AIDS patients faring better than oncology patients for example. In addition, the prognosis of PCP has been correlated with markers of inflammation rather than with organism numbers. There is now increasing evidence that lung damage occurring during PCP is a result of the type and extent of the host inflammatory response to P. carinii rather than a result of direct damage by the organism. This review will discuss the experimental and clinical data demonstrating how the host-mediated inflammatory response to infection with P. carinii determines the ultimate outcome of PCP. A better understanding of the pathophysiology of PCP should lead to the development of improved therapies for the treatment of PCP.

Pneumocystis carinii is an opportunistic infection found in patients with impaired immunity. Under favourable conditions the parasite can spread via the blood stream or lymphatic vessels and cause extrapulmonary dissemination. We report a case of P carinii infection presenting as bilateral aural polyps, otitis media and mastoiditis in human immunodeficiency (HIV)-positive patient with no history of prior or concomitant P carinii infection.

Seasonal dynamics of Pneumocystis carinii in the field vole, Microtus agrestis, and in the common shrew, Sorex araneus, were investigated in southern and central Finland by microscopical examination of methenamine silver-stained tissue sections. In both host species at both localities the number of P. carinii cyst forms was highest in late autumn (November). In S. araneus, prevalence was higher than in M. agrestis during all seasons. None of the animals was heavily infected or apparently ill, and neither species showed any extrapulmonary dissemination. In this study covering an increase phase and 4 peak host-density phases of the vole cycle, the occurrence of P. carinii seemed to be related to the population density of M. agrestis.