Several fundamental questions regarding the biology of P. carinii, such as identification of the transmissive stage and the presence of reservoirs in nature, remain to be answered, and methods need to be developed for the long-term culture and in vitro differentiation of the parasite. The use of genetic markers are likely to increase our understanding of the transmission of the organism and the mechanisms leading to severe infection.

With changes in the epidemiology and the application of newer treatments and prophylactic regimens, the types of pulmonary diseases that occur in HIV-infected persons are changing. The important advance is treatment with Zidovudine (AZT) which remains the

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most important agent in slowing the progression of the disease and has resulted in prolonging survival. New ways to assess the progression of HIV disease and new anti-retroviral treatments are available and we see an increased survival despite worsening immunosuppression (Schneider and Rosen 1997). However, the number of individuals at risk for developing PCP appears to be relatively constant as immunosuppression due to therapeutics in an increasing group of organ transplant recipients and in patients with malignancies compensates for the decrease seen in AIDS patients. The incidence of PCP and the overall mortality from PCP is declining (Montaner et al. 1994). Interestingly, compounds active against fungal cell walls are selectively active against the cyst forms of P. carinii (Bartlett et al. 1996a). With the reclassification of Pneumocystis as a fungus and with an increasing knowledge about Pneumocystis metabolism, especially its lipid metabolism, one may expect further innovative therapeutic strategies in the future (Kaneshiro 1998). Studies aiming at the characterization of metabolic pathways of the lipid metabolism of Pneumocystis are potentially of importance for the design of new therapeutic agents with anti-P. carinii activity (Kaneshiro et al. 1989).

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