MORE THAN 80 years after its identification in the lungs of rats by Chagas and Carini, and 50 years after its establishment as the cause of epidemic plasma cell pneumonitis in malnourished or premature infants,1Pneumocystis carinii continues to puzzle and surprise. Fundamental debates continue about its taxonomy (fungus or protozoan) and transmissibility. In addition, there is no reliable way to cultivate the organism in vitro. Despite these gaps in basic information, the optimal treatment and prophylaxis of P carinii pneumonia (PCP) are well established. Landmark studies by Hughes et al2-4 demonstrated the central role of sulfamethoxazole-trimethoprim in the treatment and prevention of this disease.
In the 1980s, the high rates of PCP occurring among persons infected with human immunodeficiency virus (HIV) largely overshadowed its role as a pathogen among the HIV negative. For example, in 1992, PCP accounted for 42% of all acquired immunodeficiency syndrome—indicator diseases reported
Sepkowitz KA, Brown AE, Armstrong D. Pneumocystis carinii Pneumonia Without Acquired Immunodeficiency Syndrome: More Patients, Same Risk. Arch Intern Med. 1995;155(11):1125–1128. doi:10.1001/archinte.1995.00430110015002
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