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More Patients, Same Risk

Kent A. Sepkowitz, MD; Arthur E. Brown, MD; Donald Armstrong, MD

Arch Intern Med. 1995;155(11):1125-1128.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 al^2-4 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 . . . [Full Text PDF of this Article]

Author Affiliations
Memorial Sloan-Kettering Cancer Center Cornell University Medical College 1275 York Ave Box 288 New York, NY 10021

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