Author Affiliations: Critical Care Medicine Department (Drs Kovacs and Masur) and Microbiology Service, Department of Laboratory Medicine (Dr Gill), Clinical Center, National Institutes of Health, Bethesda, Md; and Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor (Dr Meshnick).
Grand Rounds at the Clinical Center of the National
Institutes of Health Section Editors: John I. Gallin, MD, the Clinical
Center of the National Institutes of Health, Bethesda, Md; David S. Cooper,
MD, Contributing Editor, JAMA.
Pneumocystis carinii has been recognized as
a human pathogen for nearly 50 years. We present a case of P carinii infection that typifies clinical presentation in the era
of the acquired immunodeficiency syndrome epidemic. The high incidence of P carinii pneumonia in persons infected with human immunodeficiency
virus (HIV) has served to focus laboratory and clinical research efforts on
better understanding the biology of the organism and on improving diagnosis,
treatment, and prevention of this disease. Although inability to culture P carinii has hampered research efforts, molecular and
immunologic approaches have led to the recognition that the organism represents
a family of fungi with a very restricted host range and have allowed characterization
of clinically relevant antigens and enzymes. Molecular epidemiologic studies
have identified more than 50 strains of human-derived P
carinii and have suggested that recently acquired infection, as opposed
to reactivation of latent infection, may account for many cases of clinical
disease. Diagnosis has been improved by the development of organism-specific
monoclonal antibodies and, more recently, by polymerase chain reaction using
multicopy gene targets, together with induced sputum or oral wash samples.
Chemotherapeutic prophylaxis is very effective in preventing P carinii pneumonia; the combination of trimethoprim-sulfamethoxazole
remains the first-line agent for both therapy and prophylaxis. Prophylaxis
needs to be administered only during periods of high risk; in HIV-infected
patients responding to effective antiretroviral therapies, prophylaxis no
longer needs to be lifelong. Molecular studies have identified mutations in
the target of sulfa drugs that appear to represent emerging resistance in P carinii. Resistance to atovaquone, a second-line agent,
may also be developing.
Kovacs JA, Gill VJ, Meshnick S, Masur H. New Insights Into Transmission, Diagnosis, and Drug Treatment of Pneumocystis carinii Pneumonia. JAMA. 2001;286(19):2450-2460. doi:10.1001/jama.286.19.2450