Airborne spread of Pneumocystis jirovecii
Abstract & Commentary
By Dean L. Winslow, MD, FACP, FIDSA Chief, Division of AIDS Medicine, Santa Clara Valley Medical Center; Clinical Professor, Stanford University School of Medicine, Section Editor, HIV, is Associate Editor for Infectious Disease Alert.
Dr. Winslow is on the speaker's bureau for GSK and Cubist Pharmaceuticals, and is a consultant for Siemens Diagnostics.
Synopsis: Nineteen patients admitted to the hospital with Pneumocystis pneumonia had air sampling performed at distances from 1 m to 8 m from patients' heads; additional samples from patient wards and outdoors were obtained. Using real-time PCR at 1 m distance, P. jirovecii DNA was detected in 15 (79.8%). Copy number decreased with distance from the patient, but four of 12 samples (33.3%) taken at 8 m (in the corridor) were positive.
Source: Choukri F, et al. Quantification and spread of Pneumocystis jirovecii in the surrounding air of patients with Pneumocystis pneumonia. Clin Infect Dis. 2010;51:259-265.
Using liquid medium with a commercial air sampler, air was sampled at varying distances from 19 patients admitted to the hospital with Pneumocystis pneumonia. Samples were examined and DNA quantified using a real-time PCR assay targeting the large subunit ribosomal RNA gene. At 1 m distance from the patients' heads, Pnuemocystis jirovecii (PJP) DNA was detected in 15 of the 19 patients (79.8%), with fungal burdens ranging from 7.5x10e3 to 4.5x10e6 copies/me3. The levels of DNA decreased proportionately to distance from the patients' heads, but four of 12 samples (33.3%), taken at 8 m in the corridor outside the patients' rooms, were positive. Forty control samples obtained from other wards in the hospital and from outside air were negative for Pneumocystis DNA.
Commentary
Serologic surveys have shown that infection with PJP is almost universal by the time humans are about two years of age. It is a common cause of pneumonia in patients with advanced HIV infection, and was rarely seen prior to the AIDS era in other heavily immunosuppressed patients. The original hypothesis was that PJP pneumonia was due to reactivation of latent disease (similar to the pathogenesis of toxoplasma encephalitis in immunocompromised patients). However, host-to-host transmission of PJP has been demonstrated in rodents, and the original descriptions of PJP were reported in outbreak settings in malnourished orphans in Europe in the immediate aftermath of World War II, and strongly suggested patient-to-patient transmission. Recent studies have shown evidence of active subclinical PJP infection in immunocompetent patients, and genetic analysis of PJP obtained from these patients has supported the concept that reinfection with PJP occurs throughout life. Small studies and case reports have demonstrated human-to-human transmission of PJP in the hospital setting. Based on these case reports, the CDC recommends avoiding placing an immunocompromised patient in the same room with a patient with PJP pneumonia.
This study is important since it is the first study in humans to clearly show the spread of PJP in the environment, and uses modern molecular techniques to quantify the fungal burden associated with shedding from symptomatic patients. These data, and the methods used in this study, will be important in future studies to better estimate the risk of airborne transmission of PJP.
Using liquid medium with a commercial air sampler, air was sampled at varying distances from 19 patients admitted to the hospital with Pneumocystis pneumonia. Samples were examined and DNA quantified using a real-time PCR assay targeting the large subunit ribosomal RNA gene.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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