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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Clin Infect Dis. 2010 Aug 1;51(3):266. doi: 10.1086/653934

Editorial Commentary

Marilyn S Bartlett 1,(1), Chao-Hung Lee 1,(2)
PMCID: PMC3062257  NIHMSID: NIHMS202456  PMID: 20572758

In this issue of the journal, Choukri et al. [1] state that their study provides the first quantitative data on the spread of P. jirovecii in the exhaled air from infected patients. There are additional data in prior studies using air samples collected in rooms of patients diagnosed with P. jiroveceii showing that not only could the organisms be detected, but that their types correlated with types demonstrated in patients samples [2]. The air samples were compared to samples from areas close to the rooms studied as well as other control areas. We believe that airborne transmission was demonstrated with the samples and methods used. Since airborne transmission for animals had been very well established, it was the next step to show that transmission occurred in humans as well. It is important that these additional studies likewise demonstrate detection of P. jirovecii in air collected near infected patients. Concerns about isolation of infected patients have been discussed for a long time and may be reevaluated with these data.

We had a strong belief that transmission of infection was by the airborne route. When we first started working with Pneunocystis jirovecii, then called P. carinii, the only way to obtain organisms for study was to keep a large colony of Sprague Dawley rats and house new ones with the most infected ones as Dr. Jack Frenkel carefully described this in his landmark paper [3]. When we developed the first inoculated animal models (first rat and then mouse) in order to have a single strain and reproducible infection, we found that we needed strict isolation procedures to prevent airborne transmission. We housed our animals in microisolator cages and handled them in a laminar flow hood, but still had occasional cross infections. This led us to believe that there had to be airborne transmission in humans too. We reported our initial findings at the “International Workshops on Opportunistic Protists.”

We were convinced of airborne transmission because the first reports of large numbers of infections were in babies and children that were living in crowded conditions in orphanages or nurseries in European countries after World War II and were immunosuppressed due to malnutrition. One of our main concerns was whether patients diagnosed with Pneumocystis pneumonia should be isolated from other immunosuppressed individuals. The additional data provided by Choukri et al. [1] suggests that this question should be revisited.

ACKNOWLEDGMENT

This work was supported in part by National Institutes of Health grant RO1-AI-34304.

Footnotes

The authors have no conflicts of interest.

References

  • 1.Choukri F, Menotti J, Sarfati C, Lucet JC, Nevez G, et al. Quantification and Spread of Pneumocystis jirovecii in the Surrounding Air of Patients with Pneumocystis Pneumonia. Clin Infect Dis. doi: 10.1086/653933. This issue. [DOI] [PubMed] [Google Scholar]
  • 2.Bartlett MS, Vermund SH, Jacobs R, Durant PJ, Shaw MM, Smith JW, Tang X, Lu JJ, Li B, Jin S, Lee CH. Detection of Pneumocystis carinii DNA in air samples: Likely environmental risk to susceptible persons. J. Clin. Microbiol. 1997;35:2511–2513. doi: 10.1128/jcm.35.10.2511-2513.1997. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Frenkel JK, Good JT, Shultz JA. Latent Pneumocystis infection of rats, relapse, and chemotherapy. Laboratory Investigation. 1966;15:1559–1577. [PubMed] [Google Scholar]

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