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Misinformation about Pneumocystis

A recent article in Clinical and Experimental Dermatology by Saadat et al. described a purported case of botryomycosis caused by Pneumocystis carinii, which in turn prompted Mohapatra & Aggarwal to comment on the use of the name Pneumocystis carinii. Both publications contain incorrect information. Mohapatra & Aggarwal were critical of Saadat et al. for using the name Pneumocystis carinii for the human pathogen, Pneumocystis jirovecii. We concur with this opinion. However, we disagree with their opinion that there is no general consensus in the scientific community with regard to the nomenclature that should be used in reports about species in the genus Pneumocystis. P. carinii occurs in rats and has never been seen in humans, where the only species of Pneumocystis known is P. jirovecii (note the spelling of the species, it is not jiroveci). There is broad general agreement that human-associated Pneumocystis should be called P. jirovecii, a name that has been in use for nearly a decade and has been validated by the International Code of Botanical Nomenclature. However, not all authors agree with the consensus, as the letter from Mohapatra & Aggarwal illustrates. Nevertheless, Mohapatra & Aggarwal s reference to the Pneumocystis organism is a mischaracterization because there is no single organism named Pneumocystis. In addition, contrary to their statement, the species P. carinii was not renamed. It has been nearly a century since the name P. carinii was assigned to the species of Pneumocystis that is found in rats. This name has been retained; it is only the species infecting humans that has been named P. jirovecii. In the article by Saadat et al., the microbes observed were mischaracterized in several ways. In addition to referring to them as P. carinii, rather than P. jirovecii, the article indicates that the microbes in question are both protozoa and bacteria. Of course this is not possible. It should be noted that species in the genus Pneumocystis are neither protozoa nor bacteria, but true fungi. Additionally, the evidence that any species of Pneumocystis was involved in the botryomycosis formation is irreproducible and equivocal. The authors fail to indicate which of several commercially available monoclonal antibodies they used, hence the specificity cannot be gauged and the test cannot be reproduced. Additionally, it is difficult to discern the accentuated portions of the organism walls stained with Gomori methenamine silver (GMS) stain in the photomicrograph provided (Fig. 3), which they regard as a diagnostic characteristic. There are no magnification bars in this or the other micrographs, which also complicates interpretation. As GMS stains other fungi, the depicted morphology in that figure could be interpreted as arising from other fungi such as Lacazia loboi, which causes a keloidiform blastomycosis. These facts raise more questions, such as in which country was the patient examined, and where else in the world had he lived or travelled? None of this information was provided. Molecular sequence analysis could have been used to provide a definitive diagnosis of the organism. Until that is done, the report of Pneumocystis, under any species name, causing botryomycosis should be viewed with caution.