REPLY
We thank Nevez and Le Gal for their interest in our work and for underscoring its importance (1). Our results strongly suggest that Pneumocystis jirovecii, which infects humans, is sensitive to caspofungin, as are the Pneumocystis species that infect rodents used as models. Thus, we fully agree with Nevez and Le Gal that the usefulness of caspofungin to treat Pneumocystis pneumonia should be considered for clinical use. In addition, the sensitivity of P. jirovecii to the other echinocandins used clinically will have to be characterized. Indeed, Saccharomyces cerevisiae harbors three differentially regulated genes encoding the target of the echinocandins, the catalytic subunit of the 1,3-β-glucan synthase. Despite close homology, these enzymes present drastically distinct sensitivities to the different echinocandins, namely, caspofungin, anidulafungin, and micafungin (1–3). The Pneumocystis species infecting rodents proved to be sensitive to the three echinocandins (4, 5). Nevertheless, because the homology between the enzymes of the different Pneumocystis species is similar to that between the three S. cerevisiae enzymes (1), one cannot exclude the possibility that P. jirovecii is insensitive to anidulafungin and micafungin.
FOOTNOTES
This is a response to a letter by Nevez and Le Gal (https://doi.org/10.1128/AAC.01296-19).
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