LAUSR

Pneumocystis jirovecii is a transmissible fungus that causes life-threatening pneumonia in immunosuppressed patients. Pneumocystis pneumonia (PCP) remains the most frequent AIDS-defining illness in developed countries, while it is also observed with an increasing frequency in other immunocompromised patients (1). Moreover, diverse populations who do not develop PCP can frequently be colonized by P. jirovecii, the fungus being a potential comorbidity factor (2). Thus, P. jirovecii infections are still a public health issue which justifies the interest of multidisciplinary teams focusing on fundamental or applied research. It is assumed that the infection is related to the active proliferation of Pneumocystis in alveoli, and PCP is mostly associated with high fungal pulmonary burdens. PCP diagnosis is usually based on detection of asci and trophic forms in lung samples. Nonetheless, when pulmonary burdens are low, specifically in colonized patients but also in some PCP patients, detection of the fungus requires highly sensitive PCR techniques, while microscopic examination remains negative. Beyond differences in size and shape, trophic forms and asci differ by their components. (1,3)-D Glucan (BG) is absent in trophic forms, whereas it is abundant in the ascus wall. Glucan synthesis is inhibited by some echinocandins, broad-spectrum antifungal agents that have been used in Pneumocystis animal models. We read with interest the article by Cushion and colleagues, who used a “fascinating echinocandin-treated mouse model” (3). The gene expression profiles of P. murina were compared between infected untreated mice and those treated with an echinocandin. Cushion and colleagues showed that ascus formation was necessary for Pneumocystis proliferation. These findings arouse our attention since they provide additional arguments to our former investigations of P. jirovecii pulmonary colonization. In 1999, by combining an anti-ascus immunofluorescence assay (Monofluo pneumocystis kit; Bio-Rad, Marnes-La-Coquette, France), an antitrophic immunocytochemical assay (M 778; Dako A/S, Copenhagen, Denmark), and a PCR assay amplifying the mitochondrial large-subunit rRNA gene, we obtained original results showing that the stages harbored by colonized patients were trophic forms rather than asci and that ascus detection was related to PCP diagnosis (4). In 2013, by combining the same immunofluorescence and PCR assays and serum BG detection (Associates of Cape Cod, Inc., Cape Cod, MA), we showed that PCP was associated with positive BG levels but that colonization was associated with low/negative BG levels (5). The high BG levels in PCP patients may be correlated with the presence of asci in the lungs, which were effectively numerous and easily observable upon microscopic examination, whereas Citation Nevez G, Totet A, Damiani C, Le Gal S. 2018. The fascinating echinocandin-treated mouse model of Pneumocystis murina to understand Pneumocystis jirovecii. Antimicrob Agents Chemother 62:e00992-18. https://doi .org/10.1128/AAC.00992-18. Copyright © 2018 American Society for Microbiology. All Rights Reserved. Address correspondence to Gilles Nevez, [email protected]. For the author reply, see https://doi.org/10 .1128/AAC.01036-18. LETTER TO THE EDITOR