Sulfa and sulfone drugs are widely used in Pneumocystis carinii pneumonia (PCP) prophylaxis and treatment. Their enzymatic target is the dihydropteroate synthase (DHPS). Point mutations have been described in Pneumocysris carinii f.sp. hominis (P.c.hominis) DHPS gene, mainly at positions 165 and 171 [4]. Mutant P.c.hominis DHPS genotypes have been detected in patients developing PCP with or without prior sulfa or sulfone prophylaxis [3. 51. In a recent study, it was shown that P.c.hominis infected 45 immunocompetent infants diagnosed with bronchiolitis (Nevez et af. WOP-7 2001, abstract PO2). The fungus was detected in nasopharyngeal aspirates (NPAs) using a nested PCR assay amplifying a portion of the mitochondria1 large sub-unit rRNA (mtLSUrRNA) gene [6]. None of these infants received sulfa or sulfone drugs before and after P.c. hominis DNA detection. The aim of this study was to identify wild and mutant P.c.hominis DHPS genotypes in this infant population. Since no infant had a past history of sulfa or sulfone treatment, the results show that mutant types can be present among a population of P.c. hominis organisms not submitted to selection pressure. Presence of these mutant types in this infant population could result in an incidental acquisition of the fungus. These results are consistent with those previously observed in adult patients diagnosed with PCP. Indeed, mutant types have also been detected casually in these patients despite the absence of sulfa or sulfone treatment [3.5]. These observations suggest that transmission cycles of P.c.horninis in infants with bronchiolitis and adults with PCP could not be strictly independent. The acquisition of P.c.hominis in immunosuppressed patients and immunocompetent infants developing different clinical forms of P .c.hominis infection could result &om a unnmon exogenous (human or non-human) source of the fungus.
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