@article{mbs:/content/journal/jmm/10.1099/jmm.0.076257-0, author = "Vanspauwen, Marijke J. and Knops, Vera E. J. and Bruggeman, Cathrien A. and van Mook, Walther N. K. A. and Linssen, Catharina F. M.", title = "Molecular epidemiology of Pneumocystis jiroveci in human immunodeficiency virus-positive and -negative immunocompromised patients in The Netherlands", journal= "Journal of Medical Microbiology", year = "2014", volume = "63", number = "10", pages = "1294-1302", doi = "https://doi.org/10.1099/jmm.0.076257-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.076257-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", abstract = " Pneumocystis jiroveci infections can cause pneumocystis pneumonia (PCP) or lead to colonization without signs of PCP. Over the years, different genotypes of P. jiroveci have been discovered. Genomic typing of P. jiroveci in different subpopulations can contribute to unravelling the pathogenesis, transmission and spread of the different genotypes. In this study, we wanted to determine the distribution of P. jiroveci genotypes in immunocompetent and immunocompromised patients in The Netherlands and determine the clinical relevance of these detected mutations. A real-time PCR targeting the major surface glycoprotein gene (MSG) was used as a screening test for the presence of P. jiroveci DNA. Samples positive for MSG were genotyped based on the internal transcribed spacer (ITS) and dihydropteroate synthase (DHPS) genes. Of the 595 included bronchoalveolar lavage fluid samples, 116 revealed the presence of P. jiroveci DNA. A total of 52 of the 116 samples were ITS genotyped and 58 DHPS genotyped. The ITS genotyping revealed 17 ITS types, including two types that have not been described previously. There was no correlation between ITS genotype and underlying disease. All ITS- and DHPS-genotyped samples were found in immunocompromised patients. Of the 58 DHPS-genotyped samples, 50 were found to be WT. The other eight samples revealed a mixed genotype consisting of WT and type 1. The majority of the latter recovered on trimethoprim–sulfamethoxazole suggesting no clinical relevance for this mutation.", }