Dihydropteroate synthase gene mutations in Pneumocystis jiroveci strains isolated from immunocompromised patients

2011 ◽  
Vol 59 (4) ◽  
pp. 222-225 ◽  
Author(s):  
M.A. Jarboui ◽  
A. Sellami ◽  
H. Sellami ◽  
F. Cheikhrouhou ◽  
F. Makni ◽  
...  
2006 ◽  
Vol 42 (4) ◽  
pp. 582-583 ◽  
Author(s):  
D. Riebold ◽  
C. Fritzsche ◽  
M. Lademann ◽  
A. Bier ◽  
E. C. Reisinger

1998 ◽  
Vol 42 (7) ◽  
pp. 1811-1814 ◽  
Author(s):  
Leonardo K. Basco ◽  
Rachida Tahar ◽  
Pascal Ringwald

ABSTRACT In vitro sulfadoxine and pyrimethamine resistance has been associated with point mutations in the dihydropteroate synthase and dihydrofolate reductase domains, respectively, but the in vivo relevance of these point mutations has not been well established. To analyze the correlation between genotype and phenotype, 10 Cameroonian adult patients were treated with sulfadoxine-pyrimethamine and followed up for 28 days. After losses to follow-up (n = 1) or elimination of DNA samples due to mixed parasite populations with pyrimethamine-sensitive and pyrimethamine-resistant profiles (n = 3), parasite genomic DNA from day 0 blood samples of six patients were analyzed by DNA sequencing. Three patients who were cured had isolates characterized by a wild-type or mutant dihydrofolate reductase gene (with one or two mutations) and a wild-type dihydropteroate synthase gene. Three other patients who failed to respond to sulfadoxine-pyrimethamine treatment carried isolates with triple dihydrofolate reductase gene mutations and either a wild-type or a mutant dihydropteroate synthase gene. Three dihydrofolate reductase gene codons (51, 59, and 108) may be reliable genetic markers that can accurately predict the clinical outcome of sulfadoxine-pyrimethamine treatment in Africa.


PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49991 ◽  
Author(s):  
Steve M. Taylor ◽  
Steven R. Meshnick ◽  
William Worodria ◽  
Alfred Andama ◽  
Adithya Cattamanchi ◽  
...  

AIDS ◽  
2005 ◽  
Vol 19 (8) ◽  
pp. 801-805 ◽  
Author(s):  
Kristina Crothers ◽  
Charles B Beard ◽  
Joan Turner ◽  
Gena Groner ◽  
Melissa Fox ◽  
...  

2018 ◽  
Vol 51 (2) ◽  
pp. 141-145 ◽  
Author(s):  
Dorotéa de Fátima Lobato da Silva ◽  
Jedson Ferreira Cardoso ◽  
Sandro Patroca da Silva ◽  
Leda Mani França Arruda ◽  
Renato Lopes Fernandes de Medeiros ◽  
...  

2014 ◽  
Vol 63 (10) ◽  
pp. 1294-1302 ◽  
Author(s):  
Marijke J. Vanspauwen ◽  
Vera E. J. Knops ◽  
Cathrien A. Bruggeman ◽  
Walther N. K. A. van Mook ◽  
Catharina F. M. Linssen

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.


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