CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
artículos
Título:
Characterization of In Vitro-Generated and Clinical Optochin-Resistant Strains of Streptococcus pneumoniae Isolated from Argentina
Autor/es:
PAULO R. CORTES, ANDREA G. ALBARRACÍN ORIO, MABEL REGUEIRA, GERMÁN E. PIÑAS, AND JOSÉ ECHENIQUE
Revista:
JOURNAL OF CLINICAL MICROBIOLOGY
Editorial:
ASM
Referencias:
Lugar: Washington; Año: 2008 vol. 46 p. 1930 - 1934
ISSN:
0095-1137
Resumen:
Optochin susceptibility is a key test used for pneumococcal diagnosis, but optochin-resistant (Optr) pneumococci
have been reported in the last 2 decades. In this work, we characterized eight Optr clinical strains
which presented a new mutation, G47V, a predominant A49S mutation (recently reported in Brazil) and A49T.
These mutations were found in the c subunit of the F0F1 ATPase encoded by the atpC gene, and W206C was
found in the a subunit encoded by the atpA gene. The Optr clinical isolates were analyzed by BOX PCR,
multilocus sequence typing, and serotype and antimicrobial resistance profiles, and they showed no epidemiological
relationship. To characterize the Optr mutations that could emerge among clinical strains, we studied
a pool of spontaneous Optr colonies obtained in vitro from the virulent D39 strain. We compared the atpACr) pneumococci
have been reported in the last 2 decades. In this work, we characterized eight Optr clinical strains
which presented a new mutation, G47V, a predominant A49S mutation (recently reported in Brazil) and A49T.
These mutations were found in the c subunit of the F0F1 ATPase encoded by the atpC gene, and W206C was
found in the a subunit encoded by the atpA gene. The Optr clinical isolates were analyzed by BOX PCR,
multilocus sequence typing, and serotype and antimicrobial resistance profiles, and they showed no epidemiological
relationship. To characterize the Optr mutations that could emerge among clinical strains, we studied
a pool of spontaneous Optr colonies obtained in vitro from the virulent D39 strain. We compared the atpACr clinical strains
which presented a new mutation, G47V, a predominant A49S mutation (recently reported in Brazil) and A49T.
These mutations were found in the c subunit of the F0F1 ATPase encoded by the atpC gene, and W206C was
found in the a subunit encoded by the atpA gene. The Optr clinical isolates were analyzed by BOX PCR,
multilocus sequence typing, and serotype and antimicrobial resistance profiles, and they showed no epidemiological
relationship. To characterize the Optr mutations that could emerge among clinical strains, we studied
a pool of spontaneous Optr colonies obtained in vitro from the virulent D39 strain. We compared the atpACc subunit of the F0F1 ATPase encoded by the atpC gene, and W206C was
found in the a subunit encoded by the atpA gene. The Optr clinical isolates were analyzed by BOX PCR,
multilocus sequence typing, and serotype and antimicrobial resistance profiles, and they showed no epidemiological
relationship. To characterize the Optr mutations that could emerge among clinical strains, we studied
a pool of spontaneous Optr colonies obtained in vitro from the virulent D39 strain. We compared the atpACa subunit encoded by the atpA gene. The Optr clinical isolates were analyzed by BOX PCR,
multilocus sequence typing, and serotype and antimicrobial resistance profiles, and they showed no epidemiological
relationship. To characterize the Optr mutations that could emerge among clinical strains, we studied
a pool of spontaneous Optr colonies obtained in vitro from the virulent D39 strain. We compared the atpACr mutations that could emerge among clinical strains, we studied
a pool of spontaneous Optr colonies obtained in vitro from the virulent D39 strain. We compared the atpACr colonies obtained in vitro from the virulent D39 strain. We compared the atpAC
mutations of these Optr pneumococci (with or without passage through C57BL/6 mice) with those described in
the clinical isolates. This analysis revealed three new mutations, G47V and L26M in the c subunit and L184S
in the a subunit. Most of the mutations identified in the laboratory-generated Optr strains were also found in
clinical strains, with the exception of the L26M and L184S mutations, and we suppose that both mutations
could emerge among invasive strains in the future. Considering that atpAC are essential genes, we propose that
all spontaneous mutations that confer in vitro optochin resistance would not present severe physiological
alterations in S. pneumoniae and may be carried by circulating pneumococcal strains.r pneumococci (with or without passage through C57BL/6 mice) with those described in
the clinical isolates. This analysis revealed three new mutations, G47V and L26M in the c subunit and L184S
in the a subunit. Most of the mutations identified in the laboratory-generated Optr strains were also found in
clinical strains, with the exception of the L26M and L184S mutations, and we suppose that both mutations
could emerge among invasive strains in the future. Considering that atpAC are essential genes, we propose that
all spontaneous mutations that confer in vitro optochin resistance would not present severe physiological
alterations in S. pneumoniae and may be carried by circulating pneumococcal strains.c subunit and L184S
in the a subunit. Most of the mutations identified in the laboratory-generated Optr strains were also found in
clinical strains, with the exception of the L26M and L184S mutations, and we suppose that both mutations
could emerge among invasive strains in the future. Considering that atpAC are essential genes, we propose that
all spontaneous mutations that confer in vitro optochin resistance would not present severe physiological
alterations in S. pneumoniae and may be carried by circulating pneumococcal strains.a subunit. Most of the mutations identified in the laboratory-generated Optr strains were also found in
clinical strains, with the exception of the L26M and L184S mutations, and we suppose that both mutations
could emerge among invasive strains in the future. Considering that atpAC are essential genes, we propose that
all spontaneous mutations that confer in vitro optochin resistance would not present severe physiological
alterations in S. pneumoniae and may be carried by circulating pneumococcal strains.atpAC are essential genes, we propose that
all spontaneous mutations that confer in vitro optochin resistance would not present severe physiological
alterations in S. pneumoniae and may be carried by circulating pneumococcal strains.S. pneumoniae and may be carried by circulating pneumococcal strains.