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Evolution de la résistance aux aminosides chez des souches hospitalières de Serratia

Otros títulos:

Development of resistance to aminoglycosides in hospital strains of Serratia

Autor(es) y otros:
Mendoza Fernández, María del CarmenAutoridad Uniovi; Blanco Blanco, María GloriaAutoridad Uniovi; Méndez García, Francisco JavierAutoridad Uniovi; Hardisson Rumeu, CarlosAutoridad Uniovi
Fecha de publicación:
1984
Editorial:

Elsevier Masson

Citación:
Pathologie Biologie, 32(7), p. 750-754 (1984)
Descripción física:
p. 750-754
Resumen:

A study on the evolution of resistance to six aminoglycosides in Serratia as well as the relationship with the annual consumption of each drug in a hospital over the period 1974-1981 was carried out. The incidence of modifying enzymes and their genetical location was determined in 38 isolates. It was found that: The variations in the percentage of Sm clinical isolates showed no relationship with the consumption of Sm. Two different types of enzymes are involved in this resistance: AAD(3''): adenylyltransferase and APH(3''): phosphotransferase. The resistance to Nm, Km and Gm seems to be directly related with the continuous consumption of these drugs. In all the strains under study (Nm-Km)r was due to an APH(3')(5)I: phosphotransferase, Gmr to two types of acetyltransferases: AAC(3)I, only found in strains isolated before 1977 and AAC(3)II which predominates in 1981. After introducing Tm (1975) and Ak (1979) in our environment, there was an increase in the number of resistant strains. Two acetyltransferases with Tm-affinity were found: AAC(3)II and AAC(6')IV, the latter showing affinity for AKr. It was determined that five of these enzymes are plasmid-mediated. The genetical location of a sixth enzyme (AAC(6')IV) has not been clarified

A study on the evolution of resistance to six aminoglycosides in Serratia as well as the relationship with the annual consumption of each drug in a hospital over the period 1974-1981 was carried out. The incidence of modifying enzymes and their genetical location was determined in 38 isolates. It was found that: The variations in the percentage of Sm clinical isolates showed no relationship with the consumption of Sm. Two different types of enzymes are involved in this resistance: AAD(3''): adenylyltransferase and APH(3''): phosphotransferase. The resistance to Nm, Km and Gm seems to be directly related with the continuous consumption of these drugs. In all the strains under study (Nm-Km)r was due to an APH(3')(5)I: phosphotransferase, Gmr to two types of acetyltransferases: AAC(3)I, only found in strains isolated before 1977 and AAC(3)II which predominates in 1981. After introducing Tm (1975) and Ak (1979) in our environment, there was an increase in the number of resistant strains. Two acetyltransferases with Tm-affinity were found: AAC(3)II and AAC(6')IV, the latter showing affinity for AKr. It was determined that five of these enzymes are plasmid-mediated. The genetical location of a sixth enzyme (AAC(6')IV) has not been clarified

URI:
http://hdl.handle.net/10651/28521
ISSN:
0369-8114
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