Investigations of the Occurrence of Gentamicin-Resistant Staphylococcus aureus

Abstract

patients became colonized or infected with gentamicin-resistant Staphylococcus aureus (GRS). Of 63 adults, 56 had hospital-acquired GRS, whereas only 9 of 27 children had hospital-acquired GRS (P < 0.001). The other 7 adults and 18 children had GRS present on admission. More than half of those who acquired GRS in the hospital had received prior aminoglycoside therapy. Attack rates were higher in adults than in children and significantly higher on the plastic surgery service than on any other adult service. Phage typing revealed a single-strain outbreak on the plastic surgery ward involving 11 patients, whereas other isolates were of several phage types. Community-acquired GRS occurred more frequently in rural native communities (P < 0.02) and may be related to the use of topical gentamicin. Of 17 native children, 10 were from the same area but there was no common phage type. Agar dilution minimal inhibitory concentration (MIC) testing confirmed that all isolates were gentamicin resistant (MIC 2 8 ,ug/ml) and almost all were tobramycin resistant (MIC 2 8 ,ug/ml). Although the MIC distribution between gentamicin disk-susceptible and -resistant strains was significantly different, MIC's for 90% of gentamicin disk-resistant strains were c8 ,ug of amikacin per ml, and MIC's for 92% of the strains were c4 ,ug of netilmicin per ml.

Occurrence of a nonplasmid-located determinant for gentamicin resistance in strains ofStaphylococcus aureus

“…But from 1980 to the present, gentamicin resistance has appeared in a variety of strains with different phage patterns (Witte, Hummel & Rische, 1983). This observation has also been reported from other countries (Warren & Roberts, 1976;Bint et al 1977;Naidoo & Noble, 1978;Buckwold et al 1979;Greenhood et al 1979;Rosendal, Bang & Rosdahl, 1981).…”

Antimicrobial resistance of Staphylococcus aureus: genetic basis.

“…Resistance to neomycin, and to the related aminoglycosides kanamycin and paromomycin, had emerged after a delay of approximately 10 years and was attributed to the widespread topical use of neomycin on the skin and in the nose (290,419). A similar delay occurred between the introduction of the aminoglycoside gentamicin in 1964 and outbreaks of hospital infection in 1975 to 1976 caused by S. aureus strains concomitantly resistant to gentamicin and two other aminoglycosides, kanamycin and tobramycin (38,58,310,471,552); once again, extensive topical use of the antibiotic was implicated in the appearance and spread of these resistant strains (341, 552). Prior to these outbreaks, gentamicinresistant strains were rare, being obtained only as single isolates in France (470), the United Kingdom (268,390), and the United States (385).…”

Evidence for a chromosomal site specifying amikacin resistance in multiresistant Serratia marcescens

“…Resistance to gentamicin and tobramycin in gram-negative bacilli and staphylococci is a growing clinical problem (6,7,14,15,21,24,28,34). A common mechanism of aminoglycoside resistance is through plasmid-specified enzymes (5,(7)(8)(9)22) (8,9).…”