The emergence of resistance to amikacin in Serratia marcescens isolates from patients with nosocomial infection

Abstract

Administration of either amikacin (1985) or gentamicin (1984, 1986–1991) as first-choice aminoglycoside did not decrease the high incidence of amikacin-resistant Serratia marcescens (AR Sm) isolates responsible for nosocomial infections at the J.A. Fernández Hospital of Buenos Aires (42% in 1984, 31% in 1985 and 41% in 1987, differences not significant). In addition, a significant peak ( P = 0.003) was detected in 1986, with an AR Sm incidence of 70%. The incidence of AR Sm decreased by 1988–1991 for reasons not related to aminoglycoside use. In the period 1984–1987 all S. marcescens isolates carried the 6′-aminoglycoside-acetyltransferase-Ic [ aac(6′)-Ic] gene, while in addition 20% of the isolates contained the plasmid-encoded 3′-aminoglycoside-phosphotransferase-VIa[ aph(3′)-VIa] and 2% the 6′-aminoglycoside-acetyltransferase-Ib [ aac(6′)-Ib] genes. From 1988 to 1992 resistance to amikacin was associated with only 4 ARSm isolates and correlated with the appearance of Tn 1331-related sequences in these isolates. This transposon or related sequences, however, was not widely spread in the S. marcescens population under investigation. Combined use of restriction fragment length polymorphism (RFLP), ribotyping and plasmid profile analysis revealed that S. marcescens strains of the same genotype, including isolates either expressing or not the aac(6′)-Ic gene, were involved in outbreaks occurring in May 1984, May 1985 and May 1986. Furthermore, these epidemiological tools permitted discrimination of different S. marcescens clones, each bearing a particular amikacin-resistance marker.