Frequency of aminoglycoside 6'-N-acetyltransferase among Serratia species during increased use of amikacin in the hospital

The aminoglycoside-modifying enzymes present in the first 120 clinical isolates harboring extended-spectrum P-lactamases isolated in Spain were studied. Most of these isolates (84%) were gentamicin resistant. The enzymes most frequently associated and cotransferred with SHV-2 or TEM-type j-lactamases were AAC(3)V, APH(3"), and APH(3')I.Since 1983, more than 40 new plasmid-mediated 1-lactamases conferring resistance to third-generation cephalosporins have been described for members of the family Enterobacteriaceae (11). This situation is of particular concern in the treatment of more severe infections, including bacteremia in immunosuppressed patients. In such infections, aminoglycosides are frequently used in combined therapy to enhance the bactericidal activity of the treatment. Unfortunately, aminoglycoside-modifying enzymes are prevalent among strains exhibiting extended-spectrum 3-lactamases (24). In fact, the genes encoding these ,-lactamases are frequently cotransferred with other resistance markers, including those for aminoglycosides. The implication that different aminoglycoside-modifying enzymes are associated with extendedspectrum 1-lactamases has been studied by very few groups (19,22,23). In the present note, we present data on the frequency of the modifying enzymes involved in aminoglycoside resistance in the first group of strains harboring extended-spectrum 1-lactamases to be isolated in Spain.

“…Nevertheless, AAC(6')I was never cotransferred with 3-lactamases, which confirms previous observations (13). Evi frequent association of TEM-6/8 and AAC(3)V-GL was obtained.…”

supporting

confidence: 79%

Aminoglycoside-modifying enzymes in clinical isolates harboring extended-spectrum beta-lactamases

Fernández-Rodríguez

Cantón

Pérez-Díaz

et al. 1992

“…This is somewhat remarkable because we have documented within our organism population those bacteria, particularly Serratia spp., which contain the AAC-6' enzyme which is known to inactivate amikacin. Despite the presence of this enzyme in Serratia organisms, no increase and, in fact, a marked decline in the presence of Serratia organisms containing this enzyme was noted during periods of high amikacin use (8). Some institutions have noted increased resistance to amikacin with increased use of amikacin (2,12,17), while others have noted a decrease or no change in resistance (1,14).…”

Section: Resultsmentioning

confidence: 99%

Aminoglycoside resistance and aminoglycoside usage: ten years of experience in one hospital

Gerding

Larson

Hughes

et al. 1991

Self Cite

229

120

For 10 years the 700-bed Minneapolis Veterans Affairs Medical Center has conducted a policy of carefully controlled aminoglycoside usage and monitoring of resistance of over 25,000 aerobic and facultative gram-negative bacillary isolates to the aminoglycosides. On two occasions during the 1980s, our experience of introducing amikacin at a high level of usage was associated with a significant reduction in resistance to gentamicin and tobramycin among gram-negative bacilli. Rapid reintroduction of gentamicin usage in 1982 after the first amikacin period was associated with a significant and rapid increase in gentamicin and tobramycin resistance. However, in 1986, gentamicin was again reintroduced to this institution at an initially modest level, and the percentage of usage of gentamicin was gradually increased over a 15-month period without a significant change in resistance to gentamicin, tobramycin, or amikacin while maintaining an overall 68% gentamicin usage and 30% amikacin usage. Aminoglycoside usage (measured as patient days) rose steadily from under 2,000 patient days per quarter in 1980 and 1981 to over 3,000 days per quarter in 1985. Since 1985, usage has declined to under 2,500 patient days per quarter in 1990. This usage rise and fall occurred during a steadily declining daily patient census that was 590 in 1980 and 465 in 1989. A move to a new hospital building in June 1988 was associated with an additional significant decline in resistance to all aminoglycosides (P less than 0.05), continuing a trend that was evident for the year preceding the move. Resistance to aminoglycoside antibiotics is now at the lowest level in 10 years at this institution, with only one gram-negative organism, Pseudomonas aeruginosa, that exhibits more than 5% resistance to gentamicin and no gram-negative species that are more than 5% resistant to amikacin and tobramycin.

“…An increasing number of mechanisms by which GNB become resistant to amikacin are being described with the AAC(6') mechanism being the most common (8,13). Serratia strains are known to commonly produce AAC(6') (12,25). The gene coding for this enzyme has been shown to be carried on transposons which may conjugate with multiple plasmids and thereby be widely disseminated (15,29).…”

Section: Discussionmentioning

confidence: 99%

Increased resistance to amikacin in a neonatal unit following intensive amikacin usage

Friedland

Funk

Khoosal

et al. 1992

Gram-negative isolates from blood and cerebrospinal fluid were monitored for 1 year before and for 1 year after the first-line aminoglycoside in a busy pediatric department was changed from gentamicin to amikacin.In the general pediatric wards, the switch to amikacin resulted in no change in resistance of nosocomial gram-negative infections to either amikacin (0%Yo before and after) or gentamicin (23.9% [before] versus 26.5% [after]). In the neonatal unit, the switch to amikacin was followed by an outbreak of Serratia spp. that were commonly resistant to amikacin but susceptible to gentamicin. This outbreak abated spontaneously. In the year after the change in aminoglycoside usage, the resistance to amikacin of nosocomially acquired gram-negative infections increased from 7.6 to 27.7% (P < 0.001), and the resistance to gentamicin decreased from 71.2 to 60.2% (P = 0.07). The increase in amikacin resistance of gram-negative bacilli other than Serratia spp. has persisted for more than a year after the introduction of amikacin as the sole aminoglycoside. The different effects observed in the two sections of the pediatric department may be related to the more intensive usage of aminoglycosides in the neonatal unit.The effect of predominant amikacin usage on susceptibility of gram-negative bacteria (GNB) to aminoglycosides is well documented (1, 5-7, 11, 13, 17, 19, 22-24, 28, 30). Those studies showed that frequent usage of amikacin usually results in no increase or only a slight increase in resistance to amikacin and a decrease in resistance to other aminoglycosides. However, in none of those studies were communityand hospital-acquired infections analyzed separately. Also, GNB isolated from all sites were included, and except in one study (6), invasive disease was not separated from colonization without invasion. Because all infections were combined, increases in amikacin resistance of nosocomial infections may have been "diluted" by the inclusion of large numbers of community-acquired isolates. Similarly, combining isolates from all sections of a hospital may mask significant changes in a specific area.Further motivation for this study was the lack of information on antimicrobial resistance levels in relation to aminoglycoside usage in developing countries, where overcrowded hospitals with very high rates of patient turnover are common.Because of increasing resistance of GNB to gentamicin, both the neonatal and general pediatric wards of our hospital changed to amikacin as the sole aminoglycoside for suspected GNB infections.The purpose of this study was to record prospectively the effect of intensive amikacin usage on the aminoglycoside resistance patterns of invasive hospital-acquired GNB in a busy pediatric department. MATERIALS AND METHODSPatient population. Baragwanath is the major hospital serving Soweto, South Africa (population of 1 to 2 million).