Molecular epidemiology of aminoglycoside resistance in Acinetobacter spp.

Seward, Rebecca J.; Lambert, Thierry; Towner, K. J.

doi:10.1099/00222615-47-5-455

Cited by 67 publications

(62 citation statements)

References 27 publications

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“…resistance to newer semisynthetic aminoglycosides such as amikacin, tobramycin, sisomicin, and isepamicin are diverse and commonly involve production of aminoglycosidemodifying enzymes such as aminoglycoside acetyltransferases (AAC), aminoglycoside nucleotidyltransferases (ANT, or AAD), and/or aminoglycoside phosphotransferases (APH). Production of AAC(3)-I, APH(3Ј)-VI, and ANT(3Љ)-I was reported to be predominant by worldwide surveys on Acinetobacter spp., but there were considerable regional differences in their genotypes (14,15,21). In Japan, although the prevalence of amikacin resistance was estimated to be high, especially among non-carbapenem-susceptible Acinetobacter strains (25), the overall prevalence of aminoglycoside resistance and the mechanisms of resistance among Acinetobacter spp.…”

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confidence: 99%

Spread of Novel Aminoglycoside Resistance Gene aac ( 6 ′)- Iad among Acinetobacter Clinical Isolates in Japan

Doi

Wachino

Yamane

et al. 2004

Antimicrob Agents Chemother

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A novel aminoglycoside resistance gene, aac(6 )-Iad, encoding aminoglycoside 6 -N-acetyltransferase, was identified in Acinetobacter genospecies 3 strain A-51. The gene encoded a 144-amino-acid protein, which shared modest identity (up to 36.7%) with some of the aminoglycoside 6 -N-acetyltransferases. The results of highpressure liquid chromatography assays confirmed that the protein is a functional aminoglycoside 6 -Nacetyltransferase. The enzyme conferred resistance to amikacin, tobramycin, sisomicin, and isepamicin but not to gentamicin. The prevalence of this gene among Acinetobacter clinical isolates in Japan was then investigated. Of 264 Acinetobacter sp. strains isolated from geographically diverse areas in Japan in 2002, 16 were not susceptible to amikacin, and aac(6 )-Iad was detected in 7. Five of the producers of aminoglycoside 6 -Nacetyltransferase type Iad were identified as Acinetobacter baumannii, and two were identified as Acinetobacter genospecies 3. These results suggest that aac(6 )-Iad plays a substantial role in amikacin resistance among Acinetobacter spp. in Japan.Acinetobacter spp., especially Acinetobacter baumannii, are emerging pathogens responsible for causing a variety of nosocomial infections, including pneumonia, urinary tract infections, and septicemia (1). Outbreaks have been increasingly reported in the past 2 decades, particularly from intensive care units, where patients undergo invasive procedures and receive broad-spectrum antimicrobial agents, resulting in higher mortality rates (5, 27). Furthermore, because Acinetobacter spp. have an ability to readily accept foreign DNA, including genetic determinants for antimicrobial resistance, so as to adapt to and survive in environments that are hazardous to bacterial growth (6, 17), they have a propensity for developing resistance to multiple classes of useful antimicrobial agents, including broad-spectrum cephalosporins, fluoroquinolones, and aminoglycosides (1).Aminoglycosides are widely used to treat infections caused by gram-negative bacilli, including Acinetobacter spp. (1). However, resistance rates to classic aminoglycosides such as gentamicin and kanamycin are now high among Acinetobacter spp. in many geographic regions (15). The mechanisms of Acinetobacter sp. resistance to newer semisynthetic aminoglycosides such as amikacin, tobramycin, sisomicin, and isepamicin are diverse and commonly involve production of aminoglycosidemodifying enzymes such as aminoglycoside acetyltransferases (AAC), aminoglycoside nucleotidyltransferases (ANT, or AAD), and/or aminoglycoside phosphotransferases (APH). Production of AAC(3)-I, APH(3Ј)-VI, and ANT(3Љ)-I was reported to be predominant by worldwide surveys on Acinetobacter spp., but there were considerable regional differences in their genotypes (14,15,21). In Japan, although the prevalence of amikacin resistance was estimated to be high, especially among non-carbapenem-susceptible Acinetobacter strains (25), the overall prevalence of aminoglycoside resistance and the mechanisms of resista...

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confidence: 99%

Spread of Novel Aminoglycoside Resistance Gene aac ( 6 ′)- Iad among Acinetobacter Clinical Isolates in Japan

Doi

Wachino

Yamane

et al. 2004

Antimicrob Agents Chemother

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“…These are DNA elements capable of capturing genes by a site-specific recombination mechanism that often carry gene cassettes containing antibiotic resistance genes (25). Various studies have found antibiotic resistance genes located on integrons in Acinetobacter species (10,12,18,19,21,24,30). Since integrons possess an integrase gene (a site-specific recombinase) at their 5Ј end, Koeleman et al (15) postulated that PCR detection of this could be used as a simple method of identifying epidemic strains of A. baumannii.…”

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confidence: 99%

Detection and Typing of Integrons in Epidemic Strains of Acinetobacter baumannii Found in the United Kingdom

Turton¹,

Kaufmann²,

Glover³

et al. 2005

J Clin Microbiol

136

118

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Integrons were sought in Acinetobacter isolates from hospitals in the United Kingdom by integrase gene PCR. Isolates were compared by pulsed-field gel electrophoresis, and most belonged to a small number of outbreak strains or clones of A. baumannii, which are highly successful in the United Kingdom. Class 1 integrons were found in all of the outbreak isolates but in none of the sporadic isolates. No class 2 integrons were found. Three integrons were identified among the main outbreak strains and clones. While a particular integron was usually associated with a strain or clone, some members carried a different integron. Some integrons were associated with more than one strain. The cassette arrays of two of the integrons were very similar, both containing gene aacC1, which confers resistance to gentamicin, two open reading frames coding for unknown products (orfX, orfX), and gene aadA1a, which confers resistance to spectinomycin and streptomycin. The larger of these integrons had two copies of the first (orfX) of the gene cassettes coding for unknown products. The third integron, with a cassette array containing gene aacA4, which codes for amikacin, netilmicin, and tobramycin resistance; a chloramphenicol acetyltransferase, catB8; and gene aadA1, conferring resistance to spectinomycin and streptomycin, was associated with an OXA-23 carbapenemase-producing clone, which has spread rapidly in hospitals in the United Kingdom during 2003 and 2004. These integron cassette arrays have been found in other outbreak strains of A. baumannii from other countries. We conclude that integrons are useful markers for epidemic strains of A. baumannii and that integron typing provides valuable information for epidemiological studies.

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“…The majority of infections are of epidemic origin, and treatment has become difficult because many strains are resistant to a wide range of antibiotics, including broad-spectrum ␤-lactams, aminoglycosides, and fluoroquinolones (13,20,24,27). Studies of antibiotic resistance mechanisms in A. baumannii have demonstrated the presence of specific genes located on transferable plasmids and transposons (1,22,26). Natural transformation has been described in Acinetobacter calcoaceticus, but its role in the genetic spread of antibiotic resistance within clinical A. baumannii isolates has yet to be defined (15).…”

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Identification of Epidemic Strains of Acinetobacter baumannii by Integrase Gene PCR

et al. 2001

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Forty-eight clinical Acinetobacter isolates with different epidemic behavior were investigated for the presence of integrons and plasmids and for antibiotic susceptibility. Integrons were demonstrated in 50% of the strains by an integrase gene PCR. Epidemic strains of Acinetobacter baumannii were found to contain significantly more integrons than nonepidemic strains. Also, the presence of integrons was significantly correlated with simultaneous resistance to several antibiotics. Plasmids were detected in 42% of the strains. However, there was no significant correlation between the numbers of plasmids and integrons in Acinetobacter species strains, no significant difference in the number of plasmids between epidemic and nonepidemic A. baumannii strains, and no significant correlation between the presence of plasmids and antibiotic resistance. Hence, it is likely that integrons play an important role in antibiotic resistance and thereby in the epidemic behavior of A. baumannii. Because the integrase gene PCR identified almost three-quarters of the epidemic A. baumannii isolates (17 of 23), this seems to be a rapid and simple technique for the routine screening and identification of clinical A. baumannii isolates with epidemic potential.

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Molecular epidemiology of aminoglycoside resistance in Acinetobacter spp.

Cited by 67 publications

References 27 publications

Spread of Novel Aminoglycoside Resistance Gene aac ( 6 ′)- Iad among Acinetobacter Clinical Isolates in Japan

Spread of Novel Aminoglycoside Resistance Gene aac ( 6 ′)- Iad among Acinetobacter Clinical Isolates in Japan

Detection and Typing of Integrons in Epidemic Strains of Acinetobacter baumannii Found in the United Kingdom

Identification of Epidemic Strains of Acinetobacter baumannii by Integrase Gene PCR

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