Epidemiology of nosocomial infections due to Acinetobacter calcoaceticus

181

120

The gyrA gene mutations associated with quinolone resistance were determined in 21 epidemiologically unrelated clinical isolates of Acinetobacter baumannii. Our studies highlight the conserved sequences in the quinolone resistance-determining region of the gyrA gene from A. baumannii and other bacteria. All 15 isolates for which the MIC of ciprofloxacin is Ն4 g/ml showed a change at Ser-83 to Leu. Six strains for which the MIC of ciprofloxacin is 1 g/ml did not show any change at Ser-83, although a strain for which the MIC of ciprofloxacin is 1 g/ml exhibited a change at Gly-81 to Val. Although it is possible that mutations in other locations of the gyrA gene, the gyrB gene, or in other genes may also contribute to the modulation of the MIC level, our results suggest that a gyrA mutation at Ser-83 is associated with quinolone resistance in A. baumannii.

mentioning

confidence: 99%

Mutation in the gyrA gene of quinolone-resistant clinical isolates of Acinetobacter baumannii

Vila

Ruiz

Goñi

et al. 1995

181

120

“…Their contribution to nosocomial infection, however, has been increasing over the past 30 years (3,5,17). Though widely prevalent in nature (2) and generally regarded as commensals of human skin and respiratory and genitourinary tracts (1,9), they have been implicated as the cause of serious infectious diseases such as meningitis, pneumonia, tracheobronchitis, endocarditis, wound infections, and septicemia, mostly involving patients with impaired host defenses (5). Several outbreaks of hospital infection have been described, many of them due to contamination of hospital equipment and the hands of personnel.…”

mentioning

confidence: 99%

“…is complicated by the widespread multidrug resistance of the organism (4,10,13,21). Until (4,5,11,18).…”

mentioning

confidence: 99%

Antimicrobial susceptibility of Acinetobacter species

Seifert

Baginski

Schulze

et al. 1993

144

The in vitro activities of 16 antimicrobial agents against 180 Acinetobacter strains isolated from blood cultures (n = 162), central venous catheters (n = 11), and cerebrospinal fluids (n = 7) were studied. MICs were determined by a microtiter broth dilution method. Considerable differences in antimicrobial drug susceptibility against strains belonging to different species could be demonstrated. Acinetobacter baumannii isolates (n = 108) were generally more resistant than isolates identified as species other than A. baumannii. Multidrug resistance was common among A. baumannii isolates. Of the antimicrobial agents tested, imipenem was highly active against all A. baumannii isolates, and the other agents tested were only moderately active or inactive. Good activity against Acinetobacter species strain 3 was demonstrated for imipenem, amikacin, and ciprofloxacin.Most of the strains belonging to other species were susceptible to imipenem, ciprofloxacin, expanded-spectrum cephalosporins, amoxicillin-clavulanate, and the aminoglycosides but were resistant to ampicillin and older cephalosporins.

“…This organism is capable of causing life-threating infections such as bacteremia, pneumonia, and meningitis (2,3,6,32), and it is often multidrug resistant and difficult to erradicate. A progressive increase in the resistance of A. baumannii has been reported since 1980 (1,11).…”

mentioning

confidence: 99%

In vitro antimicrobial production of beta-lactamases, aminoglycoside-modifying enzymes, and chloramphenicol acetyltransferase by and susceptibility of clinical isolates of Acinetobacter baumannii

Vila

Marcos

Marco

et al. 1993

114

Antimicrobial susceptibility testing was performed on 54 epidemiologically unrelated clinical isolates of Acinetobacter baumnannii by using a standard agar dilution technique. On the basis of the in vitro activities, imipenem and doxycycline were the most active agents, whereas amikacin, isepamicin, and the new fluorquinolones ciprofloxacin and ofloxacin presented moderate activity. Cephalosporinase activity was found in 98% of the strains, whereas lactamases of TEM type 1 and one with a pI of 7 to 7.5 were present in 16 and 11% of the strains, respectively. Resistance to aminoglycosides was explained by the production of the three classes of aminoglycoside-modifying enzymes, with predominance of aminoglycoside-3'-phosphotransferase VI