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Journal of Clinical Microbiology, February 2000, p. 526-529, Vol. 38, No. 2
Department of Laboratory Medicine and
Clinical Laboratory Center1 and
Laboratory of Drug Resistance in
Bacteria,2 Gunma University School of Medicine,
3-39-22, Showa-machi, Maebashi 371-8511, Japan
Received 7 September 1999/Returned for modification 22 October
1999/Accepted 15 November 1999
Acinetobacter baumannii strains resistant to both
imipenem (IPM) and ceftazidime (CAZ) were isolated from 1994 through
1996 at Gunma University Hospital. Nine isolates from different
inpatients were examined for carbapenem-hydrolyzing activity and for
the carbapemase gene blaIMP by the PCR method.
All nine isolates were carbapenemase-producing strains that hydrolyzed
IPM and that harbored blaIMP. The
blaIMP gene was transmissible by conjugation to
an IPM-susceptible recipient strain of A. baumannii and
conferred resistance to IPM, CAZ, cefotaxime (CTX), ampicillin (AMP),
and piperacillin (PIP). Either intermediate or high-level resistance to
amikacin (AMK) was transferred from two and five strains, respectively, concomitantly with blaIMP, and gentamicin (GEN)
resistance was also transferred in one instance of high-level AMK
resistance. Comparative examination of clinical isolates for resistance
patterns to nine drugs, IPM, CAZ, CTX, aztreonam, AMP, PIP, AMK, GEN,
and norfloxacin, in addition to pulsed-field gel electrophoresis
patterns with NotI-digested genomic DNA, confirmed
nosocomial transmission of infections involving carbapenemase-producing
A. baumannii strains.
Acinetobacter baumannii
is a glucose-nonfermentative gram-negative bacillus that is widely
distributed in hospital environments and is one of the nosocomial
pathogens that often causes serious infections, especially in
immunocompromised inpatients (1, 8). Extensive use of
antimicrobial chemotherapy against bacterial infections has contributed
to the emergence and increase in the number of multidrug-resistant
strains, especially among opportunistic pathogens such as members of
the family Enterobacteriaceae and glucose-nonfermentative
bacteria. Antimicrobial susceptibility testing and biological and
genomic typing of Acinetobacter isolates have revealed the
dissemination of drug-resistant strains in various hospitals (5,
13, 14, 20, 22, 24, 26).
We have detected A. baumannii strains resistant to imipenem
(IPM) and various other We detected the carbapenemase gene, blaIMP, in
clinical isolates of IPM- and CAZ-resistant A. baumannii
strains and investigated the strains for their dissemination mode in a
single hospital.
Bacterial strains.
IPM- and CAZ-resistant isolates of
A. baumannii were obtained from different inpatients in
Gunma University Hospital from 1994 through 1996.
Media.
Sheep blood agar (BBL) was used for isolation and
purification of A. baumannii strains. Sensitivity testing
(ST) agar and ST broth (Nissui Pharmaceutical Co., Ltd.) were used
routinely for cultivation and drug susceptibility testing.
Antibacterial agents.
The abbreviations and sources of the
antibacterial agents used in the study are as follows: amikacin (AMK)
and IPM, Banyu Pharmaceutical Co., Ltd.; aztreonam (ATM), Bristol-Myers
Squibb, Inc.; CAZ, Nippon Glaxo Co., Ltd.; cefotaxime (CTX), Hoechst
Japan, Ltd.; gentamicin (GEN), Schering Corp.; norfloxacin (NOR),
Kyorin Seiyaku Co., Ltd.; piperacillin (PIP), Toyama Chemical Co.,
Ltd.; and rifampin (RIF), Daiichi Pharmaceutical Co., Ltd.
Drug susceptibility tests.
MICs were determined by an agar
dilution method with an inoculum size of 104 CFU per spot
(27).
Assay of
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Detection of Carbapenemase-Producing
Acinetobacter baumannii in a Hospital
ABSTRACT
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
INTRODUCTION
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
-lactam antibiotics including ceftazidime (CAZ). IPM is a potent -lactam, partly because of its resistance to
hydrolysis by most -lactamases except carbapenemase (2). The latter enzyme, a metallo--lactamase belonging to molecular class
B, is capable of hydrolyzing both IPM and CAZ, in addition to most
-lactam antibiotics, and confers resistance to these agents in
pathogenic bacteria (11, 19). The nucleotide sequence of the
gene encoding the carbapenem-hydrolyzing metallo--lactamase identified on a plasmid in Pseudomonas aeruginosa was
completely identical to that of the Serratia marcescens gene
named blaIMP (7, 16, 27).
Furthermore, surveillance for the identification of
blaIMP by PCR techniques revealed that the gene
was disseminated among various gram-negative pathogens, especially in
P. aeruginosa and S. marcescens (6,
15). Although IPM-resistant Acinetobacter species have
been isolated, strains that produce the carbapenemase have not yet been
reported (3, 17, 18, 21).
MATERIALS AND METHODS
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
-lactamase activity.
Exponentially growing cells
of A. baumannii in ST broth were washed with 50 mM phosphate
buffer (pH 7.0) and were disrupted by sonication. The supernatant
obtained after the cellular debris was removed by centrifugation
(15,000 × g, 15 min, 4°C) was used as the crude
enzyme extract.
-Lactamase activity was determined spectrophotometrically by
previously described methods (27). One unit of enzyme
activity was defined as the amount of enzyme that hydrolyzed 1 µmol
of substrate per min at 30°C.
PCR amplification. The PCR consisted of 25 cycles of denaturation at 94°C for 1 min, annealing at 55°C for 1 min, and amplification at 72°C for 1.5 min, followed by an additional 7 min at 72°C, with the Premix Taq reagent (Takara Shuzo Co., Ltd.) used with the Program Template Control System PC-700 (ASTEC Co., Ltd.).
The nucleotide sequences of the forward and reverse primers used for detection of the carbapenemase gene, blaIMP, were those constructed by Senda et al. (23). The PCR product was 587 bp, was derived from within the 741-bp blaIMP sequence, and was detected by agarose gel electrophoresis.Conjugation experiment. Conjugal transmissibility of blaIMP was examined with the recipient strain A. baumannii TY44Rp, a RIF-resistant mutant of strain TY44, which was a clinical isolate that lost IPM resistance after storage in Casitone medium agar.
The membrane filter method was used for conjugation. A mixture of donor and recipient cells in broth cultures at an early stationary phase of growth was filtered through membranes (pore size, 0.45 µm), and those bacterial cells that were retained were placed on ST agar plates overnight at 30°C. The transmissibility of blaIMP was determined by transfer of CAZ resistance rather than IPM resistance, because the level of CAZ resistance expressed by blaIMP was high enough to distinguish transconjugants from the recipient. Transconjugant cells were selected on agar plates containing 8 µg of CAZ per ml and 100 µg of RIF per ml. The transfer frequency was expressed as the ratio of the number of transconjugants to the number of donor cells in the conjugation mixture.Pulsed-field gel electrophoresis (PFGE). Genomic DNA was prepared in agarose plugs that had been treated with lysozyme and proteinase K by using the GenePath Reagent kit (Bio-Rad) by the procedures recommended by the manufacturer. The DNA was then digested with 12.5 U of the restriction endonuclease NotI. The DNA segments generated were separated in a 1% agarose gel and were run in Tris-borate-EDTA buffer on the pulsed-field apparatus (Gene Path System; Bio-Rad) at 6.0 V/cm for 19.7 h, with pulse times ranging from 5.3 to 34.9 s.
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RESULTS |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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Isolation of IPM-resistant A. baumannii.
A total of 251 A. baumannii strains were isolated from different inpatients
during the 3 years from 1994 to 1996 in Gunma University Hospital, and
28 of these were resistant to both IPM (MICs, 
8 µg/ml) and CAZ
(MICs, 16 µg/ml). However, the resistance was not stable, because
19 of the 28 strains lost resistance to both IPM and CAZ after storage
for a year or more in Casitone medium. The remaining nine strains that
harbored IPM and CAZ resistance are listed in Table
1. The biochemical properties of these
isolates were examined with the API NE20 system and were found to be
the same. They were isolated from various sites from different
inpatients on six wards at different times. Three of the nine isolates
were obtained from patients on intensive care units (ICUs) after they were moved there from other wards.
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Detection of carbapenemase activity and
blaIMP gene.
Nine IPM- and CAZ-resistant
isolates and one susceptible strain (TY44; MICs of IPM and CAZ, <0.5
µg/ml), whose resistance had been lost after storage, were examined
for IPM-hydrolyzing activity with crude enzyme extracts and for the
blaIMP gene by the PCR method. All of the
strains except for TY44 were capable of hydrolyzing IPM and were PCR
positive, indicating that they harbored blaIMP
(Table 2).
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Transfer of carbapenemase gene by conjugation.
The IPM- and
CAZ-resistant strains were mated with TY44Rp on membrane filters, and
transconjugants were selected on ST agar containing both CAZ and RIF.
Transconjugants were obtained at frequencies of 10
2 to
104 per donor cell from all nine strains (Table 2). For
all transconjugants, the MICs of IPM were higher than those for the
recipient strain and the gene blaIMP was
detectable by PCR (data not shown).
Susceptibilities of IPM-resistant A. baumannii strains
to various chemotherapeutic agents.
The drug susceptibilities of
the clinical isolates and their transconjugants were determined and are
shown in Table 3. The IPM MICs for nine
clinical isolates were 8 to 16 µg/ml, and IPM resistance was
accompanied by resistance to CAZ, CTX, and PIP but not always by
resistance to ATM. Seven strains were highly resistant (MICs, >128
µg/ml) or intermediately resistant (MICs, 32 to 64 µg/ml) to AMK,
and six strains were resistant to GEN (MICs, 8 to 16 µg/ml). Four
strains were obviously resistant to NOR (MICs, 8 to 16 µg/ml).
Identical drug resistance patterns were observed between TY11 and TY12
and between TY40 and TY42. The latter two strains, which were isolated
relatively late in the study, showed characteristic resistance to
multiple potent chemotherapeutic agents such as -lactams,
aminoglycosides, and quinolones.
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-lactam antibiotics IPM, CAZ, CTX,
ampicillin (AMP), and PIP was transferred concomitantly, whereas
neither ATM nor NOR resistance was transmissible. Transconjugants obtained from strains TY11 and TY12 or from strains TY40 and TY42 had
almost identical drug resistance patterns. High-level resistance to AMP
and PIP was transferred from the latter two strains. Transfer of
high-level or intermediate resistance to AMK was observed from five
strains, strains TY7, TY8, TY9, TY10, and TY15. Resistance to GEN was
transferred from TY10.
PFGE patterns of A. baumannii strains. The PFGE patterns after digestion with restriction endonuclease NotI are shown in Fig. 1, in which strains with identical patterns were placed in adjacent lanes. The following five different patterns were obtained for nine TY strains: pattern 1, strains TY11 and TY12; pattern 2, strains TY40 and TY42; pattern 3, strains TY8 and TY9; pattern 4, strains TY7 and TY10; and pattern 5, strain TY15. The two strains with pattern 1 (TY11 and TY12) and those with pattern 2 (TY40 and TY42) also had identical drug resistance patterns and transmissible drug resistance patterns (Table 3) and were isolated from the same ward and in the same month of 1994 and within a 3-month period in 1996, respectively (Table 1). The two strains with pattern 3 (TY8 and TY9) were isolated from the same ward in 1994 within 3 months of each other (Table 1), but the levels of resistance to PIP and AMK were higher for the latter strain. The drug resistance patterns of the transconjugants of these strains were identical (Table 3). The two strains with pattern 4 (TY7 and TY10) were isolated from different wards in 1994, and the AMP, AMK, and GEN MICs for the strains were different. Resistance to GEN was transferred from TY10 along with the gene blaIMP.
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DISCUSSION |
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Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
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Acinetobacter spp. are important causes of nosocomial
infections, and it has been reported that they acquire resistance to chemotherapeutic agents in various hospitals (1, 13, 20, 22,
26). Although -lactam antibiotics are potent chemotherapeutic agents, Acinetobacter strains resistant to multiple
-lactam antibiotics, mainly due to hydrolysis by -lactamases,
have been increasing (14, 25). Some -lactamases in
A. baumannii were reported to be involved in resistance to
IPM, but their catalytic activities for IPM were very low or were
barely detectable (4, 17).
We isolated A. baumannii strains resistant to multiple
-lactam antibiotics, including IPM and CAZ, and in those strains we detected IPM-hydrolyzing activity and the carbapenemase gene
blaIMP.
The blaIMP-bearing strains of A. baumannii isolated during a 3-year period in our hospital were typed according to their patterns of resistance to nine drugs and by PFGE analysis of the genome. PFGE pattern analysis has been reported to be the most discriminatory method for the genomic typing of nosocomial Acinetobacter spp. (1, 12). The restriction enzyme NotI was chosen for digestion of DNA, because the number of cutting sites associated with NotI is fewer than that associated with ApaI or SmaI, simplifying discrimination of digestion patterns.
Among nine isolates, two types each consisted of two strains from the
same ward, and the strains had identical resistance and PFGE patterns.
They were all isolated from different inpatients, indicating nosocomial
transmission. Strains of one type, strains TY40 and TY42, were
resistant to six -lactams, IPM, CAZ, CTX, ATM, AMP, and PIP, as well
as two aminoglycosides, AMK and GEN, and a quinolone. The resistance of
these strains to all -lactams except ATM was transmissible,
resulting from the transfer of blaIMP, and
intermediate resistance to AMK and GEN was transferred concomitantly. Transfer of high-level AMK resistance accompanied by transfer of
blaIMP was observed in five other isolates, two
of which, TY8 and TY9, were from the same ward and had identical PFGE
patterns, although the MICs of PIP and AMK were slightly different. The drug resistance patterns that were transferred from these two strains
were identical. They were probably derived from the same strain with
some additional changes in the MICs for strains from different hosts.
IPM resistance encoded by blaIMP appeared to be readily lost after prolonged storage in Casitone medium. Furthermore, this resistance was transmissible by conjugation to susceptible strains. These findings strongly suggest that blaIMP is a foreign gene introduced from another species of bacteria and is retained only in environments supplied with IPM.
The frequencies of conjugal transfer of blaIMP were rather high in our study. This was mainly because of the availability of the proper recipient. We used a RIF-resistant mutant of a blaIMP-negative strain, strain TY44, which was a clinical isolate that lost the gene after storage in Casitone medium agar. It was suggested that such a strain like TY44 would be a good recipient for the blaIMP gene.
We attempted to detect plasmid DNA in our isolates, but the physical identification was unsuccessful.
In Acinetobacter spp. from various geographic areas in France, dissemination of an AMK resistance gene was reported. The gene was conjugally transmissible in some strains, although the plasmids that carried the AMK resistance gene were not revealed (9).
On the other hand, one transmissible plasmid of 63 kb and another of
ca. 45 kb were reported to confer resistance to AMK and IPM,
respectively, in A. baumannii strains (10, 21).
The resistance to IPM was due to a -lactamase but not a
carbapenemase, since hydrolysis of IPM was not demonstrated by enzyme
assay but was demonstrated only by microbiological methods.
Acquisition of blaIMP and nosocomial
transmission of A. baumannii are important considerations
for chemotherapy, especially in instances of multidrug resistance to
aminoglycosides and quinolones as well as to -lactams.
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ACKNOWLEDGMENTS |
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This work was supported by a grant-in-aid for Scientific Research [grant (C) 08670300] from the Ministry of Education, Science, Sports and Culture of Japan.
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FOOTNOTES |
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* Corresponding author. Mailing address: Laboratory of Drug Resistance in Bacteria, Gunma University School of Medicine, 3-39-22, Showa-machi, Maebashi 371-8511, Japan. Phone: 81-27-220-8085. Fax: 81-27-220-8088. E-mail: siyobe{at}akagi.sb.gunma-u.ac.jp.
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Journal of Clinical Microbiology, February 2000, p. 526-529, Vol. 38, No. 2
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(2003). Presence of Pseudomonas putida Strains Harboring Plasmids Bearing the Metallo-{beta}-Lactamase Gene blaIMP in a Hospital in Japan. J. Clin. Microbiol.
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Poirel, L., Menuteau, O., Agoli, N., Cattoen, C., Nordmann, P.
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Limansky, A. S., Mussi, M. A., Viale, A. M.
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Iyobe, S., Kusadokoro, H., Takahashi, A., Yomoda, S., Okubo, T., Nakamura, A., O'Hara, K.
(2002). Detection of a Variant Metallo-{beta}-Lactamase, IMP-10, from Two Unrelated Strains of Pseudomonas aeruginosa and an Alcaligenes xylosoxidans Strain. Antimicrob. Agents Chemother.
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Lee, K., Lim, J. B., Yum, J. H., Yong, D., Chong, Y., Kim, J. M., Livermore, D. M.
(2002). blaVIM-2 Cassette-Containing Novel Integrons in Metallo-{beta}-Lactamase-Producing Pseudomonas aeruginosa and Pseudomonas putida Isolates Disseminated in a Korean Hospital. Antimicrob. Agents Chemother.
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Chu, Y.-W., Afzal-Shah, M., Houang, E. T. S., Palepou, M.-F. I., Lyon, D. J., Woodford, N., Livermore, D. M.
(2001). IMP-4, a Novel Metallo-{beta}-Lactamase from Nosocomial Acinetobacter spp. Collected in Hong Kong between 1994 and 1998. Antimicrob. Agents Chemother.
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Rossolini, G. M., Condemi, M. A., Pantanella, F., Docquier, J.-D., Amicosante, G., Thaller, M. C.
(2001). Metallo-{beta}-Lactamase Producers in Environmental Microbiota: New Molecular Class B Enzyme in Janthinobacterium lividum. Antimicrob. Agents Chemother.
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Afzal-Shah, M., Woodford, N., Livermore, D. M.
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45: 583-588
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