Table 1 - available via license: Creative Commons Attribution-NonCommercial 3.0 Unported
Content may be subject to copyright.
Aminoglycoside susceptibilities of the 58 aac(6´)-Ib-harboring Enterobacter cloacae isolates
Source publication
The aminoglycoside 6'-N-acetyltransferases of type Ib (aac(6')-Ib) gene confers resistance to amikacin, tobramycin, kanamycin, and netilmicin but not gentamicin. However, some isolates harboring this gene show reduced susceptibility to amikacin. The European Committee on Antimicrobial Susceptibility Testing (EUCAST) recommends a revision of the phe...
Context in source publication
Context 1
... whole-cell DNA was digested with XbaI, and the results were interpreted according to the cri- teria proposed by Tenover et al. [10]. Table 1 shows the antibiotic susceptibilities for the isolates. Of the 58 isolates harboring the aac(6´)-Ib gene, 49 (84.5%) were susceptible to amikacin ( ≤ 16 mg/L); 2 (3.4%), to ka- namycin ( ≤ 16 mg/L); 2 (3.4%), to tobramycin (≤ 4 mg/L); and 17 (29.3%), to gentamicin ( ≤ 4 mg/L) according to the CLSI breakpoints. ...
Similar publications
INTRODUCTION:
This study aimed to determine the role of genes encoding aminoglycoside-modifying enzymes (AMEs) and 16S rRNA methylase (ArmA) in Acinetobacter baumannii clinical isolates.
METHODS:
We collected 100 clinical isolates of A. baumannii and identified and confirmed them using microbiological tests and assessment of the OXA-51 gene. Antib...
Background: Aminoglycosides (AG) are important bactericidal antibiotics in an era of
increasing resistance. During the last decade, we observed a change in AG prescribing
patterns in our hospital. We investigated the effect of this change on AG susceptibility and
the prevalence of AG resistance genes.
Methods: Enterobacteriaceae (EB) isolated from...
We evaluated aminoglycoside resistance in 87 Acinetobacter baumannii strains isolated from four hospitals located in the North West region of Iran and typed them in sequence groups (SGs) using trilocus sequence-based scheme to compare their clonal relationships with international clones. Resistance toward aminoglycosides was assayed by minimum inhi...
Therapeutic resistance towards most of the current treatment regime by Acinetobacter baumannii has reduced the prescribing antibiotic pattern and option is being re-shifted towards more toxic agents including aminoglycosides. The present investigation aimed at to study various mechanisms towards aminoglycoside non-susceptibility in clinical isolate...
Citations
... La résistance aux aminoglycosides par les enzymes modificatrices est principalement liée à la dissémination par des plasmides qui codent généralement des gènes de multirésistance (Paterson, 2006 (Oshiro et al., 2018 ;Zhu et al., 2020). Certaines souches portant l'enzyme AAC(6')-Ib présentent une sensibilité réduite à l'amikacine (Kim et al., 2011). D'autre part, la présence de mutations au niveau de l'AAC(6')-Ib a été associée à une moindre résistance à l'amikacine (Shamara et al., 2001). ...
Enterobacter est un pathogène nosocomial à Gram négatif émergent responsable d'épidémies en réanimation néonatale (RNN). Au cours des 50 dernières années, sa taxonomie a évolué, rendant son épidémiologie ambigüe. Récemment, diverses techniques de biologie moléculaire, notamment le séquençage du génome entier, ont permis de mieux comprendre sa taxonomie et son épidémiologie. L'objectif de cette thèse était de rechercher des marqueurs microbiologiques associés à la gravité des bactériémies chez les nouveau-nés prématurés. Le premier marqueur microbiologique identifié était l'espèce. Dans ce contexte, E. xiangfangensis et E. bugandensis ont été identifiés comme les espèces les plus fréquentes en RNN. E. xiangfangensis est plus résistant aux antibiotiques que E. bugandensis. En revanche, E. bugandensis est associé à une mortalité plus élevée et semble plus virulent que E. xiangfangensis. En outre, l'analyse structurale du lipide A d'E. bugandensis a révélé la présence du 2-hydroxymyristate, une modification catalysée par l'enzyme LpxO. La présence de LpxO chez E. bugandensis était associée à la gravité de la bactériémie néonatale. L'étude du génome d'E. bugandensis a montré la présence d'autres facteurs de virulence tels que des fimbriae, des adhésines, des sidérophores et le T6SS. Ces résultats suggèrent que le potentiel de colonisation, la persistance et la virulence d'E. bugandensis sont différents de ceux des autres espèces du même genre, soulignant l'importance d'une identification précise au niveau de l'espèce, et en particulier d'E. bugandensis portant LpxO. Les incubateurs ont été identifiés comme un réservoir important pour la transmission des infections nosocomiales en RNN. Nos résultats suggèrent que les épidémies d'Enterobacter en RNN sont multi-espèces et multi-clonales. En conclusion, E. bugandensis a été identifié comme l'espèce type responsable de sepsis néonatal sévère chez les prématurés. Par conséquent, une surveillance épidémiologique des taux de colonisation chez les nouveau-nés dans la RNN devrait être mis en œuvre.
... The new subclass of intrinsic aminoglycoside nucleotidyltransferase, ANT(3")-IIa, was widely distributed and was found in almost all strains (99%), followed by the intrinsic aminoglycoside O-phosphotransferase aph(6)-Id and aph(3")-Ib found in 83 (77%) strains. To date, over a hundred AMEs have been described, and AACs represent the largest group of AMEs [41]. In the current study, AAC genes were detected in 12% of the isolates, while ANT and APH genes were distributed in almost all isolates (Table 3). ...
Carbapenem‐resistant Acinetobacter baumannii (A. baumannii, CRAb) is an emerging global threat for healthcare systems, particularly in Southeast Asia. Next‐generation sequencing (NGS) technology was employed to map genes associated with antimicrobial resistance (AMR) and to identify multilocus sequence types (MLST). Eleven strains isolated from humans in Vietnam were sequenced, and their AMR genes and MLST were compared to published genomes of strains
originating from Southeast Asia, i.e., Thailand (n = 49), Myanmar (n = 38), Malaysia (n = 11), Singapore (n = 4) and Taiwan (n = 1). Ten out of eleven Vietnamese strains were CRAb and were susceptible only to colistin. All strains harbored ant(3”)‐IIa, armA, aph(6)‐Id and aph(3”) genes conferring resistance to aminoglycosides, and blaOXA‐51 variants and blaADC‐25 conferring resistance to ß‐lactams. More than half of the strains harbored genes that confer resistance to
tetracyclines, sulfonamides and macrolides. The strains showed high diversity, where six were assigned to sequence type (ST)/2, and two were allocated to two new STs (ST/1411‐1412). MLST analyses of 108 strains from Southeast Asia identified 19 sequence types (ST), and ST/2 was the most prevalent found in 62 strains. A broad range of AMR genes was identified mediating resistance to ß‐lactams, including cephalosporins and carbapenems (e.g., blaOXA‐51‐like, blaOXA‐23, blaADC‐25, blaADC‐73, blaTEM‐1, blaNDM‐1), aminoglycosides (e.g., ant(3”)‐IIa, aph(3”)‐Ib, aph(6)‐Id, armA and aph(3’)‐Ia), phenicoles (e.g., catB8), tetracyclines (e.g., tet.B and tet.39), sulfonamides (e.g., sul.1
and sul.2), macrolides and lincosamide (e.g., mph.E, msr.E and abaF). MLST and core genome MLST (cgMLST) showed an extreme diversity among the strains. Several strains isolated from different countries clustered together by cgMLST; however, different clusters shared the same ST. Developing an action plan on AMR, increasing awareness and prohibiting the selling of antibiotics without prescription must be mandatory for this region. Such efforts are critical for enforcing
targeted policies on the rational use of carbapenem compounds and controlling AMR dissemination and emergence in general.
... Finally, a variable pattern of resistance and sensitivity were noticed to amikacin (Table-2). In consentience to this finding, many researchers confirmed that E. cloacae has a unique ability to acquire genes encoding resistance to multiple classess of antibiotics including β-lactamase inhibitor, aminoglycoside, tetracycline, and carbapenem [18,52,53,54,55,56,57,58,59] . It seems that continuous disposal of hospital waste, sewage, and other wastewater, all of which are potentially containing resistanceconferring genes, antibiotics, and their residual to the stream water, could serve as an essential contributing factor for environmental bacteria harboring antibiotic resistant [60,61,62] . ...
This study was designed to determine the extent of contamination of water storage tanks by non-lactose fermenter Enterobacter spp, and to characterize the chlorine and antibiotic resistance status. Moreover, to find the correlation between biofilm formation and resistance to chlorine. For this purpose, a total of 60 water samples were collected from residential and restaurant water storage tanks. Bacterial analysis and antibiotic susceptibility profiles of the samples were assessed by the Most Probable Number (MPN) and Vitek 2 compact tests, respectively. The biofilm formation was quantified by crystal violet staining method and chlorine resistance test by microdilution technique.
Obtained results indicated that water samples were contaminated by Escherichia coli (35%). Additionally, water samples that were assessed to be potable by the MPN test showed that (44%) positive for Enterobacter cloacae. Results of chlorine resistance test revealed variation
in resistance of E. cloacae to different concentrations of chlorine, and relatively similar antibiotic susceptibility profiles. Moreover, biofilm analysis showed the isolates that were resistant to concentration of chlorine 400 mg L-1, have formed significantly more biofilm than those that were resistant to other concentrations. A positive non-linear correlation (r = 0.72) was found between the degree of biofilm formation and the ability of isolates to resist different chlorine concentrations, and no correlation has been detected between antibiotic and chlorine resistance.
It can be concluded that the presence of chlorine resistant E. cloacae in drinking water can pose a real public health threat. The routine microbial water analysis should be modified to include detection of non-lactosefermenter Enterobacter.
... All these genetic functions synergistically make KP ST307 more resistant to antimicrobials and more difficult to treat in patients. The MIC results for amikacin in this study should be interpreted cautiously [29]. Sensitivity was confirmed in MIC and antimicrobial disk tests, but WGS analysis revealed that genes including aac (3)-lla, aph (6)-ld, and aph (3´´)-lb were resistance genes. ...
... These low rates were observed even though 73% (16/22) of aminoglycoside-modifying enzyme (AME)+isolates possessed aac (6´)-Ib, which is reported to confer amikacin resistance. Amikacin MICs below the susceptibility breakpoints are commonly observed among Enterobacter and other Enterobacteriaceae that possess aac (6´)-Ib [29,31]. The clinical significance of low MICs against bacteria carrying AMEs that are known to cause resistance has not been established, and it is unclear whether MICs or molecular markers are more relevant to treatment responses [32]. ...
Background:
A lineage of Klebsiella pneumoniae that produces carbapenemase-2 (KPC-2), sequence type (ST) 307, emerged in 2017. We analyzed the complete sequences of plasmids from KPC-2-producing K. pneumoniae (KPC-Kp) ST307, investigated the antimicrobial resistance conferred by this strain, and confirmed the horizontal interspecies transmission of KPC-carbapenemase-producing Enterobacteriaceae (CPE) characteristics among Enterobacteriaceae.
Methods:
We performed antimicrobial susceptibility testing, PCR analysis, multilocus sequence typing, curing tests, and whole-genome sequencing to characterize plasmid-derived KPC-2-producing Enterobacteriaceae clinical isolates.
Results:
Sequence analysis of KPC-Kp strain ST307 revealed novel plasmid-located virulence factors, including a gene cluster for glycogen synthesis. Three Enterobacteriaceae strains were identified in one patient: K. pneumoniae (CPKp1825), Klebsiella aerogenes (CPEa1826), and Escherichia coli (CPEc1827). The bla KPC-2 gene from K. pneumoniae ST307 was horizontally transmitted between these strains. The plasmids could be transferred through conjugation, because all three strains of bacteria contained the type IV secretion system, pilus genes, and tra genes for conjugal transfer. The bla KPC-2 gene was located on a truncated Tn4401 transposon. Plasmids containing the bla KPC-2 gene could not be artificially removed; thus, the three strains could not be cured.
Conclusions:
The ease of horizontal transfer of KPC-Kp ST307 carbapenem resistance has serious public health and epidemiological implications. This study provides a better understanding of the genetic characteristics that can contribute to the growth and spread of KPC-Kp ST307, and their association with antimicrobial resistance genes.
... From the antibiotic resistance point of view, most isolates of the E. cloacae complex constitutively produce the AmpC -lactamase and are intrinsically resistant to ampicillin, amoxicillin, amoxicillinclavulanic acid, first-and second-generation cephalosporins, and cefoxitin, while they are generally susceptible to fluoroquinolones, trimethoprim-sulfamethoxazole, chloramphenicol, aminoglycosides, tetracyclines, piperacillin-tazobactam, and carbapenems (9,10,12). Nevertheless, these organisms are capable of acquiring genes encoding resistance to multiple classes of antibiotics (12), and clinical isolates resistant to aminoglycosides by producing AMEs have frequently been reported in recent years (10,(14)(15)(16). The rapid acquisition of resistance phenotypes is most often plasmid mediated and is also associated with the dissemination of transposable elements (9). ...
Enterobacter cloacae complex are important opportunistic human pathogens capable of causing a wide variety of infections. During recent decades, the aminoglycoside-resistant E. cloacae complex isolates have increasingly been reported and become a major concern. Here we employed high-throughput sequencing in combination with specific PCR assays to investigate the prevalence of aminoglycoside resistance genes among 170 isolates of the E. cloacae complex collected from a teaching hospital in Wenzhou, China. A total of 12 known genes ( aphA-1 , strA , strB , aac(6′)-IIc , aadA2 , aac(3)-IId , aadB , aadA1 , rmtB , armA , aadA5 and aac(6′)-Ie-aph(2″)-Ia ) and 1 novel gene aac(3)-IIg were identified, with aphA-1 (71.18%), strA (55.29%) and strB (52.35%) being the most prevalent, and aac(3)-IIg was detected with a positive rate of 21.76% (37/170). The aac(3)-IIg gene was 810 bp in length and encoded a protein that shared 72-78% identities with previously known AAC(3)-II aminoglycoside 3- N -acetyltransferases. The MICs of gentamicin and tobramycin were 512 μg/mL and 64 μg/mL when aac(3)-IIg was cloned into Escherichia coli DH5a. All aac(3)-IIg -positive isolates exerted broad aminoglycoside resistance profiles mediated by coexistence of multiple resistance genes. Moreover, aminoglycoside resistance and resistance genes were found to be transferable in most strains (23/37). Nevertheless, Pulsed-field gel electrophoresis (PFGE) and dendrogram analysis showed clonal diversity among these isolates. S1-PFGE, Southern hybridization and whole genome sequencing indicated that aac(3)-IIg was located on transferable as well as non-transferable plasmids of various sizes. The analysis of genetic environment suggested that aac(3)-IIg was embedded within a class 1 integron, with IS 26 playing an important role in its mobility.
... Other studies showed that there are likely mutations (Leu119Ser, Leu120Ser, Glu167Ala, Phe171Ala, and Tyr166Ala in N-termini) occurring in Enterobacter cloacae isolates. [13][14][15] Similarly, all of the Enterobacter cloacae isolates in this study showed to be sensitive against amikacin. But there still needs further investigation for this. ...
Background: Over the past decade, numbers of Carbapenemase Producing-Carbapenem Resistant Enterobacteriaceae (CP-CRE) has been increasing worldwide and it has been becoming a threat because of its resistance against carbapenem which is considered as the “last resort” antibiotic. Therapy options for its infection are still limited. Aminoglycoside serves as one of the most commonly used antibiotics, but the resistance against it has already been presented for a long time. Aminoglycoside Modifying Enzyme (AME) is the most important resistance mechanism against aminoglycoside. AAC(6’)-Ib enzyme is one of the most common AME produced by the gram-negative bacteria.
Objectives: This study wished to identify the gene of this enzyme among CRE isolated from infected Indonesian patients in Dr. Mohammad Hoesin Hospital Palembang.
Methods: Twenty-eight isolates collected from CRE-infected patients identified by Vitek 2 Compact (bioMerieux, USA) in dr. Mohammad Hoesin Hospital Palembang during September—November 2017. AAC(6’)-Ib gene was identified using PCR method, then visualize by electrophoresis. The result is then analyzed by comparing it with a susceptibility test.
Results: Out of 28 samples, AAC(6’)-Ib is identified in 22 (78.57%) samples. Samples with AAC(6’)-Ib showed to be less resistant to various antibiotics, significantly to amikacin (p=0.023).
Conclusion: AAC(6’)-Ib gene is found in most of samples implying its frequent occurrence in Indonesian patients.
... are well recognized for their capacity to develop acquired -lactam resistance via inducible or derepressed production of AmpC -lactamases (3,4). In addition, Enterobacter isolates often manifest multiple antibiotic resistance mechanisms, including coproduction of extended-spectrum -lactamases (ESBLs), upregulation of efflux pumps, and deficiency of outer membrane porins, which may confer multidrug resistance (MDR) phenotypes (5)(6)(7)(8). More recently, carbapenem-resistant Enterobacter spp. ...
... AMK MICs in this study should be interpreted cautiously (8). Only 3% (2/65) and 11% (7/65) of the isolates were nonsusceptible to AMK using the CLSI and European Committee on Antimicrobial Susceptibility Testing (EUCAST) breakpoints, respectively (25,44). ...
... These low rates were observed despite that fact that 73% (16/22) of AMEϩ isolates possessed AAC(6=)-Ib, which is reported to confer AMK resistance. In fact, AMK MICs below the susceptibility breakpoints are commonly observed among Enterobacter and other Enterobacteriaceae that possess AAC(6=)-Ib (8,17,45,46). The clinical significance of susceptible MICs against bacteria carrying AMEs that are known to cause resistance is not established, and it is unclear if MICs or molecular markers are more relevant to treatment responses (47). ...
We compared the in vitro activity of gentamicin (GEN), tobramycin (TOB), amikacin (AMK), and plazomicin (PLZ) against 13 Enterobacter isolates possessing both Klebsiella pneumoniae carbapenemase and extended spectrum β-lactamase (KPC+/ESBL+) with activity against 8 KPC+/ESBL-, 6 KPC-/ESBL+, and 38 KPC-/ESBL-
isolates. The resistance rates to GEN and TOB were higher for KPC+/ESBL+ (100% for both) than KPC+/ESBL- (25% and 38%, respectively),
KPC-/ESBL+ (50% and 17%, respectively), and KPC-/ESBL- (0% and 3%, respectively) isolates. KPC+/ESBL+ were more likely than
others to possess an aminoglycoside modifying enzyme (AME) (100% vs. 38%, 67%, and 5%; p = 0.007, 0.06, and < 0.0001, respectively) or multiple AMEs (100% vs. 13%, 33%, and 0%, respectively; all p < 0.01). KPC+/ESBL+ isolates also had a greater number of AMEs (mean 4.6 vs 1.5, 0.9, and 0.05, respectively; all p < 0.01). GEN and TOB MICs were higher against isolates with >1 AME than with ≤1 AME.
The presence of at least 2/3 of KPC, SHV or TEM predicted the presence of AMEs. PLZ MICs against all isolates were ≤ 4 μg/mL,
regardless of KPC/ESBL pattern or AMEs. In conclusion, GEN and TOB are limited as treatment options against KPC and ESBL+
Enterobacter. PLZ may represent a valuable addition to the antimicrobial armamentarium. A full understanding of AMEs and other aminoglycoside
resistance mechanisms will allow clinicians to incorporate PLZ rationally into treatment regimens. The development of molecular
assays that accurately and rapidly predict antimicrobial responses among KPC and ESBL-producing Enterobacter spp. should be a top research priority.
... The explanation could be either impaired gene expression or that amikacin is a poor substrate for this enzyme [26]. Kim et al. [27] have also found a very high percentage of amikacinsusceptible Enterobacter cloacae isolates harbouring the aac(6 )-Ib gene (84.5% and 55.2% according to CLSI and EUCAST breakpoints, respectively), with only two isolates containing mutations associated with the loss of amikacin resistance. Recently, Almaghrabi et al. [14] did not find a correlation between AMEs and amikacin MICs or resistance in carbapenem-resistant K. pneumoniae strains. ...
The activity of eight aminoglycosides (amikacin, apramycin, arbekacin, gentamicin, kanamycin, neomycin, netilmicin and tobramycin) against a collection of 257 amoxicillin/clavulanic acid (AMC)-resistant Escherichia coli isolates was determined by microdilution. Aminoglycoside resistance rates, the prevalence of aminoglycoside-modifying enzyme (AME) genes, the relationship between AME gene detection and resistance phenotype to aminoglycosides, and the association of AME genes with mechanisms of AMC resistance in E. coli isolates in Spain were investigated. Aminoglycoside-resistant isolates were screened for the presence of genes encoding common AMEs [aac(3)-Ia, aac(3)-IIa, aac(3)-IVa, aac(6')-Ib, ant(2″)-Ia, ant(4')-IIa and aph(3')-Ia] or 16S rRNA methylases (armA, rmtB, rmtC and npmA). In total, 105 isolates (40.9%) were resistant to at least one of the aminoglycosides tested. Amikacin, apramycin and arbekacin showed better activity, with MIC90 values of 2mg/L (arbekacin) and 8mg/L (amikacin and apramycin). Kanamycin presented the highest MIC90 (128mg/L). The most common AME gene was aac(6')-Ib (36 strains; 34.3%), followed by aph(3')-Ia (31 strains; 29.5%), ant(2″)-Ia (29 strains; 27.6%) and aac(3)-IIa (23 strains; 21.9%). aac(3)-Ia, aac(3)-IVa, ant(4')-IIa and the four methylases were not detected. The ant(2″)-Ia gene was usually associated with OXA-1 [21/30; 70%], whilst 23/25 (92%) strains producing CTX-M-15 had the aac(6')-Ib gene. The most prevalent AME gene was aac(6')-Ib (18/41; 44%) in nosocomial isolates, whilst ant(2″)-Ia and aph(3')-Ia genes (20/64; 31%) were more frequent in strains of community origin. In 64.6% isolates the phenotypic profile correlated with the presence of commonly encountered AMEs.
Copyright © 2015 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved.
... We were unable to assess the previously reported impact of AAC(6=)-Ib on amikacin susceptibility since 98% (49/50) of our strains carried this enzyme. The issue was further complicated by that fact that amikacin nonsusceptibility was uncommon (14% [7/50] (40)(41)(42). The issue merits further investigation. ...
We measured in vitro activity of plazomicin, a next-generation aminoglycoside, and other aminoglycosides against 50 carbapenem-resistant Klebsiella pneumoniae strains from two centers and correlated the results with the presence of various aminoglycoside-modifying enzymes (AMEs).
Ninety-four percent of strains were sequence type 258 (ST258) clones, which exhibited 5 ompK36 genotypes; 80% and 10% of strains produced Klebsiella pneumoniae carbapenemase 2 (KPC-2) and KPC-3, respectively. Ninety-eight percent of strains possessed AMEs, including AAC(6′)-Ib (98%),
APH(3′)-Ia (56%), AAC(3)-IV (38%), and ANT(2″)-Ia (2%). Gentamicin, tobramycin, and amikacin nonsusceptibility rates were
40, 98, and 16%, respectively. Plazomicin MICs ranged from 0.25 to 1 μg/ml. Tobramycin and plazomicin MICs correlated with
gentamicin MICs (r = 0.75 and 0.57, respectively). Plazomicin exerted bactericidal activity against 17% (1× MIC) and 94% (4× MIC) of strains.
All strains with AAC(6′)-Ib were tobramycin-resistant; 16% were nonsusceptible to amikacin. AAC(6′)-Ib combined with another
AME was associated with higher gentamicin, tobramycin, and plazomicin MICs than AAC(6′)-Ib alone (P = 0.01, 0.0008, and 0.046, respectively). The presence of AAC(3)-IV in a strain was also associated with higher gentamicin,
tobramycin, and plazomicin MICs (P = 0.0006, P < 0.0001, and P = 0.01, respectively). The combination of AAC(6′)-Ib and another AME, the presence of AAC(3)-IV, and the presence of APH(3′)-Ia
were each associated with gentamicin resistance (P = 0.0002, 0.003, and 0.01, respectively). In conclusion, carbapenem-resistant K. pneumoniae strains (including ST258 clones) exhibit highly diverse antimicrobial resistance genotypes and phenotypes. Plazomicin may
offer a treatment option against strains resistant to other aminoglycosides. The development of molecular assays that predict
antimicrobial responses among carbapenem-resistant K. pneumoniae strains should be a research priority.
Enterobacter cloacae complex (ECC), espèce retrouvée dans l’environnement, est un germe commensal chez l’homme présent au niveau du tractus digestif. Capable de passer de l’état commensal à celui de pathogène opportuniste, il a pris une importance croissante du fait de son implication dans les infections des services de soins intensifs (prévalence de 5–10 %). L’espèce a été subdivisée en 13 clusters définis à partir des gènes rpoB ou hsp60 dont six avec un nom d’espèce (E. asburiae, E. kobei, E. cloacae, E. ludwigii, E. hormaechei et E. nimipressuralis). Trois clusters (III, VI et VIII) sont fréquemment retrouvés parmi les souches cliniques responsables d’infections et d’épidémies hospitalières. Le principal problème en pratique clinique réside dans la diffusion de souches d’ECC multi-résistantes aux antibiotiques. La dissémination mondiale de souches de Enterobacter résistantes aux céphalosporines de 3e génération (C3G), par hyperproduction de la céphalosporinase (AmpC) chromosomique et/ou par acquisition de gènes codant pour des β-lactamases à spectre étendu (BLSE), se complique depuis quelques années par l’émergence d’entérobactéries porteuses de carbapénémases (EPC). Les céphalosporines de 4e génération (ex. céfépime) en association avec une autre famille d’antibiotiques (notamment aminosides et fluoroquinolones) constituent le traitement de choix pour les infections sévères, ceci dû au moindre risque de sélection de mutants résistants hyperproducteurs d’AmpC par rapport aux C3G. Avec l’émergence de souches d’EPC, la mise en place d’une antibiothérapie adaptée nécessite l’utilisation d’associations à base de polymyxines, de carbapénèmes et/ou de tigécycline.
