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PubMed1991

Enterobacter bacteremia: clinical features and emergence of antibiotic resistance during therapy.

OBJECTIVES: To study the effect of previously administered antibiotics on the antibiotic susceptibility profile of Enterobacter, the factors affecting mortality, and the emergence of antibiotic resistance during therapy for Enterobacter bacteremia. DESIGN: Prospective, observational study of consecutive patients with Enterobacter bacteremia. SETTING: Three university tertiary care centers, one major university-affiliated hospital, and two university-affiliated Veterans Affairs medical centers. PATIENTS: A total of 129 adult patients were studied. MEASUREMENTS: The two main end points were emergence of resistance during antibiotic therapy and death. MAIN RESULTS: Previous administration of third-generation cephalosporins was more likely to be associated with multiresistant Enterobacter isolates in an initial, positive blood culture (22 of 32, 69%) than was administration of antibiotics that did not include a third-generation cephalosporin (14 of 71, 20%; P less than 0.001). Isolation of multiresistant Enterobacter sp. in the initial blood culture was associated with a higher mortality rate (12 of 37, 32%) than was isolation of a more sensitive Enterobacter sp. (14 of 92, 15%; P = 0.03). Emergence of resistance to third-generation cephalosporin therapy (6 of 31, 19%) occurred more often than did emergence of resistance to aminoglycoside (1 of 89, 0.01%; P = 0.001) or other beta-lactam (0 of 50; P = 0.002) therapy. CONCLUSIONS: More judicious use of third-generation cephalosporins may decrease the incidence of nosocomial multiresistant Enterobacter spp., which in turn may result in a lower mortality for Enterobacter bacteremia. When Enterobacter organisms are isolated from blood, it may be prudent to avoid third-generation cephalosporin therapy regardless of in-vitro susceptibility.

Adolescent↗

PubMed1987

Patients' endogenous flora as the source of "nosocomial" Enterobacter in cardiac surgery.

We prospectively studied Enterobacter colonization in cardiac surgery patients receiving cefazolin prophylaxis. Fifty-eight (67%) of 87 patients became colonized, 28 by the time of admission to a Cardiac Surgery Intensive Care Unit. Enterobacter cloacae was four times more prevalent than Enterobacter aerogenes. We found increased Enterobacter colonization, after prophylaxis, in 45% of surgery patients. None of 25 control patients, who underwent coronary angioplasty and received no antibiotic prophylaxis, showed increased colonization (P = .001). Both groups had similar baseline rates of Enterobacter carriage. Typing showed 50 distinct strains of E. cloacae and 11 of E. aerogenes; 25% of patients carried greater than or equal to 2 strains simultaneously. In the nine cases of horizontal transmission, source patients were intubated for greater than or equal to 5 days and had heavy throat carriage of Enterobacter. No environmental sources of transmission were found. Clinical Enterobacter infection developed in 12 patients; at least nine of these were infected with a strain that had been isolated by surveillance culture. We conclude that Enterobacter, part of the patients' endogenous flora, becomes an important pathogen when amplified by prophylactic antibiotics and is less often transmitted horizontally.

Aged↗

PubMed1988

[Biochemical typing of Enterobacter isolated from several clinical materials].

A total of 74 Enterobacter species have been isolated from the patients applying to the department of Microbiology, University of Ankara, Studying several biochemical test systems their strains have been found. 37 of these Enterobacter species have been found to be Enterobacter cloacae, 10 Enterobacter agglomerans, 13 Enterobacter aerogenes, 3 Enterobacter hafniae (Hafnia alvei), 1 Enterobacter sakazakii. 2 of the strains couldn't be classified. In conclusion most of the strains were found to be Enterobacter cloacae.

Bacterial Typing Techniques↗

PubMed1986

Enterobacter bacteremia in surgical patients.

The records of 63 surgical patients with one or more positive blood cultures for Enterobacter organisms were reviewed to determine clinical, epidemiologic, and mortality risk factors. Enterobacter bacteremia occurred, on the average, on the twenty-third day of hospitalization, most frequently in male patients (47), after antibiotic therapy (48 patients), placement of central venous catheters (38 patients), gastrointestinal tract operations (36 patients), and respiratory failure (31 patients). Portals of entry were most commonly sputum (25 patients), open skin wounds (16 patients), and central venous lines (12 patients). Mortality risk (22 patients, 35%) was increased with Enterobacter bacteremia occurring after the fifteenth day of hospitalization (18 of 45 patients versus 4 of 28 patients, p less than 0.01), a preceding Enterobacter focus (13 of 22 patients versus 9 of 41 patients, p less than 0.05), preceding non-Enterobacter bacteremia (10 of 15 patients versus 12 of 48 patients, p less than 0.02), preceding total parenteral nutrition (11 of 21 patients versus 11 of 42 patients p less than 0.01), respiratory failure (19 of 36 patients versus 3 of 27 patients p less than 0.01), and renal failure (11 of 12 patients versus 11 of 51 patients p less than 0.01). The mortality risk was not diminished by specific antibiotic therapy. Enterobacter is emerging as an important pathogen in surgical patients. Prolonged antibiotic administration, particularly that of cephalosporins, may promote Enterobacter colonization of the tracheobronchial tree and skin with subsequent invasion enhanced by respiratory failure, open skin wounds, or central venous catheters traversing the skin. Mortality risk is determined primarily by factors associated with critical illness rather than effects of Enterobacter organisms and their specific treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Cross Infection↗

PubMed2003

Population genetics of the nomenspecies Enterobacter cloacae.

The genetic heterogeneity of the nomenspecies Enterobacter cloacae is well known. Enterobacter asburiae, Enterobacter cancerogenus, Enterobacter dissolvens, Enterobacter hormaechei, Enterobacter kobei, and Enterobacter nimipressuralis are closely related to it and are subsumed in the so-called E. cloacae complex. DNA-DNA hybridization studies performed previously identified at least five DNA-relatedness groups of this complex. In order to analyze the genetic structure and the phylogenetic relationships between the clusters of the nomenspecies E. cloacae, 206 strains collected from 22 hospitals, a veterinarian, and an agricultural center in 11 countries plus all 13 type strains of the genus and reference strain CDC 1347-71(R) were examined with a combination of sequence and PCR-restriction fragment length polymorphism (PCR-RFLP) analyses of the three housekeeping genes hsp60, rpoB, and hemB as well as ampC, the gene of a class C beta-lactamase. Based on the neighbor-joining tree of the hsp60 sequences, 12 genetic clusters (I to XII) and an unstable sequence crowd (xiii) were identified. The robustness of the genetic clusters was confirmed by analyses of rpoB and hemB sequences and ampC PCR-RFLPs. Sequence crowd xiii split into two groups after rpoB analysis. Only three strains formed a cluster with the type strain of E. cloacae, indicating that the minority of isolates identified as E. cloacae truly belong to the species; 13% of strains grouped with other type strains of the genus, suggesting that the phenotypes of these species seem to be more heterogeneous than so far believed. Three clusters represented 70% of strains, but none of them included a type or reference strain. The genetic clustering presented in this study might serve as a framework for future studies dealing with taxonomic, evolutionary, epidemiological, or pathogenetic characteristics of bacteria belonging to the E. cloacae complex.

Anti-Bacterial Agents↗

PubMed2003

Evaluation of outcome in critically ill patients with nosocomial enterobacter bacteremia: results of a matched cohort study.

STUDY OBJECTIVE: To evaluate the clinical impact of nosocomial Enterobacter bacteremia in critically ill patients. DESIGN: Retrospective (January 1992 to December 2000) matched cohort study. SETTING: Fifty-four-bed ICU (including medical, surgical, cardiosurgical ICU, and burns unit) from a university hospital. PATIENTS: Sixty-seven ICU patients with Enterobacter bacteremia (case patients) and 134 control patients. INTERVENTION: Matching of control patients (1:2 ratio) was on the basis of the APACHE (acute physiology and chronic health evaluation) II system. As expected, mortality can be derived from this severity-of-disease classification system; this matching procedure results in an equal expected mortality rate for patients with Enterobacter bacteremia and control patients. RESULTS: The overall rate of appropriate antibiotic therapy in patients with Enterobacter bacteremia was high (96%) and initiated soon after the onset of the bacteremia (0.5 +/- 0.9 days). Patients with Enterobacter bacteremia had more hemodynamic instability (p = 0.015), longer ICU stay (p < 0.001), and ventilator dependence (p < 0.001). No differences between case and control patients were found in age (52 years vs 53 years, p = 0.831), prevalence of acute renal failure (16% vs 16%, p = 0.892), and acute respiratory failure (93% vs 84%, respectively; p = 0.079). In-hospital mortality rates for case and control patients were not different (34% vs 39%, respectively; p = 0.536). CONCLUSION: After accurate adjustment for severity of underlying disease and acute illness, no difference was found between ICU patients with Enterobacter bacteremia and matched control patients. In the presence of fast and appropriate antibiotic therapy, Enterobacter bacteremia does not adversely affect the outcome in ICU patients.

APACHE↗

PubMed2002

Epidemiology of extended-spectrum beta-lactamase-producing Enterobacter isolates in a Spanish hospital during a 12-year period.

Fifteen Enterobacter clinical isolates (11 Enterobacter cloacae isolates, 3 Enterobacter aerogenes isolates, and 1 Enterobacter gergoviae isolate), representing 0.4% of all Enterobacter isolates recovered in our hospital from 1989 to 2000, were suspected of harboring an extended-spectrum beta-lactamase (ESBL). These isolates were recovered from 14 different patients. ESBLs were transferred by conjugation into an Escherichia coli recipient strain. Pulsed-field gel electrophoresis (PFGE) revealed a single clone of E. aerogenes and six different clones of E. cloacae. Four of these E. cloacae clonal types were represented by only one isolate each, but the other two were represented by three and four isolates, respectively. Isoelectric focusing, susceptibility phenotyping, PCR analysis, and sequencing demonstrated the presence of three different ESBLs. The most frequent was the recently characterized CTX-M-10 ESBL, which was found in the E. gergoviae isolate and in all but one of the E. cloacae isolates. The remaining E. cloacae isolate harbored a TEM-27 ESBL, and the three E. aerogenes isolates harbored a TEM-24 ESBL. PFGE revealed that our E. aerogenes strain was indistinguishable from the French TEM-24-producing E. aerogenes endemic clone. Although a low prevalence of ESBL-producing Enterobacter isolates was found in our institution over a 12-year period, a diversity of nonepidemic E. cloacae clones was detected, as was the persistence of the CTX-M-10 beta-lactamase. The presence of the TEM-24-producing E. aerogenes French clone in our institution also demonstrates the intercountry dissemination of ESBL-producing isolates.

Bacterial Proteins↗

PubMed2002

Health and economic outcomes of the emergence of third-generation cephalosporin resistance in Enterobacter species.

BACKGROUND: This study evaluated the clinical and economic impact of the emergence of third-generation cephalosporin-resistant Enterobacter species. METHODS: Mortality, length of hospitalization, and hospital charges were examined in a cohort that was selected from a group of 477 patients with initial cultures that yielded a third-generation cephalosporin-susceptible Enterobacter species. Case patients (n = 46) had subsequent cultures yielding a third-generation cephalosporin-resistant Enterobacter species. Control patients (n = 113) who did not develop resistance were matched to cases on site of Enterobacter infection and length of hospitalization prior to isolation of the initial susceptible organism. Multivariable analyses were used to adjust for confounding. RESULTS: Twenty-six percent of cases died vs 13% of controls (P =.06). The median total hospital stay for cases was 29.5 days (interquartile range [IQR], 20-60) and 19 days for controls (IQR, 13-27; P<.001). The median hospital charge for cases was $79 323 (IQR, $34 546-$161 384) and for controls was $40 406 (IQR, $18 470-$79 005; P<.001). After adjusting for comorbidities, severity of illness, intensive care unit admission, surgery, transfer from another hospital, sex, and age, emergence of resistance was associated with increased mortality (relative risk, 5.02; P =.01), hospital stay (1.5-fold, P<.001), and hospital charges (1.5-fold, P<.001). Emergence of resistance had a median attributable hospital stay of 9 days and an average attributable hospital charge of $29 379. CONCLUSIONS: Emergence of antibiotic resistance in Enterobacter species results in increased mortality, hospital stay, and hospital charges. Minimizing resistance in Enterobacter species should be a priority.

Aged↗

PubMed2002

Impact of previous use of antibiotics on development of resistance to extended-spectrum cephalosporins in patients with enterobacter bacteremia.

This retrospective study was conducted to determine the risk factors for resistance to extended-spectrum cephalosporins (ESCs) and to examine the influence of previous use of an aminoglycoside with an ESC on resistance to ESCs in patients with Enterobacter bacteremia from January 1991 through December 2000. A total of 423 episodes of Enterobacter bacteremia among 414 patients were documented during the 10-year study period. Three hundred thirty-two (78%) isolates were Enterobacter cloacae, 72 (17%) Enterobacter aerogenes, and 19 (4%) other Enterobacter species. Causative isolates exhibited resistance to ESCs in 225 episodes and susceptibility in 198 episodes. Nosocomial acquisition was an independent risk factor for resistance to ESCs (odds ratio [OR], 3.4; 95% confidence interval [95%CI], 1.7-6.8). The median number of antibiotics used was significantly greater in cases caused by resistant isolates than in cases caused by susceptible isolates (OR, 1.8; 95%CI, 1.2-2.6). Resistance to ESCs was associated with previous use of any ESC (OR, 5.0; 95%CI, 2.5-10.2). The proportion of resistant episodes in patients treated previously with an aminoglycoside plus an ESC was not different from that in patients treated with an ESC alone. In conclusion, previous use of ESCs was associated with resistance to ESCs in patients with Enterobacter bacteremia; moreover, previous use of an aminoglycoside with an ESC did not significantly decrease the risk of resistance to ESCs.

Adult↗

PubMed2006

Enterobacter bacteremia: Clinical features, risk factors for multiresistance and mortality in a Chinese University Hospital.

BACKGROUND: This study was performed to characterize the clinical features and to identify the risk factors for multiresistance and mortality in patients with Enterobacter bacteremia. PATIENTS AND METHODS: A number of 126 patients with Enterobacter bacteremia in 1995-2004 at the Medical university-affiliated Hospital of Anhui, China were retrospectively analyzed. RESULTS: Of the 126 cases of bacteremia, 81 (64.3%) patients were identified as nosocomial infection. The overall multiresistance rate was 45.2% (57/126). Multiresistance was associated with nosocomial infection, recent invasive procedure, previous third-generation cephalosporins therapy, prolonged perioperative prophylaxis, the species of Enterobacter (E. cloacae) and polymicrobial bacteremia in univariate analysis. In multivariate analysis, previous third-generation cephalosporins therapy (OR = 13.6, p = 0.007) and prolonged perioperative prophylaxis (OR = 6.4, p = 0.029) were the strong, independent risk factors for the multiresistance. The crude 30-day mortality rate was 39.7% (50/126). Mortality directly attributed to Enterobacter spp. was 32.5% (41/126), which was significantly associated with multiresistance, nosocomial infection, recent invasive procedure, and inadequately empirical therapy in univariate analysis. Multivariate analysis revealed that only nosocomial infection (OR = 3.292, p = 0.049) was independently associated with mortality. The survival curve showed that the inappropriate initial therapy group had a lower probability of survival than the appropriate therapy group in infection-related mortality (Log Rank, p = 0.0142). CONCLUSION: Enterobacter is becoming increasingly important nosocomial pathogens. Nosocomial infection is a clinical risk factor tightly associated with multiresistance and worse outcome. More judicious use of third-generation cephalosporins may decrease the incidence of nosocomial multiresistant Enterobacter spp. in China.

Adolescent↗

PubMed2000

Clinical and molecular epidemiology of chromosome-mediated resistance to third-generation cephalosporins in Enterobacter isolates in eastern France.

OBJECTIVE: To determine both the prevalence of group I beta-lactamase-related resistance and the clinical setting in which resistance to expanded-spectrum cephalosporins occurs. METHODS: Isolates of Enterobacter spp. were sensitivity tested to a range of antibiotics, and selected isolates were DNA fingerprinted by pulsed-field gel electrophoresis. The medical records of all patients with positive cultures for Enterobacter spp. were reviewed to determine the effect of previous antibiotic treatment on the susceptibility profile of these organisms. RESULTS: The crude incidence of colonization/infection (n = 315) was 0.51 per 100 patients and 0.73 per 1000 days of hospitalization. The 4-day and 7-day Kaplan-Meier rates of colonization/infection with Enterobacter were estimated to be 7.57% (standard deviation (SD = 3.26%) and 4.16% (SD = 2.88%)), respectively. The time lag to colonization/infection with isolates producing large amounts of Bush group 1 beta-lactamase (HLBL) (27.35 +/- 27.30 days) was significantly different from that to colonization/infection with wild-type isolates (13.59 +/- 17.93 days) (P = 0.036). Ninety-six isolates (30.5%) demonstrated acquired resistance to expanded-spectrum cephalosporins: 34 isolates (10.8%) produced extended-spectrum beta-lactamase, and 62 isolates (19.7%) produced HLBL. The 89 Enterobacter isolates susceptible to third-generation cephalosporins yielded 84 major DNA patterns, and the 45 HLBL isolates yielded 38 major DNA patterns. The risk of colonization/infection with HLBL-producing Enterobacter was higher in cases of antimicrobial treatment with third-generation cephalosporins or a fluoroquinolone, and in cases of urinary tract colonization/infection. CONCLUSIONS: The judicious use in hospitals of both expanded-spectrum cephalosporins and other antibiotics such as fluoroquinolones is necessary to curtail the emergence of resistance in Enterobacter spp.

Cephalosporins↗

PubMed2001

Enterobacter species in a pediatric hospital: horizontal transfer or selection in individual patients?

Enterobacter species were studied longitudinally in a children's hospital. In total, 287 Enterobacter isolates were obtained from 171 children in 15 different wards (from March 1995 through April 1997). Strains were typed by random amplified polymorphic DNA and pulsed-field gel electrophoresis, which were concordant in outcome. In total, 97 DNA types and 199 colonization events were identified. A predominant clone was isolated 111 times from 62 children; another clone was isolated 19 times from 10 patients. These clones caused 36% of all colonizations. In 34% of the children, Enterobacter clones were found in 2-4 patients. The remaining colonizations were due to unique Enterobacter isolates. A large proportion of the Enterobacter strains was acquired through cross-transmission. This finding contrasts with the prevailing opinion that resistant Enterobacter strains are selected primarily from the patient's own gut flora.

Adolescent↗

PubMed2004

Bloodstream infections caused by Enterobacter species: predictors of 30-day mortality rate and impact of broad-spectrum cephalosporin resistance on outcome.

BACKGROUND: Enterobacter species have become increasingly important nosocomial pathogens. However, resistance to cephalosporins often complicates the treatment of Enterobacter infection. This study was conducted to evaluate the predictors of mortality and the impact of cephalosporin resistance on outcome in patients with Enterobacter bacteremia. METHODS: A total of 183 patients with Enterobacter bacteremia were retrospectively analyzed. Broad-spectrum cephalosporin resistance was defined as in vitro resistance to cefotaxime or ceftazidime. The main outcome measure was the 30-day mortality rate. RESULTS: Of 183 patients, 86 (47%) had bacteremia caused by broad-spectrum cephalosporin-resistant Enterobacter species, and their infections were classified as resistant. The 30-day mortality rate of patients with resistant infections (the resistant group) was significantly higher than that of patients with susceptible infections (the susceptible group) (33.7% vs. 18.6%; P=.021). When the 30-day mortality rates were compared according to the primary sites of infection and underlying conditions, the 30-day mortality rates of the resistant group were significantly higher than those of the susceptible group, in patients with an unknown primary site of infection, or in patients with septic shock. Multivariate analysis showed that broad-spectrum cephalosporin resistance was one of the independent risk factors associated with 30-day mortality (odds ratio [OR], 3.69; 95% confidence interval [CI], 1.01-13.52; P=.049). Presentation with septic shock and an increasing Acute Physiology and Chronic Health Evaluation II score were also independent risk factors for mortality (OR, 59.91 [95% CI, 14.93-240.15; P<.001] and 1.52 [95% CI, 1.24-1.86; P<.001], respectively). CONCLUSIONS: Broad-spectrum cephalosporin resistance adversely affects the outcome of patients with Enterobacter bacteremia, especially those with an unknown primary site of infection and those with septic shock.

APACHE↗

PubMed2005

Clinical epidemiology of ciprofloxacin resistance and its relationship to broad-spectrum cephalosporin resistance in bloodstream infections caused by Enterobacter species.

OBJECTIVES: To evaluate the clinical features of ciprofloxacin-resistant Enterobacter bacteremia and to examine the risk factors for ciprofloxacin resistance in Enterobacter species isolates causing bacteremia. DESIGN: A case-control study. SETTING: A 1,500-bed, tertiary-care university hospital and referral center. PATIENTS: All patients older than 16 years with Enterobacter species isolated from blood were enrolled. The medical records of 183 patients with clinically significant Enterobacter bacteremia from January 1998 to December 2002 were identified. We compared patients with bacteremia caused by ciprofloxacin-susceptible isolates with patients with bacteremia caused by ciprofloxacin-resistant isolates. RESULTS: Twenty-three (12.6%) of the patients had bacteremia caused by isolates resistant to ciprofloxacin. There were no significant differences in age, gender, underlying diseases, primary site of infection, or Acute Physiology and Chronic Health Evaluation II score between the ciprofloxacin-resistant and the ciprofloxacin-susceptible groups. Broad-spectrum cephalosporin resistance, defined as resistance to cefotaxime or ceftazidime in vitro, was detected in 21 (91.3%) of 23 ciprofloxacin-resistant isolates compared with 65 (40.6%) of 160 ciprofloxacin-susceptible isolates (P < .001). Multivariate analysis revealed that independent risk factors for ciprofloxacin resistance were the prior receipt of fluoroquinolones (P < .001) and broad-spectrum cephalosporin resistance (P < .001). CONCLUSIONS: In Enterobacter species isolates causing bacteremia, ciprofloxacin resistance was closely associated with the prior receipt of fluoroquinolones and broad-spectrum cephalosporin resistance. The close relationship between ciprofloxacin resistance and broad-spectrum cephalosporin resistance is particularly troublesome because it severely restricts the therapeutic options for Enterobacter species infection.

Adolescent↗

PubMed1992

Relationship between ceftriaxone use and resistance of Enterobacter species.

We investigated the relationship between the amount of ceftriaxone used in our hospital and the evolution of the rate of resistance among Enterobacter species isolates. We reviewed all positive microbiological reports for Enterobacter species and the pharmacy records for the ceftriaxone consumption during four semesters over 4 consecutive years. The resistance to ceftriaxone among Enterobacter species rose from 10 to 27% while the amount of ceftriaxone used almost trebled during the study period. In order to investigate the relationship between the use of an antibiotic and the emergence of resistance to it, we studied the development of ceftriaxone resistance in Enterobacter species and the use of this drug at the Centre Hospitalier Universitaire Vaudois (CHUV) each year between 1983 and 1986. The consumption of ceftriaxone more than doubled between 1983 and 1984, and since then has increased only slowly. Within 2 years the rate of Enterobacter species resistance to ceftriaxone has jumped from about 10% between 1983 and 1985 to 27% in 1986. As no particular modification in the preventive methods of hospital hygiene and no epidemics occurred during the period of our study, we conclude that the increase in the prescribing of ceftriaxone probably played a central role in the increased number of resistant strains of Enterobacter species.

Ceftriaxone↗

PubMed1984

Enzymatic profiles of Enterobacter sakazakii and related species with special reference to the alpha-glucosidase reaction and reproducibility of the test system.

The enzymatic profiles of Enterobacter sakazakii, Enterobacter cloacae, Enterobacter aerogenes, and Enterobacter agglomerans were determined with the API ZYM system (API System S.A., La Balme Les Grottes, France). Each assay was performed three times. A simple formula was derived and applied to assess the reproducibility of the API ZYM tests. In addition, a separate alpha-glucosidase test was performed. All E. sakazakii isolates produced alpha-glucosidase, in contrast to the other Enterobacter isolates. No phosphoamidase activity was detected in any of the E. sakazakii isolates, whereas it was present in 72% of E. cloacae, 89% of E. agglomerans, and 100% of E. aerogenes isolates. It was concluded that detection of alpha-glucosidase permits rapid and reliable differentiation between E. sakazakii and other Enterobacter species. The reproducibilities of alpha-glucosidase and phosphoamidase reactions were estimated to be 89 and 81%, respectively.

Enterobacter↗

PubMed2023

Capsular Polysaccharide Is Essential for the Virulence of the Antimicrobial-Resistant Pathogen Enterobacter hormaechei.

Nosocomial infections caused by multidrug-resistant (MDR) Enterobacter cloacae complex (ECC) pathogens are on the rise. However, the virulence strategies employed by these pathogens remain elusive. Here, we study the interaction of ECC clinical isolates with human serum to define how this pathogen evades the antimicrobial action of complement, one of the first lines of host-mediated immune defense. We identified a small number of serum-sensitive strains, including Enterobacter hormaechei strain NR3055, which we exploited for the in vitro selection of serum-resistant clones. Comparative genomics between the serum-sensitive NR3055 strain and the isolated serum-resistant clones revealed a premature stop codon in the wzy gene of the capsular polysaccharide biosynthesis locus of NR3055. The complementation of wzy conferred serum resistance to NR3055, prevented the deposition of complement proteins on the bacterial surface, inhibited phagocytosis by human neutrophils, and rendered the bacteria virulent in a mouse model of peritonitis. Mice exposed to a nonlethal dose of encapsulated NR3055 were protected from subsequent lethal infections by encapsulated NR3055, whereas mice that were previously exposed to unencapsulated NR3055 succumbed to infection. Thus, capsule is a key immune evasion determinant for E. hormaechei, and it is a potential target for prophylactics and therapeutics to combat these increasingly MDR human pathogens. IMPORTANCE Infections caused by antimicrobial resistant bacteria are of increasing concern, especially those due to carbapenem-resistant Enterobacteriaceae pathogens. Included in this group are species of the Enterobacter cloacae complex, regarding which there is a paucity of knowledge on the infection biology of the pathogens, despite their clinical relevance. In this study, we combine techniques in comparative genomics, bacterial genetics, and diverse models of infection to establish capsule as an important mechanism of Enterobacter pathogens to resist the antibacterial activity of serum, a first line of host defense against bacterial infections. We also show that immune memory targeting the Enterobacter capsule protects against lethal infection. The further characterization of Enterobacter infection biology and the immune response to infection are needed for the development of therapies and preventative interventions targeting these highly antibiotic resistant pathogens.

Humans↗

PubMed1975

[Multiple drug resistance of Enterobacter-Serratia group isolated from clinical materials (author's transl)].

We determined the drug susceptibility of Serratia-Enterobacter group isolated from clinical materials between October 1973 and May 1974 by disk method and agar plate dilution method, and compared the drug susceptibility and multiple resistance among pigment-producing Serratia, pigment non-producing Serratia and Enterobacter. We used following drugs for susceptibility tests; ampicillin, carbenicillin, sulbenicillin, cephaloridine, streptomycin, kanamycin, dibekacin, gentamicin, chloramphenicol, tetracycline, colistin, nalidixic acid, nitrofurantoin and erythromycin. Above one half of strains of Serratia and Enterobacter was isolated from sputa and pharyngeal swabs. Almost all strains of Serratia and Enterobacter wer resistant to ampicillin, cephaloridine and erythromycin, but sensitive to gentamicin and dibekacin. Resistant strains were more found in Serratia than in Enterobacter. Pigment non-producing strains of Serratia were more sesistant to chemotherapeutics than pigment producing strains. There were many multiple resistant strains in Serratia and Enterobacter, especially in pigment non-producing strains of Serratia, and the strains isolated from urine were resistant to more drugs compared with the strains from other materials.

Ampicillin↗