Epidemiological typing of Enterobacter aerogenes

Gaston, M A; Strickland, Michelle; Ayling-Smith, Beverly; Pitt, T. L.

doi:10.1128/jcm.27.3.564-565.1989

Cited by 19 publications

(6 citation statements)

References 11 publications

(10 reference statements)

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“…The smallest number of observed types occurred in a study with 200 isolates, four test strains, and 11 types of a possible 2 4 = 16; the most occurred in a study with 553 isolates, seven test strains, and 64 types of a possible 2 7 = 128. Similar levels of diversity have been reported for a variety of species (Gaston et al 1989;Senior & VOrOs 1989;Rocha & Uzeda 1990;Traub 1991;Riley & Gordon 1992).…”

Section: Bacteriocins and Allelopathysupporting

confidence: 79%

Recognition and polymorphism in host-parasite genetics

Frank

1997

Infection, Polymorphism and Evolution

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Genetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host-parasite polymorphisms: plant-pathogen interactions, nuclear-cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.

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Section: Bacteriocins and Allelopathysupporting

confidence: 79%

Recognition and polymorphism in host-parasite genetics

Frank

1997

Infection, Polymorphism and Evolution

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“…To date, outbreaks of multiresistant E. aerogenes (MREA) infection have been reported in French hospitals, especially among patients admitted to intensive care units (ICUs) (2,3,5,11,15,21,25). Phenotypic markers are not sufficiently discriminatory for Enterobacter typing (9,10), whereas arbitrarily primed PCR (AP-PCR) analysis, typing by restriction endonuclease analysis, ribotyping, and pulsed-field gel electrophoresis (PFGE) analysis have been applied successfully for epidemiologic typing of E. aerogenes strains (2,3,11,12,25).…”

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confidence: 99%

Molecular epidemiology of an outbreak of multidrug-resistant Enterobacter aerogenes infections and in vivo emergence of imipenem resistance

et al. 1997

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Molecular typing was used to investigate an outbreak of infection caused by multidrug-resistant Enterobacter aerogenes (MREA) susceptible only to gentamicin and imipenem in an intensive care unit (ICU). Over a 9-month period, ciprofloxacin-resistant E. aerogenes isolates were isolated from 34 patients, or 4.1% of ICU admissions, compared with a baseline rate of 0.1% in the previous period (P < 0.001). Infection developed in 15 (44%) patients. In vivo emergence of imipenem resistance (MIC, 32 g/ml) of organisms causing deepseated infection was observed in two (13%) of these patients following prolonged therapy with imipenem and gentamicin. Arbitrarily primed PCR (AP-PCR) analysis with ERIC1R and ERIC2 primers and pulsed-field gel electrophoresis (PFGE) analysis of XbaI macrorestriction patterns concordantly showed that outbreak-associated MREA isolates were clonally related and distinct from epidemiologically unrelated strains. AP-PCR and PFGE showed discrimination indices of 0.88 and 0.98, respectively. Space-time clustering of cases within units suggests that the epidemic-related MREA isolates were transmitted on the hands of the health care personnel. A case-control study and repeated environmental culture surveys failed to identify a common source or procedure associated with transmission. In spite of the early implementation of isolation measures, the incidence of MREA colonization remained stable until all colonized patients were discharged. This study confirms the usefulness of AP-PCR and PFGE analyses for the epidemiological study of E. aerogenes and underscores the difficulty of controlling the spread of multiresistant clones of this organism in the ICU setting. The emergence of imipenem resistance represents a threat because virtually no therapeutic option is available for such strains.

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“…The present results are in opposition to this contention, because epidemiologically related strains gave different patterns. Other phenotypic markers have been proposed for use in the typing of E. aerogenes, such as biotyping (18), serotyping with Klebsiella capsular antisera, bacteriocin typing, or phage typing (15). However, these methods often failed to type all strains and to discriminate between isolates.…”

Section: Discussionmentioning

confidence: 99%

“…Traditional techniques used for typing Enterobacter spp. have been based on phenotypic characteristics, including antibiotic resistance phenotype analysis (18), bacteriocin typing, serotyping, and phage typing (15). These techniques are often unsufficiently sensitive for typing all strains and discriminating between isolates.…”

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confidence: 99%

Epidemiological study of an outbreak due to multidrug-resistant Enterobacter aerogenes in a medical intensive care unit

et al. 1996

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In 1993, 63 isolates of Enterobacter aerogenes were collected from 41 patients in a medical intensive care unit (ICU). During the same period, only 46 isolates from 32 patients were collected in the rest of the hospital. All isolates were analyzed by antibiotic resistance phenotype, and 77 representative isolates were differentiated by plasmid restriction analysis, ribotyping, and arbitrarily primed (AP)-PCR. The extended-spectrum ␤-lactamases produced by 22 strains were characterized by determination of their isoelectric points and by hybridization of plasmid DNA with specific probes. The isolates were divided into 25 antibiotic resistance phenotypes, either susceptible (group I) or resistant (group II) to aminoglycosides, and exhibited three phenotypes of resistance to ␤-lactams: chromosomally derepressed cephalosporinase alone or associated with either extended-spectrum ␤-lactamases (mainly of the SHV-4 type) or imipenem resistance. The results of the tests divided the 77 representative isolates (group I, n ‫؍‬ 21; group II, n ‫؍‬ 56) into 15 plasmid profiles, 14 ribotypes, and 15 AP-PCR patterns. Although the resistant isolates (group II) exhibited different plasmid profiles, ribotyping and AP-PCR analysis demonstrated an identical chromosomal pattern, indicating an epidemiological relatedness. They were mainly found in the medical ICU and occasionally in other units. The susceptible strains (group I) had various and distinct markers and were mainly isolated in units other than the medical ICU. In conclusion, the presence of a nosocomial outbreak in an ICU and the spread of a multidrug-resistant epidemic strain throughout the hospital was confirmed. Ribotyping and AP-PCR represent discriminatory tools for the investigation of nosocomial outbreaks caused by E. aerogenes.

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Epidemiological typing of Enterobacter aerogenes

Cited by 19 publications

References 11 publications

Recognition and polymorphism in host-parasite genetics

Recognition and polymorphism in host-parasite genetics

Molecular epidemiology of an outbreak of multidrug-resistant Enterobacter aerogenes infections and in vivo emergence of imipenem resistance

Epidemiological study of an outbreak due to multidrug-resistant Enterobacter aerogenes in a medical intensive care unit

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