Vancomycin-Resistant
 
 Enterococcus faecium
 Strains with Highly Similar Pulsed-Field Gel Electrophoresis Patterns Containing Similar Tn
 1546
 -Like Elements Isolated from a Hospitalized Patient and Pigs in Denmark

Jensen, Lars; Hammerum, Anette M.; Poulsen, Rikke Lykke; Westh, Henrik

doi:10.1128/aac.43.3.724

Cited by 44 publications

(17 citation statements)

References 21 publications

(22 reference statements)

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“…These data strongly suggest that, in the community, VREF strains in humans mainly originate from pigs in which a high level of glycopeptide resistance has been observed [2,11,15]. This idea is consistent with observations by others that humans and pigs may harbor VREF strains with identical PFGE types [17,26]. The predominance of piglike VREF strains among humans in the community is the result of exposure and survival in the gut.…”

Section: Discussionsupporting

confidence: 86%

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Host Specificity of Vancomycin‐ResistantEnterococcus faecium

et al. 2000

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Amplified-fragment length polymorphism (AFLP) analysis was used to investigate the genetic relationships among 255 vancomycin-resistant Enterococcus faecium (VREF) strains isolated from hospitalized patients, nonhospitalized persons, and various animal sources. Four major AFLP genogroups (A-D) were discriminated. The strains of each taxon shared >/=65% of the restriction fragments. Most isolates recovered from nonhospitalized persons (75%) were grouped together with all pig isolates in genogroup A. Most isolates from hospitalized patients (84%), a subset of veal calf isolates (25%), and all isolates from cats and dogs clustered in genogroup C. Most isolates from chickens (97%) and turkeys (86%) were grouped in genogroup B, whereas most veal calf isolates (70%) clustered in genogroup D. Therefore, VREF strains are predominantly host-specific, and strains isolated from hospitalized patients are genetically different from the prevailing VREF strains present in the fecal flora of nonhospitalized persons.

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Section: Discussionsupporting

confidence: 86%

“…In several studies, genetically indistinguishable enterococci have been found in animals and humans, suggesting that animal-derived enterococci may colonize the human gut [4,9,17,22,23,[26][27][28]. Recently, Berchieri [29] showed that ingestion of a VREF strain isolated from a chicken resulted in colonization of his own gut for 20 days.…”

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confidence: 99%

Host Specificity of Vancomycin‐ResistantEnterococcus faecium

et al. 2000

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“…Of the 74 patients, 73 had vancomycin-resistant E. faecium (VRE) and only 1 patient had a vancomycinresistant strain of E. faecalis. Ten patients were from 1993, 46 from 1994, and 18 from 1995. Table 1 lists dates and isolation sites of the first isolate from each patient (primary isolates).…”

Section: Bacterial Strainsmentioning

confidence: 99%

“…14,95 Although vancomycin resistance in enterococci was first detected in France in 198652 and England,85,86 spread of the resistant bacteria has been relatively slow in most European countries,94 with the possible exception of the United Kingdom5, 27,47,95,96^France 6,8,10,34,70 So far> only sporadic clinical episodes of VRE have been described from Germany,51 Italy,7,56,87,88 The Netherlands, 34,66,67,90 Spain,84 Denmark,1,2,45,46 and Portugal.57 This is in sharp contrast to the massive epidemic spread of vancomycin-resistant strains that began in the northeastern United States in 1989 and which by now has spread to virtually all parts of the country. The number of U.S. hospitals reporting outbreaks caused by vancomycin-resistant enterococci has increased rapidly since the early 1990s.…”

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confidence: 98%

Role of Transposon Tn5482in the Epidemiology of Vancomycin-ResistantEnterococcus faeciumin the Pediatric Oncology Unit of a New York City Hospital

Lencastre¹,

Brown²,

Chung³

et al. 1999

Microbial Drug Resistance

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During a 36-month period between 1993 and 1995 in the Pediatric Oncology Unit of Memorial Sloan Kettering Cancer Center, 74 patients experienced episodes of infection or colonization caused by vancomycin-resistant enterococci (VRE). Characterization of the 74 bacterial isolates by microbiological and molecular techniques (pulsed-field gel electrophoresis and hybridization with DNA probes specific for the vanA and vanB genes and for IS1251) identified 73 Enterococcusfaecium and one Enterococcusfaecalis (vanB) among the primary VRE isolates. Most (69/73) of the E. faecium isolates carried vanA and four isolates, the vanB gene complex. The overwhelming majority (67/69) of the vanA -positive isolates also gave hybridization signal for IS1251, indicating the presence of the newly described conjugative transposon Tn5482. No hybridization with IS1251 was obtained with the four vanB-carrying isolates. About 30% of the vanA-positive strains (23/69) were represented by PFGE subtype variants of a single clone, most isolates of which were recovered during a 4-month period between April to June of 1994. The larger portion of the vanA-carrying VRE represented by close to 70% of the isolates (46/69) belonged to as many as 37 different clonal types, indicating tremendous genetic diversity. Among 67 of the 69 vanA-carrying isolates, the localization of the Tn5482-associated vanA gene complex could be unequivocally identified either on the chromosome (40/69) or in plasmids (27/69). Transconjugants recovered from filter mating experiments using either a chromosomally located or plasmid-borne vanA donor strain and a single vancomycin-susceptible strain of either E. faecium or E. faecalis were analyzed by molecular typing techniques. Seven out of 10 independent transconjugants recovered from the same cross showed extensive differences in PFGE pattern and also in the localization of the vanA hybridizing DNA fragment transferred from the common VRE donor with chromosomally located vanA. The observations suggest that the extensive genetic diversity observed among the clinical isolates of VRE may be generated during conjugation between vancomycin-resistant and -susceptible enterococcal isolates. The observations also suggest that the epidemic spread of VRE in the United States may be linked to the frequent presence of Tn5482 among the American isolates.

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“…With the use in feed of avoparcin or virginiamycin (the gly-copeptide and streptogramin used in animal husbandry), VRE or SRE was selected [15], and there was a high prevalence of VRE or SRE in poultry before and at slaughter [16], the farms were constantly contaminated, and VRE and SRE spread to new flock [17], VRE was found in poultry meat in food stores [18], and there was a prevalence of up to ∼20% of VRE in feces from nonhospitalized European individuals [19]. VRE from human infections showed the same PFGE types as strains found in pigs [20,21]. In addition, VRE and SRE (from poultry and pigs) in milk ingested by volunteers survived the acidity of the stomach and reached the gut, multiplied, and remained there for 14 days [22], and VRE and SRE transconjugants could be detected in feces 2 days after the ingestion of both a VRE/SRE donor strain and a recipient E. faecium strain in human volunteers without antibiotic treatment [23].…”

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confidence: 99%