Transferable Capacity for Gastrointestinal Colonization inEnterococcus faeciumin a Mouse Model

Abstract

A high level of gastrointestinal colonization frequently precedes invasive infection due to Enterococcus faecium. Factors other than antimicrobial resistance that promote gastrointestinal colonization by E. faecium have not been identified. We tested the ability of a colonization-proficient clinical E. faecium isolate (C68) to transfer colonizing ability to noncolonizing E. faecium recipient strains. Transconjugants derived from matings that used E. faecium D344SRF as a recipient strain colonized mouse gastrointestinal tracts in high numbers under selective pressure from clindamycin or vancomycin, compared with control strains that lacked DNA transferred from C68. We transferred DNA into a second recipient strain (E. faecium GE-1), which also colonized mice in significantly greater numbers under selective pressure from clindamycin, compared with a control strain. These results indicate that E. faecium clinical isolates express transmissible factors other than antimicrobial resistance that promote colonization of the mouse gastrointestinal tract.

Molecular Epidemiology of Vancomycin-Resistant Enterococcus faecium : a Prospective, Multicenter Study in South American Hospitals

“…The other fms genes were also frequently present at rates ranging from 67% to 97% in the VREfm isolates. The esp Efm and hyl Efm genes, which have previously been associated with CC17 (28,38), were detected in South American VR E. faecium isolates (69% and 23% of isolates, respectively). (29) 48 (14) 48 (14) 93 (27) (17) 29 (5) 29 (5) 59 (10) 0 (0) 0 (0) 88 (15) 47 (8) 41 (7) Venezuela (24) 25 (6) 25 (6) 58 (14) 4 (1) (7) 14 (1) 0 (0) 43 (3) 14 (1) 0 (0) 14 (1) 28 (2) 28 (2) Ecuador (9) 22 (2) …”

“…It was previously shown that hospital-associated E. faecium isolates from diverse geographical locations carry large, transferable plasmids containing the hyl Efm gene (which encodes a putative family 84 glycosyl hydrolase enzyme) that, additionally, are associated with vancomycin and aminoglycoside resistance genes (4). These hyl Efm -containing plasmids have emerged as important virulence and colonization determinants of CC17 of E. faecium (4,28). More recently, one of the fms clusters (fms20-fms21 [pilA]) encoding pilus-like proteins was also found to be located in a large hyl Efm -carrying plasmid in U.S. strain TX0016 (strain DO) (17).…”

“…This change in the epidemiology of enterococcal infections has been attributed to the increased ability of a genogroup of E. faecium (designated clonal cluster 17 [CC17]) to colonize the gastrointestinal tract of humans, cause disease (37), and exhibit high levels of resistance to most antienterococcal antibiotics. Several virulence and colonizing factors have been postulated to explain this increased virulence (4,25,28) and include the following: (i) the presence of an intact acm gene, which encodes a collagen adhesin and which has been associated with the pathogenesis of endocarditis in members of CC17 (25); (ii) the esp gene of E. faecium (esp Efm ), which codes for an enterococcal surface protein, which has been shown to play a role in biofilm formation (12), and which transiently aggravates experimental urinary tract infection (18); (iii) the fms (E. faecium surface protein-encoding) genes, which encode cell wall-anchored proteins, including subunits of the enterococcal pili (13,31); and (iv) the hyl gene of E. faecium (hyl Efm ; which encodes a putative glycosyl hydrolase), which is carried by transferable plasmids that have been shown to increase the ability of a laboratory strain of E. faecium to colonize the gastrointestinal tracts of mice and also enhance the virulence of a commensal strain of E. faecium in experimental peritonitis (4, 28).…”

Guidance on the safety assessment ofEnterococcus faeciumin animal nutrition

“…Strains from the community-associated clade almost never have very large plasmids containing a hyl-like gene, while hospital-associated strains often (~ 30 % in one study) harbour this gene (Rice et al, 2003). These hyl plasmids have been shown to increase colonisation of mice GI tracts and to increase lethality in a murine peritonitis model and, thus, might contribute to the success of at least some members of the hospital-associated clade (Rice et al, 2009;Panesso et al, 2011).…”

Cross-Resistance to Insecticides in a Malathion-Resistant Strain of Ceratitis capitata (Diptera: Tephritidae)

“…At present, within the Enterococcus genus, E. faecium has emerged as the most therapeutically challenging organism. C68 readily colonizes the mouse gastrointestinal tract under antimicrobial selective pressure (Rice et al, 2009). Its genome has been completely sequenced (Lam et al, 2012).…”