To the Editor: In the United States, the dissemination of amajor clone of community-associated methicillin-resistant Staphylococcusaureus (MRSA), designated USA300, and outbreaks of vancomycin-resistantEnterococcus faecalis (VREF) have been described.1,2 Community-associatedMRSA infections emerged in Colombia in 2005,3 and a total of15 community-associated MRSA infections were documented in fourcities in 2006 and 2007. All the patients presented with severeskin and soft-tissue infections, which were often complicatedby necrotizing fasciitis, bacteremia, paraspinal abscess, arthritis,or meningitis, with a mortality rate of 20%. The first knownColombian VREF isolate was recovered in a hospital in Bogotáin 2001. Since then, additional isolates have been identifiedfrom 50 patients in seven Bogotá hospitals.
The Colombian MRSA isolates were susceptible to most antistaphylococcalantibiotics, although 40% were resistant to tetracycline. Allisolates had staphylococcal chromosomal cassette mec (SCCmec)type IV, the Panton–Valentine leukocidin genes, and atleast one of the toxins associated with USA3004 but did nothave the arcA gene as a marker of the ACME (arginine catabolicmobile element) island. Pulsed-field gel electrophoresis andmultilocus sequence typing revealed that all but one of theclinical isolates were ST8 and clonally related to USA300. Theremaining isolate was a single-locus variant of ST8 (ST923)(Figure 1A). The majority of isolates carried SCCmec subtypesother than IVa, which suggests that a similar lineage of virulent,ST8, methicillin-susceptible S. aureus that independently acquiredvarious SCCmec subtypes existed in both Colombia and the UnitedStates. To our knowledge, this is the first documentation ofthe USA300 community-associated MRSA lineage as the predominant(and exclusive) clone in a country other than the United States.No community-associated MRSA isolates belonging to a differentclonal cluster have been documented by multilocus sequence typingin Colombia so far.
Figure 1. Representative Isolates of Community-Associated Methicillin-Resistant Staphylococcus aureus (MRSA) from Colombia and the United States.
Panel A shows the results of pulsed-field gel electrophoresis (PFGE) after digestion with SmaI enzyme, the city or state of origin, the toxin profile (including the presence of arcA as a marker of the ACME [arginine catabolic mobile element] island), multilocus sequence typing, and the presence or absence of staphylococcal chromosomal cassette mec (SCCmec) IV and subtypes (a, b, and c) of representative isolates of community-associated MRSA from Colombia. The strains from Texas (USA300, SCCmec IVa), North Dakota (USA400), and Nebraska (USA300, SCCmec IVb) were used as controls for typing experiments. The presence of arcA has been associated with USA300 isolates carrying the SCCmec type IVa cassette but not others, a finding that is consistent with the possibility that ST8 community-associated MRSA in Colombia acquired the SCCmec DNA independently from the U.S. isolates. ST923 is a single-nucleotide variant of ST8 in the yqiL gene. ND denotes not determined. Panel B shows PFGE results with the use of ApaI enzyme of representative isolates of vancomycin-resistant Enterococcus faecalis (VREF) ST2 from seven hospitals in Bogotá from 2001 to 2006 and isolate TX2486, the index isolate of strain HV1 (ST2) recovered from a Houston hospital in 1994, as follows: lane 1, TX2486; lanes 2 and 3, ERV-25 and ERV-31, respectively, which are representatives of the first Colombian VREF isolates recovered in 2001 (VREF isolates from 2002 and 2003 had a PFGE pattern that was identical to that of isolate ERV-31 and are not shown); lanes 4, 5, and 6, isolates ERV-62, ERV-63, and ERV-65, respectively, recovered in 2004; lane 7, ERV-81, isolated in 2005; and lane 8, ERV-116, recovered in 2006.
Pulsed-field gel electrophoresis also indicated that a singleclone of vanB VREF has been disseminated in Bogotá (Figure 1B).This clone is genetically related to an ST2 outbreak strain(HV1) of VREF described in Houston in 1994.5 In addition, theallelic profile of the antigenic or resistance-associated genesace, salA, and lsa (encoding an adhesin, a cell-wall antigen,and quinupristin–dalfopristin resistance, respectively)was identical in the two strains. Furthermore, the Houston andColombian isolates had the same pathogenicity island profile,which has been suggested as an epidemiologic marker of morevirulent clones of E. faecalis.5 To our knowledge, the onlytwo epidemic strains of ST2 vanB-type E. faecalis that havebeen described are the Houston and Bogotá strains. Ourfindings suggest a close epidemiologic relationship betweenColombia and the United States in these two pathogenic and resistantspecies.
Cesar A. Arias, M.D., Ph.D. University of Texas Medical School at Houston Houston, TX 77030 cesar.arias{at}uth.tmc.edu
Sandra Rincon, M.Sc. Universidad El Bosque Bogota, Colombia
Shahreen Chowdhury, B.S. University of Texas Medical School at Houston Houston, TX 77030
Ernesto Martínez, M.D. Hospital Universitario del Valle Cali, Colombia
Jinnethe Reyes, M.Sc. Universidad El Bosque Bogota, Colombia
Sreedhar R. Nallapareddy, M.Sc., Ph.D. Barbara E. Murray, M.D. University of Texas Medical School at Houston Houston, TX 77030
Supported in part by a grant (R37-AI47923, to Dr. Murray) fromthe Division of Microbiology and Infectious Diseases, NationalInstitute of Allergy and Infectious Diseases (NIAID), and bya K99/R00 Pathway to Independence Award (1K99-AI72961, to Dr.Arias) from NIAID.
Dr. Arias reports receiving lecture fees from Pfizer and Merckand grant support from Pfizer; Dr. Martinez, serving on advisoryboards for Merck, Wyeth, Janssen Laboratories, Pfizer, and GlaxoSmithKline;Dr. Coronell, receiving consulting fees from Wyeth, GlaxoSmithKline,Merck, and Abbot; and Dr. Murray, receiving grant support fromJohnson & Johnson, Astellas, and Intercell and consultingfees from Astellas, Theravance, Cubist, Targanta Therapeutics,Johnson & Johnson, Pfizer, AstraZeneca, and Wyeth. No otherpotential conflict of interest relevant to this letter was reported.
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