BackgroundMycobacterium intracellulare, a species of the Mycobacterium avium complex, may be the cause of severe lung, lymphatic node, skin and bone/joint infections, as well as bacteriemia. The goal of this work was to identify Mycobacterial Interspersed Repetitive Unit-Variable Number Tandem Repeat (MIRU-VNTR) markers and to study their variability in a collection of isolates of M. intracellulare collected in humans. We studied 61 isolates collected in humans between 2001 and 2008, as well as the reference strain, M. intracellulare ATCC 13950.ResultsWe identified 45 MIRU-VNTR candidates, of which 17 corresponded to the MIRU-VNTR identified in the genome of M. intracellulare ATCC 13950. Among the 45 potential MIRU-VNTR, seven were selected for use in a MIRU-VNTR assay applied to our collection of isolates. Forty-four patterns were found by MIRU-VNTR typing and the discriminatory power of the assay was high with a Hunter-Gaston diversity index of 0.98. We do not have evidence of a particular distribution of MIRU-VNTR polymorphism according to clinical situation.ConclusionsOur results suggest that MIRU-VNTR typing could be used for molecular epidemiological studies applied to M. intracellulare.
During a previous survey, five extended-spectrum -lactamase (ESBL)-producing enterobacteria (ESBLE) (two Enterobacter aerogenes isolates expressing TEM-24b, two Escherichia coli isolates expressing TEM-21 or TEM-24b, and one Klebsiella pneumoniae isolate expressing SHV-4/TEM-15) responsible for urinary tract infections (UTIs) were found among 1,584 strains collected from community patients. The aim of the present study was to elucidate the route of emergence of these typically nosocomial organisms in the community. Thus, the files of the five patients were analyzed over at least a decade, and potentially related ESBLE from hospitals or clinics were examined. Their enzymes were characterized at a molecular level, and the strains were typed by amplified-primed PCR, enterobacterial repetitive intergenic consensus PCR, and restriction plasmid profile. All patients (C1 to C5) had risk factors for ESBLE acquisition, including past history of hospitalization (2.5 to 23 months before). Four (C1 and C3 to C5) had previously received antibiotics (concomitantly to 35 months earlier), two (C1 and C3) had indwelling urinary catheters and recurrent UTIs, and three (C2, C3, and C5) formerly experienced ESBLE-induced UTIs (2 1 ⁄2 to 11 1 ⁄2 months before). The same ESBLE and/or an identical or similar ESBL-encoding plasmid was identified in the hospital ward (C1 to C4) or in a clinic (C5) where the patients had previously resided. Patients C1 and C4, infected with different ESBLE carrying a closely related plasmid, were hospitalized in the same unit. Persistence of ESBLE over at least a 5-year period was demonstrated for patient C3. Thus, community-acquired UTIs in these patients likely resulted from nosocomially acquired ESBLE or an ESBL-encoding plasmid followed by a prolonged digestive carriage.Extended-spectrum -lactamase (ESBL)-producing enterobacteria (ESBLE) have emerged at the end of the 1980s within hospitals, causing outbreaks and/or hyperendemic situations in many centers. Several recent data have suggested that ESBLE are currently emerging within the community
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