CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Virulence factors and genetic diversity of clinical and environmental Vibrio cholerae non-O1, non-O139 strains isolated in Argentina.
Autor/es:
SAKA HA, VIÑAS MR, BINSZTEIN N, CARRANZA P, SOLA C, BOCCO JL, PICHEL M.
Lugar:
Cordoba
Reunión:
Congreso; Congreso Argentino de Microbiologia; 2007
Institución organizadora:
Asociacion Argentina de Microbiologia
Resumen:
V. cholerae is the causative agent of cholera, a severe diarrhea transmitted through
contaminated food or drinking-water or by the faecal-oral route mainly in
developing countries. Cholera toxin (CT), a potent enterotoxin encoded in the
CTXphi bacteriophage and toxin co-regulated pilus (TCP), a colonization factor,
are critical in the pathogenesis of cholera. V. cholerae includes more than 200 serogroups from which only CT+
TCP+ strains from O1 and O139 serogroups are associated to cholera epidemics. The
remaining serogroups, referred to as V.
cholerae non-O1, non-O139 (VCN), mostly lack CT and
TCP. However, VCN may cause sporadic outbreaks of watery diarrhea, inflammatory
enterocolitis, sepsis and soft tissue infections. There is evidence indicating
that environmental VCN may acquire virulence genes and eventually become
epidemic. Thus, the study VCN virulence may help to understand the epidemiology
and the origin of pathogenic V. cholerae
strains. In this work, 63 VCN (clinical, 22; environmental, 38 and food, 3)
isolated in 8 provinces (1992-2003), were used to investigate the prevalence of
9 different virulence genes by PCR. A subset of 30 strains was selected to study
their enterotoxic potential in rabbit ileal loops (RIL) and their genetic
diversity by PFGE. Results obtained by PCR showed that hlyA (encoding V. cholerae cytolysin),
toxR (encoding a virulence-related
transcriptional regulator) and rtxA
(encoding RTX toxin) were the most prevalent virulence genes as they were
detected in 100%, 96.9% and 96.9% of the isolates, respectively. Only one
strain, isolated from environmental water, harbored ctxA (encoding the catalytic subunit of CT). No zot (encoding zonula occludens toxin) or
ace (encoding accessory cholera
enterotoxin) positive strains were detected. Though none of the isolates were
positive for tcpA (encoding the A
subunit of TCP), 12.7% carried tcpI (a
gene related to TCP expression), pointing out to the possibility that these
strains may have autochthonous TCP variants which could probably be functional
as receptors for CTXphi and may consequently acquire epidemic potential. The stn gene (encoding a termostable
enterotoxin) was detected in 15.9% of the isolates. The RIL assay showed that
most of the strains were capable of inducing fluid accumulation (FA), with the
highest FA values for the tcpI+ and for the stn+ strains. The PFGE
patterns revealed the existence of a wide variety of VCN clones. Interestingly,
two environmental tcpI+ isolates
presented the same PFGE pattern, two clinical isolates showed an
indistinguishable PFGE profile and other three clinical strains had a closely
related fingerprint PFGE pattern. This is the first comprehensive study about the
genetic diversity and the virulence properties of VCN in Argentina.