Biology Reference
In-Depth Information
The use of an EAF probe to detect and diagnose EPEC infection has dimin-
ished. This detection method required the infecting strain to possess the EAF
plasmid and for that plasmid not to be altered in a way which might affect probe
hybridization. Multiplex PCR approaches are now frequently utilized. These
multi-gene detections are focused on the identification of specific virulence
genes associated with EPEC classification, and those capable of distinguishing
between closely related pathotypes. The
eae
or
escV
genes are typically used
to identify EHEC, tEPEC, and aEPEC. Shiga toxin-producing strains are then
excluded based on the presence of
stx
genes. To discriminate typical from atypi-
cal EPEC, multiplex PCR detect genes of the bundle forming pili (
bfp
genes)
(
Aranda et al., 2004
;
Fujioka et al., 2012
). In addition to this method being the
most comprehensive, the ability to amplify directly from fecal samples means
that this method is also relatively quick (
Barletta et al., 2011
;
Wiemer et al.,
2011
). Quantitative PCR has recently been proposed as a tool to determine
symptomatic from asymptomatic infection as the former is associated with a
higher pathogen burden (
Barletta et al., 2011
).
Treatment
EPEC infections are usually self-limiting. Paramount attention should be paid
to correct for fluid and electrolyte loss and nutritional imbalances associated
with diarrhea; rehydration therapy alone constitutes the primary treatment. The
severity of the disease usually dictates the treatment, as oral rehydration may be
sufficient for milder cases, while more severe cases will require the inclusion of
parenteral rehydration or total parenteral nutrition (
Donnenberg, 1995
;
Nataro
and Kaper, 1998
).
Whilst antibiotic treatment for EPEC is not the primary therapeutic, EPEC
has been successfully cleared with antibiotics (
Thorén et al., 1980
;
Hill et al.,
1991
). However, the emergence of antibiotic- and multi-drug-resistant strains
has further complicated this means of treatment for severe cases. Resistance is
more prevalent in typical EPEC than atypical, largely due to coding sequences
residing on plasmids (
Laporta et al., 1986
;
Scaletsky et al., 2010b
). EPEC is
most often resistant to ampicillin, streptomycin, tetracycline, and triple sulfa
or its components (
Laporta et al., 1986
;
Lim et al., 1992
;
Guerra et al., 2006
;
Garcia et al., 2011
).
There are many existing and emerging therapies that directly target EPEC
colonization. Mixed results have been obtained in studies in which EPEC-
infected infants were treated by passive immunization with anti-EPEC bovine
immunoglobulin concentrate (
Mietens et al., 1979
;
Casswall et al., 2000
).
However, work on anti-EPEC antibody development continues. A group in
Brazil detailed the development of IgY antibodies against the O-antigens of
EPEC O111 and EHEC O111 and O157. While these antibodies were reactive
against their respective strain and inhibited the growth of the pathogen, they
remain to be tested clinically (
Amaral et al., 2008
). Extracts from medicinal
Search WWH ::
Custom Search