31 Emerging Bacterial Foodborne Pathogens and Methods of Detection 713enteriditiscaused more than 75% of the human ill-
nesses reported in England and Wales during 2000
(Liebana 2002).
Although it is the most famous of the S. enterica
serotypes, the occurrence of S. typhihas been essen-
tially eradicated in western countries over the past
100 years (Zhang et al. 2003; see Table 31.1 for
numbers). In fact, between 1992 and 1997, more
than 70% of the S. typhicases in the United States
occurred after travelling to the non-Western world
(Mead et al. 1999). Because of their prevalence in
foodborne illness, discussion in this paper will be
restricted to the S. entericaserotypes S. typhimuri-
umand S. enteriditis.
S. enteriditiscontamination is most often found in
chicken products, but the pathogen may also have a
reservoir in the rodent population. New generations
of chickens could be infected when rodents contam-
inate the feeding troughs while sleeping in them at
night (Tauxe 2002). In the United States, S. enteridi-
tiscaused about 6% of Salmonellainfections in
1980, increasing to 26% of all Salmonellainfections
by 1984. Eighty-two percent of the cases were
caused by eating eggs contaminated with the path-
ogen (Altekruse et al. 1997, Gugnani 1999).
S. typhimuriumis most commonly a foodborne
pathogen, although there have been a few cases of
outbreaks caused by contaminated water sources in
the United States. It causes enterocolitis, resulting in
diarrheal illness. As of 1998, the U.S. Centers for
Disease Control (CDC) claimed that this S. typhi-
muriumaccounted for 26% of all Salmonellaiso-
lates causing illness (Zhang et al. 2003). Both S.
enteriditisand S. typhimuriumcause nausea, vomit-
ing, abdominal cramps, diarrhea, fever, and head-
ache (Granum and Brynstad 1999).
The type III secretion system from pathogenicity
island 1 of S. typhimurium(TTSS-1) has been pro-
posed as one of the main virulence determinants
required by S. typhimuriumto cause diarrhea and
mortality among cattle. TTSS-1 is thought to work
by mediating the translocation of effector proteins
into the cytosol of the host cells. The effector pro-
teins, including SopB, SopC, and SopD, form a trans-
location complex to deliver more effector proteins
into the host cytoplasm, then cause fluid accumula-
tion and the influx of neutrophils into the intestine.
The end accumulation of fluid into the intestine may
be due to a secretory mechanism dependent on the
effector proteins, or it may be due to neutrophil-
induced tissue damage (Zhang et al. 2003). S. typhi-
muriumalso produces a number of other toxins.
However, most of these do not have equivalent ef-
fects between species and are not considered general
virulence factors.E. COLIO157:H7E. coliO157:H7 was responsible for about 3% of
the food-related deaths in the United States as of
1999 (Mead et al. 1999). E. coliO157:H7 was iden-
tified in 1976 and first described as a human path-
ogen in 1982 during two outbreaks of severe bloody
diarrheal syndrome in Oregon and Michigan (Gu-
gnani 1999, Park et al. 1998).
E. coliO157:H7 is transmitted by food or water
sources (Tauxe 2002), with secondary person-to-
person transmission. The strain produces a number
of toxins that can cause bloody diarrhea in infected
persons; 4% of those infected develop hemolytic
uremic syndrome (HUS), which can cause kidney
damage (Mead et al. 1999), and around 1% die (Park
et al. 1998). Antimicrobial therapy, such as treat-
ment with ampicillin, tetracycline, erythromycin, or
antibiotics from the quinolone family (Neill 1998,
Tauxe 2002, Wong et al. 2000, Zhang et al. 2000),
are not effective, and only supportive care can be
provided (Wong et al. 2000, Zhang et al. 2000). This
strain of E. colicontaminated the drinking water of
Walkerton, Ontario, Canada, in May 2000, causing
over 2000 people in a town of 5000 to become ill, 27
to develop HUS, and at least 6 to die (2000). In
1998, a number of illnesses attributed to E. coli
O157:H7 in Southern Ontario were due to ingestion
of contaminated salami (Williams et al. 2000).
E. coliO157:H7 is a robust organism. It is toler-
ant of cold temperatures, although it does not grow
at 4°C. The organism can survive refrigerated stor-
age for more than 2 months (Meng and Doyle 1997),
and storage at between 80 and 20°C for 9
months (Park et al. 1998). This means that when a
temperature abuse situation (6°C) does occur, it is
ideally situated to grow and replicate, resulting in
bacterial levels high enough to cause infection and
illness.
E. coliO157:H7 is also tolerant to pH values as
low as 3.6 (Meng and Doyle 1997). This acid toler-
ance has allowed the occurrence of outbreaks attrib-
uted to its contamination of highly acidic foods such
as apple cider, mayonnaise, and smoked sausage.