418 ◾ Fundamental Food Microbiology
food contamination. Clo. difficile association with meat animals and routine isolation of this organism from meats provide a strong evidence for its involvement as a foodborne pathogen.
Clo. difficile produces two toxins; Toxin A and Toxin B. Toxin A is an enterotoxin and causes
diarrhea, and Toxin B induces cytotoxicity and damages the mucus membrane. The clinical symptoms include mild self-limiting diarrhea, cramps, and abdominal pain to life-threatening pseudomembranous colitis, megacolon, and intestinal perforation. Enzyme immunoassay specific for
toxins and PCR methods are used as diagnosis and detection tools. For food-sample testing, culture methods employing suitable enrichment broth and solid agar media supplemented with antibiotics, cefoxitin, and cycloserine or moxalactam and norfloxacin are used for pathogen isolation.
escherichia coli O104:H4 17
A Shiga toxin-producing Escherichia coli (STEC) serovar O104:H4 caused the largest outbreak in
Germany, France, and other countries in 2011 resulting from consumption of fenugreek sprouts
imported from Egypt. A total of 3842 cases were reported, of which 2987 suffered from gastroenteritis (bloody diarrhea) with 18 deaths, and 855 people exhibited hemolytic uremic syndrome
(HUS) with severe kidney damage and 35 deaths. These symptoms are characteristics of enterohemorrhagic Escherichia coli (EHEC) that produce Shiga-toxin (Stx) and the prototype serovar is Esc.
coli O157:H7 (see Chapter 26). However, the serovars O104:H4 is a member of enteroaggregative
Esc. coli (EAEC), which expresses aggregative adherence fimbriae (AAF) required for attachment,
but most serovars in this group do not produce Stx. The isolate O104:H4 found in this outbreak
is a Shiga toxin–producing EAEC that has acquired the stx gene by a bacteriophage and has
been considered a newly evolved EAEC. In addition, this bacterium contained several virulence
genes that were encoded in the phage (prophage state) and in a plasmid (pAA). Whole genome
sequencing of this bacterium further revealed that it contains a colonization factor and virulence
genes that are common in both EHEC and EAEC, resulting in a highly virulent pathogen. The
pathogenesis of this Esc. coli O104:H4 was thought to be a result of increased adhesion, colonization, and damage of intestinal epithelial cells followed by increased dissemination of Stx to blood
circulation and the kidney. This may explain why high numbers of HUS patients were associated
with this outbreak. This epidemic O104:H4 strain was sensitive to antibiotics carbapenems, which
were recommended for treatment but were resistant to all penicillin and cephalosporin antibiotics.
Hepatitis E Virus 18
Hepatitis E virus (HEV), a RNA virus, is responsible for acute viral hepatitis exhibiting a mild
jaundice. The high-risk group of people who are most susceptible to HEV infection include patients
with chronic liver disease, pregnant women, and young children. HEV is a member of Hepeviridae
family, and there are four genotypes; genotype 1 and 2 are associated with human infection, and
genotype 3 and 4 are associated with humans, pigs, birds, and other species. The incubation period
for this disease is about 60 days. It is primarily a waterborne virus and caused several outbreaks
in developing countries in Asia, Latin America, and Africa. Travelers may carry the virus from
endemic zones to different parts of the world. Sporadic outbreaks are reported in the developed
countries including the United States. Though it is a waterborne virus, several recent outbreaks
were associated with consumption of deer meat and raw or undercooked swine liver in Japan. It
is now considered a zoonotic disease. Furthermore, HEV has been routinely isolated from swine
from Canada, Korea, Japan, Spain, the Netherlands, New Zealand, and the United States, implying potential future outbreak of HEV with the consumption of undercooked pork meat.
food contamination. Clo. difficile association with meat animals and routine isolation of this organism from meats provide a strong evidence for its involvement as a foodborne pathogen.
Clo. difficile produces two toxins; Toxin A and Toxin B. Toxin A is an enterotoxin and causes
diarrhea, and Toxin B induces cytotoxicity and damages the mucus membrane. The clinical symptoms include mild self-limiting diarrhea, cramps, and abdominal pain to life-threatening pseudomembranous colitis, megacolon, and intestinal perforation. Enzyme immunoassay specific for
toxins and PCR methods are used as diagnosis and detection tools. For food-sample testing, culture methods employing suitable enrichment broth and solid agar media supplemented with antibiotics, cefoxitin, and cycloserine or moxalactam and norfloxacin are used for pathogen isolation.
escherichia coli O104:H4 17
A Shiga toxin-producing Escherichia coli (STEC) serovar O104:H4 caused the largest outbreak in
Germany, France, and other countries in 2011 resulting from consumption of fenugreek sprouts
imported from Egypt. A total of 3842 cases were reported, of which 2987 suffered from gastroenteritis (bloody diarrhea) with 18 deaths, and 855 people exhibited hemolytic uremic syndrome
(HUS) with severe kidney damage and 35 deaths. These symptoms are characteristics of enterohemorrhagic Escherichia coli (EHEC) that produce Shiga-toxin (Stx) and the prototype serovar is Esc.
coli O157:H7 (see Chapter 26). However, the serovars O104:H4 is a member of enteroaggregative
Esc. coli (EAEC), which expresses aggregative adherence fimbriae (AAF) required for attachment,
but most serovars in this group do not produce Stx. The isolate O104:H4 found in this outbreak
is a Shiga toxin–producing EAEC that has acquired the stx gene by a bacteriophage and has
been considered a newly evolved EAEC. In addition, this bacterium contained several virulence
genes that were encoded in the phage (prophage state) and in a plasmid (pAA). Whole genome
sequencing of this bacterium further revealed that it contains a colonization factor and virulence
genes that are common in both EHEC and EAEC, resulting in a highly virulent pathogen. The
pathogenesis of this Esc. coli O104:H4 was thought to be a result of increased adhesion, colonization, and damage of intestinal epithelial cells followed by increased dissemination of Stx to blood
circulation and the kidney. This may explain why high numbers of HUS patients were associated
with this outbreak. This epidemic O104:H4 strain was sensitive to antibiotics carbapenems, which
were recommended for treatment but were resistant to all penicillin and cephalosporin antibiotics.
Hepatitis E Virus 18
Hepatitis E virus (HEV), a RNA virus, is responsible for acute viral hepatitis exhibiting a mild
jaundice. The high-risk group of people who are most susceptible to HEV infection include patients
with chronic liver disease, pregnant women, and young children. HEV is a member of Hepeviridae
family, and there are four genotypes; genotype 1 and 2 are associated with human infection, and
genotype 3 and 4 are associated with humans, pigs, birds, and other species. The incubation period
for this disease is about 60 days. It is primarily a waterborne virus and caused several outbreaks
in developing countries in Asia, Latin America, and Africa. Travelers may carry the virus from
endemic zones to different parts of the world. Sporadic outbreaks are reported in the developed
countries including the United States. Though it is a waterborne virus, several recent outbreaks
were associated with consumption of deer meat and raw or undercooked swine liver in Japan. It
is now considered a zoonotic disease. Furthermore, HEV has been routinely isolated from swine
from Canada, Korea, Japan, Spain, the Netherlands, New Zealand, and the United States, implying potential future outbreak of HEV with the consumption of undercooked pork meat.