slowly, and subsequently held for an
extended period of time before serving. As
withSalmonellamicroorganisms, large num-
bers of active bacteria must be ingested for
this type of foodborne illness to occur.
The spores from various strains of this
microorganism have differing resistances to
heat. Some spores are killed in a few minutes
at 100ºC, whereas others require from 1 to 4
hours at this temperature for complete
destruction.C. perfringenscan be controlled
most effectively by rapid cooling of cooked
and heat processed foods. Frozen storage at
–15ºC for 35 days provides greater than
99.9% kill of this microorganism. An out-
break of foodborne illness from C. perfrin-
gens can usually be prevented through
proper sanitation as well as appropriate
holding (≥60ºC) and storage (≤2ºC) temper-
atures of foods at all times, especially of left-
overs. Leftover foods should be reheated to
65ºC to destroy vegetative microorganisms.
Escherichia coliO157:H7 Foodborne Illness
Outbreaks of hemorrhagic colitis and
hemolytic uremic syndrome caused by E. coli
O157:H7, a facultative anaerobic, gram-neg-
ative, rod-shaped bacterium, have elevated
this pathogen to a high echelon of concern.
It is uncertain how this microorganism
mutated from E. coli, but some scientists
speculate that it picked up genes from
Shigella, which causes similar symptoms.
This microorganism is shed in the feces of
cattle and can contaminate meat during pro-
cessing. It is important to establish interven-
tion procedures during harvesting and meat
processing operations to control the prolifer-
ation of this pathogen. Until approval of an
absolute critical control point, such as irra-
diation, beef should be cooked to 70ºC to
ensure sufficient heat treatment to destroy
this pathogen. A rigid sanitation program is
essential to reduce foodborne illness out-
breaks from this microorganism.
E. coliO157:H7, which is designated by its
somatic (O) and flagellar (H) antigens, was
discovered as a human pathogen following
two hemorrhagic colitis outbreaks in 1982.
Six classes of diarrheagenic E. coliare recog-
nized. They are enterohemorrhagic, entero-
toxigenic, enteroinvasive, enteroaggregative,
enteropathogenic, and diffusely adherent.
All enterohemorrhagic strains produce Shiga
toxin 1 and/or Shiga toxin 2, also referred to
asverotoxin 1andverotoxin 2. The ability to
produce Shiga toxin was acquired from a
bacteriophage, presumably directly or indi-
rectly from Shigella(Buchanan and Doyle,
1997). The infectious dose associated with
foodborne illness outbreaks from this
pathogen has been low (2,000 cells or less),
due to the organism’s acid tolerance.
The initial symptoms of hemorrhagic coli-
tis generally occur 12 to 60 hours after eating
contaminated food, although periods of 3 to
5 days have been reported. This bacterium
attaches itself to the walls of the intestine,
producing a toxin that attacks the intestinal
lining. Symptoms start with mild, non-
bloody diarrhea that may be followed by
abdominal pain and short-lived fever. Dur-
ing the next 24 to 48 hours, the diarrhea
increases in intensity to a 4 to 10-day phase
of overtly bloody diarrhea, severe abdomi-
nal pain, and moderate dehydration.
A life-threatening complication that may
occur in hemorrhagic colitis patients is
hemolytic uremic syndrome, which may
occur a week after the onset of gastrointesti-
nal symptoms. Characteristics of this condi-
tion include edema and acute renal failure. It
occurs most frequently in children less than
10 years old. Approximately 50% of these
patients require dialysis, and the mortality
rate is 3% to 5%. Other associated complica-
tions may include seizures, coma, stroke,
hypertension, pancreatitis, and hypertension.
Approximately 15% of these cases lead to
early development of chronic kidney failureThe Relationship of Microorganisms to Sanitation 43