BACTERIAL FOOD INTOXICATION

BY
Prof. dr. Muh. Nasrum Massi, Ph.D
 INTRODUCTION
Acute infection of GI tract (diarrhea) is the
most frequent of all illnesses after common
cold.
Self-limiting (in hours and days) disease—do
not seek medical care.
High morbidity & mortality among infants and
children, -- socioeconomic and nutritional
factors
 CATEGORIES OF FOODBORNE ILLNESS
• Result from the growth microorganism in the body,
which are carried by food or water into the host
Food infection • Ex: salmonella sp., campylobacter sp.,yersinia
entercolitica

• Result from the action of mmicrobial toxin that

Food contaminated food, toxins are ingested
intoxication • Ex: staphylococcus aureus, clostridium perfiringens,
clostridium botolinum

Infection- • Results from the consumption of food containing

harmful bacteria which in the intestinal tract
mediated produce toxins that cause illness
intoxication • Ex : Shigella sp., Escherichia coli
 Bacterial toxins which are involved in
foodborne infections and intoxications
• Soluble, usually heat- • Heat stable
labile proteins found lipopolysaccharide
in the cytoplasm or in components of the
the growth medium outer membrane on
(as a result of Gram negative
autolysis). Ex: bacteria.

Exotoxins Endotoxins
 exotoxins
These are further subdivided by their mode of action:

• enterotoxins stimulate gastrointestinal cells in an

abnormal way. (e.g. cholera toxin)

• cytotoxins kill host cells by enzymatic attack. (e.g.

diphtheria toxin)

• neurotoxins interfere with normal transmission of

nerve impulses.(e.g. botulinum toxin)
 Endotoxins

These toxins have similar structures and

produce fever, shock, diarrhea and sometimes
internal hemorrhage or abortion in
hosts. Interestingly, when these toxins are
administered in sublethal levels, they can confer
enhanced resistance to bacterial infections.
 Clinical Features
(fever, vomiting, abdominal pain and diarrhea)

1. Watery diarrhea (nausea, vomiting, fever, abdominal

pain and intestinal fluid loss—caused by VC and ETEC in proximal
small intestine)—the “run”

2. Dysentery (fever, abdominal pain, cramps, tenesmus, feces

with blood and pus—produce inflammatory or destructive changes in
colonic mucosa by direct invasion or produce cytotoxins– the “squirt”

3. Enteric fever (fever and abdominal pain—mild diarrhea—

bacteremia common and cause metastatic infection in other organs---
typhoid fever in distal small bowel
BACTERIAL AGENTS OF FOOD INTOXICATION
Staphylococcus

Bacillus

Clostridium botulinum

Escherichia coli ( some strains )

Vibrio cholerae

Shigella spp

Salmonella spp

Clostridium defficile

Campylobacter jejuni

Yersinia enterocolitica
 Staphylococcus aureus
• Genus of Gram positive

• Facultavie anaerobic
bacteria that includes several
species able to synthesize
heat labile enterotoxins that
produce the food poisoning.
Bacillus cereus
 Clostridium botulinum
1. Botulism is Caused by the ingestion of a heat-labile
neurotoxin produced (most frequently) by C. botulinum.

2. Seven types of toxin, A-G, are recognized on the basis of the

serological specificity.

• A, B, E, F, and G cause disease in humans

• type C in fowls, cattle, mink and other animals

• type D is associated with forage poisoning of cattle

 Pathogenesis
Pathogenesis is due to the ingestion of C. botulinum neurotoxin.

1. These toxins are formed inside the bacterium and are released by
autolysis.

2. Botulism toxins are the most lethal substances known; a single

milligram of type A toxin will kill 15 million mice (1 mg L.D.50=30 million
mice).

3. Can be absorbed into the bloodstream through the respiratory

mucus membranes or thru the lining of the stomach.
Sources
1. C. botulinum cells and
spores are found in soils,
dust and water.

2. Spores expected in
vegetable-based products as
a result of soil
contamination.

3. foods that are handled

improperly or given
inadequate heat treatment.
 Symptoms

1. Symptoms appear between 12-72 h after the

ingestion of toxin-containing foods.
2. Nausea, vomiting, fatigue, dizziness, headache,
dry skin, mouth and throat, lack of fever,
constipation, paralysis of muscles, double vision.
Finally, respiratory failure and death.
3. The illness may linger over 1-10 days.
Pathogenic schema of diarrhoeagenic E. coli.

Pathogenic group
Enteropatogenic E coli (EPEC)
Enterotoxigenic E coli
(ETEC)
Enterohemorrhagic (verotoxin
producing) E coli (EHEC)
Enteroinvasive E coli (EIEC)
Enteroaggregative E coli (EAEC)
Diffuse aggregative E coli
(DAEC)
Escherechia coli
epidemiology
EPEC strains belong to particular O
serotypes cause sporadic cases and
outbreaks of infection in babies and
young children importance in adults less
clear
Most important bacteria cause of
diarrhea in children in developing
countries most common cause of
traveler’s diarrhea water contaminated
by human or animal sewage may be
important in spread
Serotype O157 most important EHEC in
human infections
Outbreaks and sporadic cases occur
worldwide
Food and unpasteurized milk impotant in
spread
May cause haemolytic uremic syndrome
(HUS)
Important cause of diarrhea in areas of
poor hygiene
Ionfection usually foodborne, no
evidence of animal or environmental
reservoir
Characterisitic attachment to tissue
culture cells
Cause diarrhea in children in developing
counties
Role of toxins uncertain
Laboratory diagnosis
Isolate organism from feces
Determine serotype of several colonies
withpolyvalent antisera for known EPEC
types
Adhesion to tissue culture cells can be
demonstrated
By a fluorescence actin staining test
DNA-based assays fro detection of
attacment
(virulence) factors
Isolate organisms from feces
Tests commercially available for
immunologic detection of toxins from
culture supernatants
Genes probes specific for LT and ST genes
available for detection of ETEC in feces
and in food and water samples
Isolate organisms from feces
Proportion of EHEC in fecal sample may be
very low (often <1% of E coli colonies)
Usually sorbitol non-fermenters
Shiga toxin production and associated genes
detected by biological, immunological and
nucleid acid based assays
Isolate organisms from feces
Test for enteroinvasive potential in tissue
culture cells or nucleid acid based assays
for invasion associated genes
Issue culture assays for aggregative of
diffuse adherence
Pathogenic schema of diarrhoeagenic E. coli.
 Vibrio cholerae
• Gram negative rods,often
curved
• Actively motile by a single polar
flagellum
• Nearly all produce the enzyme
oxidase and indole
• Growth is rapid in the pH range
7,4-9,6
 Pathogenic mechanism
• Produce a poten enterotoxin
 Shigella spp

• Rod-shape gram negative

bacteria

• Facultative anaerobic

• Non-spore , non-motile

• Incubation period : 1- 7 days

• Shiga toxin (vero-toxin),

cytotoxin, causes severe
diarrhea
• gram negative rod Salmonella enterica
shaped bacteria
• classified under family
enterobacteriaceae.
• Their normal habitat is
the animal intestine.
• Chicken, duck, turkey
and goose may be
infected with
Salmonella, which then
find its way into its
feces, eggs or flesh of
dressed fowl.
• Incubation period : 12-
36 hours.
 Salmonella
1. More than 1000 strains base on the O and H
antigen, but for human the most important is
Salmonella enterica.

2. There is a large contaminated food, especially

poultry and daily product

3. Salmonella infections are almost always acquired

orally in food or drink that is contaminated.
 Pathogenesis
Organism penetrates and passes through the
epithelial cells lining the terminal portion of the
small intestine. Multiplication of bacteria in the
lamina propria produces inflammatory mediators,
recruits neutrophils and triggers inflammation.
Release of LPS causes fever. Inflammation causes
release of prostaglandins from epithelial cells.
Prostaglandins cause electrolytes to flow into
lumen of the intestine. Water flows into lumen in
response to osmotic imbalance resulting in
diarrhea.
 CLINICAL PICTURE
• Sudden onset of abdominal pain, nausea, vomiting and
diarrhea, which may be watery, greenish and foul
smelling. This may be preceded by headache and chills.
• Other findings include prostration, muscular weakness
and moderate fever.
• In most cases the symptoms resolve in 2-3 days
without any complications.
 Yersinia enterocolitica
• It is a gram negative psychrophilic
• rod shaped bacterium
• motile only at temperature below 30oC.
• The major animal reservoir is pigs, but may also found in many
other animals including rodents, rabbits, sheep, cattle, horses,
dogs, and cats.
• Incriminated food : especially raw or undercooked pork products.
,unpasteurized milk or untreated water can also transmit the
infection.
 Pathogenesis
• This organism may survive and grow during refrigerated
storage. Strains that cause human yersiniosis carry a plasmid
that is associated with a number of virulence traits. Ingested
bacteria adhere and invade M cells or epithelial cells. They
exhibit resistance to complement and phagocytosis. They
produce ST only at temperatures below 30ºC. The role of ST in
the disease process remains uncertain.
• Incubation period: 4-7 days
Pathogenic mechanism of
Yersinia enterolitica
 Clinical features

• fever, abdominal pain, and diarrhea, which is often bloody.

• Illness generally lasts from 1 to 2 weeks but chronic cases may

persist for up to a year.

• A part from gastroenteritis it may also cause

pseudoappendicitis, mesenteric lymphadenitis, and terminal
ileitis.