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3) Viral Diarrhoeal  Introduction

• Non-bacterial gastroenetritis and diarrhoea are

caused by virus. In developing country non-
bacterial gastroenteritis is a major cause of death
• Although viruses appear to be commonest causes
of gastroenteritis in infant and young children,
viral gastroenteritis is not distinguishable
clinically from other types of gastroenteritis.
• The viruses are specific to human and infection
follows the general rules for fecal-oral
3) Viral Diarrhoeal  Rota Virus
• Rota virus is belong to the family
Reoviridae, they infect mamals,
including humans and birds.
• The virus (rota means ‘wheel’ in latin)
possesses a doubled-shelled capsid that
enclosed a doeble-strand RNA
composed of 11 separate segment. The
outer capsid gives the appearance of
the rim of a wheel
3) Viral Diarrhoeal  Rota Virus –
• The rotavirus is transmitted by the fecal-oral
• The incubation period for infection is 48
hour- 4 dayss. After virus replication in
intestinal cells there is acute onset of
vomiting, sometime projectil, fever and
• The virus infects the small intestine and
confines its activites to the epithelial cells on
the tips of the villi.
3) Viral Diarrhoeal  Rota Virus –
• The replicating virus damages transport
mechanism in the gut and loss of water,
salt, and glucose causes diarrhea.
• Infected cells are destroyed but there is no
inflammation or loss of blood.
• Loss of fluid during gastroenteritis leads to
severe dehydration and even death.
• Dehydrating diarrhea may last 5-7 days.
3) Viral Diarrhoeal  Rota Virus –
• Infection is commonest in those less than 2 years
old, and more frequent in the cooler months of
the years.

• IgA antibodies in colostrum give protection

during the first 6 months of life.
• Epidemic are sometime seen in nurseries
• Older children are less susceptible are less
susceptible are less susceptible, nearly all of
them having developed antibodies, but are less
susceptible occasional infections occurs in adults
3) Viral Diarrhoeal  Rota Virus –
Diagnosis, Treatment and Prevention
• Lab. method are generally not available and not
necessary in developing country, but during the
acute stage the caharacteristic 65 nm particles can
be seen in fecal sample by electron microscope
• Viral antigen can be detected in faeces by ELISA or
RIA methods
• Dehydration occurs readily in infants and
intravenous fluid replacemen can be life-saving
• There are no antiviral agent available, but live,
attenuated oral vaccine are undergoing trials
4) Food Poisoning Introduction
• Foofborne disease may be devided into 2
types : 1) food infection and 2) food poisoning
1.Food infection result from the ingeston of
m.o. (Salm.) found in the food. Salmonella
produce a toxin in host intestine that causes
gastrointestinal symptom.
2.Food poisoning are the result of ingestion
toxin that were liberated during growth of
m.o. in the food
4) Food Poisoning Introduction
• Food Poisoning : is restricted to the
disease caused by toxin elaborated by
contaminating bacteria in food before it
is consumed
• The emetic toxin of Bacillus cereus fits
this definition, as do the disease
associated with the consumption of
Staphylococcus aureus enterotoxin
and Clostridium botulinum toxin.
4) Food Poisoning Staphylococcus
• Approximately one third of the strain
S.aureus excrete into food a heat stable
exotoxin called Staphylococcus enterotoxin
• They can withstand 30 minutes of boiling and
are not inactivated by digestive enzyme
• When ingested with the food, the enterotoxin
causes a type of food poisoning that is
accompanied by vehement vomiting
(projectile vomiting), cramps, diarrhoea, and
prostration 2-8 hours after ingestion
4) Food Poisoning Staphylococcus aureus
• Enterotoxin food poisoning is rarely fatal.
• The patient is fully recocered in 24-48 hours.
• Many food support the growth of
Staphylococcus, include those that contain a
high amount of protein (ham, poultry)
• Food preparers and handlers who have
staphylococcal of the skin, especially of the
hands, and nasopharyngeal carriers are the
most likely to contaminate food. Absence of
lesions is no guarantee of safety
4) Food Poisoning  Clostridium botulinum
• Botulism is rare but serious disease
caused by the exotoxin of Clostridium
• The m.o. is widespread in the
environment and spores can be isolated
readily from soil samples and from various
animals including fish.
• Eight serologically distinct toxin have been
identified, but only 3 (A, B, and E) are
associated with human disease
4) Food Poisoning  Clostridium botulinum
• The toxin are ingested in food (often canned or re-
heated) or produce in the gut after ingestion of the
m.o.; they are absorbed in the gut into the blood-
stream and reach their site of action, the peripheral
nerve synapses.
• The action of the toxin is to block neuro-
• Three forms of botulism have been identified :
a) Food-borne botulism –toxin elaborated in food
b) Infant botulism ) ingested / implant in wound,
c) Wound botulism) multiply, elaborate toxin invivo
4) Food Poisoning  Clostridium botulinum
• The clinical disease is the same in all three
form, and is characterized by flaccid paralysis
leading to progressive muscle weakness and
respiratory arrest
• Intensive supportive treatment is urgently
required and complete recovery may take
many months.
• Laboratory diagnosis by demonstration the
presence of toxin by injecting sample of feces
and food into mice (protected with antitoxin
or unprotected). Culture of feces or wound
exudate also performed.
4) Food Poisoning  Clostridium botulinum
• Prevention with :
- polyvalent antitoxin is recommended;
- preventing germination of spore in food,
by maintaining food at an acid pH,
- or storing at <4o C,
- or destroying toxin in food by heating for
30 minutes at 80o C.
- Type A toxin : consisting neurotoxin with
hemagglutinin, that hemagglutinin protect
protects the neurotoxin from stomach
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