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 transmission 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 – Pathogenesis • The rotavirus is transmitted by the fecal-oral route • 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 diarrhoea. • 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 – Pathogenesis • 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 – Pathogenesis • 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 aureus • Approximately one third of the strain S.aureus excrete into food a heat stable exotoxin called Staphylococcus enterotoxin (A-E). • 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 botulinum. • 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- transmission. • 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 Terima Kasih