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Characteristics of Foodborne Toxicoinfections For sporeformers, ingestion of large numbers of live vegetative cells is usually necessary. Vegetative cells.

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Presentation on theme: "Characteristics of Foodborne Toxicoinfections For sporeformers, ingestion of large numbers of live vegetative cells is usually necessary. Vegetative cells."— Presentation transcript:

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2 Characteristics of Foodborne Toxicoinfections For sporeformers, ingestion of large numbers of live vegetative cells is usually necessary. Vegetative cells of sporeformers do not multiply in the digestive tract, but sporulate and release toxins. For gram-negative bacteria, after ingestion they Rapidly multiply in the digestive tract. Many cells also die, releasing toxins. Toxins of both groups(sporeformers and Gram- negative bacteria) produce the gastroenteritis symptoms.

3 Clostridium perfringens Gastroenteritis The outbreaks generally occur with some foods that were prepared in advance by heating and then kept warm for several hours before serving. As the disease produces mild symptoms, many incidents are probably not reported. Characteristics The cells are Gram-positive rods, motile and sporeformers. They grow under anaerobic conditions but can tolerate some oxygen. The vegetative cells are sensitive to pasteurization but the spores are extremely heat resistant.

4 They can grow very effectively in many protein foods. The temperature of growth of vegetative cells and germination of spores is between 10-52C. The optimum growth occurs at 45C. Habitat Spores and vegetative cells are found in soil, dust, intestinal contents of animals, birds, humans and sewage. Many foods particularly raw foods get contaminated from these sources.

5 Toxins Clostridium perfringens type A strains are predominantly involved in foodborne toxicoinfection. They produce heat-labile enterotoxin. It is an intracellular protein produced by the cells during sporulation in the intestine and released. In addition to the intestine, sporulation ane enterotoxin production can also occur in some foods.

6 Disease and Symptoms The enterotoxin causes gastroenteritis. The symptoms appear 8-24 h following ingestion of a large number of viable cells(about half million cells/g). Symptoms include diarrhea, abdominal pain, nausea, vomiting and fever. The toxin changes the permeability of intestinal cells. Fatality is rare, but it can occur in very young, elderly and sick. Symptoms disappear within 24 h. This disease is considered a mild one.

7 Food Association Raw meat from animals and birds is most commonly contaminated with the spores and cells from the digestive tract content, whereas vegetables and spices commonly get them from soil and dust. Contributing factors for outbreaks are the improper holding temperature of foods, inadequate cooking, and contaminated equipment. The foods may not show any loss of acceptance quality.

8 Prevention Proper sanitation in all phases of food preparation and handling. Food should be cooked to the highest temperature recommended to kill the cells and as many spores as possible. The food should be cooled quickly and uniformly To refrigerated temperature. If a food is stored for a long time, it is important to reheat it quickly and uniformly and keeping it hot while being served. Detection Method Enumeration of the incriminated food and fecal samples for Clostridium perfringens in a selective agar medium and incubation of plates under anaerobic conditions.

9 Bacillus cereus Gastroenteritis Charachteristics The cells are Gram-positive motile rods, which form endospores in the middle of the cells. Cells are sensitive to pasteurization. Spores can survive high heat treatment used in many cooking procedures. The organism is aerobic, but can also grow under some degree of anaerobic environment. The cells can multiply in a temperature range of 4-50C, with the optimum of 35-40C. They can grow in the presence of high salt concentration.

10 Habitat Spores and cells of B. cereus are common in soil and dust and can be readily isolated from many foods which include both raw and finished products. Intestinal tracts of 10% of healthy adult humans have B.cereus under normal conditions. Toxins The strains produce two enterotoxins(emetic and enteric). The toxins are produced during growth of cells at the growth temperature range and retained in the cells. When the cells are lysed, the toxins are released.

11 Disease and Symptoms A large number of cells(2-3 million cells/g) are needed to produce gastroenteritis. The two types of enterotoxins produce two types of symptoms: The enterotoxin associated with the diarrheal form is a heat-labile protein, and that associated with the emetic form is a heat-stable protein. In diarrheal form, symptoms occur 6-12 h following consumption of a food containing the viable cells. Symptoms include abdominal pain, profuse watery diarrhea. Recovery is usually within 24 h.

12 In the emetic form, the symptoms occur in 1-5 h following ingestion of a food containing the viable cells. As the toxin is heat stable, once the toxin forms in cells, heating food containing a large number of cells before eating can produce the symptoms. Symptoms are nausea and vomiting, abdominal pain and diarrhea may also be present. Symptoms last for 24 h.

13 Cholera Vibrio cholerae is a Gram-negative motile with monotrichous flagellum, comma-shaped, facultative anaerobic. Two serogroups of V. cholerae: 01 and 0139 they cause outbreaks but 01 serogroup causes the majority of cases. V. Cholerae 01 has 2 biotypes; Classical and El Tor Each biotype has three serotypes; Inaba, Ogawa and Hikojima. Non 01 serotype strains are isolated from coastal waters.

14 The type currently associated with cholerae epidemics worldwide is of the El Tor biotype and either Inaba or Ogawa serotype. V. cholerae is sensitive to heat and are killed by the temperature used for cooking. The optimum temperature of growth is between 30-35C. The growth rate is very rapid even at room temperature. Alkaline foods facilitate rapid growth. Survival of cells is better in cooked foods at 5-10C.

15 Habitat Cholera is a human disease. The disease results from ingestion of infective doses of V. cholerae( about one million cells) through foodsand water contaminated with feces of humans suffering from the disease. Marine environments may serve as long-term reservoirs. Both serotypes, especially non-01, have been isolated from water in U.S.

16 Toxins and Toxin Production The toxin of the 01 serotype is a heat-labile, 85-kDa cytotoxic protein with two functional units. The active A subunit stimulates adenyl cyclase in the intestinal epithelial cells to produce cyclic AMP which causes massive secretion of water along with chloride, potassium, and bicarbonate in the lining of the intestine. The non-01 serotype produces a cytotoxin and a hemolysin. Treatments consist of rapid replacement of fluids, electrolytes and administration of proper antibiotics.

17 Food Association Food can serve as a source of V. cholerae if it is contaminated directly with human feces from the patient or previously contaminated water. The handling of food by a person suffering from the disease can also contaminate food, because of poor personal hygiene. Food originating from natural reservoirs of the causative bacteria can be contaminated and spread cholera. The natural reservoirs include marine and brackish water environments. Among the types of contaminated foods are raw oysters, Crab, fish and shrimp and cooked rice.

18 Prevention Adopting proper hygienic measures. Provision of properly treated municipal water. Decontamination of suspected water by boiling. Proper disposal of sewage. Treating of infected persons with antibiotics along with replacing body fluids. Vaccination of unexposed people. Seafoods should not be eaten raw.

19 Detection Methods Isolation of V. cholerae from a sample is achieved by an initial preenrichment in alkaline peptone water, followed by streaking on a selective agar medium plate such as thiosulfate citrate bile salt sucrose agar. Suspected colonies(yellow) are biochemically and serologically tested for confirmation. The toxin is detected by immunoassay.

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