Food Poisoning

Illustrated information about food poisoning

1. FOOD POISONING Presented By: Dr. Mona Mohammed Ali 1

2. 2

3. Definition Foodborne diseases, including foodborne intoxications and foodborne infections, are terms applied to illnesses acquired through consumption of contaminated food; they are frequently and inaccurately referred to as food poisoning. 3

4. Causes The more frequent causes of foodborne illnesses are : 1) toxins elaborated by bacterial growth either: A) In the food before consumption : Clostridium botulinum . Staphylococcus aureus . Bacillus cereus . S combroid fish poisoning—associated not with a specific toxin but with elevated histamine levels . B) Or in the intestines: (Clostridium perfringens) 4

5. Causes (continued): 2) bacterial, viral, or parasitic infections : ( brucellosis, Campylobacter enteritis, Escherichia coli, hepatitis A, listeriosis, salmonellosis, shigellosis , toxoplasmosis, viral gastroenteritis, taeniasis, trichinosis, and infection with vibrios ) 5

6. Causes ( continued) : 3) toxins produced by harmful algal species : (ciguatera fish poisoning, paralytic, neurotoxic, diarrhoeic or amnesic shellfish poisoning) Or present in specific species (puffer fish poisoning, AZP). 6

7. STAPHYLOCOCCUS INTOXICATION 7

8. Causative Agent: Several enterotoxins of Staphylococcus aureus, stable at boiling temperature, even by thermal process. Staphylococci multiply in food and produce the toxins at levels of water activity too low for the growth of many competing bacteria. 8

9. Clinical Features : An intoxication (not an infection) of abrupt (within 4 hours)and sometimes violent onset, with severe nausea, cramps, vomiting and prostration, often accompanied by diarrhea and sometimes with subnormal temperature and lowered blood pressure. Deaths are rare; illness commonly lasts only a day or two, but can take longer in severe cases; in rare cases, the intensity of symptoms may require hospitalization. 9

10. Diagnosis (in an outbreak setting): Recovery of large numbers of staphylococci ( 10 organisms or more/gram of food) on routine culture media . D etection of enterotoxin from an epidemiologically implicated food item confirms the diagnosis. Absence of staphylococci on culture from heated food does not rule out the diagnosis 10

11. Diagnosis (continued): Isolation of organisms of the same phage type from stools or vomitus of 2 or more ill persons confirms the diagnosis. Recovery of large numbers of enterotoxin producing staphylococci from stool or vomitus from a single person supports the diagnosis. 11

12. Occurrence: Widespread and relatively frequent; one of the principal acute food intoxications worldwide . About 25% of people are carriers of this pathogen . 12

13. Reservoir: Humans in most instances. O ccasionally cows with infected udders, as well as dogs and fowl. 13

14. Mode of Transmission: Ingestion of a food product containing staphylococcal enterotoxin, particularly those foods that come in contact with food handlers’ hands, either without subsequent cooking or with inadequate heating or refrigeration . 14

15. Mode of Transmission (continued): When food remain at room temperature for several hours before being eaten, toxin-producing staphylococci multiply and elaborate the heat-stable toxin . 15

16. Mode of Transmission (continued): Organisms may be of human origin from purulent discharges of an infected finger or eye, abscesses, acneiform facial eruptions, nasopharyngeal secretions or apparently normal skin; or of bovine origin, such as contaminated milk or milk products, especially cheese. 16

17. Incubation Period : Interval between eating food and onset of symptoms is 30 minutes to 8 hours, usually 2–4 hours. 17

18. Treatment: No specific treatment. Fluid replacement and hospitalization if needed. 18

19. Prevention: 1) Educate food handlers about : (a) Strict food hygiene, sanitation and cleanliness of kitchens, proper temperature control, hand washing , cleaning of fingernails. (b) The danger of working with exposed skin, nose or eye infections and uncovered wounds. 19

20. Prevention (continued): 2) Reduce food-handling time (from initial preparation to service) to a minimum, no more than 4 hours at ambient temperature. If they are to be stored for more than 2 hours, keep perishable foods hot (above 60°C/140°F) or cold (below 7°C/45°F; best is below 4°C/39°F) in shallow containers and covered. 20

21. Prevention (continued): 3) Temporarily exclude people with boils, abscesses and other purulent lesions of hands, face or nose from food handling. 21

22. Control: 1) Report to local health authority Class 4 . 2) Isolation. 3)Concurrent disinfection. 4)Quarantine. 5)Immunization of contacts and Investigation of contacts and source of infection: Not pertinent. Control is of outbreaks; single cases are rarely identified . 6 ) Specific treatment. 22

23. Epidemiological Measures: Through quick review of reported cases, determine time and place of exposure and population at risk. Obtain a complete listing of the foods served and embargo, under refrigeration, all foods still available. C ollect specimens of feces and vomitus for laboratory examination. Conduct an epidemiological investigation including interviews of ill and well persons to determine the association of illness with consumption of a given food. Compare attack rates for specific food items eaten and not eaten . 23

24. Epidemiological Measures (continued ): Inquire about the origin of incriminated food and the manner of its preparation and storage before serving . Look for possible sources of contamination and periods of inadequate refrigeration and unheating that would permit growth of staphylococci. Submit leftover suspected foods promptly for laboratory examination; failure to isolate staphylococci does not exclude the presence of the heat-resistant enterotoxin if the food has been heated. 24

25. Epidemiological Measures (continued): Search for food handlers with skin infections, particularly of the hands. Culture all purulent lesions and collect nasal swabs from all food handlers. Antibiograms and/or phage typing of representative strains of enterotoxin producing staphylococci isolated from foods and food handlers and from patient vomitus or feces may be helpful. 25

26. CLOSTRIDIUM PERFRINGENS FOOD INTOXICATION ( C . welchii food poisoning, Enteritis necroticans, Pigbel) 26

27. Causative Agent: Type A strains of C. perfringens (C. welchii) cause typical food poisoning outbreaks (they also cause gas-gangrene ). Type C strains cause necrotizing enteritis. Disease is produced by toxins elaborated by the organisms. 27

28. Clinical Features: An intestinal disorder characterized by sudden onset of colic followed by diarrhea; nausea is common, vomiting and fever are usually absent . Generally a mild disease of short duration, 1 day or less, rarely fatal in healthy people . Outbreaks of severe disease with high case-fatality rates associated with a necrotizing enteritis have been documented in postwar Germany and in Papua New Guinea (pigbel). 28

29. Diagnosis( In Outbreaks Settings): Demonstration of clostridium perfringens in semiquantitative anaerobic cultures of food (10 2 /g or more) or patients’ stool ( 10 6 /g or more) in addition to clinical and epidemiological evidence confirms the diagnosis. Detection of enterotoxin in patients’ stool also confirms the diagnosis. 29

30. Occurrence: Widespread and relatively frequent in countries with cooking practices that favor multiplication of clostridia to high levels. 30

31. Reservoir: GI tract of healthy people and animals (cattle, fish , pigs and poultry). 31

32. Mode Of Transmission: Ingestion of food containing soil or feces and then held under conditions that permit multiplication of the organism. Almost all outbreaks are associated with inadequately heated or reheated meats, usually stews, meat pies, and gravies made of beef, turkey or chicken. Spores survive normal cooking temperatures, germinate and multiply during slow cooling, storage at ambient temperature, and/or inadequate rewarming. 32

33. Mode Of Transmission (continued): Illness results from the release of toxin by cells undergoing sporulation in the lower intestinal tract . Heavy bacterial contamination (more than 10 5 organisms/gram of food) is usually required to produce toxin in the human intestine for clinical disease. 33

34. Incubation Period: From 6 to 24 hours, usually 10–12 hours. 34

35. Prevention: Educate food handlers about the risks inherent in large-scale cooking, especially of meat dishes. Where possible, encourage serving hot dishes (above 60°C/140°F) while still hot from initial cooking. 35

36. Prevention (continued): Serve meat dishes hot, as soon as cooked, or cool them rapidly in a properly designed chiller and refrigerate until serving time; reheating, if necessary, should be thorough (internal temperature of at least 70°C/158°F, preferably75°C/167°F or higher) and rapid. 36

37. Prevention (continued): Do not partially cook meat and poultry one day and reheat the next, unless it can be stored at a safe temperature. Large cuts of meat must be thoroughly cooked. F or more rapid cooling of cooked foods, divide stews and similar dishes prepared in bulk into many shallow containers and place in a rapid chiller. 37

38. Control: 1) Report to local health authority Class 4 . 2) Isolation. 3)Concurrent disinfection. 4)Quarantine. 5)Immunization of contacts and Investigation of contacts and source of infection: Not pertinent. Control is of outbreaks; single cases are rarely identified . 7 ) Specific treatment. 38

39. Epidemiological Measures: Through quick review of reported cases, determine time and place of exposure and population at risk. Obtain a complete listing of the foods served and embargo, under refrigeration, all foods still available. C ollect specimens of feces and vomitus for laboratory examination. Conduct an epidemiological investigation including interviews of ill and well persons to determine the association of illness with consumption of a given food. Compare attack rates for specific food items eaten and not eaten . 39

40. Epidemiological Measures (continued ): Inquire about the origin of incriminated food and the manner of its preparation and storage before serving . Look for possible sources of contamination and periods of inadequate refrigeration and unheating that would permit growth of staphylococci. Submit leftover suspected foods promptly for laboratory examination; failure to isolate staphylococci does not exclude the presence of the heat-resistant enterotoxin if the food has been heated. 40

41. Epidemiological Measures (continued): Search for food handlers with skin infections, particularly of the hands. Culture all purulent lesions and collect nasal swabs from all food handlers. Antibiograms and/or phage typing of representative strains of enterotoxin producing staphylococci isolated from foods and food handlers and from patient vomitus or feces may be helpful. 41

42. BACILLUS CEREUS FOOD INTOXICATION 42

43. Causative Agent: Bacillus cereus, an aerobic spore former . Two enterotoxins have been identified : H eat stable: causing vomiting, is produced in food when B. cereus levels reach 10 5 colony-forming units/gram of food . H eat labile: causing diarrhea, formed in the small intestine of the human host. 43

44. Clinical Features: An intoxication characterized in some cases by sudden onset of nausea and vomiting, and in others by colic and diarrhea . Illness generally persists no longer than 24 hours and is rarely fatal. 44

45. Diagnosis (In Outbreaks Settings): Diagnosis is confirmed through quantitative cultures on selective media to estimate the number of organisms present in the suspected food (generally more than 10 5 to 10 6 organisms per gram of the incriminated food are required ). Isolation of organisms from the stool of 2 or more ill persons and not from stools of controls also confirms the diagnosis. Enterotoxin testing is valuable but may not be widely availabl e. 45

46. Occurrence: A well recognized cause of foodborne disease in the world. 46

47. Reservoir: An ubiquitous organism in soil and environment, commonly found at low levels in raw, dried and processed foods. 47

48. Mode Of Transmission: Ingestion of food kept at ambient temperatures after cooking, with multiplication of the organisms . Outbreaks associated with vomiting have been most commonly associated with cooked rice held at ambient room temperatures before reheating . Various mishandled foods have been implicated in outbreaks associated with diarrhea. 48

49. Incubation Period: From 0.5 to 6 hours in cases where vomiting is the predominant symptom. From 6 to 24 hours where diarrhea predominates. 49

50. Prevention: Foods should not remain at ambient temperature after cooking, since the ubiquitous B. cereus spores can survive boiling, germinate, and multiply rapidly at room temperature . Refrigerate leftover food promptly (toxin formation is unlikely at temperatures below 10°C/50°F); reheat thoroughly and rapidly to avoid multiplication of microorganisms. 50

51. Control: 1) Report to local health authority Class 4 . 2) Isolation. 3)Concurrent disinfection. 4)Quarantine. 5)Immunization of contacts and Investigation of contacts and source of infection: Not pertinent. Control is of outbreaks; single cases are rarely identified . 7 ) Specific treatment. 51

52. Epidemiological Measures: Through quick review of reported cases, determine time and place of exposure and population at risk. Obtain a complete listing of the foods served and embargo, under refrigeration, all foods still available. C ollect specimens of feces and vomitus for laboratory examination. Conduct an epidemiological investigation including interviews of ill and well persons to determine the association of illness with consumption of a given food. Compare attack rates for specific food items eaten and not eaten . 52

53. Epidemiological Measures (continued ): Inquire about the origin of incriminated food and the manner of its preparation and storage before serving . Look for possible sources of contamination and periods of inadequate refrigeration and unheating that would permit growth of staphylococci. Submit leftover suspected foods promptly for laboratory examination; failure to isolate staphylococci does not exclude the presence of the heat-resistant enterotoxin if the food has been heated. 53

54. Epidemiological Measures (continued): Search for food handlers with skin infections, particularly of the hands. Culture all purulent lesions and collect nasal swabs from all food handlers. Antibiograms and/or phage typing of representative strains of enterotoxin producing staphylococci isolated from foods and food handlers and from patient vomitus or feces may be helpful. 54

55. CLOSTRIDIUM BOTULINUM FOOD INTOXICATION (BOTULISM) 55

56. Causative Agent: Clostridium botulinum is an anaerobic Gram +ve , spore forming, rod. The spores are heat resistant and exist widely in the environment, and in the absence of oxygen they germinate , grow and produce toxins. 56

57. Causative Agent (continued): There are 7 distinct forms of botulinum toxins ,types A-G. 4 of these(A,B,E and rarely F cause human botulism. Type C,D,G cause illnesses in other mammals. Botulinum toxins are one of the most lethal substance known. It blocks the nerve function. 57

58. Clinical Features: Fatigue , weakness , vertigo usually followed by blurred vision, dry mouth and difficulty in swallowing and speaking. Vomiting , diarrhea , constipation and abdominal distention may occur. The condition progress to weakness in the neck and arm after which the respiratory muscles and muscles of the lower body are affected. There is no fever and no loss of consciousness. 58

59. Diagnosis: History &Examination. Laboratory confirmation including : 1) Demonstrating the presence of botulinum toxins in serum, stool or food. 2) Culture of C. botulinum from stool or food. 59

60. Occurrence: Incidence is low , but mortality rate is high 5-10% of cases. 60

61. Reservoir: Human. Other mammals and birds. 61

62. Mode Of Transmission: Consumption of improperly processed food including low acid preserved vegetables such as green beans, spinach ,mushrooms and fish including canned tuna , meat products such as sausage. Though spores are heat resistant the toxin is destroyed by boiling (for example internal temperature greater than 85 ○ C for 5 minutes. 62

63. Mode of Transmission (continued): The ready to eat foods in low oxygen packaging are more frequently involved in food borne botulism. C. botulinum will not grow in acidic conditions (PH < 4.6) and therefore the toxins will not be formed in acidic foods. However the low PH will not destroy any preformed toxin. 63

64. Incubation Period: Commonly 12- 36 hours (minimum 4 hours to 8 days maximum) 64

65. Treatment: Antitoxin. Antibiotics. Mechanical ventilation. 65

66. Prevention: Combination of low storage temperatures and salt content and or low PH are used to prevent the growth of bacteria and the formation of toxins. The vegetative forms of bacteria can be destroyed by boiling, but the spores can remain viable after boiling even for several hours. However the spores can be killed by very high temperature treatment i.e.commercial canning. 66

67. The WHO 5 keys to safer food serve as the basis for educational programmes to train food handlers and educate consumers: Keep clean. Separate raw and cooked. Cook throughly. Keep food at safe temperature. Use safe water and raw materials. 67

68. SCOMBROID FISH POISONING (SFP) ( Histamine Poisoning) 68

69. SFP: A syndrome of tingling and burning sensations around the mouth, facial flushing and sweating, nausea and vomiting, headache, palpitations, dizziness and rash occurring within a few hours after eating fish containing high levels of free histamine (more than 20 mg/100 grams of sh); this occurs when the fish undergoes bacterial decomposition after capture. Symptoms resolve spontaneously within 12 hours and there are no long-term sequelae, occasionally antihistamine may be needed. 69

70. SFP(continued): Fish in the families Scombroidea and Scomberesocidae (tuna, mackerel, skipjack and bonito) containing high levels of histidine that can be decarboxylated to form histamine by histidine-decarboxylase-producing bacteria in the fish. Nonscombroid fish and any food (such as certain cheeses) that contains the appropriate amino acids and is subjected to certain bacterial contamination ,may lead to scombroid poisoning. 70

71. SFP : Detection of histamine in epidemiologically implicated sh confirms the diagnosis . Risks appear to be greatest for sh imported from tropical or semitropical areas and sh caught by recreational or artisanal fishermen , who may lack appropriate storage facilities for large sh . Adequate and rapid refrigeration, with evisceration and removal of the gills in a sanitary manner prevents this spoilage. 71

72. CIGUATERA FISH POISONING (GFP) 72

73. GFP: A characteristic GI and neurological syndrome may occur within 1 hour after eating tropical reef sh. GI symptoms (diarrhea, vomiting, abdominal pain) occur rst , usually within 24 hours of consumption. In severe cases, patients may also become hypotensive, with a paradoxical bradycardia. Neurological symptoms, including pain and weakness in the lower extremities and circumoral and peripheral paresthesias, may occur at the same time as the acute symptoms or follow 1–2 days later; they may persist for weeks or months. 73

74. GFP: Symptoms such as temperature reversal (ice cream tastes hot, hot coffee seems cold) and “aching teeth” are frequently reported. In very severe cases neurological symptoms may progress to coma and respiratory arrest within the first 24 hours of illness. Most patients recover completely within a few weeks; intermittent recrudescence of symptoms can occur over a period of months to years. 74

75. GFP: This syndrome is caused by the presence in the fish of toxins elaborated by the dinoagellate Gambierdiscus toxicus and algae growing on underwater reefs . Fish eating the algae become toxic, and the effect is magnified through the food chain so that large predatory sh become the most toxic; this occurs worldwide in tropical areas. 75

76. Prevention: The consumption of large predatory sh should be avoided, especially in the reef area, particularly the barracuda . Where assays for toxic fish are available, screening all large “high-risk” sh before consumption can reduce risk. The occurrence of toxic sh is sporadic and not all sh of a given species or from a given locale will be toxic. 76

77. Treatment: Intravenous infusion of mannitol (1 gram/kg of a 20% solution over 45 minutes) may have a dramatic effect on acute symptoms of ciguatera fish poisoning, particularly in severe cases, and may be lifesaving in severe cases that have progressed to coma. 77

78. PARALYTIC SHELLFISH POISONING(PSP) 78

79. PSP: Is a characteristic syndrome (predominantly neurological) starting within is a characteristic syndrome (predominantly neurological) starting within minutes to several hours after eating bivalve molluscs. Initial symptoms include paresthesias of the mouth and extremities, accompanied by GI symptoms, and usually resolving within a few days. In severe cases, ataxia, dysphonia, dysphagia and muscle paralysis with respiratory arrest and death may occur within 12 hours to several hours after eating bivalve molluscs. 79

80. PSP: This syndrome is caused by the presence in shellfish of saxitoxins and gonyautoxins produced by Alexandrium species and other dinoagellates. Concentration of these toxins occurs during massive algal blooms known as “red tides” but also in the absence of recognizable algal bloom. 80

81. PSP: PSP neurotoxins are heat-stable. Surveillance of high-risk harvest areas is routine in Canada, the European Union; Japan and the USA use a standard mouse bioassay; when toxin levels in shellfish exceed 80 micrograms of saxitoxin equivalent/100 grams, areas are closed to harvesting and warnings posted in shellfish-growing areas, on beaches and in the media . 81

82. NEUROTOXIC SHELLFISH POISONING (NSP) 82

83. NSP: Is associated with algal blooms of Gymnodinium breve, which produce brevetoxin. Red tides caused by G. breve have long occurred along the Florida coast, with associated mortality in sh, seabirds and marine mammals. Symptoms after eating toxic shellfish , including circumoral paresthesias and paresthesias of the extremities, dizziness and ataxia, myalgia and GI symptoms, tend to be mild and resolve quickly and completely. Respiratory and eye irritation also occur in association with G. breve blooms, apparently through aerosolization of the toxin through wind and wave action. 83

84. DIARRHETIC SHELLFISH POISONING (DSP) 84

85. DSP: This was first reported in Japan in 1978, and thereafter worldwide. The causative toxins, dinophysistoxin-1 (DTX1), dinophysistoxin-2 (DTX2), dinophysistoxin-3 (DTX3), okadaic acid (OA), 7-O-acylDTX2 (acylDTX2), and 7-O-acylOA (acylOA) have been isolated. Illness results from eating mussels, scallops, or clams that have fed on Dinophysis fortii or Dinophysis acuminata. Symptoms include diarrhea, nausea, vomiting, and abdominal pain. O rdinary cooking such as boiling in water or steaming cannot reduce OAs. 85

86. AMNESIC SHELLFISH POISONING (ASP) 86

87. Amnesic shellfish poisoning results from ingestion of shellsh containing domoic acid, produced by the diatom Pseudonitzschia pungens . Cases were reported in the Atlantic provinces of Canada in 1987, with vomiting, abdominal cramps, diarrhea, headache and loss of short term memory. When tested several months after acute intoxication, patients show antegrade memory decits with relative preservation of other cognitive functions, together with clinical and electromyographical evidence of pure motor or sensorimotor neuropathy and axonopathy . Canadian authorities now analyze yse mussels and clams for domoic acid, and close shellsh beds to harvesting when levels exceed 20 ppm domoic acid. 87

88. PUFFER FISH POISONING (TETRODOTOXIN) 88

89. Puffer fish poisoning is characterized by onset of paresthesias, dizziness, GI symptoms and ataxia, often progressing to paralysis and death within several hours after eating. The case-fatality rate approaches 60%. The causative toxin is tetrodotoxin, a heat-stable, nonprotein neurotoxin concentrated in the skin and viscera of puffer sh, porcupine sh, ocean sunfish , and species of newts and salamanders 89

90. AZASPIRACID POISONING (AZP) 90

91. Occurrence of AZP was rst reported when mussels harvested in Ireland caused diarrhea in humans in the Netherlands in 1995. Symptoms occur 12 to 24 hours after consumption and persist for up to 5 days: they include severe diarrhea and vomiting with abdominal pain and occasional nausea, chills, headaches, vomiting, stomach cramps . Azaspiracid can cause necrosis in the intestine, thymus, and liver. 91

92. Thank you 92

93. Have a healthy meal . 93