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 .
Scombroid 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.
Detection 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.
Occasionally 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.
 Collect 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 (102
/g or more) or patients’ stool (106 /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 105 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.
For 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.
 Collect 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 :
1) Heat stable: causing vomiting, is produced
in food when B. cereus levels reach 105
colony-forming units/gram of food .
2) Heat 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 105 to 106 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 available.
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.
 Collect 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.
 Ordinary 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