This document summarizes key information about foodborne infections. It discusses Salmonella, which has over 2000 serotypes including S. typhi and S. paratyphi A, B, C. It also discusses reservoirs, transmission, clinical presentation, and prevention of various foodborne illnesses caused by Salmonella, Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, Clostridium botulinum, and Vibrio cholerae. General preventive measures are outlined such as proper food handling, processing, and sterilization to prevent transmission of bacteria and toxins through contaminated food and water.

1. Dr. Dalia El-Shafei
Lecturer, Community medicine department, Zagazig
university

2. Food born infections

5. Salmonellae have more than 2000 serotypes, of
which pathogens of Human disease is:
*Typhoidal salmonellae: S. typhi, & S. paratyphi A,
B, C.
*Nontyphoidal salmonellae, of salmonella food
poisoning and salmonellosis.

6. Causative Organism:

7. Reservoirs
Carriers
cholecystiti
s & urinary
lesions
Incubatory
Last days
of IP
(faeces)
Convalesc
ent
Temporary
10%
Chronic 2-
5%
Contact
2 wks
Healthy Sub-clinical
infection
2 wks
Cases

8. Foci and exit of infection:
 Small intestine (Peyers patches) & gall-
bladder: faeces (faecal carrier).
 Kidney: urine (urinary carrier).
 Faecal carriers:more common than
urinary
 Urinary: more frequent in endemic
Schistosomiasis Haematobium.

14. Susceptibility

15. classical untreated typhoid (4 weeks)
Prodroma
• FHMA (stepladder, evening, low pulse)
• Rash (macular rosy spots , abdomen,7th
day , 25%)
Advance
• High fever, worse physical & mental
condition,
• Abdominal distension & tenderness
Decline
• Gradual improvement
• Drop of temperature
Convalescence
• Relapse(s) after one to two weeks: 10-
20%, usually mild.

17. Atypical presentation:
infection by antimicrobial resistance
strains & in children (respiratory
symptoms & diarrhea)
Case fatality:
15-30% in untreated cases & decreases
with treatment to 1-2%.

19. Bl.
culture
1st wk
• Bacteremia
Widal
test
2nd wk
• Agglutination test (rising titer)
• High titer O & low titer H → Recent infections
• High titer H & low titer O → Past Infections
Stool &
Urine
culture 2nd
& 3rd wk
• 3 times,
• Practically valuable to detect carriers, rather
than diagnosis

22. TAB (TABC) vaccine
• Parenteral heat-killed
• Adults: 2 doses of 0.5 & 1.0ml SC, 4 weeks apart.
Children over 2 years can be given smaller dosage.
• Booster Doses: adult dose of 1.0 ml (smaller for
children) is given every 3 years.
• Protective Value: moderate (50-75%)/and may not
be protective on exposure to heavy infection
Typhoid Oral Vaccine
• Protective value is around 65%
• 4 oral doses on alternate days
Polysaccharide vaccine
• Parental vaccine containing Vi Ag in single dose

23. Vaccination in endemic areas is given to
(indications):
*Occupational groups at-risk: Food handlers,
Lab workers, HCW, waste disposal.
*Camps & other closed communities.
*Slum areas.
*At-risk communities during epidemics &
outbreaks.

24. CONTROL CASES
Release:
 3 -ve cultures of stools & urine, 24 or more
hours apart.
 1st sample: 2 weeks after drop of
temperature to normal (to exclude possibility
of relapse).

25. Control of Carriers
• Diagnosis especially among food
handlers & during pre-employment
examination: by Widal test for Vi antigen,
if +ve: stool & urine culture can be done
(repeated cultures are indicated).
• Health education.
- Not to be licensed to work in food
handling.

26.  For chronic gall-bladder carrier:
Ampicillin for 1-3 months until 3-ve
successive samples.
cholecystectomy is indicated.
 For chronic urinary carrier:
Foci surgical removal.

31. Endemic in Egypt even with increasing
incidence because of animals'
importation from different countries.

33. No man-to-man infection

35. Incubation Period: varies, usually 6-60 days.
Case fatality of untreated cases is 2% or less &
usually results from endocarditis

40.  Brucellin test:
ID hypersensitivity test (survey
studies), to show prevalence of
infection in man.

42. Prevention
Man
Milk & Meat
sanitation
Occupational
control
Airborne
infection
Animals
Veterinary
care
Sanitary
wastes
disposal
Vaccination

43. Vaccination (live attenuated) of young calves by strain
19 or RB51 of B.abortus and of young sheep & goats
by Rev-1 strain of B.melitensis in endemic areas.
Agglutination survey: +ves are infected animals, to be
slaughtered if of small percent, otherwise to be
segregated.

46. DIARRHEAL DISEASE

47. DIARRHEAL DISEASE
- Increased bowel
motions than the usual
own pattern of
individual.
OR the passage of 3 or
more abnormal loose
stools that may be
associated with fever,
vomiting & change in
color & presence of

48. Etiology: infective & no infective.
Infective include:
1- Cholera
2-Infectious food poisoning
3-Infective diarrheal disease of children
(GE)
4-Dysenteries.

51. 2315 case (2007)

52. Bio-type
Sero-group
Sero-type
Vibrio cholera
O1
Classical
3
El-Tor
3
O139

53. Causative agent:
 The organisms liberate potent exotoxins
(enterotoxins). That remain in intestine causing
destruction of mucosa.
 Current 7th pandemic: O1 sero-groups El-Tor
biotype.

56. Resistance:
 V. cholera O1 & O139 can persist in water for
long periods & multiply in moist leftover food.
 Killed within 30 minutes by heating at 56 C & within
few seconds by boiling.
 El-Tor biotype is more resistant
 The classical vibrio cause more virulent & cause
more severe clinical cases while El-Tor biotype is
less virulent causing mild cases, subclinical cases
with high carrier rate &Infectivity

58. Reservoir: Man is the only source of infection
either case or carriers.
1-Cases: inapparent, subclinical or clinical.
2-Carriers: incubatory, contact &
convalescent. Usually temporary but in El-Tor
biotype tend to be more chronic.
 Exit: Stool and vomitus of cases. Stool of
carriers.

59. Mode of transmission:
1. Ingestion of contaminated water or food.
2. Beverages prepared with contaminated water,
ice and even commercial bottled water have
been incriminated

60. Susceptibility

61. Clinical picture:
• In most cases it may be asymptomatic or causes mild
diarrhea, especially with El-Tor biotype.
• Profuse painless watery stool (rice water stool).
* Nausea & profuse vomiting early in the course of
illness.

63. Complications

64. Fatality:
- Case-Fatality is high (exceeding 50%) among
severe dehydrated cases,
- But greatly declined (less than 1%) due
to: better diagnostic facilities, better
management through dehydration and
effective chemotherapy.

65. Koll's vaccine
• Heat killed phenol
preserved
• 2 Doses (0.5&1 ml) 4 wks
apart-booster every 6 ms.
• Partial protection (50%
efficacy)
• Short duration (3-6
months)
• Only antibacterial & not
antitoxic immunity
• Not prevent asymptomatic
infection & carrier state.
• Associated with adverse
effect .
• Not recommended by WHO
Oral vaccines
• Live vaccine (strain CVD
103-HgR) & a killed
vaccine(inactivated vibrios +
B-subunit of the cholera
toxin)
• 2 dose regimen
• O1 strain
• Significant protection
• Several months
• Safe
• Travelers from industrialized
countries

67. Chemoprophylaxis
Tetracycline
• 500 mg/6
hours for 3
days
• Single
dose of
1gm
• ½ dose for
children
• Contacts
• Travelers
• Pilgrims
Doxycycline
• Single
daily dose
of 300
mg for 3
days

68. International measures:
1- Notification to WHO.
2-Chemoprophylaxis: Tetracycline or
Doxycycline for travelers coming from
endemic or infected areas.
Vaccination certificate is not required
internationally since the vaccine is not
potent

69. Cases:
 Early case finding and confirm diagnosis.
 Report to LHO & WHO.
 Isolation in fever hospital, quarantine or cordon.
 Disinfection: Concurrent disinfection of all
soiled articles & fomites, stool and vomitus
using heat & carbolic acid. Terminal cleaning is
sufficient.
 Treatment: Adequate dehydration therapy using
OR in mild cases, IV rehydration in severe
cases. Treatment of hypoglycemia.

71. Food
poisoning

72. Bacterial Food poisoning
Presence of
bacteria or other
microbes which
infect the body
after consumption .
Ingestion of toxins
contained within the
food, including
bacterially produced
exotoxins
Food infection Food intoxication

73.  Food intoxication: staphylococcal, botulism &
others (Clostridium Perfringes & Bacillus-
cereus).
 Food infection: salmonella & others.

74. Bacillus Cereus
Found in soil,
vegetation,
cereals & spices
Staphylococcus
Aureus
Found in human
nose & throat
(also skin)
Clostridium
Perfingens
Found in animals
& birds
Salmonella
Found in animals,
raw poultry &
birds
Clostridium
Botulinum
Found in the soil
& associated
with vegetables
& meats

75. SalmonellaBotulismSTAPH
- Outbreaks
- Egypt
- Rare
- sporadic cases
- Commonest
- Outbreaks
Patter
n
Non typhoidal
Salmonella
(S.typhimuriu
m &
S.enteritidis)
Exotoxin of Cl .
Botulineum
neurotoxin
Botulus= Latin
for sausage
Performed
thremostable
Enterotoxin
(Exotoxin)
Causative
agent
- Animals:
Rodents
&cattle
- Man: Cases
&carriers
- Soil: grown
vegetables, fruits
contaminated
with
spores
- Animals:
excreta
of cattle, pigs&
others
1. Man :Case or
carrier(skin or resp.
infec) > 5% of
population having
foci of skin or nose
infection
2. Cattle:
(staph.mastitis
contaminate milk)
Reservoirof
infection

76. SalmonellaBotulismSTAPH
1. Ingestion of food
from infected
cattle or swine.
2. Ingestion of food
contaminated with
excreta of animals
or rodents
3. Water polluted
with excreta of man
or animal
4-Hand to mouth
Infection “auto-
infection”
Ingestion of food
contaminated
with Performed
exotoxin of
Cl.Botulieum
(preserved
vegetables
without proper
sterilization
packed or canned
meats or
sausages
or fish)
*packing of salted
raw fish (fessikh)
Ingestion of
enterotoxin
contaminated food
or milk by resp.
discharge of food
handlers
Favored by: much
handling&
sufficient
time between
contamination &
consumption
without
Refrigeration
“koshary, belela”
Modeoftransmission
IP

77. SalmonellaBotulismSTAPH
1. Outbreaks:
GE
2. Sporadic:
salmonellosis
3. Enteric like
Picture: self-
limited disease
Paralysis of occulo-
motor & other cranial ns
causing visual
disturbances as diplopia,
loss of accommodation,
dysphagia, dysphonia &
resp. paralysis case-
fatality is high (70%) in
few days due to resp.
failure
abrupt onset
of GE (for
hours then
recovery
slight or no
fever Case-
fatality is
almost nil
C/p
- Mainly Clinically
- Culture: Stool, Vomitus& Food remains (-ve results not
exclude staph. as organism may be destroyed while the
enterotoxin is not).
Diagnosis

78. SalmonellaBotulismSTAPH
General preventive measures of food borne diseases
Preventio
n In case of botulism:
1.Proper processing, packing, canning of food after
sterilization
2. Food preservation at home
3. Suspected canned food to be spoiled (bulged from gas
formation) rejected
4. Specific prevention: Trivalent Botulism antitoxin
As food borne infection & investigation of outbreak
1. Sero-therapy by Trivalent Botulism antitoxin :limited
value (irreversible effect of exotoxin on CNS)
2.Seroprophylaxis for person sharing food with diagnosed
cases but no manifestations
3. Food remnants: destroyed after sampling for
bacteriological testing
Control

79. Botulism
 Death may occur due to
respiratory paralysis within 7
days.

80. Clostridium
Welchii
(Cl.Perfrinqens type A)
Bacillus
cereus
Anerobic spore forming
powerful enterotoxin
Aerobic spore forming 2
enterotoxins “heat labile
(diarrhea) & heat stable
(vomiting)”.
Agent
:
Animals (cattle, poultry
&fish)
Man (cases &carriers).
Spores found in the soil
“rice”.
Reservo
ir
Ingestion of spore-
contaminated meat
Ingestion of spore-
contaminated rice.
Mode of
Infectio
n
6-24 hours.1-6 hours in emetic
6-24 hours in diarrheal
cases.
IP

81. Bacillus cereus
Incubation period < 6 hours
Severe vomiting
Lasts 1-6 hours
Incubation period > 6 hours
Diarrhea
Lasts 6-24 hours
EMETIC FORM DIARRHEAL FORM

82. Investigation of outbreak of food poisoning
Reservoir
s
Food
Cases
Outbrea
k

83. Features & Circumstances of Outbreak
Many cases.
Share common food.
Very short IP (hours).
Similar manifestations.

84. 1. Enlistment & distribution of cases by
TPP.
2. Proper history taking & examination.
3. Culture of faeces & vomitus of cases.
4. Look for other cases.
Measures for cases:

85. 1. Listening of food & remnants.
2. Origin, preparation & storage.
3- Culture of suspected food remnants
4-Compare the attack rate
Attack rate for food items eaten =
no. of cases among those ate certain food x100
all who ate the same food
Food items: Greatest difference in attack rates
between those ate this food and did not eat
Measures for food
items:

86. Measures for
reservoirs:
1. Food handlers: examination e.g. for
staphylococcal infection: nose & throat
swabbing for carriers, and examining skin &
nails for lesions
2. Other possible sources of contamination
e.g. rodents & their excreta

87. Diarrheal Disease Of
Children

88. Gastro-enteritis is diarrheal disease of
children below 5 years (infants & young
children).

89. Bacterial
Escherich
ia
Enterotoxigenic
(ETEC)
Travelers’
diarrhea
Enterohaemorrh
agic(EHEC)
Hemorrhagic
colitis
Enteropathogenic
(EPEC)
Neonatal
diarrhea
Enteroinvasive
(EIEC)
Dysentery
Staphylococcus
aureus
Non-typhoidal
salmonellae
Shigellae
Campylobacter
jejuni
Viral
RotavirusHospitalized
Enteroviruses
Cocksackie
viruses,ECHO
viruses,
polioviruses,HAV
Enteric
Adenovirus
epidemicviralGE
Measles
Protozo
al
GiardialambliaGE
Entamoeba
histolytica
BalantidiumcoliDysentery

90. Reservoirs of Infection:
1- Man (cases or carrier)
2- Animals “non-typhoidal Salmonellae,
Campylobacter jejuni, E.Histolitica, B. coli”.

91. Underlying Factors:
1.Community Underdevelopment: a) Insanitary
environment. b) Illiteracy. c) Lack of effective health
services
2. Host factors: Malnutrition, especially protein-
energy malnutrition (PEM). Persisting systemic
infection “chronic otitis media & bronchitis”.
3. Season: sporadic cases may occur all the year
round.
Monthly distribution of cases in developing countries
shows 2 peaks:
• A peak of higher morbidity & mortality in summer &

92. GEforms
Epidemic diarrhea of
the newborn “E-coli”
Summer diarrhea
Flies.
Rapid multiplication of
organisms in milk &
food
Diminished acid
secretion of stomach
Weaning diarrhea.
Staphylococcal
enteritis-
Secondary enteritis
Persistent systemic
infection, specially the
respiratory & urinary
Recurrent diarrhea

93. Incubation Period: Vary according to the causative
agents usually hours to 2-4 days.
Clinical Picture:
*Mild cases: mild diarrhea (less than 5 times
throughout the day), no or mild fever, no vomiting,
no or insignificant dehydration, and no or mild
systemic manifestations (self-limited and clears up
within days)
*Moderate & severe cases: abrupt onset, with fever
(usually high), frequent liquid or rice-water stools
(up to 20 or more in a day), vomiting and

97. Basic Lines of
Treatment:
1. Rehydration therapy: 1st line to replace loss of
fluid & electrolytes, and restores fluid-electrolyte
balance by oral rehydration, or parenteral route.
a) Oral Rehydration Therapy (ORT): each of 5.5gm of
sodium chloride, sodium bicarbonate (to correct
acidosis), potassium chloride (to correct
hypokalaemia) and glucose. it is dissolved in 200 ml
water.
b) Nasogastric Rehydration: repeated uncontrolled
vomiting.

99. 2-Chemotherapy:for bacterial diarrhea cases.
3. Diet Therapy:
a) Cases having no dehydration: keep on usual
feeding, and give sufficient fluid. Supplementary
vitamin B & C.
b) Cases with dehydration:
Mild cases: given ORS and milk, alternating, until
cured.
Moderate cases: initially given rehydration, with
fasting (water can be given if necessary) for some
hours until dehydration improves, then milk, then
other foods can be given.

100. Dysentery

101. Dysentery
Inflammation of the colon (large intestine).

102. Agent
s
Bacterial
“Shigellae”
Protozoa
“Entamiba
histolytica”
Helminthis
“Scistosoma”

103. Shigellosis

104. Shigellosis (Shigella) Bacillary
Dysentery
 Acute infectious inflammatory bacterial disease
of the colon. It is a worldwide disease. It is
usually sporadic cases. Outbreaks occasionally
occur, in confined groups.
 Incidence is higher with seasonal breeding of
flies (spring, early summer and the fall)
important vector role.

106. Causative Organism
4 groups of Shigella with no cross immunity.
 Group A: S.dysenteriae (Shigella shiga), most
virulent.
 Group B: S. flexneri
 Group C: S. bouydii
 Group D: S. sonnei causing mild disease.
Relatively resistant outside the body, but readily
destroyed by heat & disinfectants.
Locally: the exotoxin is enterotoxic, causing dysentery.
* Toxaemia: the exotoxin is a neurotoxin, may be fatal

107.  Reservoir of Infection: man, cases and
carriers.
 Carriers: number is several times the
cases, and forms the main reservoir of
infection. They are contact, healthy and
convalescent carriers.
 Exit: in faeces
 Infectivity: usually for few weeks, sometimes
longer, and rarely for one or more years.

108. Incubation Period 1 -7 days (usually less than 4).
Clinical Picture:
More than one attack may occur, due to different groups and
serotypes. Infection is usually followed by type-specific immunity.
Mild disease that may pass unnoticed.
1-Acute cases : sudden onset, with fever, may be vomiting, and
dysentery (tenesmus, squeezing pain of lower abdomen, and frequent
loose scanty stools, mainly made of fresh blood, pus and mucus). Disease is
usually self-limited, with recovery in few days.
2-Severe fulminate disease: with dysentery, the case shows systemic
manifestations,
and may be dehydration and complications (uncommon), due to
exotoxin and
toxaemia, and some cases may be fatal (especially in the young,
elderly and

111. Case study
40 years old working female complained from
headache, anorexia, vomiting, and constipation
turned to diarrhea and upgrading fever few days
ago. The fever is not responding to antipyretics.
a) What are the other signs you have to look for in this
case?
b) What are the investigations you should do?
c) What is the probable diagnosis?
d) How will you manage this case?
e) When can she return to work?
f) What are the control measures you should do for
contacts?

112. Other signs
1) Fever increase at night (stepladder)
2) Bradycardia( Pulse is relatively slower to
temperature.
3) Rosy spots on the abdomen

113. Investigations
 Blood culture: (the first week):
positive culture conclusive, but the negative
not exclusive
 Widal test: (the 2nd week)
agglutination test ,rising titer which is
diagnostic
 Stool and urine culture: in 2nd & third
week valuable to detect carriers, rather than
diagnosis.

114. Management of case
 Case-finding
 Notification to the local health office.
 Isolation: allowed at home when sanitary
requirements are fulfilled, otherwise must be at
hospital.
 Disinfection
 Treatment

115. Release
 after 3 -ve cultures of stools & urine, 24 or more
hours apart.
 1st sample is taken 2 weeks after drop of
temperature to normal (to exclude possibility of
relapse).

116. measures for contacts
a) Family and Household contacts:
 Enlistment& Active immunization.
 Surveillance for two weeks, from date of last
exposure to the case, for case-finding.
 Food handlers: excluded from work, and
bacteriologic ally examined until prove not to be
carriers.
b) Nursing personnel:
 Active immunization
 personal cleanliness
 precautions on nursing the case
 not to handle or serve food to the others.

117. Case study
Three persons from a family in rural area drinking
underground water and have latrines for sewage
disposal are complaining from acute attack of
watery diarrhea with no fever.
a) What is the suspected diagnosis? Justify?
b) How will you manage this case?
c) How will you manage contacts?

118. suspected diagnosis
 Cholera as Epidemics and pandemics of it
strongly linked to unsanitary water supply, poor
sanitary conditions
 Cholera spreads easily in lower socioeconomic
group
 bad sanitary environment which act as favorite
media for endemically.

119. management of case
 Case finding.
 Notification LHO and WHO.
 Isolation in fever hospital, quarantine or cordon.
 Disinfection
 Treatment: Adequate dehydration therapy using
OR in mild cases, IV rehydration in severe
cases. Treatment of hypoglycemia
 Release after 3 -ve successive stool sample.

120. Management of contacts
 Enlistment: H.E
 Isolation for 5 days calculated from the day of
exposure.
 Release after 3 negative successive stool sample.
 Chemoprophylaxis.
 repeated stool culture to prevent carrier state.