Food born

Dr. Dalia El-Shafei
Assist.Prof., Community Medicine Department, Zagazig University

Viral
• Poliomyelitis
• Hepatitis A&E
• MCD
Bacterial
• Enteric fever
• Brucellosis
• Diarrheal diseases:
• Food poisoning
• Dysentery
• Diarrhea diseases in
children
• Cholera
Parasitic
• Ascariasis
• Entrobiasis
• Amoebiasis
• Heterophiasis
• Fascioliasis
• Hydatid cyst
• Giardiasis
• Toxoplasmosis

Fecal oral infection:
 Food-borne infection (ingestion infection).
Contaminated food: vehicles are milk & any food that
may be contaminated by handling, flies, water, or
dust, & sewage-polluted water.
 Hand-to-mouth infection
Mode of transmission

1ry
•Environment sanitation
• Health promotion
• International
measures
2ry
• Case:
• Case finding &
notification
• Isolation &
disinfection
• ttt & release
• Contacts:
• Surveillance
• Supervision
• Segregation
• Isolation
• Immunization
3ry
• Prevent complications
& care of
handicapped
Prevention

A) General Sanitation of Environment:
Safe water supply,
Sanitary wastes disposal (refuse & sewage),
 Insect control (flies & cockroaches).
Food sanitation includes control of food handlers
B)Health education :
proper clean habits (including clean hands)

I. Control of Cases “FNIDTRR”:
 Case-finding: needs efficient medical care (clinical & lab
services)
 Notification to the LHO.
 Isolation: allowed at home when sanitary requirements are
fulfilled, otherwise must be at fever hospital.
 Disinfection: - concurrent: excreta (1% crude phenol), articles
& fomites.
- terminal for objects & cleaning of the room.
 Treatment: general & specific chemotherapy.
 Rehabilitation

Polio Hepatitis A Hepatitis E
IP 7- 14 d 15- 50 d 21- 42 d
Mode of
transmission
-Faeco-oral
-Food-borne
-Oral-oral (droplet)
faeco-oral
Parenteraly
(viraemia)
Contaminated
water or food
supplies
Reservoir -Cases
-Carriers (contact,
incubatory,
convalescent)
-cases
-Incubatory Carriers
Infectivity From IP to
convalescence
Last week of IP till Jaundice
Agent -Polio virus Picorna virus

Polio HAV HEV
C/P -Inapparent 90%
-Minor (Abortive) 9%
-Major (CNS) 1%
-Inapparent (influenza-like)
-Classical: pre-icteric, icteric, post-
icteric
- Fulminate: fatal
Diagnosis -Lab: throat wash & stools
exam
-Serological: rising Ab
- Lab: stools exam
- Serological: IGM, liver enz.
Specific
prevention
-Vaccine
-Seroprophylaxis
Vaccine

An Egyptian stele shows a
priest with a deformity of
his leg characteristic of the
flaccid paralysis typical of
poliomyelitis

 Acute viral infectious disease may lead to flaccid
paralysis.
 Poliomyelitis may be near worldwide eradication.
Localized outbreaks may occur at any time.

Most
frequent
Epidemic
I Wild
Endemic
II Oct 1999
Sporadic
III
Causative Organism:
Poliovirus has 3 antigenically distinct types.

• Polioviruses have affinity to the nervous system.
• Relatively resistant & survive for long time under suitable
environmental conditions.
Destroyed by
Heat
Pasteurization
Boiling of milk
Chlorination
of water
UVR

 Cases: all clinical forms
 Carriers: all types (incubatory. Convalescent, healthy & contact who
are temporary carrier .
 In endemic area health carrier are most frequent due to polluted
environment.

Contact & healthy
carriers
Incubatory carriers
Convalescent
carriers
Cases
• About 2weeks.
• Last days of IP.
• Temporary, for some
weeks.
• Infectious for about 6-8
weeks (clinical period).

Age: incidence usually from 6 Ms-5 Ys. By compulsory vaccination
programs there is age shift to adolescents & young adults
Sex: Paralytic polio is more in males than females.
Immunity: a- Naturally acquired Immunity Maternally
acquired persists for 6 Ms. Exposure to infection by any form
of clinical disease gives lasting, type-specific immunity. 2nd
attack rarely occurs, from type-different poliovirus infection.
b- Artificially induced immunity: by immunization.

Polio
In apparent (90%)
No clinical manifestations
Acquired immunity &
carrier state
Manifest
(10%)
Abortive (minor illness)
9%
CNS (major illness) 1%
Non-paralytic (FHMA +
Meningism)
Paralytic (spinal, bulbar,
bulbo-spinal)

• Throat washing or stools
• Serological (neutralizing Ab): rising titer
In the abortive stage, is practically impossible.
Diagnosis is suspected only when non-paralytic or
paralytic picture appears.
Differential diagnosis: Other causes of acute flaccid
paralysis as Gillian-Barrie syndrome & transverse myelitis.

• Passive immunization (Sero-prophylaxis):
“non-practical”
Normal human Ig (0.3 ml/kg BW)
Exposed susceptible (pre exposure – rapidly post
exposure)
• Active immunization:
Sabin & Salk

• Oral, live attenuated trivalent vaccine made of
the 3 types, of polioviruses.
• 2, 4 and 6 Ms of age
• 3 drops orally on the tongue.
• Recently a zero dose is giving after birth as
additional dose.
• Booster Immunization: a booster dose is
given at 9 Ms, 18-24 Ms, and school age.

Live attenuated viruses of the vaccine invade
& multiply in the intestinal cells, stimulating
humoral & local cellular immunity:
 Humoral immunity: by neutralizing antibodies in
serum. It protects the CNS Against invasion by
the poliovirus.
 Cellular immunity: local tissue immunity in the
intestinal mucosa so prevents establishment of
infection in the intestine, and so prevent a carrier.

Gives humoral & tissue immunity
Excreted in stools, disseminate infection in community
Easily administrated
Used in mass immunization.
Inexpensive.
Protective value up to 95%,
Life long immunity.

Cold chain:
regenerated below 4 C
Contraindications:
Complications:
Paralysis: very rarely (1/5 million)
Pregnanc
y
Cortico-
steroids
Immune-
deficienc
y

 Trivalent vaccine, inactivated (formalin).
 Used in non-endemic areas & with Sabin vaccine in
endemic area.
 4 doses, 1.0 ml each, IM, starting at 4 months of age.
 1st 3 doses 6-8 weeks apart, 4th dose 7 months later.
 Booster dose : at school age, and whenever an epidemic
or outbreak threatens.

 Action: Salk vaccine gives humoral immunity.
No cellular immunity
 Protective Value: prevents <90% of paralytic
cases & lowers severity of paralytic effect.
 Salk is given in Egypt as quadruple Salk DPT,
IM, 2 doses at 4 &6 Ms

Due to the preventive value of polio vaccines & reluctance of
some parents to take their children for immunization, or missing
1-2 doses of 1ry immunization, periodic polio vaccination
campaigns are arranged, for better coverage & complete
immunization of infants & young children <5 ys.

Control
Cases FNIDTRR
Contacts
Enlistment
Case-finding
(2wks)
Booster v. or sero-
prophylaxis
Epidemics
Mass oral v.
Epid. study
Avoid predisposing
factors

• Sabin (1968):1ry &
booster
• Salk
Immunization
• Motivation
• Periodic campaigns
• Surveillance (1990)
Satisfactory
coverage rate

• Definition: communicable food borne acute viral disease
involving the liver endemic in developing countries, and
gives sporadic cases, usually in outbreaks in confined
groups (camps, military units, boarding school& daycare
centers).
• Causative agent: viral hepatitis A virus: RNA virus,
relatively resistant outside the body
• Reservoir: man as incubatory carriers and cases (mild or
in-apparent)

• Mode of transmission:
1-faeco-oral 2-parenteral rarely during viraemia
• IP: average 4 weeks (15-50 days)
• Clinical Picture:
1- In apparent cases: mild an-icteric cases “influenza-like picture
(non-specific syndrome) & pass unnoticed”.
2- Classical disease.
3- Severe fulminate rapidly fatal disease.

Post-icteric
Convalescence
Icteric
Jaundice (sclera) Enlarged tender liver
Pre-icteric
FHMA, myalgia, arthralgia GE, tender liver, dark urine

Clinically
• Dark urine
• Jaundice
Laboratory
• detecting
virus in
stools
Serological
tests
• IgM in
acute
cases
• ↑ liver enz.
(not
specific)

1ry
General
•Environment sanitation
•Health promotion
Specific
• Active immunization
• Sero-prophylaxis
2ry
Cases
• Case Finding.
• Notification: LHA.
• Isolation: at home
• Disinfection: feces, urine &
blood.
• Specific ttt: No
• Release
Contacts
• Enlistment & Immunization:
within 2 weeks of exposure.
• Surveillance: for 6 weeks
Epidemic measures:
• Food sanitation
• Seroprophylaxis.
• Epidemiologic study.
Prevention

Active immunization
• Inactivated vaccine
1 ml IM(deltoid) “2 doses, 4 weeks apart”
• 1- At risk: Ch. Liver Dis., travelers, lab workers.
2- Children
Sero-prophylaxis
• Human Ig
Before or few days after exp
• 1- Contacts (within 2 wks)
2- At risk: travelers (before or within 2 wks)

Bovine
Spongiform
Encephalopathy
(BSE)
Mad Cow
Disease
(MCD)
Cretuzefeld
Jacob
Disease
(CJD)

• Occurrence: It is a newly identified zoonotic disease. It 1st
appeared in England 1989 among cows that were fed by animal
meat of carcasses of died animals after their crushing. The
change in the food of the cow (herbivorous animal) into feeding
by animal tissues induced a pathological condition in the cow.
• Causative agent: Proteinaceous non-living infectious particle
that is devoid of nucleic acid (not virus or viroid)
• Modes of transmission: Ingestion of infected meat of diseased
cattle.

• Management: No specific ttt is known.
• Control measures:
1. Prevent feeding of living animals (as cattle) by died animal
tissues or bony meals.
2. At the international level:
a) All countries must ensure condemning & safe disposal of
all BSE affected animals & prevent their entry into free
countries.
b) Surveillance & compulsory notification for BSE disease.
3. Research for finding rapid diagnostic methods &
management in both animals & man.

Salmonellae have more than 2000 serotypes, of which
pathogens of Human disease is:
*Typhoidal salmonellae: S. typhi, & S. paratyphi A, B, C.
*Nontyphoidal salmonellae: Food poisoning &
Salmonellosis.

• Typhoid: Salmonella typhi (typhoid bacillus), with a big number of
serotypes
• Paratyphoid:
3 serotypes “A, B, C”
B is the most common
C is rare.
• It can remain viable in the environment (water, ice, milk, milk products,
ice-cream and other foods) for weeks.
• But it is readily destroyed by heat & disinfectants.

Reservoirs
Carriers
cholecystitis &
urinary lesions
Incubatory
Last days of IP
(faeces)
Convalescent
Temporary 10%
Chronic 2-5%
Contact 2 wks
Healthy
Sub-clinical
infection
2 wks
Cases

Fecal carriers:more common than urinary
Urinary: more frequent in endemic Schistosomiasis
Foci&exitofinfection
Small intestine (Peyers
patches) & gall-bladder Feces Fecal carrier
Kidney Urine Urinary carrier

• 10-30 ys
• Markedly ↓ with ageAGE
• Male > Female
• Females: fecal carriers 5 times > males
“cholecystitis”
SEX
• Significant ↑ during summer.SEASON
• Repeated subclinical infection (mainly), clinical
attack, or active immunizationIMMUNITY

Period of Infectivity:
1-Cases:
Infectious from the last days of IP (incubatory carriers),
throughout disease, and for varied period (months, years or
lifetime) in a percent of convalescents (convalescent carriers).
2-Contact & healthy carriers:
Infectious about 2 weeks.
Incubation Period: 8-14 days

• Onset is usually gradual.
• Picture of disease varies whether
chemotherapy is given or not.
• Treated Cases:
Chemotherapy: ↓ Disease duration
& incidence of complications.

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 1-2 weeks: 10-20%, usually mild.

Atypical presentation:
Infection by antimicrobial resistance strains & in children
(respiratory symptoms & diarrhea)
Case fatality:
15-30% in untreated cases & ↓ with ttt to 1-2%.
Intestinal
hge &
perforation
Cholecystiti
s
Thrombophlebitis
of femoral vein
Myocarditi
s
Pneumonia Osteomyeliti
s
Bone
abscesses
Complications

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
• Should be repeated for 3 times
• Practically valuable to detect carriers, rather than diagnosis
Lab diagnosis

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

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.
Travelers to endemic areas & pilgrims.

Cases
• Case-finding - Notification: LHO. - Isolation
• Disinfection - TTT - Release
Carrier
s
• Food handlers “pre-employment”
• Chronic gall-bladder carrier
Contac
ts
• Family & Household contacts
• Nursing personnel
Epidemi
c
Measure
s
• Sanitary measures - Heath education
• Epidemiologic study

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).

• Diagnosis especially among food handlers & during pre-
employment examination:
Widal test for Vi antigen, if +ve: stool & urine culture can be
done (repeated cultures are indicated).
• For chronic gall-bladder carrier:
Ampicillin for 1-3 Ms until 3-ve successive samples.
cholecystectomy is indicated.
• For chronic urinary carrier:
Foci surgical removal.

Family &
Household contacts
Enlistment & Active immunization:
Mainly during seasonal spread or
outbreak
Surveillance for 2 weeks, from
date of last exposure to the case.
Food handlers: excluded from work &
bacteriologically examined until prove
not to be carriers.
Nursing personnel
Active immunization
Personal cleanliness
Precautions on nursing & not
to handle or serve food to the
others.

Causative Organism:
Brucella organisms are relatively resistant in the environment.
Destroyed by
Heat
Pasteurization
Boiling of milk
Chlorination
of water

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

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

Diagnosis Laboratory
Blood culture
Serologic testing
Brucellin test
Clinical
Not characteristic
Fever of unknown
origin (FUO)

Brucellin test:
ID hypersensitivity test (survey studies).

Prevention
Man
Ingestion infection
Milk & Meat
sanitation
Health education
Occupational
control
PPE
Personal
cleanliness
Airborne infection
Clean animal
environment
Sanitary disposal of
infected material
Dust control
Masks
Animals
Veterinary care
Sanitary wastes
disposal
Vaccination
Agglutination
survey

Increased bowel motions
than usual own pattern
of individual.
OR
Passage of ≥3 abnormal
loose stools that may
be associated with
fever, vomiting &
change in color &
presence of blood, pus

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

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

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

• V. cholera O1 & O139 can persist in water for long periods &
multiply in moist leftover food.
• Killed within 30 min. by heating at 56 C & within few seconds by boiling.
Classical vibrio
• Less resistant
• More virulent
• More severe
clinical cases
El-Tor biotype
• More resistant
• Less virulent
• Mild cases,
subclinical cases
• High carrier rate
&Infectivity

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 & vomitus of cases. Stool of carriers.

1. Ingestion of contaminated water or food.
2. Beverages prepared with contaminated water, ice & even
commercial bottled water have been incriminated

• All ages are affected
• Attack rate is highest among childrenAGE
• Both sexes are affected.SEX
• Significant ↑ during summer & autumnSEASON
• Infection either clinical or sub clinical gives type
specific immunity.IMMUNITY

• Most cases: Asymptomatic or mild diarrhea, especially with El-Tor.
• Profuse painless watery stool (rice water stool).
• Nausea & profuse vomiting early in the course of illness.

Dehydration
Acidosis
HypoglycemiaRF
Circulatory
collapse
Case-Fatality is high
(>50%) among
severe dehydrated
cases.
But greatly ↓ (<1%)
due to better
diagnostic facilities,
better management
through dehydration
& effective
chemotherapy.

Killed “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
• Safe.
• Significant protection for
several months.
• One is a single dose live
vaccine.
• Other is a killed vaccine
consisting of in-activated
vibrios + B-subunit of the
cholera toxic, given on a 2-
dose regimen.

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

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

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.
Release after 3-ve successive stool sample.

• Enlistment by age, sex, occupation and residence.
• Isolation for 5 days calculated from the day of exposure.
• Release after 3 -ve successive stool sample.
• Chemoprophylaxis.
• Education, Case finding & repeated stool culture to prevent
carrier state.

Of the public & population at risk about mode of transmission
and preventive measures:
• Ensure safe water supply and chlorination
• Provide appropriate safe sewage disposal
• Control of house flies.
• Ensure sanitary preparation & supervision of food & drinks.
• Investigate the situation to find the epidemic variables (TPP).

Infection
• Presence of bacteria or
other microbes which infect
body after consumption.
• Salmonella.
• Shigella spp.
• Camplobacter jejuni.
• Listeria.
• E.Coli.
• Yarsinia enterocolitis.
Intoxication
• Ingestion of toxins
contained within food,
including bacterially
produced exotoxins.
• Staphylococcus aureus.
• Clostridium botulinum.
• Clostridium perfringens.
• Bacillus cereus.

SalmonellaBotulismSTAPH
- Outbreaks
- Egypt
- Rare
- Sporadic cases
- Commonest
- Outbreaks
Patter
n
Non typhoidal
Salmonella
Exotoxin of Cl .
Botulineum
neurotoxin
Performed
thremostable
Enterotoxin (Exotoxin)
Agent
-Animals: Rodents
&cattle
- Man: Cases
&carriers
-Soil: grown
vegetables, fruits
contaminated with
spores
-Animals: excreta
of cattle, pigs&
Others
- Man :Case or
carrier(skin or resp.
infec) >5% of
population having foci
of skin or nose
infection
-Cattle: staph.mastitis
contaminate milk
Reservoir

- Ingestion of food from
infected cattle or swine.
-Ingestion of food
contaminated with
excreta of animals or
rodents
- Water polluted with
excreta of man or
animal
- Hand to mouth
infection “auto-
infection”
Ingestion of food
contaminated with
Performed
exotoxin(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
38 hs12-36 hs2-6 hsI
P

-Outbreaks: GE
-Sporadic:
salmonellosis
-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

General preventive measures of food borne diseases
Prevention
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

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”.Reservoi
r
Ingestion of spore-contaminated
meat
Ingestion of spore-contaminated
rice.
Mode of
Infection
6-24 hours.1-6 hours in emetic
6-24 hours in diarrheal cases.
IP
- Intensive diarrhea, no vomiting
“self-limited”
- Necrotizing enteritis “highly fatal
in the elderly”
GIT manifestations either Emetic or
Diarrhea “self-limited”
C/P

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

Reservoir
s
Food
Cases
Outbreak

Many
cases.
Share
common
food.
Very
short IP
(hours).
Similar
C/P

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

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:
Listening of
food &
remnants.
Origin,
preparation &
storage.
Culture of
suspected
food remnants
Compare the
attack rate

1. Food handlers examination e.g. staph. infection:
nose & throat swabbing for carriers & skin & nails
for lesions
2. Other sources of contamination e.g. rodents & their
excreta

Diarrheal Disease Of Children
(Gastro-enteritis)

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

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

Reservoirs of Infection:
1- Man (cases or carrier)
2- Animals: non-typhoidal Salmonellae, Campylobacter jejuni, E.Histolitica,
B. coli.
Community
Underdevelopment
Insanitary
environment.
Illiteracy
Lack of effective
health services
Hostfactors
Malnutrition (PEM).
Persisting systemic
infection “chronic otitis
media & bronchitis”.
Season
Sporadic cases all the
year round.
Monthly distribution of
cases in developing
countries shows 2
peaks: A high peak in
summer & fall.
A small peak, during
winter months
“increased incidence
of acute respiratory
infections”.

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

IP: Vary according to the causative agents usually hours to 2-4 days.
Clinical Picture
Moderate & Severe cases
Abrupt onset, fever (usually high), frequent liquid or rice-water stools (≥20/day), vomiting
& dehydration.
Mild cases
Mild diarrhea (>5 times/day), No or mild fever, No vomiting, No or insignificant
dehydration, and No or mild systemic manifestations (self-limited & clears up within days)

Early case-finding
• Efficient health services
• Health education for
mothers.
Management of case
• Mild: outpatient service
“Started under medical
supervision &Continue at
home”.
• Sever: Hospitalization.

Rehydration
therapy
ORT
Nasogastric
Rehydration
I.V fluid
Rehydration
Diet therapy
Cases without
dehydration
Cases with
dehydration
Chemotherapy
Bacterial
diarrhea
“Shigellae &
Vibrios”
Existing
systemic
bacterial
infection
Symptomatic
Manage
symptoms,
especially fever
ttt of
Underlying
Disease
Nutritional
deficiency
diseases

Rehydration therapy
1st line to replace loss of fluid & electrolytes & restores fluid-electrolyte balance.
a) Oral Rehydration Therapy (ORT): 5.5gm of NaCl, NaHCO (correct acidosis), KCl
(correct hypokalaemia) & glucose. Dissolved in 200 ml water.
b) Nasogastric Rehydration: repeated uncontrolled vomiting.
c) IV fluid Rehydration: hospitalized severe cases
Diet Therapy
- Cases having no dehydration: usual feeding & sufficient fluid & Supplementary vit.
B,C.
- Cases with dehydration:
Mild cases: ORS & milk, alternating, until cured.
Moderate cases: initially given rehydration, with fasting (water if necessary) for some
hours until dehydration improves, then milk, then other foods can be given.

Inflammation of the colon (large intestine).
Tenesmus
Abd. pain
Frequent
stools “Bl. &
mucus”

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

Acute infectious inflammatory bacterial disease of the colon.
Worldwide disease. Usually sporadic cases. Outbreaks
occasionally in confined groups.
Incidence is higher with seasonal breeding of flies (spring,
early summer & fall).

Relatively resistant outside the
body, but readily destroyed by
heat & disinfectants.
Locally: the exotoxin is
enterotoxic, causing dysentery.
Toxaemia: exotoxin is a
neurotoxin, may be fatal
Most virulent
Mild disease
Nocrossimmunity
More than 1 attack may occur, due to different groups & serotypes.
Infection is usually followed by type-specific immunity.

• Reservoir of Infection: Man “cases & carriers”.
• Carriers: number is several times cases & forms the main reservoir of infection.
They are contact, healthy & convalescent carriers.
• Exit: faeces
• Infectivity: usually for few weeks, sometimes longer, and rarely for one or more years.
IP: 1 -7 days (usually less than 4).

Mild disease that may pass unnoticed.
Acute cases
• Sudden onset
• Fever
• Vomiting & dysentery “May be”
• Usually self-limited
• Recovery in few days.
Severe fulminate disease
• Dysentery
• Systemic manifestations
• Dehydration & complications
(uncommon) due to exotoxin
&toxaemia,
• Fatal (May be in young, elderly &
debilitated).
Dysentery: tenesmus, squeezing pain of lower abdomen & frequent
loose scanty stools, mainly made of fresh blood, pus & mucus.

PROTOZOA
Amoebiasis Giardiasis Balantidiasi
s
Causative
Agent
Entamoeba Histolytica “Endemic in
Egypt & many parts of the world”
Giardia Lamblia
“Lambliasis”
Balantidium
coli
Infective
Stage
Quadri-nucleate cyst “Resistant
outside body, but destroyed by heat,
desiccation & UVR”.
Cyst: passed with faeces
“remain viable in the
environment for months”.
Reservoir Man: chronic cases, or asymptomatic
cyst-passers. “Acute cases: non-
infectious, as they pass the fragile
vegetative form that perishes rapidly.
Even if ingested, it is destroyed by
gastric acidity & digestive enzymes”.
Rats: occasionally.
Man & mammals
(e.g. dogs, cats,
cattle, sheep)
Man & Swine
Mode of 1. Food borne infection: ingestion of food or water contaminated

Amoebiasis Giardiasis
“Lambliasis”
Balantidiasi
s
IP 3-4 weeks 1-2 weeks 3-4 days
C/P “Colon, with invasion of intestinal
wall”.
1ry amoebiasis “Dysentery”:
colon.
2ry amoebiasis: other parts of
body.
Complications:
-Intestinal: severe ulceration
“may cause perforation of colon
& intestinal hemorrhage” and
appendicitis.
-Extra-Intestinal: amoebic
abscesses, especially in the liver,
causing amoebic hepatitis
“Duodenum & Ilium,
without invasion of
intestinal wall”.
Asymptomatic.
-Gastro-enteritis of infants
& young.
“Terminal
ileum & Colon”
-
Asymptomatic.
-Mild colitis.
-Dysentery.

HELMINTHES
Ascaris Enterobius vermicularis Hymenolepis nana
Causative
Agent
Ascaris Lumbricoides “Ascariasis” “Oxyuriasis pinworm
Disease” most widespread
helminthic infection”
dwarf tapeworm
Prevalence Worldwide distribution “Preschool & school children are frequently, and may be heavily, infected
Infective
stage
Embryonated egg “resistant to
desiccation & disinfectants, and remains
viable & infective, under favorable
environmental conditions, for 3
months”.
How Ascaris eggs reach food?
-Using fresh human fertilizer.
-Promiscuous defecations.
-Flies may have potential, least role.
Egg, deposited by migrating
gravid female worm in the
perianal region.
Eggs are relatively resistant
outside the body
Eggs passed in faeces, are
immediately infective
Reservoir Man Man & Rats “occasionally’

Ascaris Enterobius vermicularis Hymenolepis nanaModeoftransmission
Food borne Infection. Hand-to-mouth infection
No Auto-infection: eggs in
faeces are not infective,
except after developing into
embryonated egg “infected
food handlers do not spread
infection”.
-Auto-infection: fingers &
nails contaminated with eggs
on scratching the anal region.
-Hands contaminated with
eggs:
* Playing with the case.
* Handling soiled fomites.
*Touching soiled toilet
fixtures.
-Auto-infection.
-Hand contaminated with
eggs when playing in rat
excreta-contaminated dirt.
Internal Autoinfection: ova
invade the intestinal wall.

ASCARIS ENTEROBIASIS HYMENOLEPIS NANA
IP 2 months 1-2 months 2-4 weeks
C/P -Mild infection may be in apparent.
-Abdominal discomfort & colic.
-Nutritional deficiency.
-Respiratory manifestations.
-Restless sleep & grinding of teeth.
Perianal pruritus &
scratching, usually
nocturnal, causing
disturbed sleep and
irritability.
Asymptomatic, mild or
vague abdominal
disturbance.
Heavy infection:
abdominal pain &diarrhea
Diagnosis
Stools examination: eggs. -Worms in anal region &
stools.
-Perianal swab to
demonstrate eggs (using
adhesive tape).
-Stool examination: not
diagnostic.
Stools examination: eggs.

TAENIASIS HETEROPHYIASIS
Causative
Agent
T.solium (pork tapeworm) & T.saginata (beef
tapeworm).
Heterophyes heterophyes.
Prevalence Worldwide. Man is usually infected with one worm only. Endemic in Egypt around Lakes Manzala
& Borollos.
Infective
stage
Cysticercus bovis in beef & Cysticercus cellulosa in
pork
Encysted metacercaria in muscles of
infected brackish-water fish (e.g. Mugil
cephalus & Tilapia nilotica)
Reservoir Man: definitive host “discharges detached gravid
segments which rupture to liberate eggs in faeces”. Egg
is infective to the intermediate host (cattle for T.saginata
& pig for T. Solium) where it hatches in the intestine of
the animal & the embryo penetrates the intestinal wall
and then carried by the circulation to various tissues
(especially skeletal muscles where it becomes
encysted).
Period of communicability so long the worm remains in
the intestine “sometimes >30 years”. T.saginata is not
directly transmitted from person to person.
Man: infected individuals pass eggs in
faeces. Fishermen in endemic areas are
particularly important for pollution of
brackish water channels where
intermediate hosts “Pyrenella conica” of
the parasite are found.
Fish-eating animals (e.g cats & dogs)
are potential reservoirs.

TAENIASIS HETEROPHYIASISModeoftransmission
Man is infected by ingestion of raw or under cooked infected
beef or pork containing the infective stage. In the intestine
the scolex (in the cysticercus) evaginates, attaches to the
mucosa and develops into mature worm.
Ingestion of the infective stage in
muscles of infected brackish-water
fish when eaten raw, or
insufficiently cooked or grilled
(Salted raw Mugil fish "fessikh",
eaten before 10 days of pickling).
IP 2-3 months. 1-15 days
C/P -Asymptomatic “except annoyance from having segments of
worms emerging from the anus”.
-Nervousness, insomnia, anorexia, weight loss, however the
disease is non-fatal.
Chronic intermittent diarrhea, with
blood and mucus in stools,
abdominal discomfort and colicky
pain.
Diagnosis Stools examination: Gravid segment or eggs Stools examination: ova

FASCIOLIASIS HYDATIDOSIS
Causative
agent
Fasciola hepatica & less commonly F.
gigantica
Echinococcus granulosus “Cystic echinococcosis”
Prevalence Worldwide especially in sheep or cattle
raising areas. “F.hepatica: Europe, America,
Australia &Middle East”,
“F.gigantica:common in Egypt”
Endemic in the Middle East and Arab North Africa
including Egypt
Infective
stage
Encysted metacercaria on aquatic plants Echinococcus eggs
Reservoir Sheep (f. hepatica), cattle (f. Gigantica),
and other large herbivorous animals. The
infection is maintained in a cycle between
animals, water, snails and aquatic plants.
Man is an accidental host “no direct man to
man transmission”
Dog is the definitive host. “Pass Eeggs in faeces”.
Intermediate Host: Sheep, cattle&other
herbivorous animals. They ingest egg-
contaminated food, to form hydatid cysts in
different organs, specially lung and liver. Dogs
infected on ingesting hydatid cyst in animal organs.
Man:Occasionally infected with eggs from dogs.

FASCIOLIASIS HYDATIDOSIS
Modeof
transmission
Food-borne infection: Eating uncooked aquatic
plants such as water cress bearing encysted
metacercaria.
Hand-to-mouth infection: usual method of infection,
when the hand gets contaminated with eggs, from
contact and playing with infected dogs.
Food-borne infection: ingestion of food or water
contaminated with excreta of infected dogs
C/P -Asymptomatic
- During liver invasion: Right upper quadrant
pain, hepatomegaly, liver function abnormalities
& eosinophilia.
-After migration to biliary ducts: biliary colic or
obstructive jaundice
No specific picture, but manifestations of slowly
growing tumor, according to location of hydatid cyst.
Diagnosis
Viable eggs in faeces or in bile aspirated from
the duodenum “detection of non-viable eggs in
faeces occurs after eating liver from infected
animal”
* Clinical examination & X-ray: nonspecific cystic
tumor “not diagnostic, but suggestive”.
* Biopsy or aspiration of cyst: is avoided, for the risk
of anaphylaxis and secondary infection.
* Casoni test “intradermal hypersensitivity test”.

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