Water borne disease

2. Food borne diseases &
toxicants
Dr Deodatt M Suryawanshi
MD Community Medicine,

3. Outline…
o Introduction
o Pathogenesis and Transmission
o Important food borne pathogens/toxins/chemicals
o Food additives ,Food fortification & Food adulteration
o Prevention of food adulteration act 1954
o Treatment and Prevention

4. 1.Introduction
• Food borne diseases-(intoxications and infections)
• illnesses acquired through consumption of contaminated food-food poisoning
• Food borne disease outbreak
Occurrence of 2 or more cases of similar illness resulting from
ingestion of common food
OR
When observed number of particular disease exceeds expected
number

5. Problem statement
o Global burden- high morbidity and mortality
❑ CDC- 76 million cases of food borne diseases in US annually with
appx.5000 deaths
❑ Infectious diarrhea- 3 to 5 billion cases and 1.8 million deaths
annually
o In India- Integrated disease surveillance Project (IDSP)
- Food poisoning outbreak reporting increased to more than double in
2009 from 2008 (120 in 2009 and 50 in 2008)

6. FOOD BORNE INFECTIONS VS INTOXICANTS
Infections
• Bacterial / Viral / parasite
• Invade and or multiply in lining of
intestine
• Incubation period- hours to days
• S/s – Diarrhoea , nausea, vomitting ,
abdominal cramps, fever
• Communicable-spreads from person to
person
• Factors-inadequate cooking, cross
contamination , poor personal hygiene ,
bare hand contact
Intoxications
• Toxins ( natural / preformed bacterial /
chemical)
• No invasion or multiplication
• Incubation period-
minutes to hours
• S/s – Vomitting , nausea, diarrhea ,
diplopia, weakness, resp. failure , numbness,
sensory/motor dysfunction
• Not communicable
• Factors-inadequate cooking , improper
handling temperatures

7. Naturally
occurring toxins
Toxins by
Bacteria
Toxins by Fungi
Food Borne
Chemical
poisoning

8. EPIDEMILOGY IN INDIA
Agent Year Region People
affected
Implicated Food
Salmonella
paratyphi A
1995 Yavatmal 33 Vegetarian food
Clostridium
butyricum
1996 Gujarat-
residential
school
34
students
Sevu
(Gram flour
crisp)
Salmonella
Enteritidis
1998 Armed
Forces
78
personnel
Frozen fowl

9. EPIDEMILOGY IN INDIA
Agent Year Region People
affected
Implicated Food
Norwalk like
Virus
2002 Delhi
Hospital
130
nurses
Salad
Sandwiches
Staph.
Aureus
2007 MP >100
children
n
adults
Bhalla ( fried
potato balls)
Salmonella
welteverden
and Wein
2008-
09
Mangalore
34
and
10
Chicken
and
Fish

10. IMPORTANT FOOD BORNE TOXINS
BY PATHOGENS
o Bacteria - Bacillus cereus , Brucella , Campylobacter, Clostridium sp ,
E.coli, Salmonella sp , Listeria , Staph aureus , Vibrio cholera and
V.parahemolyticus
o Viruses - Hepatitis A and E , Rotavirus , Norvovirus
oProtozoa – Cryptosporidium , Cyclospora , Entamoeba , Giardia , T.
gondii
o Trematodes , Cestodes and Nematodes

11. Food borne pathogens-toxins and chemicals
• Toxins - marine biotoxins , tetrodotoxin (puffer fish), pyrrolizidine alka
(Endemic ascites) , mushroom toxins , shellfish toxins , mycotoxins-
(Aflatoxins ,Ergot and Fusarium), plant intoxicants , BOAA (Lathyrism)
• Chemicals - pesticides (OPP,sb) , radionuclides , nitrites (food
preservatives) toxic metals - cd, cu, hg, pb, sn, fluoride , MSG

12. PATHOGENESIS & TRANSMISSION
• Inoculum / size of infective dose
• Can be as small as 10-100 bacterial cysts for Shigella , EHEC , Giardia,
E. histolytica
• 10^ 5-10^ 8 for Vibrio cholera, variable for salmonella
• Animals / humans harbouring infection → shed in feces →
contaminate water , fruits , vegetables →inadequate cooking /
improper storage → infection

13. COMMON BACTERIAL TOXINS
Incubation
period
Cause Symptoms Common foods
1-6 hours Staph aureus
(enterotoxin)
Nausea,
vomitting,
diarrhea
Milk n milk
products, ham,
poultry, salads,
custards
Bacillus cereus
(enterotoxin)
Nausea,
vomitting,
(emetic form)
Fried rice

14. COMMON BACTERIAL TOXINS
•
Incubation
period
Cause Symptoms Common
foods
8-16
hours
Clostridium
perfringes
(spores)
Abd.cramps,
diarrhea
Nausea and
Vomitting -rare
Meat,
poultry,
legumes.
gravies
Bacillus cereus (
diarrheal form-
preformed n stable
toxins)
Diarrhea, abd.pain,
nausea,
vomitting/fever-No

15. COMMON BACTERIAL TOXINS
Incubation
period
Cause Symptoms Common
foods
>16 hours Vibrio cholera Rice watery
stools
Water and ice
creams,
sea food
Salmonella spp Inflammatory
diarrhea
Meat , milk n
milk products,
poultry
Shigella sp dysentry Potato/raw
eggs-salad

16. EARLY DIAGNOSIS & INVESTIGATION
1.Initial assessment of cases –
Detailed clinical history including time of onset , duration of
illness , symptoms , h /o travel , recent meals , cooking and
refrigeration , details of others with similar complaints
2.Detailed clinical examination –
Vitals and degree of dehydration , systemic signs

17. LAB DIAGNOSIS
• Main objectives-
a) To confirm clinical diagnosis by isolation of causative agent from
proper samples ,
eg . stool , vomitus / gastric aspirate , food specimens
b) Ensure proper identification of disease
c) Determine causative agent if present in food sources with relevant
epidemiological markers- eg. Biotyping , serotyping , PCR , Phage
typing etc

18. COLLECTION OF FOOD SAMPLES
• Using aseptic technique n appropriate containers → samples be
refrigerated during storage and transport → must arrive lab
within 3 days of collection
• Adequate sample - minimum 100 grams
• Containers - not to be filled >75% of capacity
• Proper labelling is utmost important → labelled specimen be
placed in zip lock bag and sealed
• Vaccine carrier with ice packs for transport and cold chain
maintenance ( avoid freezing )

19. Steps of outbreak investigation
Establishing existence
Co-ordination
Collection and transport
Lab testing
Control and preventive measures
Definition of cases, population
Description of epidemiology
Possible hypotheses
Epidemiological study
Analysis of data and interpretation
Reporting

20. TREATMENT
1. Initial T/t - Assessment and reversal of dehydration ( ORT / IV Fluids )
2. Cause specific treatment if any- eg. chelating agents in case of pesticide poisoning
3. Use of antibiotics can be considered if bacterial cause is identified

21. LATHYRISM
• Disease occur by consuming large
quantities of Lathyrus sativus
(Kesari dhal)
• Lathyrism in human is referred as
Neurolathyrism
• The disease presents as Crippling
disease of nervous system
characterized by gradually

22. LATHYRISM
• It contains a toxin called Beta oxalyl amino Alanine
(BOAA)
• Lathyrus Kesari Dhal) is good source of protein.
• It is relatively cheaper.

23. INTERVENTION
Removal of toxin
• Steeping method
• Soaking the pulse in hot water for about 2 hours and the soaked water
is drained off completely
• Genetic Approach
• Development of low toxin varieties of Lathyrus
• Banning the crop
• The Prevention of food adulteration act in India has banned Lathyrus in
all forms

24. ERGOTISM
• Caused by ergot
• A filamentous fungus
• Genus Claviceps
• Parasitic
• Found in grains
• corn, wheat, barley, oats, rice, and rye
• Spread via spores
• Transported by wind, rain, insects and other animals, or by
plant-to-plant contact

25. • Infection of plants can be easily overlooked
• Mimics the shape of grains
• Fungal form is the most dangerous
• Causes ergotism
• Infection usually follows oral consumption of contaminated
food ie/ rye bread

26. HISTORY OF ERGOTISM: THE
TOLLUND MAN

27. Salem Witch Trials

28. Russia
• Ergotism very common until 1945
• Rye bread was staple food in Russia until 1945, when
potatoes were planted instead and pesticides/fungicides
introduced
• Government statistics show that areas with wet
weather and rye crops had outbreaks of trembling,
confusion, hysteria, and hallucinations
• 1926, there were 10,000 confirmed cases of ergotism

29. SIGNS & SYMPTOMS
• Ergotism can be caused by
• Acute ingestion of large amounts of fungus
• Chronic ingestion, usually via contaminated food
• 2 main categories of symptoms
• Gangrenous
• Convulsive

30. GANGRENOUS SYMPTOMS
oDry gangrene caused by tissue necrosis
oFingers and toes are affected first ,Followed by arms
and legs
oInfection may result and can lead to death
oAmputation is often the only solution
oHappens in livestock as well as in humans

31. CONVULSIVE SYMPTOMS
• Includes tingling sensation in the fingers, tinnitus,
dizziness, hallucinations, seizures, nausea and vomiting
• Mental disturbances such as mania, psychoses and
delirium may also be present

32. MECHANISM OF ACTION
oAll ergot compounds exhibit some vasospastic
properties
oEffects on serotonin and alpha adrenergic receptors in blood
vessels
oSt. Anthony’s Fire
oBody feels extremely warm due to constriction of peripheral
vessels

33. • Results in myocardial or peripheral ischemia
• Gangrene, infection, amputation, death
• Cinx in CAD, PAD, uncontrolled HTN
• Uterine smooth muscle is also affected by serotonergic
and alpha adrenergic effects
• Contractions may lead to miscarriage or preterm birth

34. Treatment
• Modern-Day Treatment
• Early detection and immediate discontinuation of exposure vital
• Severe ischemia may be irreversible
• If overdose is detected early
• Activated charcoal
• Gastric lavage if patient is conscious

35. Treatment
• Treatment of hallucinations
• Stopping exposure to
toxin usually effective
• Intracranial injection of
combination serotonin
and cholinergic drugs
successful treatment
in mice

36. Treatment
• Treatment for ischemia
• Vasodilators
• Nitroprusside, nifedipine, captopril, prostaglandins
• Anticoagulants
• Dextrin, heparin
• In extreme cases of ischemia
• Regional sympathectomy
• Hyperbaric oxygen chamber
• Hydrostatic dilation with balloon catheters

37. Prevention in community
• Proper handwashing and personal hygiene
• Proper storage (refrigeration)
• Food saftey education – community and food handlers
• Environmental measures - Discourage sewage farming for growing fruits and
vegetables

38. AFLATOXINS
❑Public health problem in India.
❑In 1975 ,400 cases of poisoning from parts of Gujarat
,Rajasthan
❑Mycotonins fungi toxins,
❑Aspergillus Flavus and A Parasiticus
❑Fungi infest food grains such as Groundnut
,maize,parboiled rice ,wheat,rice,cotton seed.
❑Caused to improper storage under damp
conditions.Moisture levels below 16% and Temp from 11
to 37%

39. EPIDEMIC DROPSY
• Epidemic dropsy is a clinical
state resulting from use of
edible oils adulterated
with Argemone mexicana seed
oil.
• Epidemic dropsy occurs as
an epidemic in places where
use of mustard oil, (from the
seeds of Brassica juncea
commonly known as Indian

40. MECHANISM OF ACTION
• ROS and Oxidative stress :.
• Pulmonary Toxicity:
• Cardiac Failure:
• Delayed clearance:

41. MECHANISM OF ACTION
• Sanguinarine and dihydrosanguinarine are two major
toxic alkaloids of argemone oil,
• which cause widespread capillary dilatation,
proliferation and increased capillary permeability.
• Other major symptoms are bilateral pitting edema of
extremities, headache nausea, loose Bowels, erythema,
glaucoma and breathlessness.

43. Test which can be used for diagnosis
• Nitric acid test
• Paper chromatography test

44. ENDEMIC ASCITES
• Caused by eating contamination of millet Panicum Miliare
(gondhili) with weed seeds of Crotalaria(jhunjunia).
• Jhunjhunia contains Pyrrolizidine alkaloids which are
hepatotoxins.
• Preventive measures:
• Education about the weed
• Deweeding of the plants.
• Sieving of millet at household level to remove seeds of jhunjunia .

45. FUSARIUM TOXINS
• Known to contaminate Food crops and pose health
hazards.
• Sorghum and rice are affected.
• Causative agent is Fusarium Incamatum.

46. CONTROL & PREVENTION
• Ensure proper storage ,prevent excessive moisture.(<
10%)
• Discard contaminated food
• Education of the population about the disease

47. FOOD ADDITIVES
• Adding of nutritious substances intentionally to increase the
appearance ,color ,texture ,flavor or storage properties of
food.
• Colouring agents: Saffron,turmeric
• Flavouring agents: Vanilla Essence
• Sweetners: sacharrin
• Preservatives: Sodium Benzoate.
• Acid Imparting agents : acetic acid,Citric acid.

48. FOOD FORTIFICATION
• Public health measure
• Process whereby nutrients are
added to foods to maintain or
improve the quality of diet of a
group.
• Health Programmes of food
fortification :
• Iodisation of salth to prevent
endemic goitre
• Fortification of milk and Ghee
with Vit A & Vit D.
• Characteristics of good
fortification
• The vehicle fortified must be consumed
regularly as part of regular diet.
• The Amount of Nutrient added must
be provide an effective supplement to
low consumers without been
hazardous to high consumers
• It should not alter the taste smell
,appearance or consistency.
• Cost of fortification should not be high

49. Food adulteration
• The process of lowering
the nutritive value of food
either by removing a vital
component or by adding
substances of inferior
quality, is called food
adulteration. The
substance that is used to

50. COMMON ADULTERANTS
o Food grains and grams- marble
pieces, sand particles, clay gilts,
soap stone pieces.
o Pulses- kesari dhal – Colours
o Wheat flow Maida-powdered
lime –
o talcum powder
o Turmeric powder (Haldi)-
metanil
o yellow
o Pepper- dry papaya seeds
o Chilli powder- coloured saw dust
o Sweets- colours not permitted
o Honey- jaggery – sugar
o Tea- coloured tea leaves after
o removing the essence

51. How dangerous are these
adulterants
• The argemone oil used to adulterate ghee and butter
is highly toxic. It causes a disease known as dropsy.
Watery fluid collecting in some parts of the body is the main
symptom. It affects the normal functioning
of the body. It may also paralyse the limbs.
• Metanil yellow used to brighten the colour of pulses, turmeric
powder and sweet meats, is a coal-tar dye. It may cause cancer.

52. ADULTERATION AND LAW
• Prevention of Food Adulteration Act , 1954-
• To Ensure pure and wholesome food and to protect from fradulent
practices
• Amendments -1964,1976,1986
• Case of proven adulteration –Minimum imprisonment of 6 months and
minimum fine of Rs 1000 envisaged
• Grievous Hurt-(320 IPC)- Death or such harm can be punished upto
Life imprisonment and fine not <Rs 5000
• Food Standards- Codex Alimentarius , Agmark standards,
• Bureau of Indian Standards
• National Nutrition Policy -1993- Food Security

53. Five keys to Safer food
1. Keep Clean –
o Wash hands before handling food and often during
preparation
o Wash hands after going to toilet
o Wash n sanitise all surfaces n equipment for food
preparation-protect kitchen from insects , pets
2. Separate raw and cooked food-
o Separate raw meat , poultry n seafood from other foods
o Use separate utensils for handling raw foods
o Store food in containers to avoid contact between raw and cooked
foods

54. Five Keys to Safer Food
3. Cook Thoroughly –
o esp. Meat , poultry , eggs and Seafood
o Bring soups n stews to boiling (ensure>70degree temp)
o Reheat cooked food thoroughly
4. Keep food at safe temperature -
o Don't leave cooked food at room temp.>2 hours
o Prompt refrigeration of cooked n perishable food
o Keep cooked food piping hot(>60 de.) prior to serving
o Don’t store food too long even in refrigerator
o Don’t thaw frozen food at room temperature

55. Five keys to safer food
5. Use safe water and raw materials-
• Use safe water
• Select fresh and wholesome fruits
• Choose foods processed for safety - pasteurised milk
• Wash fruits n vegetables if eaten raw.
• Don’t use food beyond expiry date.

65. POLIOMYELITIS
DR DEODATT M SURYAWANSHI
ASST PROFESSOR (COMMUNITY MEDICINE)

67. OUTLINE
• Definition
• Problem statement
• World scenario
• South East asia
• India
• Epidemiological factors
• Dynamics of disease
transmission
• Source
• Mode of transmission
• Incubation period
• Clinical presentation
• Treatment
• Prevention
• Polio eradication in India

68. What is Polio ?
Polio is a disease caused by polio – virus
Which cripples its victims for life.
The virus is mainly transmitted through the Faecal – oral route.
The disease can be prevented through vaccination.

69. Poliomyelitis
• First described by Michael Underwood in 1789
• First outbreak described in U.S. in 1843
• 21,000 paralytic cases reported in the U. S. in 1952
• Global eradication in near future

70. PROBLEM STATEMENT WORLD

73. PROBLEM STATEMENT : INDIA

74. Polio
Polioviruses
1,2,3
Children age
6 m to 5yrs
Unhygennic
environment
AGENT :
Poliovirus 1,2,3 serotype
Family entoroviridea
Host
Unimmunized Children
between 6 m to 5yrs
Environment
unhealthy ,lack f hygiene &
sanitation.
EPIDEMILOGY

75. AGENT FACTOR
❑AGENT :
❖ Poliovirus serotype 1,2 & 3,Enterovirus (RNA)
❖Minimal heterotypic immunity between serotypes
❖Outbreaks due to type 1
❖During eradication, first serotype to disappear is Type 2 due to better OPV,
followed by serotypes 3 & 1
❖Survives Cold environment 4 months & Faeces 6 months.
❖Rapidly inactivated by heat, formaldehyde, chlorine, ultraviolet light
❖Inactivated by pasteurization.

76. ❑Reservoir of Infection:
❖Man only known reservoir
❖Most infections subclinical dominant role in spread.(tip of the
iceberg)
❖Every 1 case there are 1000 sub clinical cases.
❖No chronic carriers

77. ❑Infectious material :
• Feces.
• Orophyarngeal secretions.

78. HOST FACTORS
❑Age
• Children> Adults
• 6 months to 5yrs
❑Sex distribution
• Male : Female 3: 1
❑Risk factors
• Fatigue, trauma, IM injections, post
tonsillectomy during epidemics of polio,
❑Immunity
• Maternal antibodies protective till 6 months
• Ig A immunity local intestinal immunity
• IgG antibodies Long lasting immunity.

79. ENVIRONMENTAL FACTORS
❖Rainy season common cause of outbreaks.
❖June to September
❖Contaminated water food and flies
❖Overcrowding and poor sanitation
❖Transmission : P to P transmission is most common where sanitation
is poor

80. DYNAMICS OF DISEASE TRANSMISSION
❑Mode of Transmission
❖Fecal oral route :contaminated fingers, contaminated food and water,
articles of daily use.
❖Droplet Infection : appears in the acute viremic phase .Close personal
contact with person can cause.
❑Incubation Period : Usually 7 to 14 days (3 to 35 days).
❑Period of communicability :
❖Infectious 7 to 10 days before and after onset of symptoms.
❖Virus is excreted commonly for almost 12 weeks from an case.

81. Poliomyelitis Pathogenesis
• Entry into mouth
• Replication in pharynx, GI tract, local lymphatics
• Hematologic spread to lymphatics and central nervous system
• Viral spread along nerve fibers
• Destruction of motor neurons

82. Travel History
❑Travel history significance
❖ Likely place of INFECTION
❖ May be even two or three places where the child has
traveled
❖ ORI needs to be done at all places.

83. CLINICAL PRESENTATION Progression of
Severity
90 TO 95% Subclinical
cases
4 to 8 % Abortive
infections
0.1 to 1%
Paralytic
polio

84. ❑Subclinical (in apparent infections)
❖90 to 95% of infections.
❖No presenting signs
❖Can be recognized only by virus isolation or rising antibody titres.

85. ❑Abortive polio
❖4 to 8 % of infections
❖Self limiting disease acute viremia
❖fever ,malaise, sore throat,anorexia and myalgia and headache.
❖Usually resolve in 3 days.
❖Cannot be diagnosed clinically.

86. ❑Non paralytic polio
❖Features of aseptic meningitis
❖Fever ,neck stiffness ,back pain.
❖Last 2 to 10 days
❖Recovery rapid.

87. Paralytic polio
• < 1% of cases
• Most common presentation of Poliomyelitis is paralytic
Poliomyelitis
• Signs of aseptic meningitis followed by severe backache,neck
pain,and by rapid onset of motor weakness.
• Biphasic disease aspectic meningitis recovery retirn of fever and
development of paralysis.This is common in children.

88. • Weakness is asymmetrical ,proximal more than distal muscles
affected Involve legs ,arm ,thoracic cage, or bulbar muscles.
• Urinary retention may occur.
• Examination reveals weakness,fasciculations,,decreased muscle tone
reduced and absent muscle tone.Absent reflexes.

89. • Tripod sign present: Difficulty in sitting and sits by supporting
hands at the back and by partly flexing the hips and the knees.
• Progression to paralysis completed by 4th day.
• Descending paralysis
• Starts at hip progresses distally to involve asymmetrical muscle
groups.
After acute phase atrophy of muscle occurs leading to life long
residual paralysis.

92. Complications;
• Bulbar paralysis :Dysphonia,dysphagia,Difficulty in handling secretions.
• Respiratory insufficiency can occur due to involvement of phrenic nerve or
intercostals nerve. Leading to aspiration of secretions and aspiration
pneumonia
• Severe medullary involvement can cause Circulatory collapse..
• Most patients with paralysis recover some function weeks to months after
infection.
• About 2/3 rd of patients have residual neurological sequel.

93. Treatment
• No specific treatment
• During acute phase treat symptomatically
• Antipyretics,
• Nursing care
• Physiotheraphy of affected limb
• Metal callipers

95. SUMMARY
• Poliovirus causes Acute, nonpersistent infections.
• Virus is transmitted only by infectious human or their
waste
• Survival of the virus in the environment is finite.
• Humans are the only reservoir.
• Trivalent vaccine interrupts virus transmission.

96. Prevention of
Polio

97. Poliovirus Vaccine
• 1955 Inactivated vaccine
• 1961 Types 1 and 2 monovalent OPV
• 1962 Type 3 monovalent OPV
• 1963 Trivalent OPV
• 1987 Enhanced-potency IPV (IPV)

98. Inactivated Polio Vaccine
• Protect against clinical disease
• Suppress pharyngeal excretion of virus
• Contains 3 serotypes of vaccine virus
• Grown on monkey kidney (Vero) cells
• Inactivated with formaldehyde
• No effect on intestinal excretion
• Therefore dose not assist in interrupting
transmission
• Impractical for mass immunization
campaigns.

99. Oral Polio Vaccine
• Live, attenuated vaccine
• Oral administration
• Mimics natural route of infection
• Contains 3 serotypes of vaccine
virus
• Grown on monkey kidney (Vero)
cells.
• Multiplies in gut & excreted in
environment
• Shed in stool for up to 6 weeks
following vaccination & transmitted
to contacts.
• Replace wild polio viruses

100. Inactivated Polio Vaccine
• Highly effective in producing immunity to poliovirus
• >90% immune after 2 doses
• >99% immune after 3 doses
• Duration of immunity not known with certainty

101. Oral Polio Vaccine
• Highly effective in producing immunity to poliovirus
• 50% immune after 1 dose
• >95% immune after 3 doses
• Immunity probably lifelong

102. Polio Vaccine Adverse Reactions
• Rare local reactions (IPV)
• No serious reactions to IPV have been documented
• Paralytic poliomyelitis (OPV)

103. Vaccine-Associated Paralytic Polio
• Increased risk in persons with immunodeficiency
• No procedure available for identifying persons at risk of
paralytic disease
• 5-10 cases per year with exclusive use of OPV
• Most cases in healthy children and their household contacts

104. Vaccine-Associated Paralytic Polio (VAPP)
1980-1998
• Healthy recipients of OPV 41%
• Healthy contacts of
OPV recipients 31%
• Community acquired 5%
• Immunodeficient 24%

105. Polio Vaccine
Contraindications and Precautions
• Severe allergic reaction to a vaccine component or following a prior dose
of vaccine
• Moderate or severe acute illness

106. Our Expectations
• Zero dose polio at birth
• Creating awareness & demand for routine immunization
• Use polio vials with VVMS
• Knowledge of vaccine vial monitors amongst all.
• Support to supplementary immunization activities
• Reporting all AFP promptly to local health authority.

107. Polio Eradication
• Last case in United States in 1979
• Western Hemisphere certified polio free in 1994
• Last isolate of type 2 poliovirus in India in October 1999
• Global eradication goal by 2005

108. Definition of Polio eradication
Demonstrated absence of
transmission of
indigenous wild poliovirus

109. KEY STRATEGIES OF POLIO ERADICATION
•ROUTINE IMMUNIZATION
•N.I.D.s
•ACUTE FLACCID PARALYSIS SURVEILLANCE
•MOP UP ROUNDS

110. Strategies of polio eradication
➢ 1985 – Routine immunization,
Individual immunity
➢1995 – NID’s (PPI / IPPI),
To replace wild with vaccine virus
➢1997 – AFP surveillance,
to identify reservoir of transmission
➢2000 – Mopping up immunization,
To eliminate last foci of transmission

111. Goal of AFP Surveillance
Identification of all reservoirs of circulating
wild poliovirus
AFP surveillance aims at identifying all cases that COULD
Be polio. By documenting all such cases, it is possible
To show that none of these “polio-like” cases were caused
by the polio virus, and therefore that polio is no longer
present.

112. Definition of AFP
• Child aged < 15 yrs who has acute onset of flaccid paralysis
for which no obvious cause found.
or
• Paralytic illness in a person of any age in which polio
is suspected

113. Acute Flaccid Paralysis
Transverse myelitis
Other enteroviruses
Echovirus
• POLIOVIRUS
Guillain- Barre syndrome
Coxsackie virus
Traumatic neuritis

114. DO NOT REPORT
• SPASTIC PARALYSIS
• CONGENITAL DEFECTS: CEREBRAL PALSY
• OBVIOUS TRUMATIC PARALYSIS
• HYPOKALEMIC PARALYSIS
• PSEUDOPARALYSIS: Osteomyelitis
Scurvy
Rickets
• Bell’s Palsy

115. HOT CASE
A case of AFP with inadequate or adequate stool
Specimens and any of the following set of conditions.
1. Age < 5 yrs + Fever at onset + Asymmetrical proximal paralysis;
2. Age < 5 yrs with rapidly progressive paralysis leading to bulbar involvement
and death
3. Any case which in the opinion of SMO looks like Polio

116. ACTION ON REPOERTED CASES
• Investigate every case within 48 hrs of report.
• Case confirmation to be done by SMO, DIO or
any designated senior pediatrician /physician
• Collect adequate stool samples in cold chain.
• Active search for more cases in the area.

117. •Assess status of immunization services In the area
and take corrective action.
• ORI after collecting stool samples.
• Follow up case after 60 days for confirmation of
diagnosis

118. Types & Timing of specimen collection
⚫ Feces ⚫Best source of virus
⚫Long duration of excretion
⚫No need for transport media
⚫Two samples ⚫Intermittent excretion
⚫14 days post
AFP onset
⚫Reduction of virus excretion with time

119. Specimen collection & Handling
Specimen 8 gms of faeces(one thumb size)
Number Two specimen, taken at least 24 hr apart.
When Within 2 wks of onset, no later than 8 wks
Method Voided faeces, preferably at least 8 gms.
Temporary storage Less than + 8°c
Transportation Less than + 8°c
Label EPID no. and ID data
Collection responsibility DIO & SMO
Storage responsibility DIO & SMO
Transportation responsibility DIO, SMO & SEPIO
Responsibility for provision of
specimen containers & specimen
carriers
DIO, SEPIO & laboratory

120. The process of AFP
surveillance
Onset of Paralysis
Detection &
notification
Case investigation &
specimen collection
Follow up examination
Specimens arrive
At national Lab
Classification of case
< 90 days of onset
Virus isolation
Result reported
Isolates sent to
Regional lab for
intra-typic
differentiation
< 28 days
< 14 days of onset
> 60 days of onset
< 3 days
of being
sent

121. Polio Eradication
You Can Help
• Physicians and other health care professionals needed for
short and long term international assignments
• Assist with surveillance evaluation, vaccination logistics, field
operations
• Details on National Immunization Program website

122. •India has been certified polio free.

123. Hepatitis A-E Viruses
An Overview
Dr Deodatt M Suryawanshi

124. A
“Infectious”
“Serum”
Viral hepatitis
Enterically
transmitted
Parenterally
transmitted
F, G, TTV
? other
E
NANB
B D C
Viral Hepatitis - Historical Perspectives

125. Source of
virus
feces blood/
blood-derived
body fluids
blood/
blood-derived
body fluids
blood/
blood-derived
body fluids
feces
Route of
transmission
fecal-oral percutaneous
permucosal
percutaneous
permucosal
percutaneous
permucosal
fecal-oral
Chronic
infection
no yes yes yes no
Prevention pre/post-
exposure
immunization
pre/post-
exposure
immunization
blood donor
screening;
risk behavior
modification
pre/post-
exposure
immunization;
risk behavior
modification
ensure safe
drinking
water
Type of Hepatitis
A B C D E

126. Hepatitis A Virus

127. Etiology
• HAV is one kind of picornavirus and used to be classified as enterovirus type72,
but recently, it is considered to be classified as heparnavirus
• Hepatitis A virion is a naked spherical particle, diameter 27nm
• Consists of a genome of linear, single-stranded RNA, 7.5kb.
• Marmoset and chimpanzee are susceptible animals

129. • Close personal contact
(e.g., household contact, sex contact, child day
care centers)
• Contaminated food, water
(e.g., infected food handlers, raw shellfish)
• Blood exposure (rare)
(e.g., injecting drug use, transfusion)
Hepatitis A Virus Transmission

130. Risk Factors in Persons with
Acute Hepatitis A
Risk Factor % of
cases
Sexual/household contact 11
International travel 17.5
Injection drug use 22.5
MSM 2.5
Day care 13.3
Suspected food/water outbreak 10.2
No risk factor identified 55.4

131. Fecal
HAV
Symptoms
0 1 2 3 4 5 6 12 24
Hepatitis A Infection
Total anti-
HAV
Titre ALT
IgM anti-HAV
Months after exposure
Typical Serological Course

132. ◼ Incubation period: Average 30 days
Range 15-50 days
◼ Jaundice by <6 yrs, <10%
age group: 6-14 yrs, 40%-50%
>14 yrs, 70%-80%
◼ Complications: Fulminant hepatitis
Cholestatic hepatitis
Relapsing hepatitis
◼ Chronic sequelae: None
Hepatitis A - Clinical
Features

133. Endemicity
Disease
Rate
Peak Age
of Infection Transmission Patterns
High Low to
High
Early
childhood
Person to person;
outbreaks uncommon
Moderate High Late
childhood/
young adults
Person to person;
food and waterborne
outbreaks
Low Low Young adults Person to person;
food and waterborne
outbreaks
Very low Very low Adults Travelers; outbreaks
uncommon
Global Patterns of
Hepatitis A Virus Transmission

134. Laboratory Diagnosis
• Acute infection is diagnosed by the detection of
HAV-IgM in serum by EIA.
• Past Infection i.e. immunity is determined by the
detection of HAV-IgG by EIA.

135. • Many cases occur in community-wide outbreaks
• no risk factor identified for most cases
• highest attack rates in 5-14 year olds
• children serve as reservoir of infection
• Persons at increased risk of infection
• travelers
• homosexual men
• injecting drug users
Hepatitis A Vaccination Strategies
Epidemiologic Considerations

136. Preventing Hepatitis A
• Hygiene (e.g., hand washing)
• Sanitation (e.g., clean water sources)
• Hepatitis A vaccine (pre and post
exposure)
• Immune globulin (pre and post
exposure)

137. Hepatitis A vaccine
• 4 inactivated vaccines are available
• Par enteral administered
• 2 doses 6-18 months apart ,> 1yr

138. • Pre-exposure
• travelers to intermediate and high
HAV-endemic regions
• Post-exposure (within 14 days)
Routine
• household and other intimate contacts
Selected situations
• institutions (e.g., day care centers)
• common source exposure (e.g., food prepared by
infected food handler)
Hepatitis A Prevention - Immune
Globulin

139. Pre-Exposure Interventions
• Vaccine is recommended for Children under 19 years old
• Travelers to countries with high rates of hepatitis A
• Drug users
• MSM
• IG is recommended for Travelers to countries with high rates of hepatitis A who
are leaving in < 2 weeks

140. Post-Exposure Interventions
(within 14 days)
• Immune Globulin
Household and other intimate contacts
• Vaccination
􀂄 Household and other intimate contacts <40
years

141. Hepatitis B Virus

143. ▪ Incubation period: Average 60-90 days
Range 45-180 days
▪ Clinical illness (jaundice): <5 yrs, <10%
5 yrs, 30%-50%
▪ Acute case-fatality rate: 0.5%-1%
▪ Chronic infection: <5 yrs, 30%-90%
5 yrs, 2%-10%
▪ Premature mortality from
chronic liver disease: 15%-25%
Hepatitis B - Clinical Features

144. ▪ Sexual - sex workers and homosexuals are
particular at risk.
▪ Parenteral - IVDA, Health Workers are at
increased risk.
▪ Perinatal - Mothers who are HBeAg positive are
much more likely to transmit to their offspring
than those who are not. Perinatal transmission is
the main means of transmission in high
prevalence populations.
Hepatitis B Virus
Modes of Transmission

145. High Moderate
Low/Not
Detectable
blood semen urine
serum vaginal fluid feces
wound exudates saliva sweat
tears
breastmilk
Concentration of Hepatitis B
Virus in Various Body Fluids

146. Spectrum of Chronic Hepatitis B Diseases
1. Chronic Persistent Hepatitis - asymptomatic
2. Chronic Active Hepatitis - symptomatic
exacerbations of hepatitis
3. Cirrhosis of Liver
4. Hepatocellular Carcinoma

147. Symptoms
HBeAg anti-HBe
Total anti-HBc
IgM anti-HBc anti-HBs
HBsAg
0 4 8 12 16 20 24 28 32 36 52 100
Acute Hepatitis B Virus Infection with
RecoveryTypical Serologic Course
Weeks after Exposure
Titre

148. IgM anti-HBc
Total anti-HBc
HBsAg
Acute
(6 months)
HBeAg
Chronic
(Years)
anti-HBe
0 4 8 12 16 20 24 28 32 36 52 Years
Weeks after Exposure
Titre
Progression to Chronic Hepatitis B Virus Infection
Typical Serologic Course

149. Symptomatic Infection
Chronic Infection
Age at Infection
Chronic Infection (%)
Symptomatic
Infection
(%)
Birth 1-6 months 7-12 months 1-4 years Older Children
and Adults
0
20
40
60
80
100
100
80
60
40
20
0
Outcome of Hepatitis B Virus Infection
by Age at Infection
Chronic
Infection
(%)

150. • High (>8%): 45% of global population
• lifetime risk of infection >60%
• early childhood infections common
• Intermediate (2%-7%): 43% of global population
• lifetime risk of infection 20%-60%
• infections occur in all age groups
• Low (<2%): 12% of global population
• lifetime risk of infection <20%
• most infections occur in adult risk groups
Global Patterns of Chronic HBV
Infection

151. Disease Severity
• 70% are jaundiced
• 40% hospitalized
• 0.5% death from acute disease
• 2-10% get chronic disease, 90% if acquired at birth
• 15-25% of those with can get liver failure/cancer

152. Diagnosis
• A battery of serological tests are used for the diagnosis of acute and
chronic hepatitis B infection.
• HBsAg - used as a general marker of infection.
• HBsAb - used to document recovery and/or immunity to HBV
infection.
• anti-HBc IgM - marker of acute infection.
• anti-HBcIgG - past or chronic infection.
• HBeAg - indicates active replication of virus and therefore
infectiveness.
• Anti-Hbe - virus no longer replicating. However, the patient can still
be positive for HBsAg which is made by integrated HBV.
• HBV-DNA - indicates active replication of virus, more accurate than
HBeAg especially in cases of escape mutants. Used mainly for
monitoring response to therapy.

153. Treatment
• Interferon - for HBeAg +ve carriers with chronic active
hepatitis. Response rate is 30 to 40%.
• Lamivudine - a nucleoside analogue reverse transcriptase
inhibitor. Well tolerated, most patients will respond
favorably. However, tendency to relapse on cessation of
treatment. Another problem is the rapid emergence of drug
resistance.
• Successful response to treatment will result in the
disappearance of HBsAg, HBV-DNA, and seroconversion
to HBeAg.

154. Hepatitis B vaccine
Plasma derived vaccine RDNA –yeast derived
vaccine
Derived from Purified from plasma of human
carriers of HBV,sub unit formalin
inactivated
Recombinant DNA
elaborated from cultures of
yeast cloned with HBsAg
Dose 1 ml dose ,3 dose at 0,1 and 6
months
1 ml at 1 and 6 months
Immunity Booster dose after 5 years Booster dose usually not
required

155. Prevention
• Vaccination - highly effective recombinant vaccines are now
available. Vaccine can be given to those who are at increased risk
of HBV infection such as health care workers. It is also given
routinely to neonates as universal vaccination in many countries.
• Hepatitis B Immunoglobulin - HBIG may be used to protect
persons who are exposed to hepatitis B. It is particular efficacious
within 48 hours of the incident. It may also be given to neonates
who are at increased risk of contracting hepatitis B i.e. whose
mothers are HBsAg and HBeAg positive.
• Other measures - screening of blood donors, blood and body
fluid precautions.

156. Hepatitis C Virus
HCV is a member of
flavivirus family.
HCV genome is a
single stranded
positive-sense RNA
and contains 9.4kb

157. hypervariable
region
capsid envelope
protein
protease/helicase RNA-dependentRNA polymerase
c22
5’
core E1 E2 NS2 NS3
33c
NS4
c-100
NS5
3’
Hepatitis C Virus

159. Symptoms
anti-HCV
ALT
Normal
0 1 2 3 4 5 6 1 2 3 4
Hepatitis C Virus Infection
Typical Serologic Course
Titre
Months Years
Time after Exposure

160. Incubation period: Average 6-7 wks
Range 2-26 wks
Clinical illness (jaundice): 30-40% (20-30%)
Chronic hepatitis: 70%
Persistent infection: 85-100%
Immunity: No protective
antibody
response identified
Hepatitis C - Clinical Features

161. Chronic Hepatitis C Infection
• The spectrum of chronic hepatitis C infection is
essentially the same as chronic hepatitis B infection.
• All the manifestations of chronic hepatitis B
infection may be seen, albeit with a lower
frequency i.e. chronic persistent hepatitis, chronic
active hepatitis, cirrhosis, and hepatocellular
carcinoma.

162. ▪ Transfusion or transplant from infected donor
▪ Injecting drug use
▪ Hemodialysis (yrs on treatment)
▪ Accidental injuries with needles/sharps
▪ Sexual/household exposure to anti-HCV-positive
contact
▪ Multiple sex partners
▪ Birth to HCV-infected mother
Risk Factors Associated with
Transmission of HCV

163. Laboratory Diagnosis
• HCV antibody - generally used to diagnose hepatitis C
infection. Not useful in the acute phase as it takes at least 4
weeks after infection before antibody appears.
• HCV-RNA - various techniques are available e.g. PCR and
branched DNA. May be used to diagnose HCV infection in
the acute phase. However, its main use is in monitoring the
response to antiviral therapy.
• HCV-antigen - an EIA for HCV antigen is available. It is
used in the same capacity as HCV-RNA tests but is much
easier to carry out.

164. Treatment
• Interferon - may be considered for patients with
chronic active hepatitis. The response rate is
around 50% but 50% of responders will relapse
upon withdrawal of treatment.
• Ribavirin - there is less experience with ribavirin
than interferon. However, recent studies suggest
that a combination of interferon and ribavirin is
more effective than interferon alone.

165. ▪ Screening of blood, organ, tissue donors
▪ High-risk behavior modification
▪ Blood and body fluid precautions
Prevention of Hepatitis C

166. HBsAg
RNA
 antigen
Hepatitis D (Delta) Virus
HDV (Delta hepatitis virus) is a kind
of defective virus
HDV is found in the nuclei of
infected hepatocytes and replicate
HDV genome is a circular single
strand RNA and contains 1.7kb

168. ▪ Percutanous exposures
▪injecting drug use
▪ Permucosal exposures
▪sex contact
Hepatitis D Virus Modes
of Transmission

169. ▪ Coinfection
– severe acute disease.
– low risk of chronic infection.
▪ Superinfection
– usually develop chronic HDV infection.
– high risk of severe chronic liver disease.
– may present as an acute hepatitis.
Hepatitis D - Clinical Features

170. anti-HBs
Symptoms
ALT Elevated
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV - HDV Coinfection
Time after Exposure
Titre

171. Jaundice
Symptoms
ALT
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV - HDV Superinfection
Typical Serologic Course
Time after Exposure
Titre

172. ◼ HBV-HDV Coinfection
Pre or postexposure prophylaxis to prevent
HBV infection.
◼ HBV-HDV Superinfection
Education to reduce risk behaviors among
persons with chronic HBV infection.
Hepatitis D - Prevention

173. Hepatitis E Virus

175. ◼ Most outbreaks associated with faecally contaminated drinking
water.
◼ Several other large epidemics have occurred since in the Indian
subcontinent and the USSR, China, Africa and Mexico.
◼ In the United States and other nonendemic areas, where
outbreaks of hepatitis E have not been documented to occur, a
low prevalence of anti-HEV (<2%) has been found in healthy
populations. The source of infection for these persons is
unknown.
◼ Minimal person-to-person transmission.
Hepatitis E -
Epidemiologic Features

176. ◼ Incubation period: Average 40 days
Range 15-60 days
◼ Case-fatality rate: Overall, 1%-3%
Pregnant women,
15%-25%
◼ Illness severity: Increased with age
◼ Chronic sequelae: None identified
Hepatitis E - Clinical Features

177. Symptoms
ALT IgG anti-HEV
IgM anti-HEV
Virus in stool
0 1 2 3 4 5 6 7 8 9 1
0
1
1
1
2
1
3
Hepatitis E Virus Infection
Typical Serologic Course
Titer
Weeks after Exposure

178. ◼ Avoid drinking water (and beverages with ice) of
unknown purity, uncooked shellfish, and uncooked
fruit/vegetables not peeled or prepared by traveler.
◼ IG prepared from donors in Western countries
does not prevent infection.
◼ Unknown efficacy of IG prepared from donors in
endemic areas.
◼ Vaccine?
Prevention and Control Measures
for Travelers to HEV-Endemic
Regions

179. Thanks