Acute infectious disease caused by toxigenic strains of Coryne bacterium diphtheriae.

1. KuldeepVyas M.Sc.
CHN
DIPHTHERIA
Kuldeep Vyas M.Sc. CHN
1Kuldeep Vyas M.Sc. CHN

2. INTRODUCTION
 Acute infectious diseasecaused
by toxigenic strains of Coryne
bacteriumdiphtheriae.
 3 major clinicaltypes-anterior
nasal, faucial, laryngeal
 Skin, conjunctiva, vulvaand
other parts may beaffected.
 Bacilli multiply locally inthroat
and produce powerfulexotoxin.
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3. HISTORY
 Took its name from greek word “diphthera”meaning
leather.
 Named in 1826 by French physician PierreBretonneau.
 In the past, disease was called as general disease or
killerdisease because therewas no treatmentand was
the cause of high mortality inchildren.
 Itwas said that thedisease killed as manyas 80% of
the children below 10yrs.
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4. PROBLEMSTATEMENT
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5. WORLD
Developed countries
rare disease dueto
routine child
vaccination
Developing countries
endemic due to lackof
adequate widespread
immunization
Reported cases in 2010- 4187
Epidemics are largely due to decreasing immunization coverage
among infants and children, waning immunity to diphtheria in
adults, movements of large groups of populations in the last few
years and irregular supplyof vaccines.
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6. INDIA
 Endemic disease
 Declining trend of diphtheria due toincreasing
coverage of child population by immunization.
Reported cases
1987- 12952
2011- 4286
112 deathsshowing acase fatality rateof about 2.61
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7. AGENT
Agent Corynebacterium diphtheria
 Gram positive motileorganism
 No invasivepower but producepowerful exotoxinafter
multiplication locally in the throat responsible for:
1. Formation of false membrane over tonsils, pharynx or larynx, with
well defined edgesand membranecannot bewiped away.
2. Marked congestion, edema, local tissuedestruction
3. Enlargement of lymph nodes
4. Toxaemic signs andsymptoms
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8.  4 types -Gravis
Mitis
Belfanti
Intermedius
 Sensitive topenicillinand readily killed by heatand
chemical agents
 Affects heart- myocarditis
nerves- paralysis
Gravis more
severe than
mitis infection
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9. SOURCE OF INFECTION
 Cases-
ranges from sub clinical toclinical
mild orsilent infections mayexhibit not more
than a mere running noseorsore throat
 Carriers-
common source of infection
may be temperoryorchronic;nasal or throatcarriers
Nasal- dangerous( frequent shedding into
environment)
Temperory- lasts for 1 month
Chronic- last for 1 yearuntil thepatient is treated
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10. INFECTIVE MATERIAL
 Naso-pharyngeal secretions
 Discharge from skinlesions
 Contaminated fomites
 Infected dusts
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11. PERIOD OF INFECTIVITY
 14 – 28 days from theonsetof disease butcarriers may
remain infective for much longerperiods.
 A case or carrier may be considered non-
communicablewhen atleast 2 culturesobtained from
nose or throat, 24 hours apart are negative for
diphtheria bacilli.
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12. AGE
Children upto
1-5 yrs
HOST FACTORS
SEX
both
IMMUNITY
Infants borne of immune
mothers are immune for
first fewweeks or monthsof
life.
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13. ENVIRONMENTAL FACTORS
 Cases occur in allseasons.
 Winter- favourable
 Kolkata- highest incidence inaugust
 Mumbai- wintermonths
 Delhi- august oroctober
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14. MODE OF TRANSMISSION
 Droplet infections
 Can also be transmitted directly tosusceptiblepersons
from infected cutaneouslesions.
 Transmission by objects contaminated by naso-
pharyngeal secretionsof patients isalso possible.
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15. PORTAL OF ENTRY
 Respiratory route- respiratory tract
 Non-respiratory route-
Portal of entry may be skin wherecuts, ulcersand
wounds not properly attended to or through
umbilicus of new born.
Siteof implantation may be eyes, genitalia or
middleear.
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16. INCUBATION PERIOD
 2- 6 days, ocassionallylonger.
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17. CLINICAL FEATURES
 Respiratory tract forms ofdiphtheria-
pharyngo-tonsillar
laryngo tracheal
nasal
combinations
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18. Pharyngo-tonsillar diphtheria
• Sore throat
• Difficulty inswallowing
• Low grade fever atpresentation
• Presence of pseudomembrane
over tonsils
• Oedema in submandibular
region
• Bull necked appearance
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20. Laryngo-tracheal diphtheria
• Preceeded by pharyngotonsillar
diphtheria
• Fever, hoarseness and croupy
cough
• Dyspnoea
• necrosis in heart
muscles, liver, kidneys
and adrenals
• vision difficulties,
speech, swallowing or
movements of armsor
legs
• paralysis of softpalate,
eye muscle or
extremities
Toxindamage
• parenchymatous
degeneration
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21. Nasal diphtheria
• Mildest form
• Localized in septum or turbinatesof one
side of nose
• Conjunctiva and genitals also sources of
infection
• Membrane extends topharynx.
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22. Cutaneous diphtheria
• Common in tropicalareas
• Secondary infection of
previous infection orskin
abrasion
• Presenting lesion-an ulcer
surrounded by erythema
and covered with
membrane.
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24. SCHICK’S TEST
 Intra dermal test
 Tests – presence of antitoxin(immunity status)and
state of hypersensitivity to diphtheriatoxin.
 Inject 0.2ml of Schick test toxin intradermallyinto
skin of forearm, while into opposite arm- control
(Schick toxin inactivated by heat) isinjected.
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25. Negative reactions
 if the person is immune, no reaction of any kind.
Positive reaction
 In testarm, acircumscribed red flush of 10-50mm
diameter appears within 24-36 hours reaching
maximum development by 4th – 7th day.
 This slowly fades intoa brown patch and skin
desquamates.
 Control arm shows nochange.
 The person is susceptible todiphtheria.
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26. Pseudo-positive reactions
 A red flush develops equally on both
arms, much less circumscribed than
true +vereactions.
 Fades by 4th day.
 allergic reaction found in certain
individuals
 Schick negative
Combined reactions
 Control arm shows pseudo positive
reaction and test armshows positive
reaction.
 The person is susceptibleto
diphtheria.
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27. CONTROL OF
DIPHTHERIA
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28. • Start active search
immediately fromfamily
and school contacts.
• Carriers can bedetected
by culture methods.
(swabs taken from nose
and throat)
CASES & CARRIERS
Early detection Isolation
all cases, suspectedcases
and carriers should be
isolated, preferably in a
hospital for atleast 14
days or until proved free
of infection.
2 consecutive throat swabs taken 24 hours apart
should be negative before terminating isolation.
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29. Treatment-
Cases
• Preliminary test dose of 0.2 ml
subcutaneouslytodetectsensitization to
horseserum.
• Followed bydip: antitoxin IM or IV in doses
ranging from 20,000-40,000 units or more
depending on severity ofcases.
• Mild early pharyngeal or laryngeal:20,000-
40,000 units
• Moderate naso pharyngeal: 40,000-60,000
units
• Severe, extensive or latedisease: 80,000-
100,000 units.
• Addition to antitoxin, penicillinor
erythromycin for 5-6 days toclearthroat.
Carriers
• Should betreated
in 10 days course
of oral
erythromycin
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30. CONTACTS
 Should be throat swabbed and immunityshould be
determined.
 Where primary immunization was received withinthe
previous 2 years- no furtheraction needed.
 Where primary course or booster dose of diphtheria
toxoid was received more than 2 years before, only a
booster dose of dip: toxoid need begiven.
 Non-immunized close contacts shouldreceive
prophylatic penicilin orerythromycin.
 They should be given 1000-2000 unitsof antitoxinand
actively immunized againstdiphtheria.
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31. COMMUNITY
 Active immunization with diphtheria toxoid of all
infants as early in life as possible with subsequent
boosterdoseevery 10 years thereafter.
 Immunization rate must be maintained athigh level.
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32. DIPHTHERIA
IMMUNIZATION
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33. Combined vaccines
• DPT
• DTP(w)
• DTP(a)
• DT(d-tetanus toxoid)
• dT(diphtheria-tetanus,
adult type)
single vaccines
• FT(formal toxoid)
• APT(alum-precipitated toxoid)
• PTAP(purified toxoid-
aluminium precipitate)
• PTAH(p:t:a: hydroxide)
• TAF(toxoid-anti toxin -
flocculus)
Antisera
Diphtheriaantitoxin
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34. DPT -VACCINE
 For immunization of infants.
 Pertussis component enhances diphtheriatoxoid.
 Types- plain and adsorbed
 Adsorption-carried out on a mineral carrier likealuminium
phosphate orhydroxide.
STORAGE
 should not be frozen
 Stored in refrigerator at 2-8 degreecelsius
 Will loose potency if keptat room temperature fora long
time.
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35. Optimum age-
 Global Advisory Group of EPI recommended that DPTan
be safelyadministered as earlyas 6 weeks after birth.
Doses-
 3 doses of DPT each is0.5ml.
Mode of admn-
 All vaccines containing mineral carriers should beinjected
intramuscular.
 DPT given in upperand outerquadrantsof gluteal region.
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36.  Immunization schedule-
 6 weeks
 10weeks
 14 weeks
 16-18 months (boosterdose)
 5 years (DT)
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37.  Reactions-
 Fever and mild local reactions
 2-6% develop feverof 39 degree or higher.
 5-10% experience swelling and induration.
 Neurological- encephalitis, prolonged convulsions,
infantile spasms, Reye’ssyndrome.
 Contra indications-
 Seriously ill children orwho need hospitalizationare not
vaccinated.
 Should not be repeated if a severe reaction occurred after
a previousdose.
 In case of DPT, subsequent DTimmunization.
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38.  For children over the age of 5 years who have not
received DPT- 2 doses of DT vaccine, 4 weeksapart,
with a boosterdose 6 months to 1 year later.
 Thosechildren who received primary courseof DPT
earlier, should receive DT as boosterat 5-6 years.
 For immunizing children over 12 years of age and
adults, preparation –dT (adult typediphtheria tetanus
vaccine).
 Contains no more than 2 Lf diphtheria toxoidper
dose.
 Admn:- 2 doses at interval of 4-6 weeks, followedby
booster 6-12 months after seconddose.
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39. SINGLE VACCINES
 Less frequentlyused.
 Good immunizing agents.
 APT- hardly used; prone togive rise tosevere
infections.
 Each doseof theseantigens generallycontain 25
loeffler(lf) units of DT.
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40. ANTI-SERA
 main stayof passiveprophylaxis and also for treatment
in diphtheria.
 diphtheria antitoxin prepared in horseserum.
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