acute infectious disease caused by toxigenic strains of corynebacterium diphtheriae.

1. Dr. RAJALEKSHMY.P.R
DEPT: OF SWASTHAVRITTA
AMRITA SCHOOL OF AYURVEDA

2. INTRODUCTION
 Acute infectious disease caused
by toxigenic strains of Coryne
bacterium diphtheriae.
 3 major clinical types-anterior
nasal, faucial, laryngeal
 Skin, conjunctiva, vulva and
other parts may be affected.
 Bacilli multiply locally in throat
and produce powerful exotoxin.

3. HISTORY
 Took its name from greek word “diphthera” meaning
leather.
 Named in 1826 by French physician Pierre Bretonneau.
 In the past, disease was called as general disease or
killer disease because there was no treatment and was
the cause of high mortality in children.
 It was said that the disease killed as many as 80% of
the children below 10 yrs.

4. PROBLEM STATEMENT

5. WORLD
Developed countries
rare disease due to
routine child
vaccination
Developing countries
endemic due to lack of
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 supply of vaccines.

6. INDIA
 Endemic disease
 Declining trend of diphtheria due to increasing
coverage of child population by immunization .
Reported cases
1987- 12952
2011- 4286
112 deaths showing a case fatality rate of about 2.61

7. AGENT
Agent Corynebacterium diphtheria
 Gram positive motile organism
 No invasive power but produce powerful exotoxin after
multiplication locally in the throat responsible for:
1. Formation of false membrane over tonsils, pharynx or larynx, with
well defined edges and membrane cannot be wiped away.
2. Marked congestion, edema, local tissue destruction
3. Enlargement of lymph nodes
4. Toxaemic signs and symptoms

8.  4 types -Gravis
Mitis
Belfanti
Intermedius
 Sensitive to penicillin and readily killed by heat and
chemical agents
 Affects heart- myocarditis
nerves- paralysis
Gravis more
severe than
mitis infection

9. SOURCE OF INFECTION
 Cases-
ranges from sub clinical to clinical
mild or silent infections may exhibit not more
than a mere running nose or sore throat
 Carriers-
common source of infection
may be temperory or chronic;nasal or throat carriers
Nasal- dangerous( frequent shedding into
environment)
Temperory- lasts for 1 month
Chronic- last for 1 year until the patient is treated

10. INFECTIVE MATERIAL
 Naso-pharyngeal secretions
 Discharge from skin lesions
 Contaminated fomites
 Infected dusts

11. PERIOD OF INFECTIVITY
 14 – 28 days from the onset of disease but carriers may
remain infective for much longer periods.
 A case or carrier may be considered non-
communicable when atleast 2 cultures obtained from
nose or throat, 24 hours apart are negative for
diphtheria bacilli.

12. AGE
Children upto
1-5 yrs
HOST FACTORS
SEX
both
IMMUNITY
Infants borne of immune
mothers are immune for
first few weeks or months of
life.

13. ENVIRONMENTAL FACTORS
 Cases occur in all seasons.
 Winter- favourable
 Kolkata- highest incidence in august
 Mumbai- winter months
 Delhi- august or october

14. MODE OF TRANSMISSION
 Droplet infections
 Can also be transmitted directly to susceptible persons
from infected cutaneous lesions.
 Transmission by objects contaminated by naso-
pharyngeal secretions of patients is also possible.

15. PORTAL OF ENTRY
 Respiratory route- respiratory tract
 Non-respiratory route-
Portal of entry may be skin where cuts, ulcers and
wounds not properly attended to or through
umbilicus of new born.
Site of implantation may be eyes, genitalia or
middle ear.

16. INCUBATION PERIOD
 2- 6 days, ocassionally longer.

17. CLINICAL FEATURES
 Respiratory tract forms of diphtheria-
pharyngo-tonsillar
laryngo tracheal
nasal
combinations

18. Pharyngo-tonsillar diphtheria
• Sore throat
• Difficulty in swallowing
• Low grade fever at presentation
• Presence of pseudo membrane
over tonsils
• Oedema in sub mandibular
region
• Bull necked appearance

20. Laryngo-tracheal diphtheria
• Preceeded by pharyngo tonsillar
diphtheria
• Fever, hoarseness and croupy
cough
• Dyspnoea
• parenchymatous
degeneration
• necrosis in heart
muscles, liver, kidneys
and adrenals
• vision difficulties,
speech, swallowing or
movements of arms or
legs
• paralysis of soft palate,
eye muscle or
extremities
Toxin damage

21. Nasal diphtheria
• Mildest form
• Localized in septum or turbinates of one
side of nose
• Conjunctiva and genitals also sources of
infection
• Membrane extends to pharynx.

22. Cutaneous diphtheria
• Common in tropical areas
• Secondary infection of
previous infection or skin
abrasion
• Presenting lesion-an ulcer
surrounded by erythema
and covered with
membrane.

24. SCHICK’S TEST
 Intra dermal test
 Tests – presence of antitoxin(immunity status) and
state of hypersensitivity to diphtheria toxin.
 Inject 0.2ml of Schick test toxin intradermally into
skin of forearm, while into opposite arm- control
(Schick toxin inactivated by heat) is injected.

25. Negative reactions
 if the person is immune, no reaction of any kind.
 In test arm, a circumscribed red flush of 10-50mm
diameter appears within 24-36 hours reaching
maximum development by 4th – 7th day.
 This slowly fades into a brown patch and skin
desquamates.
 Control arm shows no change.
 The person is susceptible to diphtheria.
Positive reaction

26.  A red flush develops equally on both
arms, much less circumscribed than
true +ve reactions.
 Fades by 4th day.
 allergic reaction found in certain
individuals
 Schick negative
 Control arm shows pseudo positive
reaction and test arm shows positive
reaction.
 The person is susceptible to
diphtheria.
Pseudo-positive reactions
Combined reactions

27. CONTROL OF
DIPHTHERIA

28. CASES & CARRIERS
Early detection
• Start active search
immediately from family
and school contacts.
• Carriers can be detected
by culture methods.
(swabs taken from nose
and throat)
Isolation
all cases, suspected cases
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.

29. Treatment-
Cases
• Preliminary test dose of 0.2 ml
subcutaneously to detect sensitization to
horse serum.
• Followed by dip: antitoxin IM or IV in doses
ranging from 20,000-40,000 units or more
depending on severity of cases.
• Mild early pharyngeal or laryngeal: 20,000-
40,000 units
• Moderate naso pharyngeal: 40,000-60,000
units
• Severe, extensive or late disease: 80,000-
100,000 units.
• Addition to antitoxin, penicillin or
erythromycin for 5-6 days to clear throat.
Carriers
• Should be treated
in 10 days course
of oral
erythromycin

30. CONTACTS
 Should be throat swabbed and immunity should be
determined.
 Where primary immunization was received within the
previous 2 years- no further action 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 be given.
 Non-immunized close contacts should receive
prophylatic penicilin or erythromycin.
 They should be given 1000-2000 units of antitoxin and
actively immunized against diphtheria.

31. COMMUNITY
 Active immunization with diphtheria toxoid of all
infants as early in life as possible with subsequent
booster dose every 10 years thereafter.
 Immunization rate must be maintained at high level.

32. DIPHTHERIA
IMMUNIZATION

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
Diphtheria antitoxin

34. DPT VACCINE
 For immunization of infants.
 Pertussis component enhances diphtheria toxoid.
 Types- plain and adsorbed
 Adsorption-carried out on a mineral carrier like aluminium
phosphate or hydroxide.
STORAGE
 should not be frozen
 Stored in refrigerator at 2-8 degree celsius
 Will loose potency if kept at room temperature for a long
time.

35. Optimum age-
 Global Advisory Group of EPI recommended that DPT an
be safely administered as early as 6 weeks after birth.
Doses-
 3 doses of DPT each is 0.5ml.
Mode of admn-
 All vaccines containing mineral carriers should be injected
intramuscular.
 DPT given in upper and outer quadrants of gluteal region.

36.  Immunization schedule-
 6 weeks
 10weeks
 14 weeks
 16-18 months (booster dose)
 5 years (DT)

37.  Reactions-
 Fever and mild local reactions
 2-6% develop fever of 39 degree or higher.
 5-10% experience swelling and induration.
 Neurological- encephalitis, prolonged convulsions,
infantile spasms, Reye’s syndrome.
 Contra indications-
 Seriously ill children or who need hospitalization are not
vaccinated.
 Should not be repeated if a severe reaction occurred after
a previous dose.
 In case of DPT, subsequent DT immunization.

38.  For children over the age of 5 years who have not
received DPT- 2 doses of DT vaccine, 4 weeks apart,
with a booster dose 6 months to 1 year later.
 Those children who received primary course of DPT
earlier, should receive DT as booster at 5-6 years.
 For immunizing children over 12 years of age and
adults, preparation –dT (adult type diphtheria tetanus
vaccine).
 Contains no more than 2 Lf diphtheria toxoid per
dose.
 Admn:- 2 doses at interval of 4-6 weeks, followed by
booster 6-12 months after second dose.

39. SINGLE VACCINES
 Less frequently used.
 Good immunizing agents.
 APT- hardly used; prone to give rise to severe
infections.
 Each dose of these antigens generally contain 25
loeffler(lf) units of DT.

40. ANTI-SERA
 main stay of passive prophylaxis and also for treatment
in diphtheria.
 diphtheria antitoxin prepared in horse serum.