Epidemiology of diphtheria

1. DIPHTHERIA
Dr.MadhuSM

2. • Diphtheria is an acute infectious disease
caused by toxigenic strain of Cornybacterium
diphtheriae.

3. • The bacilli multiply locally, usually in the throat and
elaborate a powerful exotoxin which is responsible
for -
a. The formation of a grayish or yellowish
membrane ( false membrane) commonly cover
the tonsils, pharynx, larynx with well defined edges
and membrane can not be wiped away.
b. Marked congestion, oedema or local
destruction
c. Enlargement of the regional lymph nodes
d. Signs and symptoms of toxaemia.
tissue

4. EPIDEMIOLOGICAL
DETERMINANT

5. PROBLEM STATEMENTS
•Diphtheria is rare disease in most developed
countries.
•In India:
•It is an endemic disease.
•There is a declining trend of diphtheria in the
country due to increasing coverage of child
population by immunization.
•In 1987, the incidence of the disease in the
country was about 12,952, whereas during the
year 2013, 4,090 cases and 64 deaths were
reported showing case fatality rate of about 2.61.

6. AGENT FACTORS
1. Agent -
 Corynebacterium diphtheriae is a gram positive,non-
motile organism.
 It has no invasive power,but produces a powerful
exotoxin.
2. Source of infection
a. Case – subclinical to clinical
b. Carriers – more common source of infection.
95 carriers for 5 subclinical case

7. • Carriers may be temporary or chronic; Nasal or
throat carriers.
• Nasal carriers are particularly dangerous source of
infection because of frequent shedding of organism
into the environment than throat carriers.
• Temporary carriers state may last for about a
month.
• Chronic carriers may persist for a year or
so,unless the patient is treated.

8. 3. Infective material
• Nasopharangeal secretion
• Discharges from skin lesion
• Contaminated fomites
• Infected dust
4. Period of infectivity
• Vary from 14-28 days from the onset of disease.
• But carriers may remain infectivefor much
longer periods.

9. HOST FACTORS
1. Age – particularly affects children aged 1-5.
2. Sex – both sexes affected
3. Immunity – Infant born of immune mothers
are relatively immune during first few weeks
or months of life.

10. ENVIRONMENTAL FACTORS
• It occurs in all seasons,although winter month favour
its spread.
• In Kolkata,the highest incidence was reported in
August;in Mumbai in winter months;and Delhi,
duringAugust to October.

11. MODE OF TRANSMISSION
• Mainly by Droplet infection
• It can be
susceptible
lesions.
also
person
transmitted directly to
from infected cutaneous

12. PORTAL OF ENTRY
a. Respiratory tract – common
b. Non- respiratory route – skin where cuts,
wounds and ulcers,umbilicus in new born.

13. INCUBATION PERIOD
• 2-6days
• Occasionally longer

14. CLINICAL FEATURES
• Respiratory tract forms of diphtheria consist
of -
a. Pharyngotonsillar diphtheria
b. Laryngotracheal diphtheria
c. Nasal diphtheria
d. Combination of these

15. 1.PHARYNGOTONSILLAR DIPHTHERIA
• Sore throat
• Difficulty in swallowing
• Low grade fever
• Examination of throat may shows only mild erythema,
localized exudate,or a pseudo-membrane.
• Membrane may localized or a patch of the posterior
pharynx or tonsil, may cover the entire tonsil, or less
frequently may spread to cover the soft and hard palate and
posterior portion of pharynx.

16. • In early stage, pseudomembrane may be
whitish and may be wipe off easily.
• The membrane may be extend to become
thick,blue white to gray black and adherent.
• Attempts to remove the membrane results in
bleeding.
• Patient with sever disease may have marked
oedema of the submandibular area and
anterior portion of the neck, along with
lymphadenopathy, giving a characteristic “bull-
necked” appearance

19. 2.LARYNGOTRACHEAL DIPHTHERIA
• Preceded by pharyngotonsillar disease
• Fever,hoarseness and croupy cough at presentation
• If the infection extend into bronchial tree, it is the
most severe form of disease.
• Diphtheria bacilli within the membrane continue to
produce toxin actively.
• Toxin is absorbed and result in distant toxic damage.
• in later stage, difficulty in vision, speech, swallowing
or movement of arms or legs.
• Toxin also produce nerve damage and resulting in
paralysis of the soft palate, eye, muscles or
extremities.

20. 3.NASAL DIPHTHERIA
• It is the mildest form of respiratory diphtheria.
• Usually localized to the septum or turbinates
of one side of the nose.
• Occasionally a membrane may extend into the
pharynx.

21. CUTANEOUS DIPHTHERIA
–
• Common in tropical areas.
• It often appears as a secondary infection of a
previous skin abrasion or lesion.
• The presenting lesion, often
surrounded by erythema
membrane.
an ulcer,
and covered
may be
with

22. • Non respiratory mucosal surface i.e.
conjunctivae and genitals may also be sites of
infection.

23. CONTROL OF DIPHTHERIA
1. Case and carriers
2. Contacts
3. Community

24. 1.CASE AND CARRIERS
1. Early detection of case and carriers
2. Isolation of all cases and carriers in hospital for 14 days
or until proved free of infection.
3.Treatment of cases and carriers
A. Cases -
a.Diptheria antitoxin - IM/IV in doses ranging from 20000
to 1,00,000 units or more depending upon the severity
of the case,after preliminary test dose of 0.2ml
Subcutaneously to detect sensitization to horse serum.

25. b.Penicillin or erythromycin for 5-6days
2. Carriers – treat with Erythromycinfor 10 days.
Case Diptheria antitoxin dose
Mild early pharangeal or
laryngeal
20,000-40,000 units
Moderate nasopharangeal 40,000- 60,000 units
Severe, extensive or late
( 3days or more)
80,000-1,00,000 units

26. 2.CONTACTS
• Where primary immunization or booster dose was
received within 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 diphtheria toxoid need be given.
• Non-immunized close contacts should receive
prophylactic penicillin or erythromycin and 1000-2000
units of diphtheria antitoxin
• Contacts should be placed under medical surveillance
and examined daily for at least a week.

27. 3.COMMUNITY
• Active immunization with diphteria
toxoid of all infants as early in life as
possible, as scheduled, with subsequent
booster doses every 10 years thereafter.