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DIPHTHERIA

Acute infectious disease

anterior nasal, faucial, laryngeal

exotoxin from bacilli causes

false membrane in tonsils- well defined edges, not


wiped away

congestion, oedema,

enlargement of lymph nodes

toxaemia
PROBLEM STATEMENT
GLOBALLY

fatality rate 10%


Rare in develped countries due to vaccination
improved socio economic conditions are changing the
epidemiology of diphtheria
epidemics are due to decreasing immunization
coverage
recent outbreaks- shift to older children
globally- 2012- 4,490 diphtheria cases
INDIA

Endemic

declining trend- widespread immunization

1987- 12,952 cases

2013- 4,090 cases

64 deaths

case fatality rate - 2.61


EPIDEMILOGICAL DETERMINANTS
Agent factors:
Agent- Corynebacterium diphtheria
gram positive
non motile
exotoxin +
4 types- gravis, mitis, belfanti, inermedius
gravis more severe than mitis
non toxigenic becomes toxigenic when exposed to
beta phage
bacilli sensitive to pencillin, killed by heat
toxin- myocarditis
Source of infection-

case
carriers

case

sub clinical to frank clinical cases

mild cases present with mere running nose or sore throat,


so plays more important rle in transmission
carriers-

95 carriers for every 5 cases

temperory ( 1 month) or chronic ( 1 year)

nose or throat carriers

nose carriers are more dangerous due to continuous


shedding of bacteria

incidence of carriers - 0.1-5%

immunization doesnt prevent carrier state


Infective material-

Nasopharyngeal sec

discharge from skin

fomites

infected dust
Infective period-

14-28 days from the onset of disease

carriers remain infective for a longer time

case or carrier considered non communicable when at least


2 cultures obtained from nose or throat 24 hours apart are
negative for diphtheria bacilli
Host factors:
Age-
1-5 years children
immunization widespread- shift in age fom pre school to
school age
Sex-
both sexes
Immuity:
active immunity in populatio with inapparent ifection
health efeects due to toxin
disease+ if no neutralising antitoxin in blood stream
Environmental factors;

occurs in all seasons


winter favours sspread

Mode of transmission

droplet
infe cted cutaneous lesions
objects ( thermometers, toys etc)
nasopharyngeal secretion
PORTAL OF ENTRY:

1. respiratory route
respiratory tract

2. non respiratory route


skin- cuts, wounds, ulcer
eye
genitalia
middle ear

developed countries- droplet infection

Incubation period: 2-6 days


Clinical features:
Pharyngotonsillar
-sore throat,
difficulty in swallowing,
low grade fever
local examination of throat:
pseudo membrane on tonsils - adherant, bull neck
apperance
adherant
attempts to remove causes bleeding
bull neck app- swelling of sub mandibular and
anterior part of neck
Laryngotonsillar-

preceded by pharyngotonsillar
fever,
hoarseness,
croupy cough,
dyspnoea- obstruction caused by membrane
obstruction may cause suffocation- relieved by intubatipn or
tracheostomy
bronchial tree involvement- most severe
toxins produced actively within membrane

parenchymatous degenration nd fatty infiltration of organs

nerve damage

paralysis of soft palate

eye muscles

patients who survive complications recover completely


Nasal-

localised to septum or turbinates of one side of the nose


mildest form
occasionally membrane might extend to pharynx

Cutaneous-

ulcer, erythema, membrane


tropical areas
chronic
CONTROL OF DIPHTHERIA
Cases and carriers:

Early detection-
search for cases and carriers in family nd school
contacts
swab culture from throat and nasopharynx
tests for virulence of organism

Isolation-
14 days,
atleast 2 swabs 24 hrs apart shud be negative
Treatment-
cases-

diphtheria antitoxin im/iv 20000- 100000 units after


test dose 0.2 ml s.c
pencillin or erythromycin 5-6 days

carriers-

oral erythromycin for 10 days


Contacts:

if immunization or booster recievedwithin 2 years no


further treatment

> 2 yrs booster dose is required

non imunized close contact- prophylactic pencillin or


erythromycin

under medical surveillance

bacteriological surveillance - by swabbing


Community:

active immunization of infants with diphtheria anti toxoid

subsequent booster doses every 10 years

immunise infant befre it loses its protection from maternal


antibodies

vaccine not against organism- so immunization not effective


against carrier state

non immune individuals are not protected by high level of


population immunity
vaccines

combined or mixed vaccines

DPT

DTP w

DTPa

DT

dT
Single vaccines

FT

APT

PTAP

PTAH

TAF
DPT vaccine:
Plain or absorbed on aluminium hydroxide
never frozen
stored in 2-8 C
administered at 6 , 10, 14 weeks with booster at 18-24
months and again at 5 years
0.5 ml i.m
> 12 years of age DT is given
reactions- fever , erythema, severe reactions like
encephalopathy,infantile spasms are rare
C/I anaphylaxis, epilepsy
SINGLE VACCINES:

hardly used
severe reactions
25 Lf units diphtheria toxoid

ANTI SERA:

prepared in horse serum


passive prophylaxis
THANK YOU

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