DIPHTHERIA

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7/12/2021 Dr.Bharat D.

Zinjurke 1

DIPHTHERIA
Dr. Bharat D. Zinjurke
Assistant Professor (Swasthavritta & yoga)
Smt.K.G.M.P. Ayurved Mahavidyalaya, Mumbai
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DIPHTHERIA
• Diphtheria is an acute bacterial infectious disease caused by toxigenic
strains of Corynebacterium diphtheriae.
• Three major clinical types have been described : 1. anterior nasal,
• 2. faucial 3. laryngeal;
• . The bacilli multiply locally, usually in the throat, and elaborate a
powerful exotoxin which is responsible for :
• (a) the formation of a greyish or yellowish membrane (·'false
membrane") commonly over the tonsils, pharynx or larynx (or at the
site of implantation), with well-defined edges and the membrane
cannot be wiped away;
• (b) marked congestion, oedema or local tissue destruction;
• (c) enlargement of the regional lymph nodes
• (d) signs and symptoms of toxaemia.
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DIPHTHERIA
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Greyish or yellowish membrane (·'false


membrane") commonly over the tonsils
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Congestion, oedema or local tissue


destruction
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Enlargement of the regional lymph nodes


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Problem statement
• The disease is seen occasionally among non-immunized
children in developed countries.
• During the year 2016, about 7,097 diphtheria cases were
reported globally

• INDIA : Diphtheria is an endemic disease


• In the year 2017, 5,293 cases and 148 deaths were reported
showing a case fatality rate of about 2. 79
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Epidemiological determinants
• Agent factors
• (a) AGENT: The causative agent, C.diphtheriae is a grampositive,
non-motile organism. produces a powerful exotoxin
• Four types of diphtheria bacilli - grauis, mitis, belfanti and intermedius,
all pathogenic to man.
• (b) SOURCE OF INFECTION
• (i) CASE : Cases or subclinical cases.
• (ii) CARRlER : Carriers are common sources of infection – 95%
• (c) INFECTIVE MATERIAL : Nasopharyngeal secretions, discharges
from skin lesions, contaminated fomites and possibly infected dust
• (d) PERIOD OF INFECTIVITY : 14 to 28 days
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Epidemiological determinants
• Host factors
• (a) AGE : Children aged 1 to 5.
• (b) SEX : Both sexes are affected.
• (c) IMMUNITY : Infants born of immune mothers are relatively
immune during the first few weeks or months of life.
• Environmental factors
• Cases of diphtheria occur in all seasons, although winter months
favour its spread.
• Mode of transmission – Droplet infection, direct contact
• Portal of entry
• (a) RESPIRATORY ROUTE :
• (b) NON-RESPIRATORY ROUTES : skin where cuts, wounds and
ulcers
• Incubation period - 2 to 6 days
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Clinical features
• 1. Pharyngotonsillar diphtheria :
• Sore throat, difficulty in swallowing, and low grade fever
• Examination of throat show - mild erythema, localized exudate, or a
pseudomembrane.
• Membrane - 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
• palates and the posterior portion of the pharynx.
• In the early stage the pseudo-membrane may be whitish and may wipe
• off easily.
• Then become thick, blue- white to grey- black, and adherent.
• Attempts to remove the membrane result in bleeding
• Patients with severe disease may have marked oedema of the
submandibular area and the anterior portion of the neck, along with
lymphadenopathy, giving a characteristic "bull-necked“ appearance
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Clinical features
• 2. Laryngotracheal diphtheria
• After pharyngotonsillar disease,
• fever, hoarseness and croupy cough, infection extends into
bronchial tree, it is the most severe form of disease .
• Initially it may be clinically indistinguishable from viral croup or
epiglottitis.
• Prostration and dyspnoea - obstruction caused by the
membrane.
• Suffocation if not promptly relieved by intubation or
tracheostomy.
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Clinical features
• 3. Nasal diphtheria,
• the mildest form of respiratory diphtheria, usually is localized to
the septum or turbinates of one side of the nose.
• Occasionally a membrane may extend into the pharynx.
• Non-respiratory mucosa! surface i.e., the conjunctiva and
genitals may also be sites of infection .
• Cutaneous diphtheria is common in tropical areas. It often
appears as a secondary infection of a previous skin abrasion or
infection.
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Clinical features
• The diphtheria bacilli within the membrane continue to produce
toxin actively.
• This is absorbed and results in distant toxic damage, particularly
parenchymatous degeneration, fatty infiltration and necrosis in
heart muscle, liver, kidneys, and adrenals, sometimes
accompanied by gross haemorrhage.
• Irregularities of cardiac rhythm indicate damage to the heart.
Later, there may be difficulties with vision, speech, swallowing,
or movement of the arms or legs.
• The toxin also produces nerve damage, resulting often in
paralysis of the soft palate, eye muscles, or extremities .
• Patients who survive complications recover completely
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CONTROL OF DIPHTHERIA
1. CASES AND CARRIERS
• (a ) Early detection
• (b) Isolation – 14 days
• (c) Treatment :
• (i) CASES : Diphtheria antitoxin should be given without delay, IM or IV, in
doses ranging from 20,000 to 100,000 units, AST - 0.2 ml subcutaneously to
detect sensitization to horse serum.
• For mild early pharyngeal or laryngeal disease the dose is 20,000-40,000
units
• For moderate nasopharyngeal disease, 40,000-60,000 units;
• For severe, extensive or late (3 days or more) disease, 80,000-100,000 units
• penicillin or erythromycin for 5 to 6 days to clear the throat of C.diptheriae
and thereby decrease toxin production.
• (ii) CARRIERS : The carriers should be treated with 10 days course of oral
erythromycin, which is the most effective drug for the treatment of carriers.
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CONTROL OF DIPHTHERIA
• 2. CONTACTS
• Special attention, throat swabbed and their immunity status
determined. :
• (a) where primary immunization or booster dose was received
within the previous 2 years, no further action would be needed
• (b) 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
• (c) nonimmunized close contact should receive prophylactic
penicillin or erythromycin. They should be given 1000- 2000
units of diphtheria antitoxin and actively immunized against
diphtheria.
• Contacts should be placed under: medical surveillance
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CONTROL OF DIPHTHERIA
• 3. COMMUNITY
• Active immunization with diphtheria toxoid of all infants as early
in life as possible, booster doses every 10 years thereafter.
• Immunize before the infant loses his maternally derived
immunity
• Nonimmune individuals are not protected by a high level of
population immunity.
• This implies that immunization rate must be maintained at a
high level.
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DIPHTHERIA IMMUNIZATION
• Current prophylactics
• These may be grouped as below :
• a. Combined or mixed vaccines
• - DPT (diphtheria- pertussis-tetanus vaccine)
• - DTPw (diphtheria, tetanus, whole-cell pertussis)
• - DTPa (diphtheria, tetanus, acellular pertussis)
• - OT (diphtheria-tetanus toxoid)
• - dT (diphtheria-tetanus, adult type)
• - Pentavalent (diphtheria, tetanus, pertussis,
• hepatitis Band Hib).
• b. Single vaccines
• - FT (formal-toxoid)
• - APT (alum-precipitated toxoid)
• - PTAP (purified toxoid aluminium phosphate)
• - PTAH (purified toxoid aluminium hydroxide)
• - TAF (toxoid- antitoxin flocculus)
• c. Antisera
• - Diphtheria antitoxin
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• c. ANTISERA
• Diphtheria antitoxin prepared in horse serum is still the mainstay
of passive prophylaxis and also for treatment of diphtheria.
• It has been shown, protection against diphtheria toxin is a
• quantitative phenomenon, so that a serum antitoxin titre
• that protects against a small dose of toxin may not protect
• against a large dose: for this reason, failures of diphtheria
• immunization may take place
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