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PRESENTED BY-SUBRATA DAS

DIPHTHERIA PATHOGENESIS ,DIAGNOSIS

&TREATMANT

Corynebacterium diphtheriae

• Aerobic, , Gram+ rods, Non capsulated, non- motlie• Gray-black colonies on telluride agar medium• Chinese-letter morphology with metachromatic

granules

Chinese-letter morphology in albert stain

• Toxigenic or non toxigenic (lysogenic conversion; infected by Beta phage)

Biological Features

• solely among humans• specially in children• spread by droplets• secretions • direct contact

• Poor nutrition• Crowded or unsanitary

living conditions• Low vaccine coverage

among infants and children• Immunity gaps in adults

• Incubation period -2 to 10

Pathogenesis of diphtheria

Transmission & risk factors

Pathogenesis of diphtheriaincludes two distinct phenomena:1. Invasion of the local tissues of the throat, which requires colonization and proliferation

2. Toxigenesis: bacterial production of the toxin. The diphtheria toxin causes the death eukaryotic cells and tissues by inhibition protein synthesis in the cells. The toxin is responsible for the lethal symptoms of the disease.

Mechanism of action

Diphtheria Toxin • Component :A/B fragment, joined

by S-S bond - A (catalytic domain)

- B (transmembrane and receptor binding domains) • Receptor: heparin-binding

epidermal growth factor - rich on cardiac cells and nerve cells

• Toxin diffuses throughout body via blood - Cardiac, neurologic complications - Heart/respiratory damage, paralysis

Pathogenesis of diphtheria

Diphtheria Clinical Features• Early stages: Sore throat. Low fever. Swollen neck

glands.• May involve any mucous membrane• Late stages: Airway obstruction and breathing difficulty.

Shock• Toxin causing myocarditis, polyneuritis, renal tubular

necrosis and other systemic toxic effects.

• Classified based on site of infectionanterior nasalpharyngeal and tonsillarlaryngealcutaneousoculargenital

Pharyngeal and Tonsillar Diphtheria• Exudate spreads within 2-3 days and may form “wash

leather” elevated grayish- green membrane on the tonsil with inflammation

• Removal leads to bleeding edematous submucosa• Insidious onset of exudative pharyngitis• Membrane may cause respiratory obstruction & aspiration of

the membrane• Fever usually not high but patient appears toxic• Lymphadenopathy with Bull neck appearance in severe cases

Diagnosis• Clinical: • Muscle weakness, neck rigidity• edema • a pseudomembranous material in the upper

respiratory tract characterizes• Laboratory: • Culture in the tellurite agar /loeffler’s serum• Demonstration of the organism by the albert or

methyl-blue stain

Methods of Control:

A. Preventive measures: 1. Vaccination 2. Public education3. Others

B:Control of patients, contacts and environment:

C. Epidemic Measures:4. Prompt reporting5. IG for outbreaks6. Priorities if short of vaccine

Treatment & Management

Management of a emergency case

1. DAT and antibiotics(Penicillin G/Roxithromycin) to be started immediately without waiting for lab results.

2. Rest and observation, to cover the period of potential cardiac damage and paralysis

3. Avoid limbs deformity , ensure joint mobility.

4. Tracheostomy and artificial respiration

5. Isolation : Strict for pharyn. dipth. Contact isolation for cutaneous dipth

Control and Prevention

Triple Antigen DPaT.

Preventive Measures: 1- Active immunizatn. with diph. toxoid, including an

adequate program to maintain immunity

Routine DTaP Primary Vaccination ScheduleDosePrimary 1Primary 2Primary 3Primary 4

Age2 months4 months6 months15-18 months

Interval ---4 wks.4 wks.6 months

Active protection should be maintained by administering a dose of “Td every 10 yrs.” thereafter, (esp. for persons who are at higher risk to pt. exposure e.g. health workers

Educational measures:

To inform the public and esp. parents of young children of the hazards of diphtheria and the imp. of immunization.

Control and Prevention

Thank you

QUESTIONS?