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Transcript
Diphtheria
Dr. S.M.Zahraei
Center for Communicable Diseases Control
Revised May 2009
Diphtheria
 Greek diphthera (leather hide)
 Caused by Aerobic Gram +ve rods
 Cornyebacterium diphtheriae
 Exotoxin production only if infected by
virus phage infected carrying toxin
gene
Gram +ve Bacilli and Colonies
Diphtheria Epidemiology
 Reservoir
Human carriers
Usually asymptomatic
 Transmission
Respiratory
Skin and fomites rarely
 Temporal pattern
Winter and spring
 Communicability
Up to several weeks
without antibiotics
Corynebacterium diphtheriae
 Aerobic gram-positive bacillus
 Toxin production occurs only
when C. diphtheriae infected by virus
(phage) carrying tox gene
 If isolated, must be distinguished from
normal diphtheroid
 Toxoid developed in 1920s
Pharyngeal and Tonsillar Diphtheria
 Insidious onset
 Exudate spreads within 2-3 days and may
form adherent membrane
 Membrane may cause respiratory
obstruction
 Pseudomembrane: fibrin, bacteria, and
inflammatory cells, no lipid
 Fever usually not high but patient appears
toxic
Diphtheria Clinical Features
 Incubation period 2-5 days
(range, 1-10 days)
 May involve any mucous membrane
 Classified based on site of infection
 anterior
nasal
 pharyngeal and tonsillar
 laryngeal
 cutaneous
 ocular
 genital
Thick Membrane
Pseudo membrane
‘Bull Neck’
Skin Lesions
Diphtheria Complications
 Mostly attributable to toxin
 Severity generally related to extent of
local disease
 Most common complications are
myocarditis and toxic neuritis with palsy
 Death occurs in 5%-10% for respiratory
disease
Diphtheria Antitoxin (DAT)
 Produced in horses
 First used in the U.S. in 1891
 Used only for treatment of diphtheria
 Neutralizes only unbound toxin