Corynebacteria Diphtheriae

Causes diphtheria

Characteristics/Epidemiology

Found in throat and nasopharynx of carriers and patients.

Spready by respiratory droplets, less commonly by direct contact or contaminated fomite.

Antigenic
Inhibits eukaryotic protein synthesis
Make up for 2 fragments A and B
-> Fragment B binds to certain cell receptors (identical to receptors for heparin-binding epidermal growth factor)
-> The binding causes endocytosis
-> Fragment A then dissociates and inactivate polypeptide chain elongation factor (EF-2) (with the help of NAD+)
-> Stops protein synthesis
Toxin (tox) is encoded in beta phage. Only strains containing the beta phage is virulent.
(Beta phage's DNA is carried within the the bacterial DNA, i.e. prophage in lysogenic bacteria)

Infection produces thick, grayish, adherent exudate (pseudomembrane) in the throat.

Generally the infection is local, in the throat, and may extend up to the nose or down into the bronchus -> may cause obstruction.
Later may have systemic symptom due to toxin absorption
heart and peripheral nerves most affected
* Heart: myocarditis, conduction defects
* Nerve: neuritis of CNs, and muscle group paralysis

Colonisation and exotoxin production may (but rarely) cause tissue degneneration and death.

Corynebacterium can be isolated with selective medium (e.g. Tinsdale's agar - contains potassium tellurite)

Diagnosis is clinical. No fast, reliable lab test is available.

Definitive diagnosis requires culture and tested for virulence.

Prompt neutralisation of toxin, then eradication of organism.

First treat with horse serum antitoxin first, then antibiotics.

First line: Erythromycin

Second line: Penicillin G

Formalin treatment of the toxin produces a toxoid - same antigenicity but not toxicity -> thus used to immunisation

Prevention - by immunisation (usually with tetanus toxoid and pertussis antigen i.e. DTPa)

Booster injection - every 10 years.

Things to revise/add later:

Bibliography: LWW microbiology

About
Created	20040330