Question
A 10 years old boy was admitted in pediatric ward with history of fever, toxaemia and on examination. A white patch seen of fauces which bleeds on removal. He was not immunized properly. Answer the following:
- (a) Explain the probable diagnosis and name the causative agent 2 mark(s)
- (b) Describe the laboratory diagnosis mentioning the methods of sample collection 4 mark(s)
- (c) What are the complications of the disease 1 mark(s)
- (d) How is the disease treated 1 mark(s)
- (e) Describe the method of prophylaxis briefly 2 mark(s)
Answer
a) Probable diagnosis and causative agent Diphtheria — fever, toxaemia, and a grey-white pseudomembrane over the fauces/tonsils that bleeds on attempted removal (adherent, unlike simple exudate) in an inadequately immunized child is the classical picture. Causative agent: Corynebacterium diphtheriae (toxigenic strain).
b) Laboratory diagnosis and sample collection
- Sample collection: swab taken from beneath the edge of the pseudomembrane (not the membrane surface itself, which is largely necrotic) using two swabs — one for direct smear, one for culture — collected before starting antibiotics wherever possible.
- Direct microscopy: Gram stain (Gram-positive club-shaped bacilli in Chinese-letter/palisade arrangement) and Albert’s or Neisser’s stain to demonstrate metachromatic (volutin) granules — a rapid presumptive diagnostic clue.
- Culture: on Loeffler’s serum slope (enrichment, promotes rapid growth and granule formation within 6–8 hours) and tellurite blood agar/media (selective, C. diphtheriae reduces tellurite to give black/grey colonies, differentiating biotypes gravis/intermedius/mitis by colony morphology).
- Toxigenicity testing: Elek’s gel precipitation test — confirms whether the isolated strain actually produces diphtheria exotoxin (only toxigenic strains cause the classical disease); in-vivo guinea pig toxin test is an older alternative.
- PCR for the toxin gene (tox) is available in reference laboratories.
c) Complications Toxin-mediated: myocarditis (most serious, often fatal), peripheral neuropathy/paralysis (palatal palsy, later limb paralysis); mechanical: laryngeal obstruction/suffocation from a downward-extending membrane (“diphtheritic croup”).
d) Treatment Diphtheria antitoxin (DAT), given promptly on clinical suspicion (before laboratory confirmation, since antitoxin neutralizes only free, not cell-bound, toxin) together with antibiotics (penicillin or erythromycin) to eliminate the organism and halt further toxin production; strict bed rest to reduce risk of myocarditis; supportive airway management (tracheostomy if needed for laryngeal obstruction).
e) Prophylaxis Active immunization with diphtheria toxoid (part of the DPT schedule — 3 primary doses in infancy with booster doses at 18 months, 5 years, and 10 years); contact tracing with throat swab culture and chemoprophylaxis (erythromycin) for close contacts; isolation of cases until non-infectious (culture-negative).