PE31.11 | Diphtheria Pertussis Tetanus — Summary & Reflection

KEY TAKEAWAYS

DPT infections at a glance:

• Diphtheria (C. diphtheriae): grayish adherent pseudomembrane beyond tonsillar pillars + bull-neck; toxin blocks protein synthesis (ADP-ribosylates EF-2); treatment = antitoxin FIRST (do NOT wait for cultures) + procaine penicillin G 14 days; complications = myocarditis (1–2 weeks), palatal/motor neuropathy (weeks–months), airway obstruction

• Pertussis (B. pertussis): catarrhal → paroxysmal (whoop or apnoea in infants) → convalescent; pertussis toxin causes lymphocytosis; treatment = azithromycin 10 mg/kg/day × 5 days; infants <6 months must be admitted (apnoea risk)

• Tetanus (C. tetani): trismus → risus sardonicus → opisthotonus; tetanospasmin blocks glycine/GABA → unopposed motor firing; treatment = wound debridement + TIG 3,000–10,000 IU IM + metronidazole + diazepam for spasms; neonatal tetanus = home delivery + contaminated cord + non-immunised mother

• Prevention: pentavalent (DPT+HepB+Hib) at 6/10/14 weeks; DPT booster at 16–24 months and 5–6 years; TT in pregnancy for neonatal tetanus prevention

• Key principle: antitoxin neutralises only FREE toxin — give early; toxin already bound to tissue cannot be reversed

REFLECT

Consider the concept of vaccine hesitancy in your community: all three diseases in this module are preventable with complete vaccination, yet they continue to occur. Reflect on a situation where a parent might refuse vaccination for their child. What arguments would you use to explain the real clinical consequences of diphtheria, pertussis, or tetanus? How does understanding the specific toxin mechanism — for example, that tetanus toxin causes spasms by blocking inhibitory neurotransmitters in an aware patient — help you convey the severity of the disease more effectively to a family?