A 3-year-old boy with no prior vaccinations presents to the emergency department with a 4-day history of sore throat, low-grade fever (38.5°C), and progressive barking cough with inspiratory stridor. Vital signs are HR 108/min, RR 26/min, BP 96/58 mmHg, SpO2 99% on room air. Physical examination reveals pharyngeal erythema and cervical lymphadenopathy. Direct laryngoscopy shows a gray-white adherent membrane overlying the vocal cords and trachea. Culture on Loeffler's medium yields a gram-positive rod. The child is empirically started on erythromycin and diphtheria antitoxin. Over the following 2 weeks, despite clinical recovery from the respiratory infection, the child develops progressive lower extremity weakness and loss of deep tendon reflexes. Which of the following best explains the mechanism of this late neurological complication?
- A)ADP-ribosylation of inhibitory G proteins in autonomic nerve terminals
- B)Inactivation of the 60S ribosomal subunit through depurination of ribosomal RNA
- C)Inhibition of elongation factor 2, resulting in cessation of protein synthesisGABARITO
- D)Cleavage of SNARE proteins required for acetylcholine release at the neuromuscular junction
- E)Direct bacterial invasion of the peripheral nervous system with secondary demyelination
Explicação
Diphtheria toxin irreversibly inhibits elongation factor 2 (EF-2) through ADP-ribosylation, preventing ribosomal translocation during protein synthesis. While the pseudomembrane and respiratory symptoms represent local infection, the systemic manifestations—pa... Ver explicação completa e trilha adaptativa →