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    Subjects/Microbiology/Lassa Fever Sensorineural Hearing Loss
    Lassa Fever Sensorineural Hearing Loss
    medium
    bug Microbiology

    A 28-year-old man from Sierra Leone presents to a tertiary care centre in India with a 3-week history of fever, pharyngitis with exudate, and myalgia. He was treated supportively and recovered clinically. However, 6 weeks later, he returns with complaints of progressive hearing difficulty bilaterally. Pure-tone audiometry reveals the pattern marked **A** in the diagram — bilateral severe sensorineural hearing loss across all frequencies. Which of the following best explains the pathogenesis of hearing loss in this clinical context?

    A. Ototoxicity from ribavirin therapy administered during the acute infection phase
    B. Immune-mediated inner-ear injury from cytotoxic T-cell response and immune-complex deposition, independent of acute disease severity
    C. Direct viral cytopathic destruction of cochlear hair cells during the acute viraemic phase
    D. Secondary bacterial infection of the middle ear causing ossicular fixation and conductive loss

    Explanation

    Why option 1 is correct

    The bilateral severe sensorineural hearing loss marked A in Lassa fever survivors is a distinctive late complication occurring in 25–33% of survivors, developing during convalescence or months post-recovery. The pathogenesis is immune-mediated rather than direct viral cytopathic effect. Histopathology shows minimal viral antigen in the cochlea but prominent lymphocytic infiltrate, supporting cytotoxic T-cell response and immune-complex deposition as the mechanism of inner-ear injury. Critically, this hearing loss is independent of acute disease severity — it can occur after mild or asymptomatic infection — and is independent of treatment (not prevented by ribavirin). The clinical presentation (recovered from acute illness, then develops bilateral SNHL weeks later) is pathognomonic for Lassa fever in an endemic-area returnee (WHO Lassa Fever Guidelines 2024; Harrison's 21st ed.).

    Why each distractor is wrong

    • Option 2: Direct viral cytopathic destruction would cause hearing loss during the acute viraemic phase, not weeks to months after clinical recovery. Histopathology of Lassa SNHL shows minimal viral antigen in the cochlea, ruling out direct cytopathic injury as the primary mechanism.
    • Option 3: Ribavirin is not ototoxic and does not cause SNHL. Moreover, ribavirin does not prevent or modify the course of Lassa-associated hearing loss; the loss occurs independently of whether ribavirin was given or not.
    • Option 4: The audiometric pattern A shows sensorineural (not conductive) loss across all frequencies. Conductive loss and ossicular fixation would produce a different audiometric pattern (air-bone gap) and would not explain the bilateral, severe, high-frequency-sparing pattern typical of immune-mediated cochlear injury.
    High-YieldNEET PG
    Lassa fever SNHL is a late, immune-mediated complication in 25–33% of survivors, independent of disease severity and treatment, with no specific cure — only hearing aids or cochlear implants for severe loss.

    WHO Lassa Fever Guidelines 2024; Harrison's Principles of Internal Medicine, 21st ed.

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