Jawetz Microbiology Mcq May 2026

A) HSV-1 – trigeminal ganglia – sunlight/UV B) VZV – dorsal root ganglia – emotional stress C) EBV – B lymphocytes – plasmapheresis D) CMV – salivary gland endothelial cells – trauma E) HHV-6 – microglia – rituximab therapy Answer: A – HSV-1 reactivation is classically triggered by UV light, fever, stress. VZV reactivation (shingles) often has no clear trigger but can be stress/age-related; sunlight is not classic. EBV latency in B cells; reactivation more with immunosuppression. CMV latency in monocytes; plasmapheresis not a trigger. HHV-6 in microglia; reactivation post-transplant, not rituximab specifically. 8. Spirochetes – Diagnostic Pitfall A patient with a painless genital ulcer and inguinal lymphadenopathy has a darkfield microscopy positive for spirochetes. However, the RPR is negative. Which of the following best explains this seronegative primary syphilis?

A) Flucytosine – inhibits thymidylate synthase B) Amphotericin B – binds ergosterol C) Caspofungin – inhibits β-(1,3)-D-glucan synthase D) Voriconazole – inhibits lanosterol 14α-demethylase E) Terbinafine – inhibits squalene epoxidase Answer: C – The description matches Aspergillus fumigatus (galactomannan +, green colony with red reverse). Echinocandins (caspofungin) target β-glucan, which is abundant in Aspergillus cell wall. Although voriconazole is drug of choice for invasive aspergillosis, the question asks for mechanism “specifically suited” to a unique cell wall component – β-glucan is more specific to fungal cell wall (not in human cells). Amphotericin B (B) targets ergosterol but also binds cholesterol, less specific. 6. Parasitology – Relapse Mechanism A returned traveler from Southeast Asia had 3 days of fever, chills, and sweats every 48 hours, now asymptomatic without treatment. Six months later, he develops identical symptoms. Which structure of Plasmodium vivax is responsible for this pattern, and what is its unique metabolic feature? jawetz microbiology mcq

A) Eikenella corrodens + Staphylococcus aureus – beta-lactamase protects both B) Fusobacterium nucleatum + Streptococcus anginosus – succinic acid and short-chain fatty acids inhibit phagocyte function C) Prevotella melaninogenica + Peptostreptococcus – hyaluronidase and collagenase D) Capnocytophaga + Streptococcus mitis – endotoxin synergy E) Bacteroides fragilis + Enterococcus faecalis – capsule and superoxide dismutase Answer: B – Fusobacterium + Streptococcus (especially S. anginosus group) is classic synergistic necrotizing infection (e.g., Lemierre’s, human bite). Fusobacterium produces succinic acid and short-chain fatty acids that impair neutrophil killing. Eikenella (A) is slow-growing, not typically rapid necrosis. B. fragilis + Enterococcus seen in intra-abdominal but not rapid 24h necrosis from human bite. A) HSV-1 – trigeminal ganglia – sunlight/UV B)