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DR8.1-5 | Common Viral Infections — Graded Quiz
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A 35-year-old immunocompetent woman presents with grouped vesicles on an erythematous base at the right angle of the mouth, recurring every 6–8 weeks. She reports a tingling sensation 12–24 hours before each episode. A Tzanck smear shows multinucleate giant cells. Which additional investigation would DEFINITIVELY distinguish HSV-1 from HSV-2 as the causative agent?
Correct. PCR using type-specific primers is the gold standard — it can type HSV-1 vs HSV-2 from vesicle fluid with high sensitivity and specificity. The Tzanck smear confirms herpesviruses collectively but cannot type them. Serum IgM is non-specific and cannot type. Viral culture CPE morphology also cannot reliably distinguish subtypes.
Tzanck smear detects herpesvirus cytopathic effect (multinucleate giant cells) but does not distinguish HSV-1 from HSV-2. Type-specific PCR of vesicle fluid is the gold standard for viral typing. Serum IgM cannot type the virus; viral culture morphology does not distinguish subtypes.
Only type-specific PCR can definitively distinguish HSV-1 from HSV-2. The Tzanck smear is genus-level (herpesvirus), not species-specific. Serum IgM is neither sensitive nor specific for typing. Viral culture CPE does not distinguish the two types.
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A 65-year-old diabetic man presents with a 5-day history of severe burning pain over the right side of his chest, followed 2 days ago by a band of grouped vesicles. He is not on any antiviral. He asks whether treatment can still help. The MOST accurate response is:
Correct. While early treatment (within 72 hours) is optimal, current guidelines recommend initiating systemic antivirals beyond 72 hours in high-risk groups — including the elderly, diabetics, those with ophthalmic involvement, and those still forming new vesicles. Topical therapy is insufficient.
The 72-hour window maximises antiviral benefit for zoster, but treatment is still indicated beyond 72 hours in high-risk patients (elderly, diabetic, ophthalmic zoster, severe disease, immunocompromised, new vesicle formation). Topical treatment alone is inadequate for zoster.
The 72-hour rule is the optimum window, not an absolute cut-off. In high-risk patients (elderly, diabetic, active lesions), systemic antivirals are still given beyond 72 hours. Topical aciclovir is inadequate for treating dermatomal zoster.
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An 8-year-old girl with acute leukaemia develops a generalised vesicular rash after exposure to a classmate with chickenpox. Her parents note that the lesions appeared very rapidly and are spreading to involve the palms. Which of the following management decisions is MOST appropriate?
Correct. Varicella in an immunocompromised patient is a medical emergency. IV aciclovir (not oral) is required because oral absorption may be unreliable and the risk of disseminated infection, pneumonitis, encephalitis, and hepatitis is high. Watchful waiting and oral-only therapy are inappropriate.
Varicella in an immunocompromised child (e.g., acute leukaemia) is life-threatening due to risk of visceral dissemination (pneumonitis, encephalitis, hepatitis). Intravenous aciclovir, not oral, is required. Oseltamivir has no activity against VZV.
Immunocompromised varicella requires IV aciclovir as an emergency measure — oral dosing is insufficient because of unreliable absorption and the severity risk. Oseltamivir targets influenza neuraminidase and has no activity against VZV.
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A 40-year-old man presents with multiple filiform warts on his beard area. He also has flat-topped brownish papules in a linear arrangement on his right forearm that appeared after a scratch. The linear arrangement of the flat papules best illustrates which phenomenon?
Correct. Plane warts frequently Köbnerise — new warts develop in the wake of scratching, producing linear arrays. This is the isomorphic (Köbner) phenomenon seen also in psoriasis and lichen planus at sites of trauma.
Plane warts and viral warts in general can spread linearly along scratch lines — this is the Köbner (isomorphic) phenomenon: new lesions appearing at sites of trauma or scratching. Blaschko's lines represent mosaic genetic patterns; dermatographism is urticarial whealing; pathergy is seen in Behçet's disease.
Linear warts following a scratch track = Köbner (isomorphic) phenomenon. Dermatographism is urticarial whealing after skin stroking (mast cell release). Blaschko's lines reflect embryonal cell migration patterns for mosaic disorders, not injury-induced wart spread. Pathergy is exaggerated pustular or ulcerative response to minor trauma seen in Behçet's disease.
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A 28-year-old HIV-positive man with a CD4 count of 80 cells/µL presents with extensive molluscum contagiosum — over 100 lesions covering his face and trunk, some lesions exceeding 1 cm. His antiretroviral therapy (ART) was stopped 6 months ago. The MOST important intervention is:
Correct. Giant or profuse molluscum is a cutaneous marker of severe immunosuppression (CD4 <200, often <100). The cornerstone of management is restoring immune function with effective ART. Physical treatments offer temporary clearance but cannot control recurrence without immune reconstitution. MCV is a poxvirus; aciclovir has no activity against poxviruses.
Extensive molluscum in an immunocompromised patient signals severe immunosuppression. The single most important intervention is immune reconstitution via effective ART. MCV is a poxvirus — not a herpesvirus — and aciclovir has no activity against it. Physical treatments (cryotherapy, curettage) alone are inadequate for hundreds of lesions when immune function is not restored.
Extensive molluscum in an HIV patient = immune failure marker → restart ART. Cryotherapy alone to 100+ lesions is impractical and will not prevent recurrence. Imiquimod may be used as adjunct but cannot substitute for immune reconstitution. Aciclovir targets herpesviruses (HSV/VZV) — MCV is a poxvirus and is NOT susceptible to aciclovir.
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A 25-year-old man presents with a single painless papule on the shaft of the penis. Examination shows a 3 mm dome-shaped pearly papule with a central dimple. A second lesion is present on his lower abdomen. He is sexually active. The correct interpretation is:
Correct. The central umbilication on a pearly dome-shaped papule = molluscum. In a sexually active adult with anogenital lesions, molluscum is transmitted sexually and is classified as an STI. Genital warts (condyloma acuminata) are cauliflower-surfaced without umbilication. HSV causes vesicles/ulcers. Syphilitic chancre is a painless indurated ulcer, not a dome-shaped papule.
Molluscum contagiosum in the anogenital region of a sexually active adult is classified as an STI. It must be distinguished from genital warts (condyloma acuminata — rough, cauliflower-surfaced, lack central dimple) and from primary HSV (vesicles, tender) and syphilis (indurated, non-tender ulcer).
The central umbilication is the diagnostic key. Condyloma acuminata are rough, cauliflower-like, and lack the central dimple. HSV lesions are vesicular-ulcerative and painful. Syphilitic chancre is a clean-based indurated ulcer. The clinical context (sexually active, anogenital site) classifies this molluscum as an STI.
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A medical student is reviewing a case of herpes zoster in an elderly patient and notes that the rash is on the left V1 dermatome (periorbital and nasal tip). The correct clinical concern and priority action is:
Correct. Hutchinson's sign — vesicles on the tip or side of the nose in V1 zoster — indicates nasociliary nerve involvement, which is the same branch that innervates the eye. This predicts a high risk of herpes zoster ophthalmicus with corneal, iris, and posterior segment complications. Urgent ophthalmology referral and systemic antivirals are mandatory.
Herpes zoster ophthalmicus (V1 involvement) with Hutchinson's sign (lesion on nasal tip = nasociliary branch) has a high risk of ocular complications including keratitis, uveitis, and visual loss. Urgent ophthalmology review and systemic IV/oral aciclovir are required — do not delay for investigation.
V1 zoster is NOT mild — it carries significant risk of sight-threatening ocular complications (keratitis, uveitis, retinitis). Hutchinson's sign (nasal tip lesion) = nasociliary involvement = high eye risk. Topical steroids are contraindicated. Do not delay referral for Tzanck confirmation — the clinical picture mandates immediate action.
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You are comparing the pathogenesis of viral warts (HPV) and molluscum contagiosum (MCV). Which statement CORRECTLY differentiates them?
Correct. HPV (papillomavirus) replicates in the nucleus and uses E6/E7 proteins to stimulate keratinocyte proliferation; koilocytes are its histological marker. MCV (poxvirus) replicates entirely in the cytoplasm, producing Henderson-Paterson bodies; it does not integrate, does not establish neural latency, and does not produce koilocytes.
HPV integrates episomally and drives keratinocyte proliferation via E6/E7 oncoproteins. MCV is a poxvirus that replicates in the cytoplasm, does not integrate or establish neural latency, and produces Henderson-Paterson (molluscum) bodies. Koilocytes are HPV's histological hallmark; multinucleate giant cells belong to herpesviruses.
Neural latency (ganglion reservoir + reactivation) is a herpesvirus feature — neither HPV nor MCV establishes it. MCV replicates in the cytoplasm (not the nucleus); multinucleate giant cells are from herpesviruses. Henderson-Paterson bodies = MCV (poxvirus); koilocytes = HPV.
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A 14-year-old girl presents with 12 flat, smooth, slightly brownish papules distributed in a linear streak along the forearm, appearing 2 weeks after she scratched the area. Which wart type does this represent, and what is the underlying HPV type group?
Correct. Plane warts are caused by HPV types 3 and 10. They are flat-topped, smooth, and minimally keratinised, and frequently Köbnerise along scratch tracks. HPV 1/2 cause plantar and common warts; HPV 6/11 cause anogenital condylomata; HPV 16/18 are high-risk oncogenic types.
Flat-topped, smooth, minimally keratinised papules in a linear Köbner pattern on a teenager's forearm = plane warts (verruca plana), caused predominantly by HPV 3 and 10. HPV 6/11 = condylomata acuminata; HPV 16/18 = high-risk oncogenic types; HPV 1/2 = plantar/common warts.
The flat-topped, smooth, linearly arranged lesions on the forearm in a teenager = plane warts. Plane warts are caused by HPV 3/10. HPV 6/11 → anogenital warts; HPV 16/18 → high-risk (oncogenic); HPV 1/2 → plantar/common warts.
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Comparing varicella (chickenpox) and smallpox (variola) — a distinction historically critical and still examined — which feature DEFINITIVELY separates varicella from smallpox?
Correct. The key distinctions: VZV (herpesvirus) vs variola (poxvirus); polymorphic rash (multiple stages simultaneously, centripetal) in varicella vs monomorphic rash (all same stage, centrifugal, includes palms/soles) in smallpox. These differences are the basis of the classic distinction taught for outbreak recognition.
The two defining features distinguishing varicella from smallpox: (1) causative virus — VZV (herpesvirus) vs variola (poxvirus); (2) rash morphology — varicella is polymorphic (all stages simultaneously) with centripetal distribution; smallpox is monomorphic (all lesions in same stage) with centrifugal distribution including palms/soles.
Smallpox is a poxvirus (not herpesvirus). Its rash is monomorphic (all same stage) with centrifugal distribution including palms/soles. Varicella rash is polymorphic (multiple stages) with centripetal distribution (sparing palms/soles). Options C and D have the distributions reversed.
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