Kaposi varicelliform eruption: an unusual presentation caused by varicella zoster virus in a healthy adult patient - a case report.

BACKGROUND: Kaposi Varicelliform Eruptions (KVE), also known as eczema herpeticum, is a rare and potentially life-threatening dermatological condition primarily attributed to herpes simplex virus (HSV) infection, with less frequent involvement of Coxsackie A16, vaccinia, Varicella Zoster, and smallpox viruses. Typically associated with pre-existing skin diseases, especially atopic dermatitis, KVE predominantly affects children but can manifest in healthy adults. Characterized by painful clusters of vesicles and sores on the skin and mucous membranes, it often masquerades as other dermatological disorders. Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for pain relief and inflammation, though their potential role as KVE triggers remains uncertain. CASE REPORT: Here, we present a case of an 18-year-old female with KVE attributed to Varicella Zoster virus (VZV) and successfully treated with oral acyclovir within a week, underscoring the significance of early recognition and intervention. KVE can manifest with systemic symptoms like fever, fatigue, and lymphadenopathy and may involve multiple organ systems, necessitating possible antibiotic use for complications. CONCLUSION: This case underscores the importance of prompt KVE identification and consideration of antiviral therapy to enhance patient outcomes. Further research is warranted to elucidate predisposing factors for this rare condition.

T helper 1 effector memory CD4+ T cells protect the skin from poxvirus infection.

Poxvirus infections of the skin are a recent emerging public health concern, yet the mechanisms that mediate protective immunity against these viral infections remain largely unknown. Here, we show that T helper 1 (Th1) memory CD4+ T cells are necessary and sufficient to provide complete and broad protection against poxvirus skin infections, whereas memory CD8+ T cells are dispensable. Core 2 O-glycan-synthesizing Th1 effector memory CD4+ T cells rapidly infiltrate the poxvirus-infected skin microenvironment and produce interferon γ (IFNγ) in an antigen-dependent manner, causing global changes in gene expression to promote anti-viral immunity. Keratinocytes express IFN-stimulated genes, upregulate both major histocompatibility complex (MHC) class I and MHC class II antigen presentation in an IFNγ-dependent manner, and require IFNγ receptor (IFNγR) signaling and MHC class II expression for memory CD4+ T cells to protect the skin from poxvirus infection. Thus, Th1 effector memory CD4+ T cells exhibit potent anti-viral activity within the skin, and keratinocytes are the key targets of IFNγ necessary for preventing poxvirus infection of the epidermis.

Is molluscum contagiosum related to zinc deficiency in children? Effectiveness of oral zinc sulfate therapy in lesion regression.

OBJECTIVES: Molluscum contagiosum (MC) is viral skin infection that is most commonly observed in children. Zinc homeostasis is essential for proper immune function, especially in host-virus interactions. This study aimed to investigate the effectiveness of oral zinc sulfate treatment in children with MC. METHODS: The subjects included 23 children with MC and 30 age/sex-matched healthy children as controls. Children with MC received oral zinc sulfate for 2 mo, and serum zinc levels were measured before and after the treatment period. Patients were examined every 4 wk for evidence of partial or complete lesion regression. Lesion numbers were recorded before treatment and during follow up. RESULTS: The mean serum zinc levels in children with MC did not differ from those in controls (80.57 ± 10.14 vs 81.90 ± 8.47 µg/dL, respectively, P = 0.370). After zinc sulfate supplementation, the mean serum zinc levels increased from 80.57 ± 10.14 to 100.5 ± 9.95 µg/dL (P < 0.001) in subjects with MC. After a 2-mo treatment period, six subjects exhibited resolution of lesions at the 1-mo follow up, 10 subjects at the 2-mo follow-up, and three subjects at the 3-mo follow up. Disease recurrence was not observed. A 6-y-old boy and two 4-y-old girls without other systemic symptoms had MC lesions that persisted after zinc sulfate therapy and throughout the 1-y follow up. One female subject experienced complete recovery in after treatment month 4, but recurrence was observed in month 7 and persisted for 18 mo. CONCLUSIONS: Our findings support the use of oral zinc sulfate as a therapy for children with MC.