Development of sacral/buttock retiform purpura as an ominous presenting sign of COVID-19 and clinical and histopathologic evolution during severe disease course.

Retiform purpura has been described as a relatively frequent cutaneous finding in patients with coronavirus disease 2019 (COVID-19). The etiology is hypothesized to be related to thrombotic vasculopathy based on lesional biopsy specimen findings, but the pathogenesis of the vasculopathy is not completely understood. Here, we present a case of a retiform purpuric patch on the sacrum/buttocks in a hospitalized patient prior to subsequent diagnosis of COVID-19 and an eventual fatal disease course. Two lesional biopsy specimens at different time points in the disease course revealed thrombotic vasculopathy, despite therapeutic anticoagulation. Detailed histopathologic evaluation using immunohistochemical markers suggest the etiology of the vasculopathy involves both persistent complement activation and platelet aggregation, which possibly promote ongoing thrombus formation. This case highlights that sacral/buttock retiform purpuric patches may be a presenting sign of infection with SARS-CoV-2 virus and may represent an ominous sign supporting a future severe disease course. In addition, biopsy specimen findings at separate time points demonstrate that cutaneous vasculopathy may persist despite adequate systemic anticoagulation, possibly due to the combination of persistent complement and platelet activation. Finally, occlusive thrombi in sacral/buttock retiform purpuric patches may contribute to future ulceration and significant cutaneous morbidity in patients who survive COVID-19.

Characterization of human papillomavirus type 154 and tissue tropism of gammapapillomaviruses.

The novel human papillomavirus type 154 (HPV154) was characterized from a wart on the crena ani of a three-year-old boy. It was previously designated as the putative HPV type FADI3 by sequencing of a subgenomic FAP amplicon. We obtained the complete genome by combined methods including rolling circle amplification (RCA), genome walking through an adapted method for detection of integrated papillomavirus sequences by ligation-mediated PCR (DIPS-PCR), long-range PCR, and finally by cloning of four overlapping amplicons. Phylogenetically, the HPV154 genome clustered together with members of the proposed species Gammapapillomavirus 11, and demonstrated the highest identity in L1 to HPV136 (68.6%). The HPV154 was detected in 3% (2/62) of forehead skin swabs from healthy children. In addition, the different detection sites of 62 gammapapillomaviruses were summarized in order to analyze their tissue tropism. Several of these HPV types have been detected from multiple sources such as skin, oral, nasal, and genital sites, suggesting that the gammapapillomaviruses are generalists with a broader tissue tropism than previously appreciated. The study expands current knowledge concerning genetic diversity and tropism among HPV types in the rapidly growing gammapapillomavirus genus.

Disseminated herpes simplex infection in a HIV+ patient.

UNLABELLED: Genital herpes, a viral infection caused by Herpes simplex virus (HSV), is the most common cause of genital ulceration. Patients with a severe decrease in cellular immunity, such as patients positive for Human immunodeficiency virus (HIV) infection, are more likely to develop atypical, severe, disseminated and/or chronic HSV infections. On the other hand, there is an increase incidence of HIV detection among patients positive for HSV infection, as genital ulcers represent a potential portal of entry of HIV into the host. A case of a 52-year-old homosexual man with a two-month history of multiple erythematous ulcerative lesions on the perianal area, the buttocks, and the third left finger is presented. According to the clinical history, the clinical findings and the laboratory results, a diagnosis of HSV infection was made and treatment with valaciclovir was started, which led to complete regression of lesions 30 days later. The atypical features of the herpetic lesions, along with a past history of atypical pneumonitis one year prior to our observation, prompted to a diagnosis of concurrent HIV infection, later confirmed by laboratory RESULTS: Atypical and disseminated HSV infections occur relatively often in HIV+ patients. This article discusses clinical presentation, diagnosis and management of HSV infection in such cases.

Isolation of herpes simplex virus from the genital tract during symptomatic recurrence on the buttocks.

OBJECTIVE: To estimate the frequency of isolation of herpes simplex virus (HSV) from the genital tract when recurrent herpes lesions were present on the buttocks. METHODS: Data were extracted from a prospectively observed cohort attending a research clinic for genital herpes infections between 1975 and 2001. All patients with a documented herpes lesion on the buttocks, upper thigh or gluteal cleft ("buttock recurrence") and concomitant viral cultures from genital sites including the perianal region were eligible. RESULTS: We reviewed records of 237 subjects, 151 women and 86 men, with a total of 572 buttock recurrences. Of the 1,592 days with genital culture information during a buttock recurrence, participants had concurrent genital lesions on 311 (20%, 95% confidence interval [CI] 14-27%) of these days. Overall, HSV was isolated from the genital region on 12% (95% CI 8-17%) of days during a buttock recurrence. In the absence of genital lesions, HSV was isolated from the genital area on 7% (95% CI 4%-11%) of days during a buttock recurrence and, among women, from the vulvar or cervical sites on 1% of days. CONCLUSION: Viral shedding of herpes simplex virus from the genital area is a relatively common occurrence during a buttock recurrence of genital herpes, even without concurrent genital lesions, reflecting perhaps reactivation from concomitant regions of the sacral neural ganglia. Patients with buttock herpes recurrences should be instructed about the risk of genital shedding during such recurrences. LEVEL OF EVIDENCE: II-2.

Concurrent reactivation of varicella zoster virus and herpes simplex virus in an immunocompetent child.

Latency within the nervous system is a characteristic feature of herpesviridae infection. It is reactivated by triggering factors such as UV exposure, stress, and trauma. Simultaneous reactivation of herpes simplex and herpes zoster is uncommon, however, an observation provably explained by differences in the triggering mechanism. Concurrent reactivation of herpes simplex virus (HSV) and varicella zoster virus (VZV) is occasionally encountered in immunosuppressed patients; on the other hand, it is rarely reported in immunocompetent individuals. We present the case of an immunocompetent 8-yr-old female patient with concurrent reactivation of HSV on the face and VZV on the right L2 dermatome.

Identidad genómica entre virus herpes simplex aislados de lesiones glúteas y genitales / Genomic identity among herpes simplex virus isolated from buttock and genital injuries

El herpes glúteo es originado por el HSV-2 en más del 70 por ciento de los casos y un 58 por ciento de los pacientes refiere antecedentes de herpes genital. Con el fin de investigar la existencia de identidad genómica entre los HSV aislados de lesiones glúteas y genitales, se estudiaron 21 HSV: 9 obtenidos de lesiones glúteas; 8 de lesiones genitales y 4 de secreción vaginal. Estos aislados provenían de 5 pacientes portadores de herpes glúteo y genital. El estudio se realizó mediante aislamiento viral, tipificación con anticuerpos monoclonales y análisis genómico con enzimas de restricción. Se demostró que, 18 aislados correspondían a HSV-2 y 3 a HSV-1. El estudio con enzimas de restricción corroboró los resultados obtenidos con anticuerpos monoclonales y permitió definir la existencia de 4 tipos de patrón HSV-2 y dos de HSV-1. Se estableció la existencia de doble infección herpética en dos de las pacientes analizadas. Los pérfiles de los genomas virales obtenidos de aislados glúteos se correspondieron en forma idéntica con el de los aislados genitales y de secreción vaginal en cada una de las pacientes estudiadas. Los resultados anteriores nos permiten confirmar la hipótesis que lesiones herpéticas genitales y glúteas pueden ser originadas por la misma cepa viral y tener un origen de infección común