Abstract
Reactive cutaneous coccidioidal skin manifestations are commonly noticed during the early stage of coccidioidomycosis. These skin lesions are devoid of any active coccidioidal organism, and the immune trigger mechanisms are not elucidated. We describe 6 cases of unusual reactive cutaneous coccidioidal manifestation, characterized by painful vesiculobullous lesions known as erythema sweetobullosum. The biopsy of the lesions revealed neutrophilic dermatosis with inflammatory cells resulting in a cleft and elevation of the most superficial layer of the skin forming a bulla. The reactive cutaneous lesion is self-limited and requires no specific therapy.
Highlights
Immune-mediated skin reactions to coccidioidomycosis manifest commonly as erythema nodosum and erythema multiforme.[1]
Coccidioidomycosis is caused by Coccidioides immitis and posadasii, which result in an identical spectrum of illness
The organism can be demonstrated at the site of the lesion with organism-specific manifestations whereas the reactive cutaneous manifestation is usually a delayed-type immune reaction.[1,8]
Summary
Immune-mediated skin reactions to coccidioidomycosis manifest commonly as erythema nodosum and erythema multiforme.[1]. A 42-year-old male presented with painful, pruritic vesiculobullous rash on his bilateral forearms for 15 days (Figure 6). The coccidioidal serology showed reactive ID-IgM and ID-IgG with CF antibody titer
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Journal of Investigative Medicine High Impact Case Reports
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.