The avian schistosome Trichobilharzia franki in mice: Migration, pathogenicity, and the host immune response

Abstract

Cercarial dermatitis (CD; swimmer's itch) is a re-emerging skin disease caused by avian schistosomes, including Trichobilharzia franki. Here, we present morphological, genetic, and experimental evidence confirming the involvement of T. franki in recent CD outbreaks across Czechia. Ocellate furcocercariae were collected from Radix auricularia at four sites and identified as T. franki through ITS1 sequencing. Despite minor morphological differences from previously reported specimens, all isolates belonged to the genetically uniform T. franki “auricularia” clade. Experimental infection of mice with T. franki resulted in a ∼ 60 % penetration rate, accompanied by early-onset scratching and transient weight loss. Gross pathology demonstrated hemorrhages on lung surfaces and splenic atrophy at 2 days post-infection (dpi), along with a prominent enlargement of parotid lymph nodes at both 2 and 7 dpi. Histological examination of the skin revealed viable schistosomula, moderate leukocyte infiltration, epidermal hyperplasia, and the formation of hyperkeratotic crusts at 2 dpi. By 7 dpi, parasites were no longer detectable, but epidermal pathology persisted. In the lungs, eosinophil-rich foci and multifocal hemorrhages were observed at 2 dpi, transitioning to neutrophil-dominated lesions at 7 dpi, despite the absence of detectable schistosomula. Splenocytes from infected mice responded to homologous and heterologous cercarial antigens by producing IFN gamma, IL-4, and IL-10, indicating a mixed Th1/Th2/Treg profile and notable species cross-reactivity. However, parasite-specific IgG remained undetectable at 7 dpi. These findings confirm T. franki as the causative agent of CD outbreaks and underscore its capacity to induce localized and systemic pathology and immune response, cross-reacting with other schistosomes.