No abstract

The development of nasal avian schistosomes of the genus Trichobilharzia in their final host is poorly known. Therefore, an experimental infection of ducklings (Anas platyrhynchos f. dom.) by T. regenti was performed. The infection resulted in leg paralysis and orientation/balance disorders of birds. The examination of the duck's spinal cord and brain confirmed the presence of developing parasites in pre-patent as well as patent periods. The absence of the worms in other tissues strongly supports our hypothesis that the parasite migrates through the central nervous system (CNS) to its final location in bird nasal mucosa. The injury level is probably dependent on number of parasites as well as yet unknown host factors. The affinity to the CNS seems to be high; also by exposure of experimental animals to low cercarial doses the growing worms in the CNS were found. In addition to the generally accepted view that bird schistosomes may cause cercarial dermatitis of mammals (including man), there is evidence of a partial development of T. regenti in mouse CNS; in certain cases leg paralysis was also recorded. Therefore, the pathogenesis spectrum caused by bird schistosomes in birds/mammals needs to be reconsidered.

No abstract

Avian schistosomes are the primary causative agent of cercarial dermatitis in humans, but despite its worldwide occurrence, little is known of the immune mechanism of this disease. Using a murine model, hosts were exposed to primary (1×) and multiple (4×) infections of Trichobilharzia regenti via the pinna. Penetration of larvae into the skin evoked immediate edema, thickening of the exposure site, and an influx of leukocytes, including neutrophils, macrophages, CD4+ lymphocytes, and mast cells. A large proportion of the latter were in the process of degranulating. After 1× infection, inflammation was accompanied by the release of IL-1β, IL-6, and IL-12p40. In contrast, in 4× reinfected animals the production of histamine, IL-4, and IL-10 was dramatically elevated within 1 h of infection. Analysis of Ag-stimulated lymphocytes from the skin-draining lymph nodes revealed that cells from 1× infected mice produced a mixed Th1/Th2 cytokine response, including abundant IFN-γ, whereas cells from 4× reinfected mice were Th2 polarized, dominated by IL-4 and IL-5. Serum Abs confirmed this polarization, with elevated levels of IgG1 and IgE after multiple infections. Infection with radiolabeled cercariae revealed that almost 90% of larvae remained in the skin, and the majority died within 8 days after infection, although parasites were cleared more rapidly in 4× reinfected mice. Our results are the first demonstration that cercarial dermatitis, caused by bird schistosomes, is characterized by an early type I hypersensitivity reaction and a late phase of cutaneous inflammation, both associated with a polarized Th2-type acquired immune response.