Fasciola and fasciolosis in ruminants in Europe: Identifying research needs

Abstract

Fasciola hepatica is a trematode parasite with a global distribution, which is responsible for considerable disease and production losses in a range of food producing species. It is also identified by WHO as a re-emerging neglected tropical disease associated with endemic and epidemic outbreaks of disease in human populations. In Europe, F. hepatica is mostly associated with disease in sheep, cattle and goats. This study reviews the most recent advances in our understanding of the transmission, diagnosis, epidemiology and the economic impact of fasciolosis. We also focus on the impact of the spread of resistance to anthelmintics used to control F. hepatica and consider how vaccines might be developed and applied in the context of the immune-modulation driven by the parasite. Several major research gaps are identified which, when addressed, will contribute to providing focussed and where possible, bespoke, advice for farmers on how to integrate stock management and diagnosis with vaccination and/or targeted treatment to more effectively control the parasite in the face of increasing the prevalence of infection and spread of anthelmintic resistance that are likely to be exacerbated by climate change.

Keywords: Fasciola hepatica; Galba; diagnosis; fluke; fluke vaccine; flukicide resistance; helminth immunomodulation; research gaps; socio-economics of parasite infection; transmission.

Figure 1

Immune responses to Fasciola hepatica; (a) as the life cycle begins within the mammalian host progressing from ingested metacercariae to NEJ to adult fluke multiple immunological events occur. (b) Alternatively activated macrophages (AAMφ) quickly emerge and are characterized by arginase‐1 and IL‐10 expression. These cells have been implicated in examples of host immunomodulation and bystander suppressive effects shown in (c). In parallel the adaptive response becomes detectable within 3–4 weeks post‐infection when both IL‐4 and IgG1 can be measured (e); however, only IgG1 levels are sustained. Simultaneously lymphocyte proliferation (f) is readily detected overlapping with NEJ presence in the intestine, the peak response is quickly reached and dissipates rapidly. IL‐4 (e) and TGF‐β (d) are thought to have T‐cell sources during infection and a plateau of TGF‐β appears to coincide with IL‐4 but only TGF‐β levels are maintained. Significantly, IL‐10 levels (d) are slower to rise in comparison with TGF‐β but remain during experimental infection. IgG1, lymphocyte proliferation and cytokine responses are correlated with the parasite burden indicating a strong role for antigenic load in driving these responses