| Abstract: | Co‐infection of tuberculosis (TB) and helminths is recognized as a significant problem in regions where such pathogens are endemic and chronic cases exist. Co‐infection can modulate the immune system leading to interference with diagnostic tests, increased pathological impacts and pathogen persistence. However, research has found that such interactions between pathogens can be context and species specific. Recent studies have suggested that liver fluke, Fasciola hepatica, infection may impact on immunological responses and diagnostics for bovine tuberculosis (bTB; caused by Mycobacterium bovis) in cattle. Where evidence of such interaction exists, there would be an onus on policy makers to adjust eradication programs to minimize impacts. We assessed the association between herd‐level bTB breakdown risk and seasonal variation in liver fluke exposure based on 5,753 bulk tank milk (BTM) samples from 1,494 dairy herds across Northern Ireland. BTM was tested by an IDEXX antibody specific enzyme‐linked immunosorbent assay (ELISA) using the ‘f2’ antigen as a detection agent. The ELISA determined the result based on a sample to (known) positive ratio (S/P%) from which binary status and categories of exposure were derived. Associations were tested using multivariable random effects models. Models predicting bTB risk were not improved with the inclusion of liver fluke exposure levels. Variations in modelling liver fluke exposure (S/P%, binary, categories of exposure) and bTB risk (skin test breakdowns, post‐mortem confirmed breakdowns, breakdown size and lag effects) also failed to support associations (neither positive nor negative) between the pathogens at herd‐level. These results, along with previously published animal‐level data from Northern Ireland, suggest that the nexus between bTB and F. hepatica may have small size effects at the population‐level. However, our results also highlight the high prevalence of F. hepatica in cattle in our study population, and therefore we cannot fully discount the potential hypothesis of population‐level depression of immune response to M. bovis due to co‐infection. |
