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Understanding the diagnostic tests and challenges in host genetic selection against Johne's disease in New Zealand
Venkatesh Km1, Vsr Dukkipati2, S K Gupta3
1School of Agriculture and Environment, Massey University, Palmerston North, New Zealand.
Abstract:
Johne's disease (JD) is a common endemic gastrointestinal disease of ruminants caused by Mycobacterium avium subspecies paratuberculosis (MAP). With no effective treatment or vaccine preventing infection, control is currently based on the identification of infected animals and prevention of the spread of infection. The aim of this review is to critically assess the diagnostic tests currently used to detect MAP infection in NZ dairy cattle and to evaluate the current understanding of the host's genetics in preventing the disease. Multiple diagnostic tests for MAP infection, such as ELISA and faecal quantitative PCR, are currently available in NZ, but none are close to a gold-standard test. The lack of new tests in NZ has resulted in the development of multiple testing strategies such as parallel and serial testing with combinations of tests to improve specificity and sensitivity, pooling samples to reduce costs, whole herd testing to optimise culling before drying off, or selection of cows to produce replacements. However, these strategies need further testing to confirm their cost-benefit, especially in relation to varying infection pressures at the individual cow and herd levels. There is limited understanding of how the host's genetic variation contributes to the range of responses - the JD phenotype - seen in animals in contact with MAP. Canonically, this is described in terms of susceptibility, resistance and resilience. However, within field studies, it is very difficult to identify animals with these characteristics. For example, the combination of repeated and combined diagnostic testing, together with longitudinal production data required to identify resilient animals, can be very expensive. This review shows that more NZ-based research is required around strategies that optimise the use and value of what are inevitably imperfect diagnostic tests. Such work should be undertaken alongside a focus on identifying the genetic differences behind the JD phenotypes.
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