Triclabendazole (TCBZ) has been the drug of choice for treating liver fluke infections in livestock for over 20 years. More recently, it has been used successfully to treat human cases of fascioliasis, but will no longer be available for human use as Novartis is stopping its production (Curtale, 2006). In farm animals, resistance to TCBZ first appeared in Australia in the mid-1990s and since then has been reported in a number of European countries (Ireland, the UK, The Netherlands and Spain)(Fairweather, 2005). To date, no confirmed cases of TCBZ resistance have been documented in humans. Should resistance develop further in livestock, the heavy reliance on a single drug to maintain productivity and animal health puts future treatment strategies at risk. This is particularly worrying given the recent rise in the prevalence and spread of the disease. Climate change has been blamed for this phenomenon, providing more favourable conditions for the survival of the snail host (Mitchell, 2002). The aim of this short review is to summarise work being carried out to elucidate the mechanism of resistance. Different, yet parallel, approaches (molecular, morphological, pharmacological and proteomic) are being used by different laboratories to obtain a more complete picture of resistance.
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