FASCIOLOSIS (Fasciola hepatica infection) has increased in some European countries up to 12-fold in recent years and there is evidence to suggest it’s increasing in the UK.1
The primary underlying cause appears to be climate change, i.e. the trend towards wetter, milder weather, favouring the survival and development of the free-living stages of the liver fluke and its intermediate host, Galba truncalata, the mud snail.
As a result, the seasonality of disease is becoming less well defined, more prevalent and the geographical occurrence of fasciolosis is also changing. Strategic control programmes will need to be adapted, and be based more on recent weather conditions and local forecasts, particularly rainfall and average temperature data, rather than just on farm systems and traditional or historical timings.
Fluke proliferation and links to weather
The complex life-cycle of fluke makes it very dependent on high rainfall and mild temperatures to flourish. There have usually been two key periods of host infection with liver fluke in the UK: summer infection and winter infection.
Adult sheep/cattle carriers will shed fluke eggs onto pasture and when the ambient temperature exceeds 10°C the eggs will hatch. Meanwhile, the intermediate host, the mud snail Galba truncatula, will also start multiplying in numbers as the weather warms up. This generally occurs between May and October.2
Hatched eggs release miracidium which then infects the snails and develops within them. In wet summers there will be huge snail populations which are infected by miracidium from May to July.
If wet weather continues the snails shed massive numbers of metacercariae onto pasture, which go on to infect sheep/cattle over summer and early autumn time.
This “summer infection” results in outbreaks of acute and sub-acute disease in late autumn and winter when immature fluke migrate through the liver causing widespread tissue damage. In a dry or cold spring and early summer, the snail population will remain low and fewer fluke eggs will hatch. Therefore pasture contamination in late summer/autumn is much lower and disease risk is much reduced.2
“Winter infection” occurs when eggs excreted by carrier animals in late autumn and encysted metacercariae survive over winter on pasture and resume development in early spring, once conditions become favourable. This will lead to cases of sub-acute and acute disease in the host from as early as July.1
Disease patterns and climate changes
In the UK, recent average temperatures have consistently increased by between 1°C and 4°C, compared to the past 30 years figures.3 This degree of climate change very much supports the development of fluke which requires a mean temperature above 10°C to complete its life-cycle.2
Mild, wet weather also promotes proliferation of the mud snail. This may well be the reason why fasciolosis has spread geographically across the UK in the past 40 years.
Disease patterns have changed from a restricted distribution in the 1970s with only occasional cases seen in the west, to current levels now, where large areas of the UK are seeing outbreaks.1
It’s also thought that the introduction of infected sheep has helped spread fluke into eastern areas.4
Climate change has also seen a trend towards wetter, milder winters,2 allowing more fluke stages to survive over winter on pasture. This coincides with reported changes in the timing of infection, with a steady increase in the mean risk in winter infection and outbreaks of disease occurring earlier in the year as a consequence.1
Anecdotal reports suggest that there is an increase in cases of acute fasciolosis before midsummer.1
Predictions
According to some predictions, the UK may experience unprecedented levels of liver fluke infection over the next 60 years, with overall future risk being higher in all regions than it is currently.
Serious epidemics may well be the norm by 2020 in parts of Scotland and by 2050 in parts of Wales. Winters are predicted to become even milder and more months will have a mean temperature above 10°C.
As a consequence, outbreaks in late spring/early autumn can be expected. These will initially be restricted to the far south, but will slowly spread north over time. With some parts of the UK experiencing longer windows for fluke development, fasciolosis infection could extend from being seasonal to a year-round disease.
Updating control strategies
A tailored strategic approach to fluke control based on current local risk factors (i.e. the weather) and NADIS forecasts now seems to be more appropriate for optimal results.
For example, years with normal or below average rainfall can be considered low risk years. As such, consider treating for adult fluke in January then late April/early May. In addition, treat for adult and immature fluke in October.
Years with above average rainfall can be considered high risk. Therefore it would be prudent to treat for adult fluke in January then late April/early May. In addition, treat for both adult and immature stages of fluke in June (4-6 weeks after the last treatment), October and again four weeks later in November.
Rotation and choosing the right product is obviously important too. For example, Closantel (Flukiver 5% w/v Oral Suspension, Elanco) will kill adult fluke and immature flukes down to 5-6 weeks of age. In addition it will delay egg shedding for up to 13 weeks after treatment, which will help reduce infection of snails.
Resistance to closantel has not been reported in the UK. Triclabendazole will kill all stages of fluke but resistance is established in the UK and once fluke become resistant they do not return to susceptibility.4 Other examples of adult flukicides include nitroxynil and oxyclosanide, although they have limited activity against immature stages.5
The strategic control of fluke is becoming more complex as climate conditions appear to favour the spread and survival of liver fluke across the UK. Ideally, it is best to assess the risk of disease based on local weather conditions and parasite forecasts, (see NADIS website) before deciding on the frequency and timing of flukicide administration.
References
- Fox, N. J., White, C. L., McClean, C. J. et al (2011) Predicting impacts of climate change on Fasciola hepatica risk. PloS ONE 6 (1): e16126. (www.plosone.org/article/info%3Adoi %2F10.1371%2Fjournal.pone.0016126)
- Taylor, M. (2009) Changing patterns of parasitism in sheep. In Practice 31: 474-483.
- Van Dijk, J., Sargison, N. D., Kenyon, F. et al (2010) Climate change and infectious disease: helminthological challenges to farmed ruminants in temperate regions. Animal 4 (3): 377- 392.
- Borgsteede, F. H. M., Moll, L., Vellema, P. et al (2005) Lack of reversion of triclabendazole-resistant Fasciola hepatica. Vet Record 156: 350-351.
- National Animal Disease Information Service (NADIS), Liver Fluke Control in Sheep 2013: www.nadis.org.uk/bulletins/liver-flukecontrol-in-sheep.aspx.
