more than 1 billion Euros are spent annually on chemical helminth control in the
EU (www.parasol-project.org). The annual cost of gastro-intestinal parasites to the
British sheep industry is estimated at £84 million, making parasitic gastro-enteritis
(PGE) the most costly disease afflicting small ruminants (Nieuwhof and Bishop
2005 ). A health plan for 1,500 lambs in a 1,000 ewe lowland flock would typically
include a £300 annual allocation for the treatment and prevention of gastro-intestinal
nematode infections (Scott et al. 2007 ). In recent years, climate change and the advent
of milder wetter weather in some geographical areas have resulted in a dramatic
resurgence of fasciolosis (liver fluke) in sheep and cattle (Mitchell 2002 ;SAC
Veterinary Services 2008 ). The emergence of anthelmintic resistance is leading,
gradually, to direct production losses resulting from lack of efficacy of available
anthelmintics. Resistance of gastro-intestinal nematodes and liver fluke has indeed
become a global issue in sheep, and evidence is mounting that it is an emerging
problem in cattle as well (Coles et al. 2001 ; Demeler et al. 2009 ;www.parasol-project.
org). Another trend that adds to the economic and welfare relevance of nematode
infections is the growing importance of organic farming, wherein the routine use of
anthelmintics is restricted. Some cases of poor management in this production
segment have resulted in clinical parasitism being reported in sheep (Waller 2006 ).
The life-cycle of gastro-intestinal nematodes starts with production of eggs by
adult worms in the host. The eggs are expelled from the host in the faeces and
contaminate the pasture. First-stage larvae hatch from the eggs and moult twice
before they become infective. Third-stage larvae are capable of migrating from
dung pats and soil onto moist grass. Eggs develop into infective third-stage larvae
1–2 weeks after excretion from the host. Larvae can survive up to a year on pasture.
Infection occurs when third-stage larvae are consumed with the grass during the
grazing season. Immature worms migrate into the gut mucosa and cause significant
damage to the mucosal lining when they re-emerge as immature adults. The cycle
completes when the immature forms reach the adult stage in the gastro-intestinal
tract of the host. Third-stage larvae turn into adults over a period of 3–4 weeks
unless they become inhibited and their development is arrested, typically for
several months, in the gut mucosa (a phenomenon known as hypobiosis).
Worm control programmes rely on whole-herd anthelmintic dosing strategies,
which are timed to minimise or suppress worm burdens that have resulted from
exposure to infective larvae on pasture. Gastro-intestinal nematode infections of
cattle involving the abomasal-dwelling species (the abomasum is the fourth and final
stomach compartment in ruminants)Ostertagia ostertagi,Trichostrongylus axeiand
Haemonchus placei, and the intestinal-dwelling speciesCooperia onchophoraand
Nematodirus spp.are ubiquitous throughout Europe. In the first grazing season
calves, infection withO. ostertagican cause severe PGE, characterised by diarrhoea,
reduced feed intake and deterioration of body condition. Chemoprophylaxis with
anthelmintic drugs during the first half of the grazing season (April–October)
provides effective control of PGE, whilst lowering pasture contamination with
nematode larvae in late summer. The use of anthelmintics in lactating dairy cows
after turnout from winter housing on to pasture controls sub-clinical gastro-intestinal
nematode infections and results in improved milk production (Gross et al. 1999 ;
Population Medicine and Control of Epidemics 115