Parasitic Gastroenteritis
Introduction
Parasitic gastroenteritis (PGE) is a disease complex associated with a number of nematode species (mostly strongyles), either singly or in combination. It is characterised by:
- diarrhoea
- less than optimum productivity (sub-clinical disease)
- seasonal appearance
- hypoalbuminaemia.
PGE is of considerable economic importance in grazing livestock. It is a potential welfare problem, particularly on organic farms. Losses are associated with the cost of:
- replacement stock
- disruption of breeding programme
- impaired productivity, e.g. weight-gain, wool clip, milk yield, etc.
- treating clinically affected stock, e.g. drugs, labour, veterinary bills
- prophylaxis (prevention), e.g. drugs, labour, pasture management.
Aetiology
Strongyle nematodes are the main cause of PGE in grazing animals and, in particular, those found in two superfamilies, i.e. Trichostrongyloidea and Strongyloidea. Non-bursate nematodes are rarely responsible for PGE, although Strongyloides species (a member of the family Rhabditoidea and NOT a strongyle) may sometimes contribute to the disease.
Normally, only a few of the many roundworm species that are found in the alimentary tract of grazing stock are important as causes of PGE, e.g. in first season calves in northern Europe, Ostertagia species (an abomasal nematode) is the primary pathogen with Cooperia and Nematodirus species (intestinal nematodes) acting as contributory factors; other worms are rarely of clinical significance.
Epidemiology
Introduction
The epidemiology and pathogenesis of many strongyle infections of grazing animals are very similar. Infection by ingestion of an infective larva (L3), development to L4 and adult stages is generally restricted to gastric or intestinal mucosa (although a few species migrate around the body), adult worms eventually emerge to lie on the mucosal surface. The prepatent period is normally 2weeks, though may be 6+months for certain species or if development is "arrested".
Risk of disease depends on the balance between:
- rate of infection if the host; and
- host immunity.
Rate of Infection
The rate of infection of the host by infective L3 depends upon:
- host appetite (under normal circumstances this is fairly constant, increasing with host liveweight); and
- numbers of infective larvae (L3) on pasture (there are marked fluctuations in the number of L3 on pasture grazed by livestock during the year which help to explain the seasonal occurence of PGE).
Development from L1 → L2 → L3 is temperature dependent. Also, the L3 cannot feed as it is ensheathed (i.e. enclosed in the shed L2 cuticle). Its life-span therefore depends on how quickly its food stores are used up, and this too is temperature dependent as it is more active in warm weather.
a) Infective larvae (L3) overwinter on pasture:
- if infected stock grazed pasture previous year
- longer lifespan in colder weather
b) Larval numbers decline in the spring:
- heavy mortality of overwintered L3 (food reserves soon depleted as temperatures rise)
- diluted by spring grass growth
Host infected at turnout, patent infections develop and pasture contaminated:
- stock ingest remaining overwintered L3
- strongyle eggs passed out with faeces onto pasture
c) Development from egg to L3:
- strongyle eggs passed in host faeces for most of the grazing season
- development of egg to L3 depends on dung-pat microclimate and requires:
- high relative humidity (nearly 100%) - dungpat acts as a "buffer" against drought; and
- warmth (optimum temperature 25°C) - dungpat cannot buffer against changes in macroclimate temperature.
- development is therefore influenced largely by macroclimate and temperature. Net result = concertina effect.
d) Translation of infective larvae
- movement of larvae from dungpat onto grass in order to infect final host
- L3 must cross a zone of repugnance around the dungpat (up to 45cm) - normally left ungrazed
- L3 cross zone by swimming in a film of moisture. Also, beetle and earthworm activity, rain splash, soil migration, etc.