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== Introduction ==

== 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:

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 and hypoalbuminaemia.

*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:

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, the treatment of clinically affected stock e.g. drugs, labour, veterinary bills and finally, prophylaxis (prevention) e.g. drugs, labour, pasture management.

*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.

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. 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.

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.

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 2 weeks, although it may be >6 months for certain species or if development is "arrested".

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 metabolism is faster in warm weather.

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:

Acquired host immunity affects both the establishment of recently ingested infective larvae as well as the course of infection of developing worms. When considering the effects that host immunity has on a worm burden, remember that animals grazing at pasture are continuously exposed to infection and not just challenged by a single large infection.

*'''rate of infection''' if the host; and

*'''host immunity'''.

=== Rate of Infection ===

Effects of host immunity on worm burden are reduction in establishment of larvae e.g. fewer L3 establish in an immune adult cow than a parasite-naive calf. There is also expulsion of an existing worm burden ("self cure"), due to immediate-type hypersensitivity reaction to antigen from incoming L3. Arrested development has a minor role only; arrested development is mainly caused by climatic changes e.g. temperature changes (''Ostertagia'') or drought (''Haemonchus'').

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.

Factors adversely affecting host immunity include nutrition; gross deficiency or mineral/trace element deficiency e.g. cobalt. Also there is a periparturient relaxation in immunity" (PPRI) seen in breeding ewes and sows, which is due to impaired cell-mediated immune response associated with an increase in blood prolactin levels and a shift of [[IgA]] from gut mucosa to mammary gland around parturition. Drug treatment, repeated anthelmintic and corticosteroid treatment also affects host immunity, as does concurrent infection; where the pathogenic effects of ''Nematodirus'' infection are exacerbated by concurrent [[Coccidiosis - Sheep|coccidia infection in lambs]].

a) ''Infective larvae (L3) overwinter on pasture'':

*if infected stock grazed pasture previous year

Diarrhoea, which is often profuse and characteristic depending on the parasite involved, e.g. dark  if ''Trichostrongylus ''and greenish if ''Nematodirus''. There may also be weight loss, or reduced weight gain plus, oedema in severe chronic cases. In acute cases, the only clinical sign may be sudden death.

*longer lifespan in colder weather

*heavy mortality of overwintered L3 (food reserves soon depleted as temperatures rise)

Clinical signs, seasonal incidence and history are indicative of the condition.

Faecal samples should be taken to examine to eggs in the faeces. Only a number above a threshold for eggs to cause clinical disease is a positive diagnostic indicator.

*strongyle eggs passed out with faeces onto pasture

In an outbreak of PGE on a farm, anthelmintic treatment should be given to all stock. If diarrhoea is very severe then supportive therapy, such as providing an electrolye solution, may be given. Affected animals may need to be brought in and housed for a short period of time.

*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.

*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

This means in most cases, control strategies work around the presence of a Contaminated Pasture. You will need to dose lambs two or three times at 3-weekly intervals in May or June. Optimum timing may be predicted by a forecasting system based on soil temperatures during March.

*L3 cross zone by swimming in a film of moisture. Also, beetle and earthworm activity, rain splash, soil migration, etc.

 

Another way to manage worm control is to provide alternate grazing of sheep and cattle. Good worm control is possible by alternating the grazing of fields on an annual basis with each host due to the relative insusceptibility of cattle to sheep nematodes and vice versa.

 

Tannin-Rich Forages are a new thinking into worm control. Condensed tannins, found in clover, lucerne, trefoil, etc. protect plants against microbial and parasitic attack and have recently been found to protect dietary protein against rumen breakdown and they posses some anthelmintic activity. To date, trials investigating the anthelmintic activity of tannin-rich forages have shown variable results between studies; faecal worm egg output was reduced in most studies and worm numbers in some. Clearly, further research is required, though such forages do offer potential as a long-term epidemiological tool and may reduce farmers' dependence on anthelmintics.  

 

<big><b>Also see:

 

 

Radostits, O.M, Arundel, J.H, and Gay, C.C. (2000) '''Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs, goats and horses,''''' Elsevier Health Sciences. ''

 

 

 

 

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