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

Strongyle nematodes are the main cause of PGE in grazing animals and, in particular, those found in two superfamilies; 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. 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.

Pathogenesis and Epidemiology

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".

Risk of disease depends on the balance between the rate of infection of the host and host immunity. 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 the 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 occurrence 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 metabolism is faster in warm weather.

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.

It is important to remember that a worm burden inside an animal grazing at pasture does not remain static, but is continually changing i.e. as older adult worms are lost, more infective larvae are recruited. A state of equilibrium is reached i.e rate at which L3 establish = rate at which adult worms are lost. In an immune animal, the same equilibrium exists, except that fewer of the L3 ingested become established.

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).

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 coccidia infection in lambs.

Clinical Signs

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.

Diagnosis

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.

Treatment and Control

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.

Clean Pasture would be ideal but this requires no lambs having grazed that pasture the previous year, and so is impractical in many cases.

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.

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.

References

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing.
Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition), Elsevier Science.
Fox, M and Jacobs, D. (2007) Parasitology Study Guide Part 2: Helminths, Royal Veterinary College.
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.