Ostertagiosis - Cattle

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Introduction

Ostertagiosis is a parasitic worm disease in cattle caused by Ostertagia

Pathogenesis

'Type I Ostertagiasis: Ostertagia ostertagi is ingested by calves in their first year at grass. The parasites colonise the gastric glands of the fundus and pylorus and then 17-21 days after ingestion, the parasites reach maturity and emerge from the gastric glands. Emergence in sufficient numbers causes extensive pathological changes - chronic gastritis. A thickened, hyperplastic, non-functional gastric mucosa is formed, meaning impaired function in the gut resulting in diarrhoea and hypoalbuminaemia.

'Type II Ostertagiasis: Ostertagia ostertagi may become hypobiotic in the Autumn and if these infestation are heavy, lots of hypobiotic larvae reactivate in the Spring. This causes severe acute gastritis (fibrinous or haemorrhagic), and even sudden death.

Epidemiology of Ostertagiosis (Dairy Herds)

Calves are weaned early and put out to graze with other calves of similar age. Disease risk is high if not controlled, and most frequently occurs when calves graze permanent pasture, especially if kept at high stocking rates.

Type 1 Disease: Occurs in calves during their first grazing season between mid-July and October. The disease caused by L3 ingested 3-4 weeks earlier. There will be a high morbidity/ low mortality. Clinical signs include diarrhoea, weight loss and reduced appetite.

Pre-Type 2 Phase: Calves at end of first grazing season (from October) accumulate large population (greater than 100,000) of Ostertagia EL4 (arrested stage). Disease is caused by L3 ingested in late autumn. There are usually no clinical signs.

Type 2 Disease: Occurs in yearlings housed after first grazing season (February-May). The disease happens due to resumed development of waves of previously arrested EL4 ingested as L3 the previous autumn. There is low morbidity/high mortality and the clinical signs include diarrhoea, weight loss, reduced appetite and submandibular oedema.

Epidemiology of Ostertagiosis (Beef Suckler Herd)

Calves suckle and graze with their dams. Calves are susceptible, but cows are immune. Overt disease is much less common than in dairy herds because:

Spring-Calving Herds: Spring mortality of L3 occurs before calves eat significant amounts of grass. Immune cows pass very few worm eggs, leading to development of very few L3 therefore disease very unlikely.
Autumn-Calving Herds: Calves graze before spring mortality of L3 occurs, and will contaminate pasture. There are relatively few calves on pasture (as most of the grass is needed by the cows, therefore, relatively few eggs dropped onto pasture, so disease risk higher but still low compared with dairy herds.


Acquired immunity is slow to develop (takes whole grazing season) and immunity may wane during winter housing, but is rapidly re-established upon turnout. Adult cattle are solidly immune (no significant role in epidemiology of disease) and only deposit a very small number of eggs onto the pasture.

Diagnosis

Clinical signs, seasonal incidence and previous grazing history are suggestive. Response to worming treatment is also a positive diagnostic tool.

Faecal examination, worm egg count is definitive if there are >1000 e.p.g. (eggs per gram) in type 1 disease and variable or sometimes zero in type 2 disease.

Blood pepsinogen or gastrin can also be measured. Findings will show it to be elevated if disease is present. This is a specific indicator of abomasal damage in groups of animals and is useful when assessing how much of the herd is affected.

Post mortem examination will show fundic nodule, an increased gastric pH, there will be a putrid smell and you will see the presence of >40,000 adult worms in lumen on mucosal surface if the animal has clinical ostertagiosis. Pathological signs will also include raised hyperplastic nodules, 2-3mm in diameter with a central orifice (the opening to the parasitised gastric gland), a “moroccan leather” or “crazy paving” appearance in heavy infestations and necrosis of the epithelium following emergence of the larvae.

Treatment and Control

Anthelmintic treatment is required along with supportive therapy such as electrolyte solutions if diarrhoea is very severe.

Type 1 Disease: Use clean pasture (e.g. new leys, pasture not grazed by cattle previous year - but not always available) or delay turnout until after spring mortality of L3 (but uneconomical use of pasture/supplementary feeding). Dose and move to aftermath (hay/silage) in mid-July (but will not control early season disease). 

If there is no alternate grazing available then use repeated anthelmintic treatment monthly from mid-July (but temporary control of egg output only, cattle reinfected) or before mid-July on 2 or 3 occasions, e.g. ivermectin 3, 8 and 13 week treatment post-turnout (relies on residual activity of at least 2 weeks and 3 week worm prepatent period, but labour intensive).

Intra-ruminal anthelmintic devices (minimise pasture contamination and size of autoinfection peak), examples include Paratect Flex (Pfizer), Autoworm (Schering-Plough), Ivomec SR bolus (Merial) and Panacur bolus (Hoechst), they are expensive.

Type 2 Disease: Cattle are exposed to low challenge at pasture in late autumn so are unlikely to require treatment at housing. Cattle exposed to medium/high challenge in late autumn or animals of unknown origin are likely to require treatment at housing using an anthelmintic active against hypobiotic larvae.


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References

Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) Bovine Medicine (Second edition), Blackwell Publishing

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




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