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Endoparasites - Ostertagia

Ostertagia ostertagi: Brown stomach worm

General Description: Adults are brownish and thread-like growing to 9mm in length.

Life Cycle: Adults in the abomasum lay eggs that pass in faeces. Once hatched, larvae undergo two moults to become infective third-stage larvae, which migrate onto herbage and are ingested by grazing cattle. Once ingested, these parasitic larvae grow and moult twice more to become egg-laying adults. Environmental conditions of cold or excessive dryness may trigger a condition know as hypobiosis, in which larval development is arrested so that maturation may take several months. Prepatent period is 17 to 21 days.

Location: Abomasum.

Geographical Distribution: Worldwide in cattle raising areas.

Significance: Brown stomach worm is a widespread parasite of cattle. Affected cattle not only lose weight but often die of overwhelming clinical ostertagiasis.

Effect on Host: Ostertagiasis occurs in two forms, Type I and Type II disease. Type I form occurs in calves during their first grazing season as a result of maturation of ingested larvae in the abomasum. Type II disease occurs in animals over age 9-12 months as a result of resumed development of larvae which have undergone arrested development, or hypobiosis, which occurs from early autumn to late winter-spring. Ingested larvae enter the glands of the abomasum, where they grow and moult to become adults (17 to 21 days), at the same time causing erosion of the cells. (Larvae that undergo hypobiosis stay in the cells for longer periods). Cells damaged by the larvae are replaced by rapidly dividing cells that lack the function of producing hydrochloric acid and the enzyme pepsinogen. In a normal abomasum, the pH of the contents is maintained at 2 to 2.5. When large numbers of the parietal cells are lost, the pH of the abomasal contents may rise to 7. Consequences of this are (a) pepsinogen is not activated to its active form, pepsin, (b). proteins are not denatured and digested, (c) there is an increase in the number of bacteria in the abomasum, (d) there is leakage of blood and blood-proteins into gut. Dietary energy and protein which would otherwise be used for growth must be used to replace these proteins. Weight loss is the result. Albumin in the intestine also inhibits fluid absorption by the gut, causing diarrhoea. Severe infections may cause death. The loss of albumin also causes body fluids to collect in lower parts of the body such as under the jaw (bottle jaw) or in the abdomen (ascites). The disease condition produced by these worms is known as ostertagiasis and is characterised by severe diarrhoea, oedema, and weight loss leading to emaciation.

Diagnostic Information: Strongyle-type eggs appear in the faeces; third-stage larvae cultured from them may be identified as Ostertagia. Elevated blood pepsinogen levels may be diagnostic of Type II ostertagiasis.

Control: Avoid overstocking, use pasture management to avoid the accumulation of infective larvae on herbage, and treat regularly with an anthelmintic known to be effective against the inhibited fourth larvae stage.

   
Ostertagia – anterior end   Scanning electron microscope photo – anterior – Ostertagia   Ostertagia – male, posterior end
   
Hypobiotic larva in abomasum   Effect of Ostertagia infection on wall of the abomasum   Adult male Ostertagia and L4 larva

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