genome size estimate for O. ostertagi is ~58 MB, based on T. circumcincta (Ostertagia circumcincta), whose genome is 58.6 MB and on H. contortus at 52 MB, based on flow cytometry. There are 7,006 identified expressed sequenced tags (ESTs), representing 2,564 genes. Disease Clinical ostertagiosis normally occurs in first grazing season calves but can affect mature animals. Subclinical infection results in reduced weight gain and growth rate, reduced reproductive efficiency and reduced milk production. The primary clinical symptom of fulminant bovine ostertagiosis is watery diarrhoea and is usually accompanied by reduced appetite. Infected animals are characterised by dull, rough coats and hindquarters soiled with faeces as a result of the profuse diarrhoea. Cattle are frequently co-infected with many gastrointestinal nematodes including species of the following genera: Ostertagia, Haemonchus, Bunostomum, Oesophagostomum, Trichuris, Trichostrongylus, Cooperia, and Nematodirus. The clinical signs between these species of nematodes are difficult to distinguish from each other, and are often referred to as a syndrome called parasitic gastroenteritis. Clinical ostertagiosis can be observed under two sets of circumstances referred to as type I and type II disease. Type I disease Type I disease occurs in young cattle grazing on pastures for their first time during the period of high pasture contamination. This syndrome usually occurs in the summer and fall months in the Northern hemisphere and during the winter and spring months in the Southern hemisphere. Infective larvae are ingested daily by the young stock on pasture. The pathological and clinical signs are due to the direct development of large numbers of L3 larvae to adult worms over a relatively short period of time (approximately 3 weeks) in young animals with an immune system naïve to Ostertagia infections. The young adult worms then break out of the gastric glands, causing substantial damage to the abomasal wall. Mild cases result in reduced growth or production and severe cases can result in fulminating disease characterized by profuse watery diarrhoea, rapid weight loss, submandibular oedema ("bottle jaw"), anemia and death. Type II disease Type II disease can occur in yearlings and older cattle. It is the result of arrested L4s resuming their development to immature adults and leaving the gastric glands. This can occur weeks or months after being ingested as L3s and is a consequence of favourable environmental conditions. The larvae will then resume maturation gradually or in bursts. The clinical signs are identical to type I disease and