the severity depends on the magnitude of the eruptions. In the Northern hemisphere type II disease is often seen in the early spring, and in the fall in the Southern hemisphere. Pathology Worms can readily be seen and identified in the abomasum, and small petechiae (blood spots) may be visible where the worms have been feeding. The most characteristic lesions of Ostertagia infections are multiple small, white, raised umbilicated nodules 1–2 mm in diameter. These may be discrete, but in heavy infections they tend to coalesce and give rise to a "cobblestone" or "morocco leather" appearance. Nodules are most marked in the fundus region but may cover the entire abomasal mucosa. In severe cases, edema may extend over the abomasum and into the small intestine and omentum. When examined histologically, abomasal gastric glands contain larvae in varying stages of development, which results in hyperplasia and distention of the glands, and flattening of the glandular epithelium. Affected glands lack differentiated acid-producing parietal and pepsinogen producing chief cells. Type I and type II disease is often differentiated by the presence of increased numbers of globule leucocytes, eosinophils and focal aggregates of lymphoplasmocytic cells in animals with type II disease. Pathophysiology Consequences of the damage done to the gastric gland by O. ostertagi include: Pepsinogen is not activated to its active form, pepsin, due to decreased acid production caused by the loss of parietal cell function, resulting in an increase in abomasal pH. Due to increased abomasal pH, proteins are not denatured and digested. Dietary energy and protein, which would otherwise be used for growth, must be used to replace these proteins. Weight loss is the result. Also due to the increased abomasal pH, there is an increase in the number of bacteria in the abomasum, which can contribute to the diarrhoea seen in clinical cases. Movement of serum proteins, particularly albumin from the circulating blood into the abomasal lumen due to compromised intracellular junctions occur. The increased albumin decreases fluid absorption by the gut, causing diarrhoea. 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 increased abomasal pH also stimulates the production of gastrin and thus hypergastrinemia, which is closely associated with the inappetence. This parasite-associated drop in intake has been shown to be largely responsible for impaired weight gain. Immune response