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 and host defence Gastrointestinal nematodes may elicit a variety of host immune responses depending on the initial immune status of the host, parasite species, and environmental conditions. The body has several physical defense mechanisms against parasites including the continual sloughing of the gut
epithelium to prevent parasite attachment. However, once an infection has occurred, the host's immune system attempts to limit the damage caused by the worm. Apart from the importance of the extrinsic factors of weather, climate and grazing management, the immune status of cattle is perhaps the most significant of all host factors influencing infection with
O. ostertagi. Unlike other common gastrointestinal nematodes of cattle, who are subject to a quick host immune response after relatively short periods of exposure and immune system memory, a protective host immune response against
O. ostertagi requires far longer periods of exposure and is not always permanent. The failure to respond quickly to
Ostertagia may be a result of the suggested immunosuppression or impairment of antibody and cellular responses.
O. ostertagi has been shown to induce cytokines and T-cells in the adaptive immune response in cattle, and recent advances have been made to produce suitable vaccines targeting adult stage
Ostertagia. The major limitations to reducing parasitic load using vaccines is the complex and dynamic host-parasite interaction that is unique to each species of host and parasite, which is often influenced by several environmental factors. ==Diagnosis==