[2] The parasitic stage of the life cycle begins when warm moist conditions cause the L3 larvae to migrate onto herbage surrounding the fecal pat, which are ingested during grazing.
In the host's rumen, the L3 larvae shed their protective sheath and pass into the abomasum, where they penetrate the gastric glands.
The young adult worms then emerge from the gastric glands and continue their maturation on the mucosal surface of the abomasum.
[6] The cuticle in the anterior region is striated transversely whereas the rest of the body is unstriated and bears around 36 longitudinal ridges.
[7] The Ostertaginae are characterized by a reduced buccal capsule and square head, and well-developed copulatory bursa in the male.
[15] The primary clinical symptom of fulminant bovine ostertagiosis is watery diarrhoea and is usually accompanied by reduced appetite.
[16] 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.
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.
[21] The young adult worms then break out of the gastric glands, causing substantial damage to the abomasal wall.
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.
The failure to respond quickly to Ostertagia may be a result of the suggested immunosuppression or impairment of antibody and cellular responses.
[36] 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.
[42][43] Enzyme-linked immunosorbent assays (ELISAs) have been used as a diagnostic tool to quantify the impact of gastrointestinal nematodes in dairy cattle by measuring antibodies in milk.
Higher levels of antibodies measured by ELISA methods, referred to as optical density ratios (ODRs), are associated with decreased milk production in dairy cattle.
The most common in the cattle industry are macrocyclic lactones, which include ivermectin and eprinomectin, benzimidazoles, and imidazothiazoles are also used to a lesser extent.
There is a broad range of current literature reporting developing resistance of O. ostertagi to all major classes of anthelmintic worldwide including the United States, New Zealand, Brazil, Argentina, and the UK.
[55][56][57] As recently as January 2016, O. ostertagi anthelmintic resistance was reported to all three major drug classes on 20 dairy farms in Southern Australia[58] The two most widely accepted anthelmintic resistance diagnosis methods for O. ostertagi are in vivo methods: the fecal egg count reduction test (FECRT) and the controlled efficacy test (CET).
The World Association for the Advancement of Veterinary Parasitology (WAAVP) has provided guidelines on the detection of anthelmintic resistance.