[1] Infections with C. oncophora may result in mild clinical symptoms, but can lead to weight loss and damage of the small intestine, especially when co-infections with other nematodes such as O. ostertagi occur.

[2][3] Infections are usually treated with broad-spectrum anthelmintics[4] such as benzimidazole, but resistance to these drugs has developed in the last decades and is now very common.

Free-living L3 stage larvae residing on the pasture are taken up by grazing cattle and pass to the small intestine.

Like other trichostrongylids, early C. oncophora L4 larvae are able to arrest their development under unfavourable environmental conditions such as low temperatures and high dryness, a process termed hypobiosis.

Arrested development is characterized by a large number of individuals stopping at the same stage of development, a bimodal distribution of worm sizes, and a recent exposure of the host animal to the infectious agent prior to the prepatent period of the infectious agent.

Arrested development can be triggered by the following situations: seasonal influences on the larvae while outside the host, the normal host immune response interrupting the normal parasitic phase of the life cycle, or overpopulation of adults that leads to negative feedback preventing the further development of more larvae.

It is advantageous for nematodes to enter arrested development as they can survive in hostile environments, cause disease in the host by a large portion of the larvae resuming development, produce large numbers of infectious eggs when the environmental conditions are once again favorable, and avoid susceptibility to various anthilmentics.

The genomic data might prove as an invaluable resource for fundamental biological research, comparative genomics and provide new insights in genetic mechanisms involving drug susceptibility, resistance, host parasite relationships, host immunity, possibility to maintain the life of currently available drugs and improved molecular diagnostics.

[9] Recent transcriptomic data of C. oncophora from different developmental stages identified protein and domain families that are important in stage-related development.

These proteins have been shown extreme diversity in occurrence and function in prokaryotes and eukaryotes, which includes involvement in several processes like reproduction, cancer and immune regulation,[11] though they await experimental characterization.

However, the pathology caused by Cooperia coupled to its wide range of distribution has huge economic impact to cattle producers.

Infection causes appetite reduction and inefficient uptake of necessary nutrients which effects body weight, reproduction and can lead eventually to calf death.

[16] Although C. oncophora does not feed on host-blood, it has the capacity to burrow through the gut wall, especially in the proximal location (duodenum) which can lead to anemia[17] in the host.

Ruminants respond to C. oncophora infection using multiple mechanisms, and the degree of response varies based on various host-parasitic factors.

These are capable of clearing the parasite rapidly, so that no eggs are detected in the feces, or there is only a very low worm burden after 42 days post infection (p.i.)

Although they can significantly reduce egg output after 35–42 days while worm burden in the intestine remains in range of low to high number.

[18] IgA/antigen complex can bind to the Fc receptor of the eosinophil and thereby induce the release of anti-inflammatory mediators and cytokines which can in turn reduce the worm load.

[19] On the other hand, response to secondary exposure involves increase in CD4+ T-cell in the lymph node, in the peripheral blood and in Payer's patches of the proximal gut.

Acute inflammation in the primed proximal gut occur earlier and eosinophil level normalizes before 14 days of infection.

Some other genes encoding cell adhesion molecules including CDH26, collectins and gelectins are up-regulated in infected ruminants.

These include maintaining a healthy herd, pasture management, careful grazing, plowing the field, avoiding congested and humid environments, keeping calves separately and ensuring hygiene.

Moreover, levamisole and several macrocyclic lactones (e.g. abamectin, doramectin, eprinomectin, ivermectin, moxidectin) are reported to be effective.

After multiple rounds of exposure adult ruminants can overcome the adverse effects of the parasite however still it act as reservoir for new infection.

[26] Resistance has been reported to all broad spectrum anthelmintics, which are benzimidazoles (BZs), levamisole/morantel (LEV) and macrocyclic lactones (ML).

[29] MLs bind irreversible to Glutmate gated chloride ion (GluCl) channels, leading to hyperpolarisation.

Pharyngeal and somatic muscle cells get paralyzed, which results in starvation of the worms and also their removal from the gastrointestinal tract.

This includes transporters which are part of the xenobiotic metabolism by absorbing, distributing and eliminating external substances and their metabolites.