Etiology

• Nematodes are roundworms and the parasitic species that cause PGE are many.
• The most common ones in cattle are Ostertagia ostertagi Ostertagia ostertagi, Cooperia oncophora Cooperia spp, Nematodirus battus Nematodirus spp (primarily a sheep parasite but may affect cattle co-grazing with sheep) in temperate regions and Haemonchus spp Haemonchus spp in tropical and subtropical zones. However, there are other Trichostrongyle spp that can cause production losses and clinical illness Trichostrongylus axei.

Predisposing factors

General

• Naïve cattle of any age, although the younger animals are at higher risk of developing clinical disease.
• Intensive grazing systems with high stocking density.
• Suitable environmental and climatic conditions that allow the parasites to survive on pasture.

Specific

• Depending on the farm and grazing systems used, naïve cattle are exposed to worms at different ages, eg in an all year round calving herd, batches of similar age calves are turned out at different stages during the grazing season, whereas in block calving herds (spring or fall) the groups will be larger and more uniform, affecting stocking density and susceptibility.
• Other underlying diseases will increase susceptibility in cattle of any age, allowing the parasites to fully develop their opportunistic behavior.

Pathophysiology

• When infective larval stages are ingested, they establish in the gut mucosa, develop and feed in different parts of the GI tract, depending on their species.
• Mixed infections are the most common presentation, although typically one or more Nematode species predominate.
• The parasites will cause varying levels of damage to the mucosa and (for those residing in the small intestine) the villi.
• O. ostertagi Ostertagia ostertagi is able to encyst and persist within the abomasal wall for several months. The exact mechanisms and environmental factors that initiate and terminate the encysted stage are still somewhat unclear, although external temperatures have been shown to contribute.
• Severity of the clinical disease often correlates to worm burdens. Immunity develops relatively slowly following exposure, and it is often not fully protective against reinfection, requiring a constant challenge to maintain freedom from clinical signs.
• Gastrointestinal parasites can modulate and down regulate the host immune response to a variety of other infectious challenges, and this ought to be considered when planning vaccination schedules.

Timecourse

• Once infective stage larvae have been ingested, the pre-patent period for most of the parasite species is around 3-4 weeks. Pathology and clinical signs can be observed before the end of the pre-patent period, as soon as juvenile worms cause damage to the GI tract.
• Duration: the clinical signs will persist for as long as the animals remain untreated. Normally they will recede within few days or weeks of receiving the appropriate anthelmintic.

Epidemiology

• Life cycles :
  • The nematodes responsible for PGE have a direct life cycle with no intermediate hosts.
  • Eggs shed by infected hosts hatch on pasture and have to complete a number of developmental larval stages before becoming infective (the infective stage is usually an L3 larva).
  • Transmission is via the orofecal route by ingestion of the L3 stages, which travel through the gastrointestinal tract until they reach their final destination, either the abomasum or the small intestine.
  • In these sites the larvae need to complete other juvenile stages before sexual maturity, at which point they will mate and produce eggs (the number of eggs and frequency varies with the species of nematode).
  • The host sheds eggs with their feces on the pasture, where the cycle starts again.
• The pre-patent period for the most common species of nematodes that can cause PGE is about 3-4 weeks, although in field conditions this number is only relevant at the very beginning of grazing season, ie diarrhea in young calves turned out the week before examination is unlikely to be caused by nematodes. However, further along the grazing season the pre-patent period is less important because reinfection occurs daily; unless the veterinarian is monitoring progression of treatment by repeated FEC. In this case, a post-treatment sample needs to be collected before the end of the pre-patent period.
• Depending on which species of nematode, they will inhabit different organs in the host. Helminth infections are most often mixed. Ostertagia ostertagi Ostertagia ostertagi and Haemonchus contortus Haemonchus spp attach to the abomasal mucosa, whereas Nematodirus battus Nematodirus spp and Cooperia oncophora Cooperia spp live in the small intestine. All species of nematodes cause varying degrees of damage to the mucosa.
• Larvae are able to overwinter both within host and on pasture:
  • Within the host they become encysted as L4 shortly after ingestion at the end of the warm grazing season. Their mass re-emergence after 3-6 months causes Type II Ostertagiosis (O. ostertagi), an acute disease that affects a small proportion of animals in a group.
  • On pasture they are able to survive many months, up to 2 years, in fairly harsh climatic conditions (they survive better under light snow cover than in mild conditions, though prolonged freezing should kill most). This enables the parasites to be already present on the grass in spring and initiate the cycle.
• The immune response develops with sufficient exposure to the parasites in the first two grazing season of the animal and is both innate and acquired. Nematodes possess a number of antigenic surface molecules and also produce other substances (Excretory/Secretory molecules, ES) that are able to elicit an immune response in the host.
• Until immunity develops, the young host is most susceptible to parasite damage and likely to show clinical signs of clinical PGE. The burdens can be high, both in the number of worms within the GI tract and the number or eggs produced.
• Different species of worms will have different prolificacy; egg numbers and frequency will change over time. Often clinical PGE is observed during the pre-patent period, when most of the damage is caused by a fast-growing population of juvenile worms. 
• As the host develops immunity, the number of parasites surviving within decreases. Once immunity is established, most cattle will harbor few worms but rarely in numbers high enough to cause clinical disease – unless other underlying conditions impair the systemic immune response.
• Local and systemic antibodies (IgA and IgG) are produced within approximately 3 weeks of infection and remain detectable in serum for many months after initial infection.