Bovis ISSN 2398-2993

Ostertagiosis: Types 1 and 2

Synonym(s): Stomach worm associated disease, Brown stomach worm associated disease, Parasitic gastroenteritis (In mixed infections)

Contributor(s): Rob Kelly , Andrew Forbes

Royal Dick School Veterinary Studies logo


  • Cause: Ostertagia ostertagi Ostertagia ostertagi.
  • Clinical signs: sudden onset loss of appetite, profuse green watery diarrhea/fecal staining and possibly loss of condition.
  • Subclinical infections: common in cattle of all ages, often associated with production and weight. 
  • Diagnosis: clinical signs associated with increased serum pepsinogen.
  • Treatment: albendazole, doromectin, eprinomectin, febantel, fenbendazole, ivermectin, levamisole, moxidectin, netobimin and oxfendazole.
  • Prognosis: type I typically has high morbidity and low mortality; Type II has low morbidity and potentially high mortality. 



  • Ostertagia ostertagi (specifially emergence of L4 stages from gastric glands within the abomasum and associated pathology).

Predisposing factors


  • Naïve cattle grazing pasture for the first time can acquire large burdens of O. ostertagi, which can result in disease.
  • Suitable environmental and conditions: requirement of temperate climate for development of eggs at pasture between 5-35OC. 
    • Hypobiosis occurs not only over temperate winters, but also over the dry-season in the sub-tropics, where the mechanism is more likely to relate to aridity rather than temperature. 
    • The mechanisms for both initiation of hypobiosis and reactivation are inevitably complex. Whilst it has been shown that pre-treatment (temperature exposure) of infective larvae can  induce hypobiosis in northern temperate environments, the means by which ‘resumption messages’ get to the larvae in the abomasal gastric glands is currently unknown.
  • Immunity to O. ostertagi will develop post-infection when first exposed at grazing and is usually life long. Hence low burdens of O. ostertagi are protective against clinical ostertagiosis. 


  • Two clinical presentations occur with ostertagiosis dependent upon when youngstock are exposed: 
    • Type I ostertagiosis: first grazing season within summer months (July- September in the UK) in suitable climatic conditions.
    • Type II ostertagiosis: previous grazing pasture where suitable climatic conditions occur at the end of the grazing season (summer grazing in the UK). Increase in temperatures (>5OC) after a cold period are associated with a mass emergence of L4 stages (in UK often in late winter or spring). Although the exact trigger for emergence is unclear. Cattle are usually yearlings by this stage due to nature of production systems.
  • Hence disease presentations are dependent upon the grazing system employed within the production system and understanding of the grazing system is vital for diagnosis of ostertagiosis.


  • The life cycle is direct without involvement of intermediate host species .
  • Egg are passed from adult female worms in the feces where they develop through various stages over a period of 1 to 2 weeks under optional temperatures; longer if too cold.
  • During pasture development period larvae hatch from eggs and go through 2 stages from first stage (L1) to second stage (L2) to third stage larvae (L3). The L3 stage is the infective stage to cattle. Larval development at pasture is dependent upon moisture within the fecal pat and environmental temperatures within a maximum range of 5-35OC.
  • Cattle ingest L3 from the pasture and L3 exsheaths in the rumen to invade gastric glands within the abomasum. Two further moults occur and L5 emerge from the gland and sexually mature as adults on the abomasal mucosa.  The pre-patent period (PPP) of ostertagiosis is 3-4 weeks.
  • Clinical syndromes: 
    • Type I ostertagiosis: where large burdens of O. ostertagi cause significant damage to gastric glands within the first grazing season.
    • Type II ostertagiosis: where large encystsed/ hypobiosed burdens of O. ostertagi merge from gastric glands causing significant pathology.
  • Presence and severity of disease is dependent on parasite burden and subsequent pathology. 


  • The pre-patent period (PPP) of ostertagiosis is 3-4 weeks. Development of L4 within abomasal gastric glands can arrest for a 2-6 month period.
  • Recovery from disease, post-treatment, is dependent upon O. ostertagi burden and the extent of pathological damage to the abomasum.


  • Predominately a parasite of cattle and buffalos.
  • Occasional transmission to goats and wild ruminants although these species rarely involved in transmission to cattle.
  • Epidemiology is largely dependent upon grazing systems implemented and climatic conditions for parasite development. Although eggs can develop to L3 in housing on straw.
  • Parasite survival within the environment: L3 parasites can survive winter periods in the UK on pasture and these are the main source of infection to stock when they are turned out in spring.
  • Rain can enable L3 stages to migrate from feces onto the pasture to facilitate ingestion by cattle when grazing.
  • Parasite survival within the host: L4 stages also overwinter as dormant parasites (Hypobiosis) within gastric glands of the abomasum; if mass emergence occurs type II disease occurs. If trickle emergence occurs disease is unlikely however parasites will contribute to pasture burden after turnout. 
  • Development of immunity from exposure O. ostertagi at pasture is important to prevent development of disease. Development of immunity is dependent upon O. ostertagi challenge; therefore it is a balance within the host between developing immunity or clinical disease. 
  • Small numbers of overwintered L3 contribute to establishing disease in summer months by going through various host cycles and multiplying within the host to increase burden on pasture over the grazing period.
  • Type I ostertagiosis: 
    • As mentioned previously build-up of eggs on pasture from the start of summer, through numerous life cycles, can lead to sufficient parasite burdens to cause disease (hence why type I ostertagiosis is seen from July onwards in the UK).
    • In dairy heifer replacement cattle this is a common presentation.
    • Not common in spring calving suckler herds, where challenge is low, as egg production in adult cattle is relatively low. Also in suckler herds, milk is the main source of nutrition to the calf, prior to weaning and so herbage/larval intake is low during this period.
    • Disease can occur post-weaning in both spring and autumn born calves.
  • Type II ostertagiosis: 
    • Risk of disease where youngstock are grazed on heavily contaminated pastures in autumn. Dry early summer then wet late summer can facilitate mass emergence of L3 on pasture.
  • Sub-clinical ostertagiosis: 
    • This is the most common presentation of ostertagiosis as animals of all ages harbour worm burdens and have associated abomasal pathology.
    • Losses can only be accurately quantified through comparisons between treated and untreated animals.
  • Ostertagiosis in association with cooperiosis: 
    • Mixed infections of O. ostertagi and other trichostrongyle species are common usually with Cooperia oncophora (small intestine ) and occasionally Trichostrongylus axei (abomasum).
    • Ostertagia ostertagi is usually most significant pathogen,  but co-infections with C. oncophora are predominant in first-grazing season calves and together result in parasitic gastroenteritis. 
    • C. oncophora is responsible for the majority of eggs counted in fecal samples in calves over the first half of the grazing season.
    • Clinically treatment and control are similar for O. ostertagi and mixed trichostrongyle infections. 
  • Ostertagiosis in older adult cattle: 
    • Ostertagiosis is common in all ages of cattle. 
      • In older animals infection often presents as sub-clinical disease with associated production losses.
      • Immunity can also drop during the peri-parturient period in cattle potentially resulting in a brief disease incident at calving. Although this is rare and usually there is no need to routinely treat older adult cattle.
      • If cattle have never been exposed to O. ostertagi, hence have never developed immunity to the parasites, adults can develop disease similar to youngstock.


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading


Refereed Papers

  • Recent references from PubMed and VetMed Resource.
  • Berk Z, Bishop S C, Forbes A B & Kyriazakis I (2016) A simulation model to investigate interactions between first season grazing calves and Ostertagia ostertagi. Vet Parasitol 226 pp 198–209.
  • Charlier J, De Waele V, Ducheyne E, Van der Voort M, Vande Velde F et al (2015) Decision making on helminths in cattle: diagnostics, economics and human behaviour. Ir Vet J 69 (14).
  • Crilly J P & Sargison N (2015) Ruminant coprological examination: beyond the McMaster slide. In Pract 37 pp 68–76.
  • Mihi B, van Meulder F, Vancoppernolle S, Rinaldi M, Chiers K et al (2014) Analysis of the mucosal immune responses induced by single and trickle infections with the bovine abomasal nematode Ostertagia ostertagi. Parasite Immunol 36 pp 150–156.
  • Delafosse A (2013) The association between Ostertagia ostertagi antibodies in bulk tank milk samples and parameters linked to cattle reproduction and mortality. Vet Parasitol 197 pp 212–220.
  • Knox M R, Besier R B, Le Jambre L F, Kaplan R M, Torres-Acosta J F J et al (2012) Novel approaches for the control of helminth parasites of livestock VI: Summary of discussions and conclusions. Vet Parasitol 186 pp 143–149.
  • Charlier J, Höglund J, von Samson-Himmelstjerna G, Dorny P & Vercruysse J (2009) Gastrointestinal nematode infections in adult dairy cattle: Impact on production, diagnosis and control. Vet Parasitol 164 pp 70–79.
  • Claerebout E & Vercruysse J (2000) The immune response and the evaluation of acquired immunity against gastrointestinal nematodes in cattle: a review. Parasitology 120 pp 25-42.
  • Ghadirian E & Arfaa F (1973) First report of human infection with Haemonchus contortus, Ostertagia ostertagi, and Marshallagia marshalli (family Trichostrongylidae) in Iran. J Parasitol 59 pp 1144–1145.

Other sources of information

  • COWS (2013) Control of Worms Sustainably. COWS technical manual for veterinary surgeons and advisors. [online] Available at:
  • Scott P R, Penny C D & Macrae I M (2011) Cattle Medicine. 1st Edn. London. Manson Publishing.
  • Sutherland I & Scott I (2010) Gastrointestinal nematodes of Sheep and Cattle: Biology and Control. 1st Edn. Oxford. Wiley-Blackwell.
  • Taylor M A, Coop R L & Wall R L (2007) Veterinary Parasitology. 3rd Edn. London. John Wiley and Sons Ltd.
  • Andrews A H, Blowey R W, Boyd H & Eddy R G (2004) Bovine Medicine: Diseases and Husbandry of Cattle. 2nd Edn. Oxford.


  • Royal (Dick) School of Veterinary Studies, University of Edinburgh, UK.