Bovis ISSN 2398-2993

Ostertagia ostertagi

Synonym(s): Stomach worm, Brown stomach worm

Contributor(s): Rob Kelly , Andrew Forbes

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Introduction

Classification

Taxonomy

  • Nematoda; Trichostrongyloidea; Ostertagia ostertagi.

Etymology

  • Ostertagia ostertagi is one of the most important gastrointestinal parasites in cattle with infections reported in cattle populations across the globe.
  • Ostertagiosis is readily seen in temperate climates in various disease presentations and is occasionally seen in sub-tropical climates. Immunity is acquired over two grazing seasons, so disease is primarily seen in youngstock.
  • Specifically, a parasite of cattle and buffalos. Occasionally goats and deer. A related parasite, Telodorsagia circumcincta, infects and can cause disease in sheep. 

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Clinical Effects

Epidemiology

  • Predominately a parasite of cattle and buffalos. 
    • Occasional transmission to goats and wild ruminants although these are 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, with improved survival in colder winters. However, overwintered parasites are unlikely to contribute to clinical disease in the UK. 
      • In mild conditions, larval mortality increases through higher metabolic rate and depletion of glycogen stores. Survival is better if the winter is cold and with a covering of snow.
  • Under favourable conditions L3 can survive on pasture for up to 2 years.
    • However small numbers of overwintered parasites can contribute to sub-clinical disease the next spring in naïve animals.
  • Requirement of temperate climate for development of eggs at pasture between 5-30°C. 
    • Encysted stages can hypobiose for 2-6 months L3 stages can survive on pasture under snow for long periods.
  • 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. 
  • Development of immunity from exposure O. ostertagi at pasture is important to prevent development of disease.
    • Development of immunity is dependent upon O. ostertagi exposure and typically requires two complete grazing seasons to be functional. 
  • 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.

Lifecycle

  • The life cycle is direct without involvement of intermediate host species .
  • Egg are passed from adult parasites into the feces contaminate the pasture and develop through various stages within feces over approximately 2 weeks.
  • During pasture development period larvae hatch from eggs and go through 2 exsheathing 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 between 5-35OC.
  • Cattle ingest L3 from the pasture and L3 exsheaths in the rumen to invade gastrin glands within the abomasum. Two further exsheathing stages occur and L5 migrate out of the gland and sexually mature on the mucosa of the abomasum. The pre-patent period (PPP) of ostertagiosis is 3-4 weeks.
  • If external temperatures drop < 5OC L4 larvae can encyst/ hypobiose for between 2-6 months. Clinical syndromes:
    • Type I ostertagiosis: where large burdens of O. ostertagi cause significant damage to gastric glands during the grazing season.
    • Type II ostertagiosis: where large encystsed/ hypobiosed burdens of O. ostertagi remerge from gastric glands causing significant pathology.
    • Subclinical forms occur where there may be marked loss in production.
  • Presence and severity of disease is dependent on parasite burden and subsequent pathology.
  • Development of immunity is dependent upon sufficient exposure to parasites over first and second grazing season at pasture.
  • Development of immunity is dependent upon sufficient exposure to parasites over first and second grazing season at pasture.
  • Certain husbandry systems can impact on the risk of ostertagiosis occurring. Such as suckler cows grazing with calves at foot that will provide low levels of exposure to calves so they develop immunity. While at the same time dams co-grazing will limit number of infective larvae on pasture. However in highly stock pasture, cows can contribute significantly to pasture contamination due to their high fecal output. 
  • 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 when L3 are exposed to temperatures below 5°C in the autumn.
Transmission
  • Eggs are shed onto pasture and development of L1 through L2 to L3 stages occurs within the fecal pat at temperatures between 5-35°C at 60-70% humidity.
  • Infective L3 stages are found on pasture where cattle are grazed and attach to herbage.

Disease presentations

  • Further information about clinical Ostertagiosis can be found by following this link: Ostertagiosis types 1 and 2 .
  • Type I ostertagiosis:
    • As mentioned previously, build up of larvae 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 low and provides a level of immunity to a low exposure to younger cattle. Yet can be a problem in autumn born calves.
  • Type II ostertagiosis:
    • Typically the risk of type II disease is where youngstock are grazed on pasture in early summer, cattle are taken off, and returned to the same pasture in late summer. This can facilitate a build up of O. ostertagi L3 on pasture and large burdens which are associated with disease. 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 and can be seen in cattle of all ages, whether naïve or immune.
    • Subclinical infections typically arise when larval intake is insufficient to cause clinical disease, but abomasal pathology and associated biochemical changes, an increase in gastrin for example, lead to inappetance and suboptimal production.
    • Can be associated with the low numbers of overwintered larvae present on pasture.
  • Ostertagiosis in association with cooperiosis:
    • Mixed infections of O. ostertagi and other trichostrongyle species are common usually with Cooperia oncophera (abomasum) and occasionally Trichostrongylus axei (abomasum).
    • Ostertagia ostertagi is usually most significant pathogen, but occasionally C. oncophera can important in its own right or in association with O. ostertagi. 
    • Clinically treatment and control are similar for O. ostertagi and mixed trichostrongyle infections. 
  • Ostertagiosis in older adult cattle:
    • O. ostertagi is ubiquitous on pasture-based cattle farms and infection is present in animals of all ages. Through acquired immunity, worm burdens tend to be lower in adult cows, but typically >90% of normal, ‘healthy’ adults have abomasal pathology, sometimes quite extensive.
    • Clinical disease is uncommon, but production losses (lower milk yield) are common in cows. 
    • There is limited evidence for a peri-parturient decline in immunity in cattle, but it has been observed, though without clinical signs.

Pathological effects

  • Pathology is predominately associated after ingested L3 have invading gastric glands within the abomasum and growing in size, through successive moults to L5 stage, which emerges from the gland.
  • Round nodules sometimes win a pin-prick centre are noted within the mucosal surface of the abomasum. Caused by development of L3-L5 within gastric glands. Inhibited larvae are very small and do not provoke and inflammatory or immune response, nor any visible pathology. In active disease there is often edema present within the folds of the abomasum and can be pale or necrotic. Hardened nodules may be evident from historic infections. Pathology is colloquially described as “Moroccan leather” due to the gross appearance of the abomasal surface .
  • Recovery from disease, post-treatment, is dependent upon O. ostertagi burden and the extent of pathological damage to the abomasum.

Other Host Effects

  • High morbidity in outbreaks but mortality is usually low. Prompt anthelmintic treatment usually results in clearance of susceptible parasite stages.
  • Severely affected cattle may have extremely retarded growth rates and may never reach their live weight gain potential.
  • Co-infections are common with Trichostrongylus axei Trichostrongylus axei and Cooperia species Cooperia species such as C. oncophora which may or may not contribute to clinical disease. Reports of co-infection with F. hepatica F. hepatica have reported to potentially add to the detrimental effects of high parasitic burdens.

Control

Control via animal
  • Development of immunity is dependent upon sufficient exposure to parasites over the first two grazing seasons at pasture.
  • Certain husbandry systems will limit the impact of ostertagiosis occurring. Such as suckler cows grazing with calves at foot that will provide low levels of exposure to calves so they develop immunity. While at the same time dams co-grazing will minimise number of infective larvae on pasture.
Control via chemotherapies
Type I ostertagiosis
  • Anthelmintic treatment of clinical cases such as albendazole, doromectin, eprinomectin Eprinomectin, febantel, fenbendazole Fenbendazole, ivermectin Ivermectin, levamisole Levamisole, moxidectin Moxidectin, netobimin and oxfendazole are efficacious against the active stages of the parasites. 
  • Treated animals should be moved onto pasture that has not grazed youngstock the previous year. 
Type II ostertagiosis
  • Appropriate anthelmintic treatment of clinical cases is required as not all stages are active against encysted/ hypobiotic larvae. Macrocyclic lactones (ML), such as Doromectin, Eprinomectin Eprinomectin, Ivermectin Ivermectin and Moxidectin Moxidectin are highly effective. The efficacy of benzimidazoles such as albendazole, Fenbendazole Fenbendazole and Oxfendazole is highly variable against arrested encysted/ hypobiosed L4 and Levamisole Levamisole is ineffective.
  • In severely dehydrated cases, rarely seen with cases of type II ostertagiosis, Fluid therapy Fluid therapy may be required to counterbalance hydration.
  • Provide additional nutrition to support improvement of growth rate. Additional protein provided within the diet can be useful to counterbalance protein losses in recovering animals.
  • For lactating cattle products are available without milk withholds.
  • Strategic treatment with anthelmintics can be useful to prevent against clinical or sub-clinical ostertagiosis. Although targeted and sustainable use of anthelmintics is strongly recommended to avoid selecting for anthelmintic resistance. Some examples are provided below: 
    • Preventative treatments are generally given to minimise egg output and hence larval contamination. The timing of such treatments is based on assumptions regarding to seasonal epidemiology, rather than diagnostic tests.
    • Strategic treatments at turn out or housing where indicated (the latter for type II ostertagiosis).
    • Targeted selective treatment (TST) of animals with evidence ostertagiosis within a group. 
      • Such as measuring poor weight gain, increased blood pepsinogen, FWECs or loss body condition and only treating animals affected.
      •  Taking care to also monitor for other diseases such as Lungworm Lungworm (D. viviparus) and Liver fluke Liver fluke (Fasciola hepatica) and treat where necessary.
    • Prolonged action anthelmintics can be useful in high challenge. 
  • Overall an integrated approach should be adopted as necessary to avoid over reliance on anthelmintic treatments and to avoid selecting for anthelmintic resistance.
Control via environment
  • Due to the specific risk period for ostertagiosis related to grazing at specific times of year; a review of yearly pasture management of youngstock should be adopted where ostertagiosis is a problem. Avoiding overuse of pastures where intensive grazing strategies may lead to heavy pasture burdens.
  • Due to the development of immunity in adult cattle alternate year grazing has been advocated in some instances between adult and youngstock. Also such rotational grazing practices as between sheep, cattle and crops on an annual basis. Thus minimising pasture burden that might be useful in organic herds. However such control practices maybe contraindicated where lungworm is present, as rotational grazing may result in waning of protective immunity and result in outbreaks of parasitic bronchitis. 
Other countermeasures
  • Treatment failures: 
    • Under dosing of anthelmintic which may select for anthelmintic resistance if undertaken repetitively.
    • Anthelmintic resistance. Benzamidazole resistance One Health has been reported for O.ostertagi, C. oncophora and T. axei in the UK, Europe, Australia, New Zealand, USA and South Africa.
    • ML- resistant O. ostertagi also reported in Europe and elsewhere, though currently incidence is quite low.
    • Suspected cases of anthelmintic resistance should be investigated as appropriate. Refer to COWS guidelines of how to do this and how to minimize selection for anthelmintic resistance.

Diagnosis

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Further Reading

Publications

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 pp198–209. 
  • 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 pp 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 Suppl: S25-42.
  • Burden D J, Hughes D L, Hammet N C & Collis K A (1978) Concurrent daily infection of calves with Fasciola hepatica and Ostertagia ostertagi. Research in Veterinary Science 25 (3) pp 302–6. 

Other sources of information

  • Taylor M A (2013) COWS technical manual for veterinary surgeons and advisors. [online] Available at: http://beefandlamb.ahdb.org.uk.
  • 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.

Organisation(s)

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

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