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Eimeria alabamensis infection

ISSN 2398-2993

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Synonym(s): pathogenic coccidial parasite oocyst coccidiosis diarrhea diarrhoea calf

Introduction

  • Cause: Eimeria alabamensis.
  • Signs: with acute presentation, clinical signs may include soft/loose feces, inappetence, lethargy, diarrhea, abdominal discomfort and tenesmus. With chronic presentation calves may show no clinical signs or weight loss/poor weight gain and ill-thrift may be reported.
  • Diagnosis:
    • Fecal microscopy smear (presence of coccidial species, pathogenic and non-pathogenic).
    • Fecal microscopy salt floatation (quantitative of coccidial species, pathogenic and non-pathogenic with higher counts suggestive of disease with clinical signs).
    • Follow up PCR speciation (differentiate between species present).
  • Treatment: diclazuril, toltrazuril, decoquinate, fluid therapy.
  • Prognosis:
    • Where outbreaks occur, relatively high morbidity in groups of susceptible individuals (commonly 3 weeks to 3 months of age). If left untreated or treated too late, clinical cases may continue to present with chronic ill-thrift with absence of resolution.
    • Low mortality, even in outbreaks.

Geographic incidence

  • Ubiquitous in populations of cattle.
  • Increased risk of disease in naïve cattle, hence higher incidence in youngstock rearing systems where there is intense infection pressure (both indoor and outdoor grazing systems). Pasture infections are anecdotally more common with E. alabamensis than other pathogenic bovine gastrointestinal Eimeria species.

Age predisposition

  • Eimeria bovis Eimeria bovis, zuernii Eimeria zuernii and alabamensis are the most pathogenic coccidial species in cattle. Eimeria alabamensis is less well known and is commonly associated with diarrhea in calves one to two weeks after turnout and sometimes later in the grazing season.
  • Generally seen in calves between 3 weeks to 3 months of age, although has been diagnosed in cattle up to a year of age. Occurrence is therefore likely related to previous exposure and infection pressure, with generally strong immunity developed after initial exposure.

Cost considerations

  • Mainly impact on weight gain in growing calves kept as replacements or as fattening stock. In one study, over a 24-day period post-exposure, affected calves lost 18 kg compared to unexposed calves that gained 6-18 kg.

Special risks

  • Limited.
  • See Coccidiosis for further information on co-morbidities.

Pathogenesis

Etiology

  • In the UK and Europe, Eimeria alabamensis is a less common cause of bovine coccidiosis Coccidiosis compared to E. bovis and E. Zuernii.
  • Oocysts in the feces are the infective stage .
  • The life cycle of E. alabamensis has 3 major stages; the first 2 stages are internally within the host (asexual and sexual replication), followed by an environmental stage (sporulation) which is infective to the bovine host .
  • Internal host stages take 5-8 days (shorter than other Eimeria species).
  • The life cycle is completed within 1 host.
  • Ingestion of a sporulated oocyst to the intestine. Each sporulated oocyst contains a total of 8 infective sporozoites which are released into intestinal contents. Each single sporozoite invades one enterocyte where replication starts by several asexual replication cycles, also known as schizogony or merogony.
  • The schizogony is a multiple fission, leading to a varying number of daughter parasite cells derived from one initial stage. During each schizogony, 100-1000s of merozoites are formed in each host cell.
  • After completion of one schizogony cycle, the merozoites leave the host cell by rupturing it to infect a new enterocyte. The merozoites form either a microgamont, which is the male stage, or a macrogamont, the female parasite stage. Once matured the microgamont ruptures into many microgametes which fertilize the macrogamont. This leads to the formation of a zygote that matures into the oocyst. Infection is self-limiting as once the life cycle is complete, there are no stages left inside the gastrointestinal tract.
  • The oocyst leaves the host cell and is excreted by the host by defecation. Oocysts are required to sporulate to become infective, which does not occur at temperatures beyond 4-37°C/39.2-98.6°F.
  • The environmental oocysts are transmitted directly by fecal-oral infection route, the susceptible hosts ingesting contaminated feed, pasture, drinking from contaminated water sources and fomites .
  • In many outbreaks of disease, intercurrent diseases or nutritional problems are present which may result in a multiple cause for ill-thrift (chronic disease). Possibly related to an associated immunosuppression on neutrophil function. For example, the cumulative immunosuppressive effects often seen in tandem with pneumonia outbreaks in housed calves.

Predisposing factors

General

Specific

  • Bovines are the primary host of E. alabamensis, being fairly host-species specific. This includes all domestic species of cattle and wild bovids such as bison.
  • Bovine coccidiosis Coccidiosis (any pathogenic Eimeria species) occurs in areas of high stocking density with significant fecal contamination, both indoors and outdoors. Particularly where conditions are moist and warm, with areas where youngstock gather such as around feed and water troughs.
  • Environmental and management factors, such as weather, housing, feeding practices and stocking densities can predispose infection. Management stresses have also been thought to predispose outbreaks.

Pathophysiology

  • The lifecycle of E. alabamensis occurs within the nuclei of intestinal cells in the distal ileum with occasional extension to the cecum and proximal colon in severe infections.
  • The highly pathogenic species E. bovis and E. zuernii cause the most severe lesions. Compared to these species, E. alabamensis pathology is dependent upon infective burden. In general, meronts might be visible by the naked eye as white plaques containing 100,000s merozoites. Severe to chronic bovine coccidiosis Coccidiosis results in extensive epithelial destruction resulting in hemorrhagic and diphtheritic enteritis localized to the part of the intestine affected (E. alabamensis distal ileum with occasionally cecum and proximal colon).
  • After exposure to pathogenic Eimeria species, immunity is protective for a particular species. The animal will then be resilient to infection but a few parasites can still develop and therefore continue to contaminate the environment. By and large, clinically affected animals contribute the most oocysts to the environment with resilient individuals maintaining presence of infection.

Timecourse

  • Unlike other bovine gastrointestinal coccidial species the pre-patent period for E. alabamensis is much shorter of 5-8 days compared with 15–21 days with E. bovis and zuernii.
  • For all pathogenic species disease can present for 5-17 days during or after the pre-patent period.
  • For E. alabamensis, peak shedding of oocysts may only last for 2-3 days, although can continue for 3 weeks.

Epidemiology

  • In the UK, disease caused by E. alabamensis is often seen in the early summer months, when youngstock are turned out to pasture or in single age cohorts. But susceptible cattle can subsequently acquire infection at any time of year, with clinical coccidiosis dependent on previous exposure. In the UK, coccidiosis was the second out of 8 most frequent reason for bovine post-mortem submissions to national veterinary surveillance laboratories between 2015-2022 between July and September.
  • Risk of disease in an environment can be related to contamination the previous year. Oocysts will survive over-winter on the grass and can remain infective in hay or other preserved fodder products.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Bangoura B & Bardsley K D (2020) Ruminant coccidiosis. Vet Clin N Am Food Anim Pract 36 (1), 187–203 SciDirect.
  • Taylor M (2000) Protozoal disease in cattle and sheep. In Practice 22 (10), 604-617 SciDirect
  • Svensson C & Olofsson H (1996) Eimeria alabamensis coccidiosis in grazing calves: control by a long-acting baquiloprim/sulphadimidine bolus. Appl Parasitol 37 (3), 168-176 PubMed.
  • Svensson C, Uggla A & Pehrson B (1994) Eimeria alabamensis infection as a cause of diarrhoea in calves at pasture. Vet Parasitol 53 (1–2), 33-43 SciDirect.
  • Foreyt W J (1989) Diagnostic parasitology. Vet Clin N Am Small Anim Pract 19 (5), 979-1000 SciDirect.
  • Soekardono S, Ernst J & Benz G W (1975) The prepatent and patent periods of Eimeria alabamensis and further description of the exogenous stages. Vet Parasitol 1 (1), 19-33 SciDirect.

Other sources of information

  • Deplazes P, Eckert J, Mathias A, von Samson-Himmelstjerna G & Zahner H (2016) Parasitology in Veterinary Medicine. First edit. Wageningen, Netherlands.
  • Taylor M A, Coop R L & Wall R L (2007) Veterinary Parasitology. 3rd edn. John Wiley and Sons Ltd, USA.
  • MSD Veterinary Manual. Coccidiosis of Cattle - Digestive System. Website: https://www.msdvetmanual.com.
  • SRUC. Coccidiosis due to Eimeria alabamensis. Website: https://www.sruc.ac.uk.

Organisation(s)

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