Difference between revisions of "Babesiosis - Horse"

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Also known as: '''''Equine Piroplasmosis — Biliary fever
 
Also known as: '''''Equine Piroplasmosis — Biliary fever
  
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|literature search = [http://www.cabdirect.org/search.html?q=(title:(Babesiosis)+OR+title:(Piroplasmosis)+OR+title:(%22Biliary+fever%22))+AND+od:(horses) Babesiosis in horses publications]
 
|literature search = [http://www.cabdirect.org/search.html?q=(title:(Babesiosis)+OR+title:(Piroplasmosis)+OR+title:(%22Biliary+fever%22))+AND+od:(horses) Babesiosis in horses publications]
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[[Category:Piroplasmida]]
 
[[Category:Piroplasmida]]

Latest revision as of 15:43, 5 January 2023

Also known as: Equine Piroplasmosis — Biliary fever

Introduction

Equine babesiosis is a tick-borne protozoal infection of donkeys, mules, horses and zebra characterised by acute haemolytic anaemia. The disease is caused by the intraerythrocytic protozoa Theileria equi (formerly Babesia equi) and Babesia caballi and is transmitted primarly by ixodid ticks. Equine babesiosis is present in most tropical and sub-tropical regions of the world where tick vectors are present. Only the United States, Canada, Australia, Japan, England and Ireland are not considered to be endemic areas. The disease is associated with high economic losses relating to treatment costs, loss of performance, abortion and death.

Aetiology and Pathogenesis

B. caballi and T. equi are transmitted by ticks, which become infected when they ingest parasites in the blood of infected horses. Approximately 15 species of ticks in the genera Dermacentor, Hyalomma and Rhipicephalus can be vectors for these organisms. T. equi can also be transmitted by Boophilus microplus. Currently, there is no evidence suggesting transmission by other insects. Infected adult ticks host several cycles of replication of Babesia spp. and final maturation of the parasite occurs when the tick attaches to a new host. For this reason, the tick must remain attached to the host for a period of time (up to a few days) before infection can occur. Equine babesiosis may also be transmitted via contaminated surgical instruments, blood products or syringes. Following recovery from infection, horses may become lifelong carriers of the disease and represent a potential reservoir of parasites.

Clinical signs

Clinical signs are generally dependent on the causative parasite. Infection with B. caballi tends to result in a milder form of disease that is often clinically unapparent whereas T. equi results in a more serious disease. The clinical presentation of the disease is variable and dependent on the immunological status of the affected animal. In rare cases, the presentation may be peracute with animals found dead within 24-48 hours of the onset of clinical signs. More often cases occur acutely with clinical signs including depression, pyrexia, inappetance, icterus, haemoglobinuria, conjunctival petechial haemorrhages amd anaemia. Small and dry faeces are often reported. Other common clinical signs include tachypnoea, ataxia and oedema of the head.

The subacute form of the disease has a similar but less severe presentation, characterised by intermittent fever, anorexia, weight loss, signs of mild colic and oedema of the distal limbs. Chronic infections are typically accompanied by varying clinical presentations including mild inappetance, weakness, weight loss and mild anaemia.

Diagnosis

The clinical signs of babesiosis are variable and diagnosis may not be straightforward. Babesiosis should be considered in any horse that is pyrexic and icteric and has been imported from an endemic area. Direct identification of the parasites in blood using a Giemsa-stained blood smear is a commonly used method of diagnosis but is not suitable for identification of babesiosis in carrier horses. For these animals, serology using an indirect fluorescent antibody test or ELISA is recommended and these are the basis of pre-import tests required by many countries. PCR in combination with reverse line blot (RLB) allows simultaneous detection and identification of different species infecting horses.

Pathology

At post mortem, the acutely affected horse is usually emaciated, icteric and anaemic. Gross lesions include hepatomegaly and splenomegaly, pericardial effusion and a pale, flabby heart. Petechial haemorrhages may be present on the kidneys with oedema of the renal capsule a common feature.

Treatment

Specific anti-Babesia antibiotics (imidocarb diproprionate) are used to treat the disease. Higher success rates are associated with treatment of B. caballi compared with T. equi. It has recently been reported, that even high dose treatment with imidocarb may not be capable of eliminating B. caballi and T. equi from healthy carriers. However, success with high doses of imidocarb has also been reported.[1]

Control

In non-endemic areas, carrier horses should not be imported. If they are, they should be identified using serological testing, quarantined and treated.


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References

  • Butler, C. M., Nijhof, A. M., van der Kolk, J. H., de Haseth, O. B., Taoufik, A., Jongejan, F., Houwers, D. J. (2008) Repeated high dose imidocarb dipropionate treatment did not eliminate Babesia caballi from naturally infected horses as determined by PCR-reverse line blot hybridization Veterinary Parasitology 151:320–322
  • Knottenbelt, D. D., Pascoe, R. R. (2003) Diseases and Disorders of the Horse Elsevier Health Sciences
  • Radostits, O. M., Arundel, J. H., Gay, C. C. (2000) Veterinary Medicine: A Textbook of the diseases of cattle, sheep, pigs goats and horses Elsevier Health Sciences
  • Sellon, D. C., Long, M. T. (2007) Equine Infectious Diseases Elsevier Health Sciences



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