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Home \ INFEQUUS \ Equine piroplasmosis



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Differential diagnosis of infectious diseases of equidae

Equine piroplasmosis disease information
Disease
Equine piroplasmosis

Synonyms
Equine malaria Equine babesiosis Equine theileriosis Equine biliary fever

Vector
Hyalomma spp. Dermacentor spp. Rhipicephalus spp.

Agents
Theileria equi
 Acronym: T. equi
 Type: Parasite
 Family: Theileriidae
 Gender: Theileria
Babesia caballi
 Acronym: B. caballi
 Type: Parasite
 Family: Babesiidae
 Gender: Babesia

Clinical signs
Fever Death Anaemia Jaundice Weakness Anorexia Lethargy Tachypnea Tachycardia Weight loss Petechiation Splenomegaly Bilirubinuria Liver disease Renal failure Hemoglobinuria Thrombocytopenia Peripheral oedema Disseminated intravascular coagulation

Equine piroplasmosis
Figure 1: Theileria equi blood smear. SEVISEQ


Equine piroplasmosis
Figure 2: Babesia caballi blood smear. SEVISEQ


Equine piroplasmosis

Etiology

Equine piroplasmosis (EP) is an infectious disease caused by the intraerythrocytic protozoan parasites B. caballi and T.equi. Previously, T. equi was known as Babesia equi. These parasites are transmitted by ixodid ticks of the genera Dermacentor, Hyalomma and Rhipicephalus; although iatrogenic transmission can also occur. In the case of T. equi, a placentary transmission has been described. Horses that survive can become inapparent carriers for a long time (4 years for B. caballi or lifelong for T. equi) and they can act such a source of infection for the ticks, which will parasite more horses. This disease is important since it is the main restriction on the export of horses to other countries.


Epidemiology

EP is an endemic disease  present in tropical and subtropical regions. By contrast, Canada, Iceland, Australia and Japan are free countries currently. In the US, the infection would be limited to one or more areas.
B. caballi and T. equi present a indirect biological cycle. The cycle starts when sporozoites are transmitted through the infected tick saliva to the equid host.

  • B. caballi: sporozoites invade erythrocytes directly and they reproduce asexually first to trophozoites and then to merozoites. The merozoites continue to reproduce asexually causing the rupture and invasion of new red blood cells.
  • T equi: sporozoites invade peripheral blood mononuclear cells (PBMCs), they reproduce asexually first to schizonts and then to merozoites and they cause the rupture of these cells. The merozoites invade the erythrocytes, which continue to reproduce asexually and invade new red blood cells.
In both cases, the merozoites will be ingested by a tick, in whose midgut they will reproduce sexually until the zygote phase. The zygote will reach the salivary gland of the tick and the sporozoites will form.


Pathogeny

EP is characterized by an haemolytic anemia, which results from the lysis of erythrocytes (due to merozoites multiplication) as well as from removal of infected  erythrocytes by the spleen. It has been seen that nonparasitized erythrocytes are also eliminated, but the reason is unknown. Thrombocytopenia, alter coagulation, vasculitis, and formation of microthrombi within small vessels may also be observed. Transplacental transmission can result in abortions (late gestation most common), stillbirths, or birth of an infected foal, but not all foals from infected mares will be affected. Colostral antibodies against both parasites may persist in the foal for 4 to 5 months. Horses infected with T.equi produce antibodies against equi merozoite antigen (EMA-1) and those infected with B. caballi to rhoptry associated protein 1 (RAP 1).


Clinical signs

The clinical signs are variable and nonspecific. In general, the infection with T. equi results in more severe clinical disease than the infection with B. caballi. The presentation can be hyperacute, acute or chronic. The hyperacute form is rare and horses may be found dead. Signs of acute infection can vary from fever, anorexia, lethargy and peripheral edema to anemia, jaundice, tachycardia, tachypnea, hemoglobinuria and/or bilirubinuria, thrombocytopenia and petechiae on mucous membranes. Chronic infection may result in weight loss, lethargy, partial anorexia and splenomegaly on rectal palpation.


Diagnosis

During the acute state of the infection, EP can be diagnosed through a thin blood smear stained to identify the parasites within the erythrocytes (although this method has a low sensitivity), PCR and through several serologic tests such as the complement fixation test (CFT can detect seroconversion approximately 8 to 11 days after infection) and the indirect fluorescent antibody test (IFAT may detect seroconversion 3 to 20 days after infection). The competitive enzyme-linked immunosorbent assay (c-ELISA) is considered to be the most sensitive test for chronic infection or identifications of carriers, detecting seroconversion 21 days after infection.


Treatment

Several drugs have proved to alleviate clinical signs, being imidocarb dipropionate (ID) administered intramuscularly, together with a correct hydration of the animal, the most effective. ID has anticholinesterase activity, so reactions to the drug as sweating, signs of agitation, colic and diarrhea are often present. Other drugs used against equine piroplasmosis are diminazene aceturate and diaminazene diaceturate, but upon administration they can cause severe muscle damage. The antibiotic oxytetracycline administered intravenously is effective against T. equi, but not against B. caballi. Finally, buparvaquone is no longer commonly utilized in practice.


Prevention and control

There are no vaccines available for these parasites. The regular evaluation of the animal, the elimination of the ticks and the use of acaricides can help to prevent the infection.


Public Health Considerations

Equine piroplasmosis is a non-zoonosic disease, but it is included in the OIE list of notifiable diseases.


References