Equine Babesiosis - A Review

Russell Z. Edwards, DVM; Holly Moore, DVM; Bruce E. LeRoy, DVM, PhD; and Kenneth S. Latimer, DVM, PhD

Class of 2005 (Edwards) and Department of Pathology (Moore, LeRoy, Latimer) College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388

Introduction

Equine babesiosis is an acute, subacute, or chronic infectious hemolytic disease caused by the intraerythrocytic protozoa Babesia equi and Babesia caballi. The disease is also known as equine piroplasmosis and "biliary fever." Endemic in most tropical and subtropical regions of the world, this infection has been documented in horses, mules, donkeys, and zebras. The occurrence of equine babesiosis has been tied closely with the geographic distribution and seasonal activity of its biological vectors: species of ticks in the genus Dermacentor, Rhipicephalus, and Hyalomma. Historically, babesiosis has had the greatest impact in southern Africa, where it was first described around the turn of the century as "anthrax fever," "biliary fever," a "billous form" of African Horse Sickness, or "equine malaria." In recent times, equine babesiosis has spread from its endemic tropical and subtropical zones to more temperate regions as global transport of equids has increased greatly. For example, both species of Babesia affecting horses were introduced into the United States around 1958 with the importation of Cuban horses to Florida. Equine babesiosis is now considered endemic in some areas of the southeastern United States.

Etiology

Babesiosis in the horse is caused by two protozoal piroplasms, Babesia equi and Babesia caballi. These organisms currently are the only erythroparasites of clinical significance in North American horses. B. caballi is a relatively large member of the genus and its appearance has been likened to B. bigemina, the species responsible for Texas Cattle Fever. The development of B. caballi in the host occurs exclusively in erythrocytes. The trophozoites appear as round, oval, or elliptical basophilic structures that measure 1.5 to 3µm in diameter. The organisms are intraerythrocytic within the cytoplasm of erythrocytes (Fig.1). Pairs of organisms are commonly found in a single erythrocyte oriented such that they form an acute angle. Babesia equi, in contrast, is a smaller member of the genus and has been found to have an extraerythrocytic stage of shizogony occurring in host lymphocytes. Similarities to the bovine pathogen Theileria have stimulated debate over the rightful taxonomic classification of this organism. Trophozoites of B. equi appear as oval, round, elliptical, or spindle-shaped basophilic structures that measure up to 3µm in diameter (Fig. 2). The merozoite stage appears as two or four pyriform parasites together within the erythrocyte, each with a length of only 1.5 µm on average. When four Babesia equi merozoites are present together in one cell, they frequently form a characteristic "Maltese cross" (Fig. 3).

Figure 1. Babesia caballi in equine erythrocyte.

Figure 2. Babesia equi in equine blood smear.	Figure 3. Babesia equi merozoites form "Maltese cross."

Transmission

Horses become infected with the Babesia organism when they are parasitized by feeding ticks that harbor the sporozoites in their salivary secretions. Ticks acquire the organism by taking a blood meal from infected horses. Infected adult ticks host several successive cycles of replication of Babesia sp., and gut epithelial cells, ova, and salivary glands become infected with the organism. Replication involves the eventual liberation of sporozoites into the salivary gland lumen in the offspring upon reaching the feeding nymph stage. Transmission to the horse occurs when these infected nymphal ticks inject the sporozoites into the new host during feeding. Competent tick vectors for Babesia caballi and Babesia equi are listed below.

In addition to transmission via infected ticks, babesiosis also may be spread iatrogenically by blood-contaminated needles or surgical instruments. At the present time, there is no evidence of transmission by other insects.

Clinical Signs

Rarely, a peracute form of the disease occurs in which horses die within 24-48 hours of the onset of clinical signs. Clinical signs of equine babesiosis generally follow a variable incubation period of 5 to 21 days.

The acute form of the disease usually involves fever, malaise, anorexia, depression, icterus, hemoglobinemia / hemoglobinuria, pale mucous membranes, tachycardia, and tachypnea. Additional features that may or may not be seen include sweating, colic, lacrimation, incoordination, cardiac murmurs, and subcutaneous edema around the head and eyelids.

Subacute cases are characterized by intermittent fever, anorexia, weight loss, tachycardia, tachypnea, with variable degrees of icterus, hemoglobinuria, and bilirubinuria.

Chronic infections typically result in variable clinical presentations involving inappetance, weight loss, weakness, and mild anemia. Of the two causative organisms, B. equi is considered the more pathogenic. While B. caballi is known to produce a more persistent fever and anorexia, B. equi is responsible for a greater incidence of hemoglobinuria and death. A variety of secondary complications may result from babesiosis including acute renal failure, colic, enteritis, laminitis, pneumonia, infertility, and abortion. Important differential diagnoses that should be considered in cases with suspect clinical signs of babesiosis include equine infectious anemia (EIA), monocytic ehrlichiosis, red maple toxicosis, and hepatic disease.

Pathogenesis and Pathologic findings

The exact pathogenesis of equine babesiosis is not known completely, but metabolic stress placed on the parasitized erythrocytes may cause hypophosphatemia and weakening of erythrocytic cell membranes causing hemolysis. Parasitized red cells lyse intravascularly, producing hemoglobinemia in the acute phases of the disease. The intravascular hemolysis causes a marked hyperbilirubinemia and icterus can be pronounced in many cases. Hemoglobinuria seems to occur more frequently and severely with Babesia equi infections, but can be seen in horses infected with either species. In addition to regenerative hemolytic anemia, a significant monocytosis and eosinopenia may be observed in horses with babesiosis. In severe disease, the intravascular hemolysis produced by the infection may disturb capillary blood flow enough to cause disseminated intravascular coagulation (DIC) and resulting signs of coagulopathy.

Along with appropriate clinical signs and pathologic findings of hemolytic anemia, the identification of the parasitized erythrocytes on routinely stained blood smears is diagnostic (Fig. 4). In cases of chronic or subacute babesiosis, it may not always be possible to visualize the organisms on blood smear examination. In these situations, PCR, ELISA, serology, or a combination of these tests is used to establish a diagnosis. The most commonly used serologic tests are the complement fixation (CF) and indirect fluorescent antibody (IFA) tests. Gross necropsy findings of horses with babesiosis include thin watery blood, icterus, effusions of the body cavities and pericardium, hepatomegaly, and splenomegaly.

Figure 4. Equine blood smear with B. caballi in erythrocyte

Treatment and Prevention

If equine babesiosis is diagnosed and treated early, there is an excellent chance of recovery. However, Babesia equi infections are known to be more refractory to treatment than those caused by Babesia caballi. Imidocarb is a babesiacidal drug that is administered at a dosage of 2.2mg /kg. Two treatments are administered at a 24-hour interval. For cases of Babesia equi that are resistant to therapy, a dose of 4mg /kg is administered 4 times at 72-hour intervals. This regimen is often effective in treating the infection. Prevention of babesiosis requires control of tick infestations and avoiding iatrogenic transfer of infected blood during routine surgical and medical procedures. Vaccines are not commercially available at this time to prevent disease or boost immunity to Babesia spp. infections.

References

Coetzer JAW, Thomson GR, Tustin RC (eds): Infectious Diseases of Livestock, vol. 1. Oxford University Press, New York, 1994.

Cowell RL, Tyler RD: Cytology and Hematology of the Horse, 1st ed. American Veterinary Publications, Inc., California, 1992.

Hendrix CM: Diagnostic Veterinary Parasitology, 2nd ed., Mosby, Inc. St. Louis, 1998.

Jain NC: Essentials of Veterinary Hematology, Lea & Febiger, Philadelphia, 1993.

Levine ND: Veterinary Protozoology. Iowa State University Press, Ames, Iowa, 1985.

Jones TC, Hunt RD, King NW: Veterinary Pathology, 4th ed., Lea & Febiger, Philadelphia, 1972.

Smith BP: Large Animal Internal Medicine, 3rd ed., Mosby, Inc., St. Louis, 2002.

Acknowledgement

The image "Running Dream" (© 2003 Kaija Savinainen Mountain) is from the Willow Creek Studio website and is used with permission.

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