Babesiosis is an important tick-borne disease that occurs worldwide. It ranges from a relatively mild to a fatal disease. Although haemolytic anaemia is the hallmark of the disease, a number of variations and complications can occur. The genus Babesia was named after Victor Babes, who in 1887 established the aetiology of the cattle disease in Romania. The first report of canine babesiosis was in South Africa in 1885 by Hutcheon; however, the parasites were only recognised by Purvis and Koch, in 1896 and 1897 respectively. Feline babesiosis has been reported from France, Germany, Thailand, and Zimbabwe, but only appears to cause clinical disease in South Africa.

EPIDEMIOLOGY

Three subtypes of Babesia canis are recognised, namely: B. c. canis, B. c. vogeli, and B. c. rossi. The former 2 subtypes occur in Europe and North Africa respectively, whereas the latter subtype occurs in Southern Africa. Babesia gibsoni occurs in Asia, North America, and North-and East Africa.

Feline babesiosis is caused by B. felis, which is a small Babesia parasite and has been reported from France, Germany, Thailand, and Zimbabwe, but only appears to cause clinical disease in South Africa.

Canine babesiosis is tick transmitted whereas feline babesiosis is assumed to be tick transmitted, as the vector has never been isolated. Babesia c. canis is transmitted by Dermacentor reticulatus; B. c. vogeli and B. gibsoni by Rhipicephalus sanguineus; and B. c. rossi by Haemaphysalis leachi.

A seasonal variation occurs with the highest incidence in the summer months. The source of infection is carrier ticks or ticks feeding on dogs that are either ill or incubating the disease and then feeding on a susceptible dog. Other possible sources of infection are carrier dogs or blood transfusions.

Although canine and feline babesiosis can occur in animals of all ages, the majority of cases are young animals.

GENERAL LIFE CYCLE OF THE BABESIAS

In the adult tick, schizogony occurs in the gut epithelial cells, resulting in the formation of large merozoites. These merozoites then undergo successive cycles of schizogony within a variety of cell types, including the oocytes. In the salivary glands, schizogony results in the formation of small, infective merozoites. After the tick has attached to a host and feeds, the merozoites in the tick's saliva enter the host erythrocytes with the aid of a specialised apical complex. Once inside the erythrocyte, the merozoite transforms into a trophozoite, from which further merozoites develop by a process of merogony. Once divided they leave the cell to enter other erythrocytes. Both trans-stadial and trans-ovarial transmission can occur and it is believed that a tick can remain infective for a number of generations.

CLINICAL MANIFESTATIONS

Canine babesiosis

The disease can be clinical classified into uncomplicated and complicated forms. Uncomplicated cases typically present with signs relating to acute haemolysis, including fever, anorexia, depression, pale mucous membranes, splenomegaly, and a water-hammer pulse. This form is further divided into mild, moderate or severe disease, according to the severity of the anaemia.

The complicated form of babesiosis refers to clinical manifestations that are not easily explained by the haemolytic disease process alone. Possible complications included acute renal failure, cerebral signs, coagulopathy, icterus and hepatopathy, immune mediated haemolytic anaemia, acute respiratory distress syndrome, haemoconcentration, hypotension, cardiac involvement, and pancreatitis. Overlap between the different categories of the complications can also occur.

Babesia canis canis, B. c. vogeli, and B. gibsoni usually result in mild-to-moderate disease; whereas B. c. rossi results in severe and complicated disease.

Feline babesiosis

Common clinical signs include anorexia, weight loss, and anaemia. Less common signs can include icterus, vomition, pica, and respiratory signs. The disease can be protracted and often clinically silent until fairly far advanced.

CLINICAL PATHOLOGY

Canine babesiosis

The primary haematological abnormalities are anaemia, thrombocytopaenia, and leucocytosis.

Urine analysis may show hypersthenuria, bilirubinuria, haemoglobinuria, proteinuria, granular casts, and renal tubular epithelial cells.

Alterations in biochemical parameters will vary depending on the severity of the case. Typically, uncomplicated cases can have no biochemical changes. However, elevated liver enzymes, hypokalaemia in more severely affected cases, and elevated serum urea with a normal serum creatinine may be evident. In the complicated case, biochemical changes will reflect the underlying complication.

Feline babesiosis

Anaemia is the most consistent haematological finding, whereas white cell and thrombocyte counts can be variable and inconsistent.

The most remarkable changes on serum biochemistry are elevated ALT activity and hyperbilirubinuria. Other biochemical parameters are generally variable and inconsistent.

DIAGNOSIS

The diagnosis of babesiosis is made by demonstrating Babesia organisms within infected erythrocytes on a blood smear stained with a Romanowsky-type stain.

Large (2x5μm) pear-shaped organisms usually present in pairs are indicative of B. canis infection, whereas smaller (1x3μm), singular, round to oval organisms are B. gibsoni. Babesia felis parasites are approximately 1/3 of the size of B. canis and various shapes can be seen.

In less endemic areas, serology and PCR may be more reliable methods for detecting occult parasitemia.

THERAPY

Antibabesial therapy for canine babesiosis

Diminazene is administered intramuscularly at a dosage of 3,5 mg/kg once only. Diminazene has a low therapeutic index, with toxicity resulting in neurological signs 24 to 48 hours after an overdose and are irreversible and potentially fatal.

Imidocarb can be administered either intramuscularly or subcutaneously at a dose of 6mg/kg. Toxicity can cause severe renal tubular and hepatic necrosis.

Trypan blue suppresses parasitemia, alleviates clinical signs, but does not eliminate infection. It is administered strictly intravenously at a dose of 10 mg/kg.

Promising therapy for B. gibsoni is a combination of atovaquone at 13 mg/kg orally tid and azithromycin at 10mg/kg orally oid, both for 10 days. In a small group of dogs this therapy cleared infection (as detected by PCR) for over 56 days.

Antibabesial therapy for feline babesiosis

The drug of choice is the anti-malarial drug, primaquine phosphate, given at 1 mg per cat every 36 hours for 4 treatments, then 1 mg per cat every 7 days for 4 treatments. The drug does not sterilise the infection. Another drug that reportedly has some effect is doxycycline given at 5-mg/kg bid for 21 days.

Blood transfusions

Transfusions are indicated in cases that have a life-threatening anaemia. The decision to transfuse should be based on clinical signs, history and haematological testing. Packed red blood cells are the component of choice for babesiosis.

Supportive therapy

Supportive therapy should be based on thorough patient assessment and ongoing monitoring, appropriate laboratory testing and accepted therapeutic principles for the complications that may be present.

PREVENTION

The primary means of disease prevention is the control of the vector tick by routinely dipping or spraying pets, using tick collars, or spot-on preparations, and spraying of the premises. Ectoparasitic agents (such as fipronil) are also effective.

A vaccine against a specific, avirulent canine babesiosis strain (Pirodog®) is available in France; however, cross-immunity between the different strains of Babesia appears not to occur. It has recently been shown that protective immunity to a virulent strain is possible thus making vaccines from different parasite strains feasible.

Premunity has been recognised as important in controlling clinical signs of the virulent form of the disease in endemic areas, therefore complete eradication of parasites from infected animals may not be advantageous in these areas; and thus the use of drugs to sterilise the infection may be undesirable. The role that premunity plays in areas with less virulent strains is not know.

As Babesia organisms can be transmitted by blood transfusions, it is important that all blood donors are negative for babesiosis.