Bovine babesiosis

After an incubation of usually 8 to 15 days, cattle develop high fever, then dullness, loss of appetite, weakness and reluctance to move. B. bigemina produces a rapidly developing anaemia with red urine. With B. bovis, red urine often appears as disease progresses but may be late or absent; jaundice, diarrhoea, abortion, muscle wasting, tremors and recumbency follow, and some animals show nervous signs such as hypersensitivity, nystagmus, circling, head pressing, aggression and convulsions. At necropsy B. bovis cases show a greatly enlarged spleen, a swollen yellow-brown liver with thick bile, enlarged kidneys and cherry-pink cerebral grey matter; B. bigemina carcasses are pale and watery-blooded, often with pulmonary oedema.

Bovine babesiosis is caused by tick-transmitted intraerythrocytic protozoa of the genus Babesia (order Piroplasmida), chiefly Babesia bovis and B. bigemina, with B. divergens in parts of Europe. The two main species damage the host differently. B. bigemina disease is driven almost entirely by rapid, sometimes massive intravascular haemolysis, so anaemia and haemoglobinuria dominate, and infected red cells do not sequester. B. bovis is the more pathogenic despite parasitaemias usually below 1%: parasite products trigger release of vasoactive substances and coagulation activation, producing hypotensive shock and vascular stasis, while infected red cells lodge in capillaries, including those of the brain, causing nervous signs. Recovered cattle are immune to the same species for life.

Cattle are the main host; water buffalo are usually infected with few or no signs. B. bovis and B. bigemina are widespread in Africa, Asia, Australia and the Americas, transmitted mainly by one-host ticks of the genus Rhipicephalus (Boophilus); Ixodes ricinus carries B. divergens. In Egypt, Babesia is described as the most endemic blood parasite of cattle and buffalo, spread by R. annulatus and R. microplus; in a May-September clinical survey in north-central Algeria the few B. bovis cases (6 of 299) clustered in July. Calves rarely show disease, and Bos indicus cattle are more resistant than Bos taurus, so outbreaks follow when susceptible adult or imported cattle meet infected ticks. Surviving B. bovis cases can remain carriers. It is a WOAH-listed disease.

Anaplasmosis, especially in cattle with anaemia and jaundice but no red urine; leptospirosis, chronic copper poisoning and plant toxicities, which also cause haemolysis and red urine; and theileriosis, which co-circulates with Babesia in north Africa. The cerebral form of B. bovis resembles heartwater, cerebral theileriosis, sporadic bovine encephalomyelitis, plant or organochlorine poisoning and thiamine-deficiency cerebrocortical necrosis. Demonstrating parasites in Giemsa-stained blood films (capillary blood for B. bovis) or brain smears confirms Babesia; PCR differentiates species and detects carriers.

Red blood cells and blood vessels, spleen, liver, kidneys, brain (cerebral capillaries), lungs, mucous membranes

Live attenuated vaccines in calves under 1 year: immunity in 3-4 weeks, lasting at least 4 years in most cases (WOAH) vs 4-6 weeks, lasting years for B. bovis but may wane for B. bigemina (Anipedia); tick control; resistant Bos indicus breeds.

Cerebral B. bovis cases are almost always fatal and acute cases can die within days. Early specific antiprotozoal treatment helps. Non-fatal cases take weeks to regain condition but usually recover fully and become immune.