It is a tick transmitted haemoprotozoan infection of cattle, buffalo, horse, sheep, goat, dog, pig, wild animals and man characterized by fever, anaemia, haemoglobinuria and haemoglobinuria.
Distribution
Babesia was first reported in 1885 in South Africa.
The disease is world wide in distribution. The disease has got a serious economic impact due to obvious reason of death, decreased production and lowered working efficiency. In India, babesiosis is one of the important diseases and has been reported from all the States. There is high percentage of sero reactors among cattle of different States of India.
The genus Babesia was named after Victor Babes who in 1987 established its aetilogy.
Aetilogy
Cattle, Buffalo – Babesia bigemina; Babesia bovis; Babesia divergens; Babesia major
Horse – Babesia equi; Babesia caballi
Sheep – Babesia motasi; Babesia ovis
Pig – Babesia trautmanni
Dog – Babesia canis; Babesia gibsoni
Cat – Babesia felis
Babesia parasite has been placed on record for the first time by Babes in 1888 from blood from African cattle.
In dog, three subtypes of Babesia canis have been recorded. They are B.C. canis. B.C. vogeli and B.C rossi. The canis and vogeli subtypes occur in Europe and Sough Africa. Whereas rossi occur in Sough Africa. B. gibsoni occurs in Asia, North America and North and East Africa.
Feline Babesia is caused by B. felis do occur in France, Germany, Thailand and Zimbabwe, Canine Babesia is tick transmitted but cat babesia’s vector seldom is available. Babesia C. canis is transmitted by Dermacentor reticulatus B.C vogeli and B. gibsoni by Rhipicephalus sanguineus and B.C. rossi by Haemophysalis leachi. Though the disease may occur in any age in dog and cat but majority cases suffer in younger age group.
Susceptible Hosts
The disease has been recorded in all breeds of cattle but more commonly in exotic and cross bred rather than indigenous one. In cattle, highest infection rate is observed in 6-12 months of age. In general, cattle under one year of age are infected with B. bigemina and cattle over two years of age by B. bovis.
The disease is also seen in water buffalo, horse, sheep, goat, pig, dog, wild animals and man. Seroprevalence of Babesia bigemina infection in buffalo has been reported from India. It has been recorded in a 14 days old cow calf in sub-acute manner. Some workers reported it in 2 days to 1 month of age in calf.
Mode of Transmission
The disease is transmitted under natural conditions from affected to healthy animals through ticks.
Transmission is not merely a mechanical process as parasites undergo developmental stages within the body of ticks before they are conveyed in the saliva in an infective form. Many species of ticks have been incriminated to be the natural vectors of babesiosis. Beephilus microplus and as vector of clinical cases of Babesia bigemina. In horse, Dermacentor Hyalomma and Rhipicephalus are responsible for transmission of both Babesia spp. Babesiosis is transmitted by Rhipicephalus haemaphysalis, Dermacentor and Ixodes ticks. Porcine babesiosis through transovarial route by Rhipicephalus sanguineus is possible. Canine babesiosis is transmitted by the ticks of the genera Rhipicephalus, Dermacenor, Hyalomma and Haemaphysalis. In general, the disease is transmitted transovarially or trans-stadially. A carrier state in dog following recovery has been suggested. The disease can also be transmitted by parenteral injection of infected blood or organ emulsion or blood transfusion. Blood donors should be negative for babesiosis.
Pathogenesis
The incubation period varies depending on the species of Babesia involved and it ranges from 5-10 days. Following infection multiplication of protozoa occurs in peripheral vessels and there is intravascular haemolysis. It has been pointed out that proteolytic enzymes are liberated from the infected erythrocytes and these enzymes interact with components of blood and thus lead to increased erythrocytic fragility, hypotensive shock and disseminated intravascular coagulation.
It is also postulated that coating of RBC by parasitic antigen neutralizes the normal surface charge and thereby favours autoagglutination of RBC. Parasitaemia, fever and haemoglobinuria are the main clinical attributes. Death occurs due to anaemic anoxia.
Clinical Findings
The babesiosis is characterized by high fever, anorexia, depression and weakness. There is increased heart and respiratory rate. The conjunctival mucous membrane is brick red in the initial stages and pale in the terminal stage. In the terminal stage of the disease, there is severe jaundice and haemoglobinuria. But, jaundice is not common in B. gibsoni infection.
In young animals, the disease is associated with subclinical manifestation due to age resistance. Experimental splenectomised animals show depression, inappetence followed by high rise of temperature, haemoglobinuria and marked anaemia.
In sizeable percentage of cases, the temperature comes down to lower level within 6-8 hours of the appearance of haemoglobinuria. The febrile period is characterized by tremors of skeletal muscles. When the temperature recedes, the animals assume either lateral recumbency or prostration. In B. bovis infection, spasms of anal sphincter and ‘Pipe stem’ faeces are observed. In fatal cases, the animals are unable to stand on their feet in spite of support. A few hours before death, tremors of the neck muscles, involuntary movements of the fascial muscles accompanies by shallow, jerky respiration are observed. B. bovis infection may involve the central nervous system leading to ataxia, paddling of limbs and coma. This is associated with sludging of parasitized RBC in brain capillaries. In recovering cases of fall of temperature is gradual. They can stand of their feet without support in spite of debility. Haemoglobinuria in such cases last for a day or two. The clinical pictures of ovine and caprine babesiosis are similar to bovine babesiosis.
In dog, five forms of the disease may be encountered.
Alimentary form – Characterized by stomatitis, gastritis and enteritis
Respiratory form – Characterized by respiratory distress
Circulatory form – Characterized by oedema
Ocular form – Characterized by keratitis and iritis
Muscular form – Characterized by muscle weakness
Atypical signs like convulsion, locomotor disturbance, ascites, dyspnoea, cough, enlarged tonsils and bleeding from muzzle may be observed in some cases.
Disease has been classified as (a) complicated form and (b) uncomplicated form.
(a) Complicated form in dog: This results due to haemolytic process. Complications comprise of acute renal failure, cerebral signs, coagulopathy, icterus, hepatopathy, immune mediated haemolytic anaemia, acute respiratory distress, haemoconcentration, hypotension, cardiac involvement and pancreatitis.
(b) Uncomplicated form in dog: Acute haemolysis, fever, anorexia, depression, pale mucous membrane, splenomegaly and severe depending on the severity.
In horses, haemoglobinuria is rare in occurrence and jaundice is more common hence it is known as ‘biliary fever’.
Clinical Pathology
Haematology
- There is severe anaemia. The mean PCV, total erythrocyte count and haemoglobin values drop by 16, 20 and 24% within 48 hours.
- There is increased leucocyte count associated with moderate neutrophilia.
- There is presence of albumin and bile pigment in the urine.
- There is increased level of blood glucose, total serum bilirubin and SGOT level.
Lesion
Carcass is anaemic. There is frothy exudate in the trachea and bronchi and oedema of the lungs. Blood stained fluid occurs in the pericardium. There is degenerative changes in the liver and kidneys. Gall bladder is distended with dark green bile. Subcutaneous tissues and muscles are pale. Presence of serous fluid in the thoracic and abdominal cavities. Minute haemorrhages are seen in kidneys, liver, gall bladder and lymph nodes. Streaks of haemorrhages may be present in gastrointestinal mucosa. There is embolism of brain capillaries and sign of encephalitis. In dogs, splenomegaly and hepatomegaly are the characteristic signs.
Diagnosis
This is base on the following criteria:
(1) Clinical signs – haemoglobinuria is the cardinal signs
(2) Examination of the blood smear: This is the simplest diagnostic method. But, some species of babesia are less readily found in the peripheral circulation. This difficulty can be ruled out by preparing thick blood smear. The smear may be stained with Giemsa stain.
(3) Clinical pathology: Low erythrocyte count, low packed cell volume, low haemoglobin level and increased red blood cell sedimentation.
(4) Serological tests: Following tests have been done with success
- Capillary agglutination test
- Latex agglutination test
- Slide agglutination test
- Curd agglutination test
- Complement fixation test
- Indirect haemagglutination test
- Indirect Fluorescent antibody test
- Radio immunoassay
- Enzyme linked immunosorbent assay
Treatment
B. bigemina and B. major are more sensitive to drug and require low doses. Following drugs are used.
- Quinuronium derivatives: Acaprin, Babeson and Piravan are used @ 1 ml/50 kg body weight.
- Aromatic diamidines: Berenil @ 4 mg/kg body weight through intramuscular route.
- Imidocarb: This is used @ 1 mg/kg body weight. Dog has been treated with Imidocarb @ 3-6 mg/kg body weight with success.
- Dimenazine: This has been used @ 12 mg/kg body weight by deep intramuscular injection in cattle and 3.5 mg/kg once daily in dogs.
- B. gibsoni can be treated with atovaquone @ 13 mg/kg orally and azithromycin @ 10 mg/kg orally for 10 days.
Supportive Treatment
Following supportive therapy has been advocated.
- Analgesic antipyretic for control of fever and abdominal pain.
- Glucose saline for dehydration.
- Liver extract and vitamin B complex to correct anaemia.
- Iron orally or parenterally where liver extract with vitamin B complex do not give adequate response.
- Whole blood therapy to correct severe anaemia.
Control
- Programme is to be taken to control tick population as far as possible as it is a tick borne disease.
- A herd can be made tick free by dipping or spraying at periodical interval with acaricide.
- Vaccination
Following vaccines have been used.
- Live vaccine: Immunity of babesiosis based on ‘premunition’. Dwivedi and Gautam (1980) observed mild resistance in calves receiving hyperimmune B. bigemina antiserum.
- Killed vaccine: The killed vaccine gives partial protection against challenge with B. bigemina.
- Inactivated from cell culture: This vaccine has been advocated by Smith et. al., 1979.
- Irradicated vaccine: Irradicated B. bigemina vaccine has been used with success. It has been pointed out that this vaccine is capable of triggering optimum and protective immune response.
- Canine vaccine (Pirodog) is available in France.
Zoonotic Aspect
Human cases of Babesiosis have been recorded and some of human cases have died.
