Babesiosis

Babesiosis is a first vector borne disease of cattle, sheep, pigs, horses and dogs and is characterized by fever, intravascular haemolysis causing a syndrome of anaemia, haemoglobinaemia and hemoglobinuria.

Babesiosis is caused by Babesia species of family Babesidae and transmitted by ixodid ticks.

Morphology

The Babesia species is pleomorphic in nature and occurs in RBC as ovoid, round, elongate, pyriform and pear shaped form lieing in pairs with an acute narrow angle. Large forms lie with their narrow ends at an acute angle and small forms at obtuse angle.

Babesia Species

Life Cycle

Epidemiology

Virulence of parasite
- Babesia bigemina and Babesia bovis are highly pathogenic, B. divergens and B. canis – relatively pathogenic; B.major and B.ovis – mildly pathogenic producing transient anaemia.
Breed susceptibility: All breeds are equally susceptible.
Inverse age resistance: young animals are less susceptible than older animals
Immune status of host
- In endemic area the young animals acquire immunity through colostrums of the dam as a result of transient infection with mild clinical signs. The active immunity is depends on persistence of carrier status, and the phenomenon was termed as premunity.
Carrier status: infected animal act as carrier for over 2 years, if infected constantly, they act as carrier for life
Level of tick challenge
- In endemic area host immunity is maintained at high, when more number of ticks present in that area. Where there is few ticks or limited ticks, the population immunity is low. In these circumstances, the number of ticks suddenly increases due to favourable environmental condition or reduced dipping frequency. The incidence of clinical cases increases sharply. This situation is known as enzootic instability.
Risk factors: In endemic area occasional outbreak of disease often associated with stress such as parturition or presence of other diseases.

Transmission

Transovarian transmission occur in one host tick & Transtadial transmission occur in two or three host tick.
Intra uterine transmission in B. bigemina and B. bovis.
Mechanically by contaminated needles and surgical instruments. eg. B. bigemina and B. equi. also B. bovis.

Pathogenesis

The multiplication of parasite in red blood cells causes rapid destruction of erythrocytes with accompanying haemoglobinaemia, hemoglobinuria and fever.
The Babesia bovis is most pathogenic than Babesia bigemina.
Babesia bovis infection is associated with sludging of RBCs in the small capillaries. In the cerebrum this causes blockage of the vessels by clumps of infected RBC leading to anoxia and tissue damage. The activation of certain plasma components (kinin, kallikrein) results in vasodilatation and accompanied by increased permeability leading to circulatory stasis, shock and intravascular coagulation.
Infection with Babesia cabbali in horses causes Clogging of the capillaries of various organ by parasitized cells and free parasites, the stasis from this sludging causes degeneration of the endothelial cells of small blood vessels causes anoxia and accumulation of toxic metabolic products, capillary fragility, eventual escape of erythrocytes and macroscopic haemorrhage.
Babesia canis and babesia gibsoni causes multiorgan dysfunction by generation of cytokines, Nitic oxide and free radicals by host.

Clinical manifestation

Cattle

High fever (rectal temp. Reaching 41.5⁰c).
Anorexia and ruminal atony.
Cattle stand with arched back, rough hair coat, dyspnoea and tachycardia.
Reddened mucous membrane initially later become pale and icteric.
Profound diarrhoea followed by constipation.
Anemia occur rapidly with 75% of erythrocyte destruction or more.
Weakness and loss of condition is due to anemia.
Profound diarrhoea followed by constipation.
Advanced stages: Severe anaemia, haemoglobinuria, jaundice, dark red to brown colour urine with a very stable froth and death after 24 hours.
Drop in milk production.
Abortion in pregnant animals.
Incoordination, convulsions, depressions and death occur in cerebral babesiosis apart from fever, anemia and hemoglobinuria.

Sheep and goat

Clinical signs similar to cattle.

Dog and cat

Peracute form

Rapid onset of collapse with hypotensive shock.
Pale mucous membrane (sometimes cyanotic).
Tachycardia, weak pulse, weakness and depression.
Hemoglobinuria.
Multiple organ dysfunction with hypotension, hypoxaemia leading to coma and death.

Acute form

Fever, anemia, jaundice,marked thirst inapetence, prostration and death.
Petechial and ecchymotic haemorrhage may be observed on gums or ventral abdomen.
Involvement of circulatory system may produce edema, purpura, ascites and there may be gastritis and stomatitis.
Involvement of respiratory system may cause catarrah and dyspnoea.
CNS involvement causes locomotor disturbances, paresis or epileptic forms.
Cerebral babesiosis may be confused with rabies.

Chronic form

Fever is not high, mild jaundice and severe anemia, affected animals become weak and emaciated.

Horse

Pale mucous membrane, anemia and icterus.
Hemoglobinuria is rare.
Gastroenteritis.
Posterior paralysis.

Necropsy Findings

Subepicardial and endocardial petechial haemorrhage.
Liver is yellowish brown colour.
Lungs are congested and edematous.
Pericardial sac may contain serosanguineous fluid.
Splenomegally with dark pulpy consistency.
Kidneys are pale often edematous.
Bladder is distended with dark reddish brown colour urine.

Sample collection

Live animals: peripheral blood smear and paired sera sample.
Dead animals: smear from heart muscle, kidney, liver, lung, brain and from a blood vessels in an extremity.

Diagnosis

Based on clinical signs.
Examination of piroplasms in RBC of peripheral blood smear stained with giemsa stain during acute phase of infection.
Presence of heavy infestation with ticks.
Haematology: TEC – less than 2 million/ cmm, Hb: less than 3.0gldl and neutrophilia.
Biochemical changes: Reduced calcium, phosphorous, total serum protein; Increase in blood glucose, total serum bilirubin and SGOT in liver damage.
FAT: Acridine orange fixed with blood smear the organism appeared as red with yellow nucleus
Necropsy: Splenomegaly, jaundice, haemoglobinuria, myocardial ecchymoses –highly suggestive.
Molecular diagnosis by PCR in chronic infection.
Immunodiagnosis in subclinical infections.
IHA: 80% effective in field infections.
IFA, ELISA, FAT, CFT, IHA and Capillary agglutination tests are used to identify the antibodies in serum.
Others: Latex agglutination tests, Card agglutination test, ELISA, Microplate enzyme immuno assay. IFA differentiates antibodies due to vaccination and natural infection.

Differential diagnosis

Eperythrozoonoses
Theileriosis
Leptospirosis
Anaplasmosis
Trypanosomosis
Bacillary haemoglobinuria
Phosphorous deficiency
Copper toxicity
Rabies

Treatment

The most commonly used drugs are Diaminacine aceturate at 3.5 mg/ kg b.wt I/M, Imidacarb at 1.2 mg/Kg S/C, Amicarbalide at 5-10mg/kg and trypan blue at 10 mg/kg b.wt (1% solution).
For cerebral babesiosis added dose is required. Diaminacine aceturate should be given on 2^nd day of treatment.
Imidacarb @ 3.0 mg/Kg b.wt provide protection for 4 weeks and completely eliminate the B.bigemina and B.bovis from carrier animals.
The trypan blue is not effective against B. bovis.
Imidocarb has been successfully used as a chemoprophylactic that will prevent clinical infection for 2 months.
Injections of long acting oxytetracycline @ 20 mg/kg.
Sheep- Diaminazene aceturate @ 3.5mg/Kg on two successive days or 12mg/Kg as single dose.
Horse- Combination of imidocarb and buparvaquone appears to be effective and capable of eliminating B.equi and B.caballi from horse. (For B.caballi -Imidocarb @ 2mg/Kg two doses at 24 hrs interval and Buparvaquone @ 4-6mg/Kg to control acute babesiosis due to B.equi).
Dog- For Babesia canis- Imidocarb dipropionate @5.0 to 6.6 mg/Kg b.wt I/M.
For Babesia gibsoni- Tab.Atovaquone 13.4 mg/Kg TID and Azithromycin @10 mg/Kg once in day for 10 days with fatty meal. PCR testing was repeated at 30 and 60 days after the end of treatment.
Clindamicin can be effective against babesia gibsoni @ 25 mg/kg b.wt bid PO for 14 days.
For Babesia felis -Primaquine phosphate @ 0.5 mg/Kg twice at 24 hrs interval.

Control

Vaccination is commonly practised by inoculating blood from donor animals, that has recently recovered from infection.
A regime of four injections of long acting oxytetracycline at 20 mg/kg at weekly intervals during their first month of grazing on tick infested pastures.
Control of ticks by spraying or dipping of animals in acaricidal agent at regular intervals.
Segregation and treatment of animals harbouring infection.
Killed vaccine- irradiated Babesia sp with freund’s incomplete adjuvant.
Chemoimmunization- administration of imidocarb and vaccines simultaneously.
Blood transfusion in severe anemic animals.