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It has previously been shown that dogs can be vaccinated against heterologous Babesia canis infection using a vaccine containing soluble parasite antigens (SPA) from in vitro cultures of B. canis and B. rossi that are adjuvanted with saponin. In the present study the onset and duration of immunity of vaccinated dogs were studied. Results showed that 3-26 weeks after initial vaccination, dogs effectively limit the level of SPA in plasma upon challenge infection, which was reflected in limited duration and extent of clinical manifestations. There was no statistically significant effect of vaccination on the parasite load in the circulation, which was determined from blood smears. It was further shown that the level of immunity of primary vaccinated dogs (priming and booster vaccination with a 6-week interval) and that of repeatedly vaccinated dogs (a single additional vaccination 6 months after primary vaccination) is comparable. From this study it is concluded that vaccination with this preparation induces protective immunity against clinical babesiosis from 3 weeks after booster vaccination onwards, and remains effective for a period of at least another 6 months. A single booster vaccination is sufficient to maintain immunity for at least another 6 months.

Soluble parasite antigens (SPA) from European Babesia canis can be used to protect dogs against a homologous but not heterologous challenge infection. In this study it is shown that when dogs are vaccinated with a mixture of SPA from both, a European B. canis isolate and a South African Babesia rossi isolate, protective immunity against heterologous B. canis infection is induced. Three groups of five beagle dogs each were vaccinated twice with graded doses of SPA derived from in vitro cultures of B. canis and B. rossi, with a 3-week interval. Saponin was used as adjuvant. Three weeks after booster vaccination immunological responsiveness against heterologous B. canis antigen was measured by seroconversion against infected erythrocytes and lymphocyte transformation using SPA. Upon vaccination dogs produced antibodies against infected erythrocytes and lymphoblastogenic responses against SPA in a dose-dependent manner. Dogs were then challenged with heterologous B. canis parasites. Dogs appeared to be protected against challenge infection, which was reflected in less severe decrease of packed cell volume (PCV) and reduced clinical signs. The level of protection to clinical signs (but not excessive PCV drop) was related to the level of SPA in plasma and spleen size, and not related to peripheral parasitaemia. The results suggest that vaccination with this bivalent vaccine primes T-helper cells that recognise common epitopes on SPA from an antigenically distinct B. canis isolate. These cells provide the essential Th signal to mount an effective and timely antibody response against SPA and parasites or parasitised erythrocytes, which prevents the further development of clinical babesiosis.

This paper describes the clinico-pathological parameters measured in dogs that were vaccinated against Babesia canis using soluble parasite antigens (SPA) and then challenged. The packed cell volume (PCV) and the plasma creatinine value decreased immediately after challenge. Actual PCV values could be predicted in the first 5-6 days of the infection, assuming that creatinine values were modulated by increase of plasma volume. This association no longer existed after that time, and observations indicated splenic involvement in reduction of numbers of circulating erythrocytes. The anaemia due to B. canis infection appears to be the result of a multifactorial process including plasma volume increase, erythrocyte retention in the spleen and erythrocyte destruction, partly due to parasite proliferation. Vaccination limited the reduction of PCV values, and the development of splenomegaly. Differences in protection between vaccinated and control animals became apparent 6 days after infection, when a memory immune response becomes operative, and the onset of recovery of vaccinated animals correlated with the onset of antibody production against SPA.

Groups of five dogs were vaccinated with Babesia canis antigens from in vitro culture in combination with saponin as adjuvant. Protection against challenge infection was evident as diminished clinical disease, decrease in parasitaemia, and a less marked fall in haematocrit values. Recovery from infection occurred at the time a memory immune response became effective (from Days 5 to 6 after challenge infection onwards). The effect was dose dependent, the highest antigen dose being most effective. A lysate of normal erythrocytes did not have protective activity, indicating that a parasite component was responsible for protection. Unlike the malaria situation, disease was not associated with elevated levels of tumour necrosis factor in the plasma, nor with hypoglycaemia. Disease appeared to be the result of the activity of a parasite product, which could have triggered reactions which led to sequestration of erythrocytes from the peripheral venous blood. As a result, the packed cell volume decreased, and organs such as lymph nodes and spleen became congested. As soon as immunity had developed there was a rapid increase in the peripheral erythrocyte number, and congestion of the spleen diminished, indicative of restored capillary blood flow. The results further suggest that vaccination with a soluble parasite product blocks the trigger of this pathological process.