The thesis describes observations carried out on
infections caused by various Babesia spp. in mice, rats
and cattle with particular reference to a study of
parasitaemias after acute infection.
Of mice infected with Babesia rodhaini, 95% died.
The mortality rate was not affected by decreasing the
number of parasites inoculated, although the time to
death was proportionately increased.
Rats infected with B. rodhaini usually survived
after varying degrees of illness and moderate parasitaemias. Parasitaemias fell rapidly from peak levels to
latency. In most rats persistent infections were not
detectable by subinoculation or splenectomy beyond ten
days after the onset of latency. Subinoculation was
shown to be an extremely sensitive means of detecting
infection. Rats which naturally effected a sterile cure
were immune to homologous challenge for at least a year.
All mice infected with B. microti recovered. The
primary parasitaemia declined in a series of progressively
smaller recrudescences. Persistent parasitaemias remained
patent in some mice for as long as a year. The magnitude
and occurrence of chronic patent parasitaemias did not
decrease with increasing time from infection. B- methasone
administration had no significant effect on chronic
parasitaemias.
Babesia divergens infection in splenectomised calves
was characterised by moderate parasitaemias accompanied
by fever, anaemia, haemoglobinuria and some deaths. The
decline in packed cell volume (P.C.V.) was associated
with the fall in parasitaemia rather than with its rise.
There was a positive correlation between the degree of
anaemia and the level of maximum parasitaemia. In non - splenectomised cattle, infection produced only low and
transient parasitaemias.
Chronic parasitaemias were monitored daily in splenectomised calves by the examination of thin blood smears
stained with acridine orange. In this way, 105 erythrocytes in each smear could be quickly examined. Parasitaemias fluctuated with frequent and regular spontaneous
recrudescences. The pattern of recrudescences was not
affected by the administration of B- methasone or adrenocorticotrophic hormone (A.C.T.H.), but recrudescences
were provoked by beginning to handle and sample the
cattle. Relapse parasitaemias were of low magnitude and
were not accompanied by anaemia or other clinical signs.
The indirect fluorescent antibody (I.F.A.) test was
used to determine the antibody titres in primary and
chronic infections. The response of splenectomised calves
and non -splenectomised cattle was similar. After
infection, antibodies were not detectable until maximum
parasitaemias were reached. Titres continued to rise as
parasitaemias fell, maximising 30 -40 days after infection.
There was no difference between mean maximum titres of
splenectomised and non -splenectomised cattle. Titres
persisted for at least 500 days. Changes in titre were
detected neither in association with recrudescent parasitaemias nor with A.C.T.H. and B- methasone administration.
In Nigeria, B. bigemina was isolated from latently
infected indigenous cattle. The original isolate contained six other species of haemoparasite. These contaminants were eliminated by a series of rapid passages in
splenectomised calves, and a pure isolate of B. bigemina
was obtained. Six non -splenectomised adult steers were
infected with the impure isolate of B. bigemina, and ten
similar cattle were infected with the pure isolate.
In splenectomised calves, moderate parasitaemias
caused severe disease with fever, anaemia, haemoglobinuria
and death in 3/5 animals. The onset of anaemia was associated with the crisis of parasitaemía rather than with
its rise. In non -splenectomised steers, infection caused
low parasitaemias and minimal symptoms of disease with a variable degree of anaemia. The depression of P.C.V. was
correlated positively with the magnitude of maximum
parasitaemia.
The I.F.A. response was similar in splenectomised
and non -splenectomised cattle. Antibody was first
detected between one and five days after maximum parasitaemia. Maximum titres were not significantly different
in splenectomised and non -splenectomised cattle and were
reached between 16 and L10 days after infection.
In the six steers infected with an impure isolate of
B. bigemina, chronic parasitaemias were monitored for 115
days. Anaplasma marginale was frequently patent during
this time and a reciprocal relationship was noted between
it and B. bigemina, with the former parasite apparently
dominant. Falls in A. marginale parasitaemia were
followed by recrudescences of B. bigemina. B- methasone
administration was followed by B. bigemina recrudescent
parasitaemias in 2/6 animals. In the other four animals
a response appeared to be abolished by the presence of
A. marginale.
In the ten steers infected with a pure isolate of
B. bigemina, parasitaemias generally remained latent
after primary parasitaemia. Relapse parasitaemias were
provoked in 8/8 animals treated with B- methasone although
a pre -existing infection of A. marginale in some cattle
inhibited this response. Two animals showed minor
recrudescences of B. bigemina after A.C.T.H. treatment.
The chronic B. bigemina parasitaemia in one splenectomised calf was observed for 79 days. Throughout this
period the parasitaemia remained patent and fluctuated
periodically. The feeding of non -infected ticks did not
affect the parasitaemia, but B- methasone treatment was
followed by a major recrudescence which caused a moderate
fall in P.C.V.
Exotic cattle imported to Nigeria were regularly bled
for serum over a 14 month period during which they were
exposed to limited natural tick infestation. Five out of
fifty cattle became infected with B. bigemina as was
evidenced by a change in their I.F.A. status, but none
was clinically ill nor was the milk yield affected.
