The present study evaluated aspects of the class-specific antibody response
of rabbits experimentally infected with Trypansoma evansi.
Using sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE)
and "Western" blotting adapted to detecting class-specific antibody response and
optimized for the T. evansi system, humoral responses to T. evansi were observed
to be directed to both the surface and non-surface components of the parasite.
Using 125l-iodination, two components with molecular weights of 67,000 and 60,500
daltons were found to be associated with the surface of the parasite with their detection
varying between different stocks of T. evansi. Both the surface and non-surface
components elicited skin reactions in animals, with the most intense reactions observed
with the surface components and in animals drug c\ired of T. evansi infections.
Class-specific antibody response to the surface components involved the
production of the three immunoglobulin classes studied - IgG, IgM and IgA while
responses to the non-surface components were predominantly IgG, an observation
that was thought to be linked with the role of IgM in bringing about trypanolysis
and IgG in neutralising the products of such lysis.
Based on clinical signs, animals were classed as resistant or susceptible with
the serum from the resistant animals detecting more antigens of T. evansi and
earlier than those of the susceptible animals. The detection of the surface and many
non-surface components of the parasite was associated with resistance. Crossinfection studies demonstrated absolute protection of animals to homologous challenge,
which was found to be associated with the production of specific antibodies.
Partial protection to heterologous challenge was associated with the presence of
cross-reacting antibodies to one of the surface and some of the non-surface components.
There were also indications that non-antibody factors may be important in the
induction of protection while complete absence of antibodies to antigens of the
challenge parasites was associated with non-protection.
Studies on complement demonstrated the depletion of C3 during infection with C3
in circulation returning to near preinfection levels after drug treatment and during
periods of low parasitaemia. C3 activation was observed in infected animals and
using an in vitro system, C3 was activated mainly through the classical and also
the alternative pathways, with the complexes formed with IgG being more efficient
in activating C3 than those formed with IgM. C3 was also found to be important
during secondary responses as rabbits with depleted C3 responded poorly by producing lower levels of antibodies than C3 intact, control animals.
cing lower levels of antibodies than C3 intact, control animals.
Histopathological studies revealed that changes in organs of infected animals
could be the direct effect of the parasites or consequences of the host defence
response, some of which could lead to the depression of the host's immune responses.
Observations warranting an investigation of a possible transmission of T. evansi
through a sexual mode and also the importance of an integrated approach in the
investigation of host/parasite relationships in T. evansi infections were made.