Abstract
The effect of tick-borne fever (TBF) on antibody formation and lymphocyte proliferation in sheep was studied following experimental infection with Ehrlichia phagocytophila. All infected sheep developed fever within three to four days. The sheep recovered clinically within eight days. Both infected and non-infected control sheep were immunised twice with different antigens, that is, on days 9 and 35 following the experimental infection. The levels of antibodies produced against tetanus toxoid and influenza virus in the infected sheep were significantly lower than in the control animals. The findings indicated that a TBF-infection may impair both primary and secondary antibody responses for up to six weeks. Immunisation with Actinomyces pyogenes resulted in significantly higher antibody titres in the TBF-infected group than in the control group, as measured by an enzyme-linked immunosorbent assay ( ELISA). It is believed that TBF-induced neutropenia may lead to increased exposure to A pyogenes-antigens and thereby enhance antibody production. Antibodies to E phagocytophila were measured by the indirect fluorescent antibody test and by an ELISA. The inoculated sheep responded with the formation of antibodies to E phagocytophila at one week (P<0·025), and showed a peak response at four weeks (P<0·0005) after inoculation. The antibody titre decreased between four and six weeks, but was still high at six weeks (P<0·0005). The lymphocyte responses to phytohaemagglutinin (PHA) concanavalin A (Con A) and pokeweed mitogen (PWM) were lower than in the control group and this difference was significant at most time points after infection. The lower responses to Con A and PWM were demonstrated within six weeks after the inoculation, whereas the lower response to PHA was shown within four weeks. Serum from one sheep, collected four weeks after infection, suppressed the in vitro lymphocyte response to Con A strongly, and the response to PHA and PWM moderately. This indicates that unidentified serum factors may at least be partly responsible for the suppressed mitogen responses.
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