This thesis describes studies that were undertaken to evaluate the effect of T.
parva infection on the reproductive function of Boran/Friesian cross heifers. The
study was conducted in four separate experiments. In Experiments 1 and 2, the
animals were monitored for cyclical status post-infection. In Experiments 3 and 4, the
infected animals were divided into two groups: one group was monitored for cyclical
status and the other for both cyclical and pregnancy status after exposure to a bull.
The reproductive function was assessed by routine monitoring of oestrus behaviour,
palpation of the genital reproductive tract per rectum and determination of serum
progesterone (P4) concentrations. Further, in view of observed acyclicity in the early
work, attempts were made to assess the pituitary response to gonadotrophin releasing
hormone (GnRH) in a group of animals (Ch. 5) in an attempt to explain partly the
mechanisms involved in the impairment. Animals were monitored for the progression
of disease by clinical and parasitological responses. Further, subject to death or
sacrifice, a macroscopic and histological examination of target and various other
organs and tissues was undertaken in an effort to establish the part played by
observable pathological changes in the development of impaired reproductive function.
In Experiment 1, ten heifers were infected with 1:20 T. parva stabilate while
four others remained as uninfected controls. Two of the infected animals died, one
each on days 17 and 29. Clinical reactions in the recovered animals ranged from mild
to moderate. P4 profiles and ovarian structures revealed that three of eight recovered
animals had luteal dysfunction post-infection although two of the three showed clinical
oestrus during this particular period. The other five recovered animals cycled
regularly. The results from clinical and pathological studies did not indicate any direct
adverse effect of infection on reproductive function. All the four controls cycled
throughout the study period.
In Experiment 2, ten animals were infected with an undiluted stabilate while
four others acted as uninfected controls. Eight of ten infected animals died of severe
disease. Of the eight fatal cases, six were cyclic pre- and post-infection based on P4
profiles, ovarian structures and/or behavioural data. P4 profiles and ovarian structures
revealed that the other two animals were acyclic before and after infection although
clinical oestrus was detected in both pre-infection. Both of the recovered animals
underwent extended periods of acyclicity post-infection. There was no evidence
linking the acyclicity to the active parasitosis or pathological changes observed in the
reproductive organs. All control animals cycled throughout the study period.
In Experiment 3, 14 heifers were infected with undiluted stabilate and treated at
the height of clinical reaction. One of eight animals subjected to serial kill, was acyclic
before and after infection based on P4 profile and ovarian changes although it was seen
in heat pre-infection. Of the remaining seven, one animal became acyclic while all the
other six revealed clinical oestrus or/and cyclical ovarian changes after infection. Two
of six animals exposed to a bull became pregnant while the others were cycling
regularly at seven months post-infection. All controls cycled throughout the study
In Experiment 4, eight animals were immunized by infection and treatment
method while four others acted as uninfected controls. Three of four animals
monitored for cyclicity cycled regularly post-immunization. The other had a persistent
corpus luteum which regressed spontaneously after an extended luteal period of 42
days and cycled regularly subsequently. One of four animals exposed to a bull became
pregnant while the others cycled regularly to week 20 post-immunization. All the
controls cycled throughout the study period.
The evidence from the four experiments indicated that T. parva did not directly
affect reproductive function. Pathological lesions were observed in the reproductive
organs but these were mild and did not affect normal reproductive physiological
activity. It is postulated that the impaired reproductive function was due to an indirect
effect linked to loss in condition following infection.