Studies on the effects of trypanosoma congolense infection on the reproductive function of the ram
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Date
1993-12
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University of Glasgow
Abstract
This thesis describes a series of studies carried out in Scottish blackface rams
experimentally infected with Trypanosoma congolense stabilates 57/10 and 57/11
(originally imported from ILRAD, Kenya as ILRAD 1180) with the primary aim of
determining the effects of infection on the function of the hypothalamo-pituitary-gonadal
axis. The studies also investigated the possibility that pyrexia is responsible for inducing
gonadal endocrine and exocrine dysfunctions in infected animals. In addition the effect
of infection on the function of the hypothalamo-pituitary-adrenal (HPA) axis was
assessed in order to determine whether reproductive dysfunction generally seen during
trypanosomiasis is related to stress caused by the infection.
Chapter I comprises an introduction and a literature review on trypanosome-
induced reproductive dysfunctions with emphasis on pyrexia and changes in the HPA
axis.
Chapter II describes the two experiments carried out in rams infected with T.
congolense and the general materials and methods used in these studies.
Chapter III describes the effects of infection on semen characteristics and
pathology of various reproductive organs such as the testis, cauda epididymis, prostate
and pituitary gland. It was found that T. congolense induced a progressive deterioration
of semen quality in terms of an increased percentage of abnormal spermatozoa in the
ejaculate.
Progressive non-inflammatory degenerative changes were observed in the
testis and prostate gland. The cauda epididymis showed varying degrees of decreased
sperm reserve. Trypanosome-induced pyrexia led to an elevation of scrotal temperature
in infected rams, suggesting that the changes in the gonads could have been due to
increased testicular temperature. Indeed, similar changes were observed in the semen
and gonads of uninfected rams following artificial elevation of testicular temperature by
scrotal insulation.
The pituitary gland showed changes associated with increased
basophilic degranulation in infected rams.
Changes in plasma concentrations of reproductive hormones in the same rams are
described in Chapter IV.
It was observed that soon after the onset of parasitaemia,
which occurred within 1-2 weeks of infection, plasma testosterone concentration
declined and levels remained low throughout the infection period. This reduction in
plasma testosterone concentration was associated with a progressive and marked decline
in
testosterone pulse
amplitude
and
testosterone secretion
after injection of
gonadotrophin-releasing hormone (GnRH) was also depressed throughout the infection
period. By four weeks after infection, declining plasma testosterone concentration was accompanied by a significant increase in plasma luteinizing hormone (LH) pulse
amplitude and increased pituitary responsiveness (LH secretion) to exogenous GnRH.
As the infection progressed up to 8 weeks, the plasma LH concentration declined. This
could not be associated with some aspects of gonadal steroid feedback as similar LH
changes were observed in infected rams which had been castrated. Neither was the
decline in plasma LH concentration caused by the inability of the pituitary gland to
secrete and release LH as secretion of LH in response to exogenous GnRH was not
impaired throughout the infection period. It was therefore concluded that the decline in
plasma LH concentration after 8 weeks of infection was possibly induced by a
progressive impairment of the ability of the hypothalamus to synthesize and/or release
GnRH.
Gonadal steroidogenesis in infected rams was investigated in the in vitro
experiments described in Chapter V. This work showed that the alteration in plasma
testosterone concentration following infection was associated with a decline in Leydig
cell steroidogenesis, possibly mediated by increased testicular temperature affecting
testosterone biosynthetic enzymes. However, by 4 weeks after infection, reduced plasma
testosterone in infected animals was exacerbated by the impaired ability of the testes to
release testosterone into the circulation resulting in a significant increase in
intratesticular testosterone content. A similar increase was also observed in scrotal-
insulated rams and it was therefore suggested that changes in intratesticular testosterone
in infected rams at 4 weeks of infection was associated with a trypanosome-induced
increase in testicular temperature perhaps through an effect on testicular blood flow.
The effects of T. congolense infection on the function of the HPA axis in rams
and the relationship between this and the changes in the hypothalamo-pituitary-gonadal
axis are described in Chapter VI. The onset of parasitaemia stimulated a significant
increase in plasma cortisol concentration which was followed within 3-6 week of
infection by a decline in plasma cortisol levels and a reduced ability of the pituitary to
secrete adrenocorticotrophin hormone (ACTH) after injection of corticotrophin-releasing
hormone (CRH). Thereafter, the activity of the HPA axis was increased in step with the
fluctuating parasitaemia.
CRH stimulation of the HPA axis had no effect on LH
secretion but reduced the plasma concentration of testosterone indicating the possible
aggravation of T. congolense-induced reproductive disorders by stress-induced cortisol.
The general discussion and conclusions drawn from all the experiments are.
presented in Chapter VII.
It can be concluded that T. congolense causes a very profound dysfunction of the
hypothalamo-pituitary-gonadal axis in rams through actions at various sites. These
effects may be partly associated with trypanosome-induced pyrexia and are exacerbated
by increased plasma cortisol concentrations resulting from the activation of the HPA
axis.
Description
Thesis
Keywords
Trypanosoma congolense infection