Studies on the effects of trypanosoma congolense infection on the reproductive function of the ram

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University of Glasgow


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.




Trypanosoma congolense infection