Effects of castration on luteinizing hormone secretion and response to gonadotrophin-releasing hormone in sheep infected with Trypanosoma congolense.

The effects of trypanosomiasis on the endocrine function of the hypothalamo-pituitary-gonadal axis were investigated before and after castration of Scottish Blackface rams infected with Trypanosoma congolense and uninfected controls. Blood samples were collected at 15-min intervals for 6 h before and at 10, 20, 40, 60, 80, 100 and 120 min after injection of synthetic gonadotrophin-releasing hormone (GnRH, 20 micrograms iv) 2 days before infection and 26 and 54 days after infection, with castration being performed 28 days after infection. Mean luteinizing hormone (LH) pulse amplitude was higher (3.3 +/- 0.2 vs 2.6 +/- 0.3 ng/ml) and mean plasma testosterone concentration was lower (4.1 +/- 0.6 vs 7.6 +/- 1.2 nmol/l) in infected vs control rams 26 days after infection (p < 0.05). Mean plasma LH concentration and pulse amplitude increased in both groups after castration but both were significantly lower in infected compared to control rams (6.6 +/- 1.5 and 13.0 +/- 2.2 ng/ml, p < 0.01; 7.7 +/- 0.9 and 11.6 +/- 0.9 ng/ml, p < 0.001), respectively. However, LH responses to exogenous GnRH were similar in infected and control rams at each stage of the experiment, suggesting that the smaller increase in plasma LH after castration in infected rams was not caused by reduced responsiveness of the pituitary to GnRH but by alterations in GnRH secretion by the hypothalamus or its transport to the adenohypophysis. These results also demonstrate that impairment of testosterone secretion within 4 weeks of T. congolense infection in sheep may be due to testicular rather than pituitary effects.