Research Article: Plasma ACTH concentration and pituitary gland histo-pathology in rats infected with Trypanosoma brucei brucei

Date Published: December , 2017

Publisher: Makerere Medical School

Author(s): Charles Irungu Maina.


Human African trypanosomiasis is one of the neglected and re-emerging infectious diseases in Africa with over 60 million people being at risk of contracting the disease.

To investigate the effects of Trypanosoma brucei brucei infection on secretion of adrenocorticotropic hormone (ACTH) and histology of the pituitary gland and paraventricular nucleus in rats.

Rats were randomly divided into two groups, control and experimental. Experimental rats were injected intraperitonially with 0.2ml of blood containing 1.0 × 104 live T.b.brucei parasites. Tail blood samples were collected weekly for the determination of plasma concentration of ACTH. The pituitary gland and coronal section of brain were processed histologically and observed microscopically.

There was a significant difference (p = 0.0190) in plasma ACTH concentration between the control and experimental rats. Histological alterations were observed in both the pituitary and paraventricular nucleus of experimental rats.

T.b.brucei infection causes histological changes in both the paraventricular nucleus and pituitary gland in rats. These histological changes could account for the decrease in corticotropin releasing hormone (CRH) and ACTH production in the infected rats.

Partial Text

Human African trypanosomiasis (HAT), better known as sleeping sickness, is one of the neglected and re-emerging infectious diseases in Africa. Over 60 million people are at risk of contracting the disease, and 300,000 to 500,000 cases are reported annually, with at least 60,000 deaths1. The disease is caused by protozoan parasites of the genus Trypanosoma and is transmitted by the bite of an infected tsetse fly of the genus Glossina.

The PVN is one of the neuronal nuclei in the hypothalamus. It is highly vascularised and is protected by the blood-brain barrier, although its neuroendocrine neurons extend to sites beyond the blood-brain barrier, notably, in the median eminence. The PVN contains multiple subpopulations of neurons that are activated by a variety of stressful and/or physiological changes.

This study has demonstrated that T.b. brucei infection causes an initial increase, and then a decrease, in concentration of plasma ACTH in infected rats. The infection also causes histological changes in the PVN and pituitary corticotrophs of the rats. These histological changes cause the PVN and the pituitary corticotrophs to produce less CRH and ACTH, respectively.




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