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Experimental African Trypanosomiasis: Effects on Plasma Melatonin Concentration and Pineal Gland Histology in Rodents

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Experimental African Trypanosomiasis: Effects on Plasma Melatonin Concentration and Pineal Gland Histology in Rodents JIPBS Journal of Innovations in Pharmaceuticals and Biological Sciences www.jipbs.com Original Article Experimental african trypanosomiasis: effects on plasma melatonin concentration and pineal gland histology in rodents Charles I. Maina*1, Apolonary O. Oucho2, Chebii Kiptanui3, Samuel M. Kimani1 1Department of Biological Sciences, Egerton University, P.O. Box 536 - 20115, Egerton, Kenya. 2 Department of Biological Sciences, University of Eldoret, P.O. Box 1125 - 30100, Eldoret, Kenya. 3Department of Human Pathology, Moi University, P.O. Box 1146 – 30100, Eldoret, Kenya. Abstract Trypanosomiasis remains a major public health problem to man over much of tropical Africa. The disease is caused by protozoan parasites of the genus Trypanosoma and is fatal if untreated. The effects of T.b.brucei infection on plasma melatonin concentration and pineal gland histopathology was investigated in male albino rats. Twelve rats were each infected intraperitoneally with 0.2ml of infected blood containing approximately 1.0 x 104 live T.b.brucei parasites. Twelve other rats served as uninfected controls. Trypanosomes were detected in the blood of infected rats 5-8 days post-infection. There was a significant difference (P=0.0382) in plasma melatonin concentration between control and experimental rats. Histopathological changes in the pineal gland of experimental rats included tissue degeneration and pinealocytes with pyknotic nuclei. These histopathological changes were responsible for the decrease in plasma melatonin concentration in the experimental rats. Keywords: Trypanosomiasis, Melatonin, Pineal gland, Histopathology *Corresponding Author: Charles I. Maina, Department of Biological Sciences, Egerton University, P.O. Box 536 - 20115, Egerton, Kenya. Tel +254 728425209. Email : [email protected] 1. Introduction bite of an infected tsetse fly of the genus Glossina. It is estimated that over 66 Human African trypanosomiasis, million people in 37 African countries are commonly known as sleeping sickness, is at risk of contracting the disease, 300,000- one of the neglected and re-emerging 500,000 people are currently affected, and infectious diseases in Africa that has been 48,000 deaths can be attributed to the accorded little attention and priority [1]. disease each year [2]. The disease The disease is caused by flagellate continues to be a major health problem protozoan parasites of the genus throughout sub-Saharan Africa and is Trypanosoma and is transmitted by the ©JIPBS, All rights reserved Innovational Publishers www.innovationalpublishers.com Charles Maina et al, JIPBS, Vol 1 (1), 01-09, 2014 likely to be so for the foreseeable future The production and secretion of [1]. melatonin follows a circadian rhythm, with the levels being higher during the night There are two distinct forms of and lower during the day [8,9]. Research human African trypanosomiasis; the into melatonin secretion patterns in the chronic West African form which occurs in vertebrates, as well as in humans, has west and central Africa, and the acute East shown that melatonin levels rise with African form, which occurs in east and onset of darkness and fall with the onset of southern Africa. West African daylight [10. 11, 12, 13, 14]. As daylight trypanosomiasis is caused by approaches, light perceived by the retina is Trypanosoma brucei gambiense and encoded, and this information is relayed to accounts for about 95% of the reported the pineal gland. Light serves to suppress cases of sleeping sickness [3]. East African pineal activity, and subsequently, trypanosomiasis is caused by T.b. melatonin levels decrease to very low rhodesiense and accounts for about 5% of levels and remain there until production the reported cases of sleeping sickness in and secretion are once again stimulated by Africa [3]. There is an early or the onset of darkness [15]. Although the haemolymphatic stage, when the circadian pattern of melatonin secretion trypanosomes are restricted to the blood has been established, little has been and lymph system, and a late or reported on the changes of melatonin encephalitic stage, when the parasites secretion in various pathological cross the blood-brain barrier to invade the conditions. This study was, therefore, central nervous system [3]. In the absence carried out to investigate the effects of of treatment, sleeping sickness patients die T.b.brucei infection on the plasma within months when infected with T. b. concentration of melatonin, and pineal rhodesiense or within years when infected gland histology in rats. with T. b. gambiense. 2. Materials and Methods The most characteristic symptom of human African trypanosomiasis is the Experimental Setup severe disturbance in the sleep/wake cycle with typical diurnal somnolence (which Twenty four male albino rats, aged gave the disease its other name, sleeping 3-3½ months and weighing 200-220g, sickness) and in many cases nocturnal were used in this study. The rats were insomnia [4]. Melatonin (5-methoxy-N- randomly divided into two groups of acetyltryptamine), the principle hormone twelve rats each. The first group of twelve secreted by the pineal gland, is a key rats constituted the uninfected controls regulator of the sleep/wake cycle, and while the other twelve were inoculated other circadian rhythms [5]. Melatonin with a T.b. brucei (ILTat1.4) isolate and functions as a synchronizer of the constituted the infected experimental biological clock by providing information group. These laboratory rodents were about night-length [6,7]. It is apparent that chosen because they allow easy handling melatonin and the pineal gland have and present an acute infection that has widespread effects and optimal strong similarities with the human disease functioning of the pineal gland is essential [16]. to our well-being. 2 Innovational Publishers www.innovationalpublishers.com Charles Maina et al, JIPBS, Vol 1 (1), 01-09, 2014 The rats were housed at room rats. The donor rat was put in a cage and temperature (25.2±3.6 0C) in the mini- transported to the University of Eldoret, laboratory animal house of the where the study was carried out. Department of Biological Sciences, University of Eldoret, Kenya. They were The donor rat was monitored for housed three per cage and were exposed the presence of parasites daily by direct to 12/12hours of light/dark cycle microscope observation of trypanosomes throughout the study period. The rats in wet smears of blood samples obtained were provided with food (Mice Pencil, from tail bleeds. When parasitaemia was Unifeed Millers Ltd, Kisumu, Kenya) and established, the donor rat was water ad libitum. anaesthetised with ether and 2ml of blood obtained from it through cardiac puncture. Two weeks prior to baseline data One millilitre (1ml) of this blood was collection, the rats were observed and diluted with 2ml of phosphate buffered accustomed to routine handling. They saline (PBS) solution (pH 7.4). Then, 0.2ml were also screened for ectoparasites of this blood, containing approximately 1.0 besides being injected subcutaneously x 104 live T.b. brucei parasites was injected with 0.02ml of Ivermectin (Ivermin®, intraperitoneally to each of the twelve rats Sinochem Ningbo Ltd., China), a broad- in the experimental group. The number of spectrum parasiticide that effectively parasites was determined using the controls both endoparasites and Neubauer haemocytometer method [19]. ectoparasites. The research committee of Tail blood samples were collected daily the Department of Biological Sciences, from the infected rats and screened for University of Eldoret, Kenya, approved this trypanosomes using wet and thin blood study and the animals were handled in smear films [20]. The rats were also accordance with internationally accepted observed for any abnormal behaviour principles for laboratory animal care and and/or any clinical signs of infection. The use [17]. rats were infected after four weeks of pre- infection baseline data collection. Control Inoculation of Experimental Rats rats were, concurrently, injected An isolate of the parasite intraperitoneally with 0.2ml normal saline. Trypanosoma brucei brucei (ILTat1.4) was Determination of Plasma Concentration obtained from the International Livestock of Melatonin Research Institute (ILRI), Nairobi, Kenya. This strain was used because it allows a Tail blood samples were collected long disease course (30 days on the weekly for the determination of plasma average) with central nervous system concentration of melatonin. Blood involvement by around twenty one days in samples were collected from all the twenty mice [18]. The parasite was originally four rats at night, between 10.00pm and obtained from the blood of a naturally 2.00am. This time was chosen because infected cow in Uhombo village, Kenya. melatonin is a hormone of darkness; its The isolate was inoculated blood levels are essentially undetectable intraperitoneally to a donor rat for the during the day, but rise sharply during the purpose of harvesting enough parasites for night [21]. subsequent inoculation into experimental 3 Innovational Publishers www.innovationalpublishers.com Charles Maina et al, JIPBS, Vol 1 (1), 01-09, 2014 Using the tail snip method, about Data Analysis 1ml of blood from each of the twenty four rats was collected in a vacutainer coated Data collected from this study was with ethylene diamine tetra acetate summarized as mean ± standard deviation (EDTA). The blood sample was promptly and the difference between the means centrifuged for 5 minutes at 12,000
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