Comparative Studies on the Infectivity and Pathogenicity of Experimental Trypanosoma Brucei Brucei Infection in Mice, Rats, Rabbits and Guinea Fowls

Comparative Studies on the Infectivity and Pathogenicity of Experimental Trypanosoma Brucei Brucei Infection in Mice, Rats, Rabbits and Guinea Fowls

ABSTRACT

The study compared the infectivity and pathogenicity of experimental Trypanosoma brucei brucei infection in mice, rats, rabbits and guinea fowls. A total of 10 each of the following animals‟ mice, rats, rabbits and guinea fowls of both sexes were used for the study. Each group of the animal species was divided into two groups (infected and control) of five animals each. The mice, rats, rabbits and guinea fowls in the infected groups were individually inoculated with blood containing 1 x10⁶ Trypanosoma brucei brucei (Fadere stock). All animals in the control groups were not infected. Patent parasitaemia as determined by the haematocrit centrifugation technique was between 3-4 days in the mice and rats, while it was 7-8 days in rabbits. No parasitaemia was seen in the infected Guinea fowl throughout the study. The mean body weights of mice, rats and rabbits decreased in the infected group as compared to the control group. All animals in the infected group except guinea fowls showed an increase in body temperature. In the mice and rats, there were significant differences (SD) (p < 0.05) in the overall mean PCV, HGB and RBC between the infected groups (IG) as compared to the control group (CG). In the rabbits there were SSD (P < 0.05) in the overall mean PCV, HGB and RBC between the IG (36.1 ± 0.6%, 12.11 ± 0.8 g/dl and 5.9 ± 0.4×10⁶) and CG (43.7 ± 0.5%, 14.1 ± 0.9 g/dl and 7.23 ± 0.3×10⁶ respectively). There was no SD (P > 0.05) between the overall mean PCV, HGB and RBC of the infected guinea fowls and those of the control group throughout the experiment. Also, no mortality was recorded among the infected guinea fowls as a consequence of the infection. A decrease in mean total white blood cell (WBC) counts of the rats and the rabbits were observed while mice and guinea fowls groups showed no significant difference between the WBC of the infected and control groups. Microscopic lesions observed in the mice, rats and rabbits included congested central vein and perivascular cuffing, congestion and mononuclear cellular infiltration around blood vessels of the lungs, depletion of lymphoid cells, congested intertubular spaces and focal necrosis of the renal tubular epithelium. In the guinea fowls, the spleen revealed haemosiderosis. The study thus demonstrated that mice, rats and rabbits are, in order of susceptibility better laboratory models than the guinea fowls which tend to show some measure of resistance to Trypanosoma brucei brucei used in the experiment. Therefore rabbits could be used in our laboratory to preserve Trypanosoma brucei brucei.

CHAPTER ONE

INTRODUCTION

1.1 Background of the Study

Trypanosomosis is a disease of man, domestic (Fajinmi et al., 2011; WHO 2015) and wild animals (Abenga et al., 2006; Mbaya et al., 2009; 2011). It is transmitted by tsetse flies (Glossina spp.) and characterized by anaemia, oedema, cachexia, intermittent fever and death (Yakubu et al., 2014). In Africa including Asia and South America, it is transmitted by several biting flies like Tabanus, Hippobosca, Stomoxys (WHO 2015; Yakubu et al., 2014).

The Trypanosoma species affecting man and his domestic animals have been subdivided into two groups, the haematic group (Trypanosoma congolense, T. vivax) which remain in the blood plasma and the tissue invading group (T. brucei brucei, T. brucei gambiense, T. brucei rhodesiense and T. equiperdum) that are found in extra and intravascular spaces (Abubakar et al., 2005; Chretien and Smoak, 2005; Ngure et al., 2008). Because of their presence in the blood, these invading parasites produce numerous changes in the cellular and biochemical constituents of blood (Taiwo et al., 2003). Infection with Trypanosoma brucei infection like other Trypanosoma infection precipitate red blood cell destruction which results in anaemia as well as tissue damage (Ekanem and Yusuf, 2008; Akanji et al., 2009).

Clinically, the effects of trypanosomosis in animals range from anaemia, immunosuppression, depression with the inability to rise, pyrexia directly associated with parasitaemia, paleness of mucous membrane, rapid pulse beat, retarded growth, the roughness of haircoats. Reduced capacity to work leading to morbidity and mortality in the absence of treatment (Batista et al., 2012; Silva et al., 2013).

In addition is an enlargement of peripheral lymph nodes, reduced milk production, low meat quality, and weight loss as well as reproductive disorders such as infertility, abortion, stillbirth.

In a review by Ibrahim et al., (2015), some of the pathological changes in animals (mice, rats and rabbits) include splenomegaly, hepatomegaly and nephritis, in addition, cardiomegaly has been reported in rabbits. The histopathology changes include degenerative changes in both liver and kidneys, The spleen of the mice showed giant macrophages, that of the rats showed epithelioid giant cells, while those of the rabbits showed haemosiderosis and eosinophilic infiltrations. However, exclusive to the rabbits was hydropic degeneration, necrosis and mononuclear cellular infiltrations in the myocardium. Also observed was that the liver of the mice showed central vascular congestion with sheathed artery, that of the rats showed sinusoidal haemorrhages and nuclear vacuolation while that of the rabbits showed very mild, but widespread vacuolar degeneration of hepatocytes with periportal mononuclear cellular aggregations and presence of scattered megalocytes. The report also indicated that the kidneys of the mice infected with T. brucei showed interstitial haemorrhages and necrosis of the tubular epithelial cells, that of rats showed multi-focal glomerular degenerations and tubular ballooning in the cortex while that of rabbits showed mild but diffuse interstitial mononuclear cell infiltration, especially at the corticomedullary junction.

1.2 Statement of Research Problem

Although T. brucei brucei is primarily a parasite of domestic animals as well as man, laboratory animals are often used to establish the course of infection and the degree of pathogenicity of the parasite, and these animals, therefore, serve as models in different experimental designs to study the disease it causes. However, it has been reported from experimental studies that the course of infection and severity depends on some factors such as the host species and the strains of the parasite. These studies have not given much information on the degree of infectivity and pathogenicity of T. brucei brucei infection in laboratory animals such as mice, rats, rabbits and guinea fowls.

Laboratory mice and rats especially have been used in laboratories to preserve Trypanosoma brucei brucei for experimental studies and some degree of pathogenicity and sometimes death have been reported (Lawal et al., 1999). It is therefore important to explore the possibility of using other animal species as experimental models for the Trypanosoma brucei brucei infection for appreciable periods with minimum loss of such animals and hence the parasites.

1.3 Justifications

Extensive work has been done on animal trypanosomosis due to Trypanosoma vivax, Trypanosoma congolense and Trypanosoma brucei (Adeiza et al., 2008; Adamu et al., 2008) but little has been done to determine and compare the degree of pathogenicity of these parasites in different laboratory animals. Laboratory animals (mice and rats) are used as models in many types of research. Therefore, there is a need to establish the infectivity rate and pathogenicity of Trypanosoma brucei brucei infection in these animals with the view of establishing the best laboratory animal model for use in trypanosomosis research.

The ability of laboratory animals to serve as in vivo models depends partly on the capacity to withstand experimental infection. This needs to be established in different laboratory animal models.

Laboratory rats and mice have over the years been used extensively in the preservation of Trypanosoma brucei parasites but the pathogenicity of the parasites sometimes result in a sudden loss of both the animals and the parasite hence the need to explore the possibility of using other animal models in comparison with mice and rats for this purpose.

1.4 Aim and Objectives of the study

1.4.1 Aim of the study

This research aimed to compare the infectivity and pathogenicity of Trypanosoma brucei in mice, rats, rabbits and guinea fowls

1.4.2 Specific objectives of the study

The objectives of the study were to determine and compare the:

a. Parasitaemia and its onset in mice, rats, rabbits and guinea fowls following experimental infection with Trypanosoma brucei.

b. Changes in rectal temperature induced by experimental Trypanosoma brucei infection in mice, rats, rabbits and guinea fowls.

c. Hematological changes induced by experimental Trypanosoma brucei infection in mice, rats, rabbits and guinea fowls.

a. Microscopic lesions and their distribution in the laboratory animals experimentally infected with Trypanosoma brucei

1.5 Research Hypothesis

Ho; There is no difference in the course of experimental Trypanosoma brucei infection in mice, rats, rabbits and guinea fowls.

Ha; There is a difference in the course of experimental Trypanosoma brucei infection in mice, rats, rabbits and guinea fowls.

References

Shehu, S.A., Ibrahim, N.D.G., Esievo, K.A.N. and Mohammed, G. (2006). Role of erythrocyte surface sialic acid inducing anaemia in Savannah Brown bucks experimentally infected with Trypanosoma evansi. Veterinarski Arhiv,26(6): 521-530.

Silva, T.M., Olinda, R.G., Rodrigues, C.M., Camara, A.C., Lopes, F.C., Coelho, W.A., Ribeiro, M.F., Freitas, C., Teixeira, M.M. and Batista, J.S. (2013). Pathogenesis of reproductive failure induced by Trypanosoma vivax in experimentally infected pregnant ewes. Veterinary Research, 44 (1): 1-5.

Singh, B.P. and Mishra, S.K. (1986). Haematology changes in Trypanosoma evansi infection in calves. Indian Journal of Veterinary Medicine 6, 108-109.

Snow, W., Wachand, T. and Rawlings, P. (1996). Observations on the prevalence of trypanosomosis in small ruminants, equine and cattle about tsetse challenge, in the Gambia. Veterinary Parasitology, 66: 1-11.

Stephen, L.E. (1986). Trypanosomiasis: A veterinary perspective. Pergamon,Oxford. 511 pp.

Stevenson, P., Munga, L., Baylis, M. and Alushula, L.(1991). The control of tsetse and trypanosomiasis by deltamethrin treatment of ranch animals in Kenya. Proceedings of 21st ISCTRC Meeting at Yamoussoukro, Ivory Coast. Pp.201.

Taiwo, V. O., Olaniyi, M. O., and Ogunsanmi, A. O. (2003). Comparative plasma biochemical changes and susceptibility of erythrocytes to in vitro peroxidation during experimental Trypanosoma congolense and T. brucei infections in sheep. Israel Journal of Veterinary medicine, 112-117.

Thompson, J.W., Mitchel, M., Rees, R.B., Shereni, W., Schoenfeld, A.H. and Wilson, A. (1991). Studies on the efficacy of deltamethrin applied to cattle for the control of tsetse flies (Glossina spp.) in Southern Africa. Tropical Animal Health and Production, 23: 221-226.

Umar, I.A., Ogenyi, E., Okodaso, D., Kimeng, E., Stancheva, G.I., Omage, J.J., Isah, S. and Ibrahim, M.A. (2007). Amelioration of anaemia and organ damage by combined intraperitoneal administration of vitamins A and C to Trypanosoma brucei brucei-infected rats. African Journal of Biotechnology, 6:2083-2086.