- Email: [email protected]
Effects of melarsamine hydrochloride (Cymelarsan®) and diminazene aceturate (Berenil®) on the pathology of experimental Trypanosoma brucei infection in red fronted gazelles (Gazella rufifrons)
Veterinary Parasitology 163 (2009) 140–143
Contents lists available at ScienceDirect
Veterinary Parasitology journal homepage: www.elsevier.com/locate/vetpar
Short communication
Effects of melarsamine hydrochloride (Cymelarsan1) and diminazene aceturate (Berenil1) on the pathology of experimental Trypanosoma brucei infection in red fronted gazelles (Gazella rufifrons) A.W. Mbaya a,*, M.M. Aliyu b, C.O. Nwosu a, V.O. Taiwo c, U.I. Ibrahim b a b c
Department of Veterinary Microbiology & Parasitology, University of Maiduguri, Nigeria Department of Veterinary Medicine, University of Maiduguri, Nigeria Department of Veterinary Pathology, University of Ibadan, Nigeria
A R T I C L E I N F O
A B S T R A C T
Article history: Received 22 September 2008 Received in revised form 12 March 2009 Accepted 19 March 2009
An experimental infection of red fronted gazelles (Gazella rufifrons) with Trypanosoma brucei strain MKAR/84/NITR/6 was carried out. Two waves of parasitaemia which corresponded with a significant decline (p < 0.05) in packed cell volume (PCV) was encountered in the infected untreated controls and those treated at day 8 post-infection with a sub-optimal dosage of diminazene aceturate (Berenil1) at 3.5 mg/kg body weight. At postmortem, hepatomegally, splenomegally, lymphadenopathy, nephritis, myocardial degeneration with pulmonary oedema was observed in the two groups. Similarly, histopathological studies of some organs revealed interstitial haemorrhages, severe degenerative changes with cellular infiltrations. On the other hand, those treated by day 8 post-infection with melarsamine hydrochloride (Cymelarsan1) at 0.3 mg/kg, 0.6 mg/kg or diminazene aceturate (Berenil1) at 7.0 mg/kg body weight had apparently normal organs at the end of the experiment. These results suggest that, T. brucei can cause severe pathological changes in untreated red fronted gazelles (Gazella rufifrons). However, treatments at the onset of parasitaemia, by day 8 post-infection with melarsamine hydrochloride (Cymelarsan1) at 0.3 and 0.6 mg/kg or diminazene aceturate (Berenil1) at 7.0 mg/kg body weight ameliorated the deleterious effects of the infection in the gazelles. ß 2009 Elsevier B.V. All rights reserved.
Keywords: Pathology Trypanosoma brucei Red fronted gazelle Cymelarsan1 Berenil1
1. Introduction The pathogenesis of trypanosomosis in wild animals has remained a subject of controversy due to their trypanotolerant trait. The breakdowns in the premunity associated with trypanosomosis rarely occur under freeliving conditions. On the other hand, there is tremendous increase in susceptibility to the infection by wild animals under conditions of captivity. In the semi-arid zone of
* Corresponding author at: Department of Veterinary Microbiology and Parasitology, Faculty of Veterinary Medicine, University of Maiduguri, Bama Road, P.M.B.1069, Maiduguri, Nigeria. Tel.: +234 8036011774. E-mail address: [email protected] (A.W. Mbaya). 0304-4017/$ – see front matter ß 2009 Elsevier B.V. All rights reserved. doi:10.1016/j.vetpar.2009.03.036
Northeastern Nigeria, 1(16.67%) stripped hyeanas (Hyeana hyeana) and 7(50%) red fronted gazelles (Gazella rufifrons) maintained under captive conditions suffered infection with Trypanosoma brucei (Mbaya et al., 2008). The greater susceptibility to trypanosomosis exhibited by captive than free-living wild animals has been attributed to the increased secretion of cortisol by captive animals in response to the stress of captivity (Mbaya, 2007). In the semi-arid zone of Northeastern Nigeria, red fronted gazelles (Gazella rufifrons) are easily semi-domesticated and frequently reared together with sheep and goats in households (Mbaya, 2007). Consequently, as a result of the importance attached to the ownership of red fronted gazelles (Gazella rufifrons) and their known susceptibility to trypanosomosis under captive conditions,
A.W. Mbaya et al. / Veterinary Parasitology 163 (2009) 140–143
there is need to have a detailed understanding of the pathology of the infection in the animals as well as develop suitable control measures against it. In this study, free-living red fronted gazelles (Gazella rufifrons) were subjected to captivity for the first time with a view to negate any trypanotolerance that the animals may have and infected with T. brucei to investigate the pathology of the subsequent disease as well as develop suitable chemotherapeutic regimen for its control. 2. Materials and methods Thirty apparently healthy free-living red fronted gazelles (Gazella rufifrons) aged between 2 and 3 years and weighing between 20 and 25 kg were captured directly from the wild for the first time and screened according to standard criteria (Soulsby, 1982). They were found to harbour a mixed infection of T. brucei, T. vivax, Strongyles, and Anaplasma marginale and routinely treated according to standard methods (Soulsby, 1982). The animals were housed in concrete floored and fly-proof pens throughout the experiment and allowed 40 days to
Fig. 1. Parasite counts (103 mL
1
141
acclimatize to their new environment. They were fed on wheat bran supplemented with bean husks, guinea corn and chopped cucumber while water was provided ad libitum. Prior to the commencement of the study, the animals were randomly divided into six groups (A, B, C, D, E and F) of five gazelles each. Trypanosoma brucei brucei (Strain Mkar/84/Nitr/6) used for the study, was obtained from the Nigeria Institute for Trypanosomosis Research (NITR) in Kaduna, Nigeria. The stabilates were passaged twice in rats and then transferred into two red Sokoto goats that served as donors. Infected blood from the donor goats was diluted with phosphate buffered glucose saline (PBSG, pH 7.2). Each gazelle in groups A, B, C, D and E was inoculated, via the jugular vein, with the infected blood containing 1.5 x 106 trypanosomes. Groups A and B were respectively treated subcutaneously with melarsamine hydrochloride (Cymelarsan1) at a single standard dose rate of 0.3 and 0.6 mg/kg body weight, while groups C and D were treated intramuscularly with diminazene aceturate (Berenil1) at a single standard dose rate of 3.5 and 7.0 mg/kg body weights. All treatments commenced at the onset of
) and packed cell volume (%) of red fronted gazelles infected with T. brucei and their treatments.
142
A.W. Mbaya et al. / Veterinary Parasitology 163 (2009) 140–143
parasitaemia by day 8 post-infection. Group E served as infected untreated control and Group F the uninfected control. The experimental gazelles were monitored daily for the development of clinical signs of trypanosomosis. The initial detection of parasitaemia was by the wet film and haematocrit buffy–coat methods (Murray et al., 1983) while the degree of parasitaemia (Herbert and Lumsden, 1976) and packed cell volume (PCV) (Shalm et al., 1995) was estimated every other day. All gazelles that died from the infection or were humanely killed at the end of the study were subjected to detailed necropsy. The vital organs were carefully removed, washed, weighed and examined for lesions. Tissue sections of the organs were processed according to standard criteria (Drury and Wallington, 1976). The data obtained from the study were summarized as means standard deviation and differences between them determined at the 5% level of significance (Graph Pad Instat, 2000). 3. Results All the infected gazelles developed acute trypanosomosis with a pre-patent period of 8 days. Clinical signs observed were fluctuating pyrexia (40–42.8 8C), progressive loss in body weight, dullness, inapetence and palour of buccal and ocular mucous membranes. There were elevated parasite counts and a general decline in packed cell volume (PCV) (Fig. 1). These changes were however, significant (p < 0.05) during the first and second waves of parasitaemia, following sub-optimal treatment with diminazene aceturate (Berenil1) at 3.5 mg/kg body weight and in the infected control with the death of all the gazelles in the two groups occurring between days 46 and 52 postinfection. The signs of the infection were however, effectively modulated in the groups treated with either melarsamine hydrochloride (Cymelarsan1) at 0.3 and 0.6 mg/kg or with diminazene aceturate (Berenil1) at 7.0 mg/kg body weight, with no mortality recorded in these groups. Vital organs of the infected control and those treated with 3.5 mg/kg of diminazene aceturate (Berenil1), were enlarged with petechial and echymotic haemorrhages on serosal surfaces while the heart appeared pale and hypoplastic. Similarly, various degrees of degenerative changes with cellular infiltrations were encountered in tissue sections of the vital organs of the infected controls (Figs. 2–5) and in those treated with diminazene aceturate (Berenil1) at 3.5 mg/kg body weight. The vital organs of the gazelles treated with melarsamine hydrochloride (Cymelarsan) at 0.3 and 0.6 mg/kg or diminazene aceturate (Berenil1) at 7.0 mg/kg body weight were apparently normal.
Fig. 2. Heart of untreated control showing focal areas of hyaline degeneration of myocardial fibers (arrows) (H&E; 450).
the higher dosage (7.0 mg/kg body weight) was curative. The cardiomegally encountered in the early phase of the infection in the untreated and sub-optimally treated groups is probably associated with cellular infiltrations in the myocardial or endocardial layers. However, the terminal shriveling of the heart may have been due to myocardial fiber degeneration as described by Egbe-Nwiyi et al. (2005). The anaemia observed, may, have contributed in part to the widespread degenerative changes in the vital organs. Tissue hypoxia due to ischaemia, disseminated intravascular coagulation by micro-thrombi or immune complexes have been identified as factors indirectly involved in the pathology of organ damage in trypanosomosis (Igbokwe, 1995). The severe organ and tissue damage usually associated with trypanosomosis have been attributed to the fact that the trypanosomes mechanically traumatize cells and create tiny holes on the plasma membranes by the lashing
4. Discussion The results of the study showed that various degrees of organ and tissue damage occurred in the infected untreated gazelles, which experienced two waves of parasitaemia. The trend of parasitaemia observed in the gazelles treated with diminazene aceturate (Berenil1) at 3.5 mg/kg is probably due to a sub-optimal dosage, since
Fig. 3. Liver of untreated control showing widespread vacuolar degeneration of hepatocytes (H&E; 450).
A.W. Mbaya et al. / Veterinary Parasitology 163 (2009) 140–143
Fig. 4. A highly reactive spleen of infected untreated control showing Tlymphoblastic halos (A) numerous macrophages (B) in red pulp (H&E; 450).
143
The highly reactive spleen of the infected gazelles may indicate an intense antigenic stimulation while the B-lymphophagocytosis observed in the centre of the follicles is a clear evidence of immunosuppression. Red fronted gazelles (Gazella rufifrons) subjected to captivity for the first time have been reported to show evidence of stress with a resultant increased blood cortisol secretion leading to compromised trypanotolerance (Mbaya, 2007). In conclusion, therefore, the findings of this study suggest that the trypanotolerance of free-living red fronted gazelles (Gazella rufifrons) may become compromised in captivity with severe clinical and pathological changes and death when such animals infected with T. brucei remain either untreated or are treated with sub-optimal (3.5 mg/ kg) doses of diminazene aceturate (Berenil1). Treatment with higher doses (7.0 mg/kg) of Berenil1 or melarsamine hydrochloride (0.3 and 0.6 mg/kg) may be used to control the development of clinical disease in such animals under captive conditions. Acknowledgement Financial support from the University of Maiduguri Central Research Committee is gratefully acknowledged. References
Fig. 5. Kidney of infected control showing widespread glomerular degeneration with presence of pinkish casts in Bowman’s capsules (A) and tubular lumens (B) H&E; 450).
actions of their powerful locomotory flagella, the microtubule-reinforced body or as they penetrate tissues through the interstices Igbokwe (1995). Furthermore, indirect evidences of tissue damage in trypanosomosis have been associated with peroxidative damage to tissues by free radicals such as allylic hydrogen atoms from amethylene carbons of polyunsaturated fatty acids, which are produced through the activity of phospholipids A1 released by trypanosomes (Igbokwe, 1995).
Drury, R.A.B., Wallington, E.A., 1976. Carleton’s Histological Techniques, 4th ed. Oxford University Press, London, pp. 21–70. Egbe-Nwiyi, T.N., Igbokwe, I.O., Nwosu, C.O., 2005. Effects of oral copper sulphate supplementation on the severity of Trypanosoma brucei and T. congolense infection of rats. Nig. Vet. J. 26, 8–17. Graph Pad Instat., 2000. Version 3, 00 for Windows, Graph pad software, San Diego, CA, USA, www.graphpad.com. Herbert, W.J., Lumsden, W.H.R., 1976. Trypanonosoma brucei: a rapid matching method for estimating the host’s parastaemia. Exp. Parasitol. 40, 427–432. Igbokwe, I.O., 1995. Nutrition in the pathogenesis of African trypanosomiasis. Protozool. Abst. 19, 797–807. Mbaya, A.W., 2007. Studies on trypanosomosis in captive red fronted gazelles (Gazella rufifrons) in Nigeria, PhD Thesis. University of Maiduguri, 271 pp. Mbaya, A.W., Aliyu, M.M., Nwosu, C.O., Ibrahim, U.I., 2008. Captive wild animals as potential reservoirs of haemo and ectoparasitic infections of man and domestic animals in the arid-region of Northeastern Nigeria. Vet. Archiv. 78, 429–440. Murray, M., Trail, J.C., Nad d’ Letern, G.D.M., 1983. Trypanotolerance in cattle and prospects for the control of trypanosomosis by selective breeding. Revue Scientifique et technique Del, Office International Des Epizooties 9, 369–386. Shalm, O.W., Jain, N.C., Carroll, E.J., 1995. Veterinary Haematology, 3rd ed. Lea and Fabiger, Philadelphia, pp. 498–512. Soulsby, E.J.L., 1982. Helminths, Arthropods and Protozoa of Domesticated animals, 7th ed. Bailliere Tindall and Company, London, pp. 800–809.
Contents lists available at ScienceDirect
Veterinary Parasitology journal homepage: www.elsevier.com/locate/vetpar
Short communication
Effects of melarsamine hydrochloride (Cymelarsan1) and diminazene aceturate (Berenil1) on the pathology of experimental Trypanosoma brucei infection in red fronted gazelles (Gazella rufifrons) A.W. Mbaya a,*, M.M. Aliyu b, C.O. Nwosu a, V.O. Taiwo c, U.I. Ibrahim b a b c
Department of Veterinary Microbiology & Parasitology, University of Maiduguri, Nigeria Department of Veterinary Medicine, University of Maiduguri, Nigeria Department of Veterinary Pathology, University of Ibadan, Nigeria
A R T I C L E I N F O
A B S T R A C T
Article history: Received 22 September 2008 Received in revised form 12 March 2009 Accepted 19 March 2009
An experimental infection of red fronted gazelles (Gazella rufifrons) with Trypanosoma brucei strain MKAR/84/NITR/6 was carried out. Two waves of parasitaemia which corresponded with a significant decline (p < 0.05) in packed cell volume (PCV) was encountered in the infected untreated controls and those treated at day 8 post-infection with a sub-optimal dosage of diminazene aceturate (Berenil1) at 3.5 mg/kg body weight. At postmortem, hepatomegally, splenomegally, lymphadenopathy, nephritis, myocardial degeneration with pulmonary oedema was observed in the two groups. Similarly, histopathological studies of some organs revealed interstitial haemorrhages, severe degenerative changes with cellular infiltrations. On the other hand, those treated by day 8 post-infection with melarsamine hydrochloride (Cymelarsan1) at 0.3 mg/kg, 0.6 mg/kg or diminazene aceturate (Berenil1) at 7.0 mg/kg body weight had apparently normal organs at the end of the experiment. These results suggest that, T. brucei can cause severe pathological changes in untreated red fronted gazelles (Gazella rufifrons). However, treatments at the onset of parasitaemia, by day 8 post-infection with melarsamine hydrochloride (Cymelarsan1) at 0.3 and 0.6 mg/kg or diminazene aceturate (Berenil1) at 7.0 mg/kg body weight ameliorated the deleterious effects of the infection in the gazelles. ß 2009 Elsevier B.V. All rights reserved.
Keywords: Pathology Trypanosoma brucei Red fronted gazelle Cymelarsan1 Berenil1
1. Introduction The pathogenesis of trypanosomosis in wild animals has remained a subject of controversy due to their trypanotolerant trait. The breakdowns in the premunity associated with trypanosomosis rarely occur under freeliving conditions. On the other hand, there is tremendous increase in susceptibility to the infection by wild animals under conditions of captivity. In the semi-arid zone of
* Corresponding author at: Department of Veterinary Microbiology and Parasitology, Faculty of Veterinary Medicine, University of Maiduguri, Bama Road, P.M.B.1069, Maiduguri, Nigeria. Tel.: +234 8036011774. E-mail address: [email protected] (A.W. Mbaya). 0304-4017/$ – see front matter ß 2009 Elsevier B.V. All rights reserved. doi:10.1016/j.vetpar.2009.03.036
Northeastern Nigeria, 1(16.67%) stripped hyeanas (Hyeana hyeana) and 7(50%) red fronted gazelles (Gazella rufifrons) maintained under captive conditions suffered infection with Trypanosoma brucei (Mbaya et al., 2008). The greater susceptibility to trypanosomosis exhibited by captive than free-living wild animals has been attributed to the increased secretion of cortisol by captive animals in response to the stress of captivity (Mbaya, 2007). In the semi-arid zone of Northeastern Nigeria, red fronted gazelles (Gazella rufifrons) are easily semi-domesticated and frequently reared together with sheep and goats in households (Mbaya, 2007). Consequently, as a result of the importance attached to the ownership of red fronted gazelles (Gazella rufifrons) and their known susceptibility to trypanosomosis under captive conditions,
A.W. Mbaya et al. / Veterinary Parasitology 163 (2009) 140–143
there is need to have a detailed understanding of the pathology of the infection in the animals as well as develop suitable control measures against it. In this study, free-living red fronted gazelles (Gazella rufifrons) were subjected to captivity for the first time with a view to negate any trypanotolerance that the animals may have and infected with T. brucei to investigate the pathology of the subsequent disease as well as develop suitable chemotherapeutic regimen for its control. 2. Materials and methods Thirty apparently healthy free-living red fronted gazelles (Gazella rufifrons) aged between 2 and 3 years and weighing between 20 and 25 kg were captured directly from the wild for the first time and screened according to standard criteria (Soulsby, 1982). They were found to harbour a mixed infection of T. brucei, T. vivax, Strongyles, and Anaplasma marginale and routinely treated according to standard methods (Soulsby, 1982). The animals were housed in concrete floored and fly-proof pens throughout the experiment and allowed 40 days to
Fig. 1. Parasite counts (103 mL
1
141
acclimatize to their new environment. They were fed on wheat bran supplemented with bean husks, guinea corn and chopped cucumber while water was provided ad libitum. Prior to the commencement of the study, the animals were randomly divided into six groups (A, B, C, D, E and F) of five gazelles each. Trypanosoma brucei brucei (Strain Mkar/84/Nitr/6) used for the study, was obtained from the Nigeria Institute for Trypanosomosis Research (NITR) in Kaduna, Nigeria. The stabilates were passaged twice in rats and then transferred into two red Sokoto goats that served as donors. Infected blood from the donor goats was diluted with phosphate buffered glucose saline (PBSG, pH 7.2). Each gazelle in groups A, B, C, D and E was inoculated, via the jugular vein, with the infected blood containing 1.5 x 106 trypanosomes. Groups A and B were respectively treated subcutaneously with melarsamine hydrochloride (Cymelarsan1) at a single standard dose rate of 0.3 and 0.6 mg/kg body weight, while groups C and D were treated intramuscularly with diminazene aceturate (Berenil1) at a single standard dose rate of 3.5 and 7.0 mg/kg body weights. All treatments commenced at the onset of
) and packed cell volume (%) of red fronted gazelles infected with T. brucei and their treatments.
142
A.W. Mbaya et al. / Veterinary Parasitology 163 (2009) 140–143
parasitaemia by day 8 post-infection. Group E served as infected untreated control and Group F the uninfected control. The experimental gazelles were monitored daily for the development of clinical signs of trypanosomosis. The initial detection of parasitaemia was by the wet film and haematocrit buffy–coat methods (Murray et al., 1983) while the degree of parasitaemia (Herbert and Lumsden, 1976) and packed cell volume (PCV) (Shalm et al., 1995) was estimated every other day. All gazelles that died from the infection or were humanely killed at the end of the study were subjected to detailed necropsy. The vital organs were carefully removed, washed, weighed and examined for lesions. Tissue sections of the organs were processed according to standard criteria (Drury and Wallington, 1976). The data obtained from the study were summarized as means standard deviation and differences between them determined at the 5% level of significance (Graph Pad Instat, 2000). 3. Results All the infected gazelles developed acute trypanosomosis with a pre-patent period of 8 days. Clinical signs observed were fluctuating pyrexia (40–42.8 8C), progressive loss in body weight, dullness, inapetence and palour of buccal and ocular mucous membranes. There were elevated parasite counts and a general decline in packed cell volume (PCV) (Fig. 1). These changes were however, significant (p < 0.05) during the first and second waves of parasitaemia, following sub-optimal treatment with diminazene aceturate (Berenil1) at 3.5 mg/kg body weight and in the infected control with the death of all the gazelles in the two groups occurring between days 46 and 52 postinfection. The signs of the infection were however, effectively modulated in the groups treated with either melarsamine hydrochloride (Cymelarsan1) at 0.3 and 0.6 mg/kg or with diminazene aceturate (Berenil1) at 7.0 mg/kg body weight, with no mortality recorded in these groups. Vital organs of the infected control and those treated with 3.5 mg/kg of diminazene aceturate (Berenil1), were enlarged with petechial and echymotic haemorrhages on serosal surfaces while the heart appeared pale and hypoplastic. Similarly, various degrees of degenerative changes with cellular infiltrations were encountered in tissue sections of the vital organs of the infected controls (Figs. 2–5) and in those treated with diminazene aceturate (Berenil1) at 3.5 mg/kg body weight. The vital organs of the gazelles treated with melarsamine hydrochloride (Cymelarsan) at 0.3 and 0.6 mg/kg or diminazene aceturate (Berenil1) at 7.0 mg/kg body weight were apparently normal.
Fig. 2. Heart of untreated control showing focal areas of hyaline degeneration of myocardial fibers (arrows) (H&E; 450).
the higher dosage (7.0 mg/kg body weight) was curative. The cardiomegally encountered in the early phase of the infection in the untreated and sub-optimally treated groups is probably associated with cellular infiltrations in the myocardial or endocardial layers. However, the terminal shriveling of the heart may have been due to myocardial fiber degeneration as described by Egbe-Nwiyi et al. (2005). The anaemia observed, may, have contributed in part to the widespread degenerative changes in the vital organs. Tissue hypoxia due to ischaemia, disseminated intravascular coagulation by micro-thrombi or immune complexes have been identified as factors indirectly involved in the pathology of organ damage in trypanosomosis (Igbokwe, 1995). The severe organ and tissue damage usually associated with trypanosomosis have been attributed to the fact that the trypanosomes mechanically traumatize cells and create tiny holes on the plasma membranes by the lashing
4. Discussion The results of the study showed that various degrees of organ and tissue damage occurred in the infected untreated gazelles, which experienced two waves of parasitaemia. The trend of parasitaemia observed in the gazelles treated with diminazene aceturate (Berenil1) at 3.5 mg/kg is probably due to a sub-optimal dosage, since
Fig. 3. Liver of untreated control showing widespread vacuolar degeneration of hepatocytes (H&E; 450).
A.W. Mbaya et al. / Veterinary Parasitology 163 (2009) 140–143
Fig. 4. A highly reactive spleen of infected untreated control showing Tlymphoblastic halos (A) numerous macrophages (B) in red pulp (H&E; 450).
143
The highly reactive spleen of the infected gazelles may indicate an intense antigenic stimulation while the B-lymphophagocytosis observed in the centre of the follicles is a clear evidence of immunosuppression. Red fronted gazelles (Gazella rufifrons) subjected to captivity for the first time have been reported to show evidence of stress with a resultant increased blood cortisol secretion leading to compromised trypanotolerance (Mbaya, 2007). In conclusion, therefore, the findings of this study suggest that the trypanotolerance of free-living red fronted gazelles (Gazella rufifrons) may become compromised in captivity with severe clinical and pathological changes and death when such animals infected with T. brucei remain either untreated or are treated with sub-optimal (3.5 mg/ kg) doses of diminazene aceturate (Berenil1). Treatment with higher doses (7.0 mg/kg) of Berenil1 or melarsamine hydrochloride (0.3 and 0.6 mg/kg) may be used to control the development of clinical disease in such animals under captive conditions. Acknowledgement Financial support from the University of Maiduguri Central Research Committee is gratefully acknowledged. References
Fig. 5. Kidney of infected control showing widespread glomerular degeneration with presence of pinkish casts in Bowman’s capsules (A) and tubular lumens (B) H&E; 450).
actions of their powerful locomotory flagella, the microtubule-reinforced body or as they penetrate tissues through the interstices Igbokwe (1995). Furthermore, indirect evidences of tissue damage in trypanosomosis have been associated with peroxidative damage to tissues by free radicals such as allylic hydrogen atoms from amethylene carbons of polyunsaturated fatty acids, which are produced through the activity of phospholipids A1 released by trypanosomes (Igbokwe, 1995).
Drury, R.A.B., Wallington, E.A., 1976. Carleton’s Histological Techniques, 4th ed. Oxford University Press, London, pp. 21–70. Egbe-Nwiyi, T.N., Igbokwe, I.O., Nwosu, C.O., 2005. Effects of oral copper sulphate supplementation on the severity of Trypanosoma brucei and T. congolense infection of rats. Nig. Vet. J. 26, 8–17. Graph Pad Instat., 2000. Version 3, 00 for Windows, Graph pad software, San Diego, CA, USA, www.graphpad.com. Herbert, W.J., Lumsden, W.H.R., 1976. Trypanonosoma brucei: a rapid matching method for estimating the host’s parastaemia. Exp. Parasitol. 40, 427–432. Igbokwe, I.O., 1995. Nutrition in the pathogenesis of African trypanosomiasis. Protozool. Abst. 19, 797–807. Mbaya, A.W., 2007. Studies on trypanosomosis in captive red fronted gazelles (Gazella rufifrons) in Nigeria, PhD Thesis. University of Maiduguri, 271 pp. Mbaya, A.W., Aliyu, M.M., Nwosu, C.O., Ibrahim, U.I., 2008. Captive wild animals as potential reservoirs of haemo and ectoparasitic infections of man and domestic animals in the arid-region of Northeastern Nigeria. Vet. Archiv. 78, 429–440. Murray, M., Trail, J.C., Nad d’ Letern, G.D.M., 1983. Trypanotolerance in cattle and prospects for the control of trypanosomosis by selective breeding. Revue Scientifique et technique Del, Office International Des Epizooties 9, 369–386. Shalm, O.W., Jain, N.C., Carroll, E.J., 1995. Veterinary Haematology, 3rd ed. Lea and Fabiger, Philadelphia, pp. 498–512. Soulsby, E.J.L., 1982. Helminths, Arthropods and Protozoa of Domesticated animals, 7th ed. Bailliere Tindall and Company, London, pp. 800–809.