– Clinical and Haematological Studies in Dogs with Single and Mixed Experimental Trypanosoma Brucei and Ancyclostoma Caninum Infection –
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ABSTRACT
Trypanosomosis is one of the most devastating diseases of animals caused by infection with a protozoan parasite trypanosome, which is transmitted by tse-tse fly. Besides anaemia, which is a cardinal symptom of the disease, infection also impairs the immune system of animals and renders them more susceptible to other.
Under natural field condition, in areas where trypanosome and helminth parasites are endemic, mixed infection appears to be common.
A study was conducted to determine the clinico-haematological manifestations in dogs experimentally infected with Trypanosoma brucei and Ancylostoma caninum singly and in combination. Twenty young local dogs were used in the study.
They were randomly grouped into 4 with 5 dogs in each group; group A (uninfected control), group B (infected with A. caninum), group C (infected with T. brucei) and group D (mixed infection with A. caninum/T. brucei).
For the mixed infection, dogs were initially infected with A. caninum and then T. brucei infection superimposed 23 days later by the time of patency of Ancylostoma eggs in the stool.
Results of this study showed that the prepatent period (PP) of A. caninum infection in the dogs was 24.5±0.4 days. The PP of T. brucei infection alone was 5.0±0.0 days, but was 4.6±0.22 days in the mixed infection.
Clinical signs of dullness, inappetence, anorexia, weakness, pale mucous membrane due to anaemia, rough hair coat were encountered in both infections.
Additionally, specific signs of bloody diarrhea and sunken eyes were present in A. caninum infected dogs while fever, swollen face, bilateral ocular discharge and corneal opacity accompanied T. brucei infection. A combination of these signs in a more severe form characterized the mixed infection of both parasites.
There was a significant decrease (P<0.05) in the packed cell volume (PCV) in all the infected groups (B, C and D) as from day 19 post infection (p.i.).
Infection with Ancylostoma caninum caused significant increase (P<0.05) in the total leucocyte count of the dogs in group B from day 29 p.i., whereas significant decrease were recorded in trypanosome infected dogs group C and in mixed infection group (D) on days 38 and 34 p.i., respectively.
The absolute neutrophil counts significantly increased (P<0.05) in group B by day 29 p.i. whereas significant decreases were recorded in groups C and D from day 34 p.i.. There was no variation in the absolute lymphocyte count except on day 20 p.i. when an increase was detected only in the mixed infection group (D).
The absolute eosinophil counts significantly increased (P<0.05) in group B from day 14 p.i. in contrast to a significant decrease (P<0.05) in the mixed infection group (D) by day 34 p.i. There was no significant variation (P<0.05) in the absolute monocyte counts of the infected dogs.
The results of the egg per gram (EPG) of faeces on days 28, 34 and 39 were 20300±12195, 81233±26410 and 67683±13971 for group B, and 34325±8044, 54425±24764 and 55800±12304 for group D, respectively, and showed
no significant difference (P>0.05).
It was concluded that concurrent infection of T. brucei and A. caninum resulted in enhanced pathogenicity manifested in remarkable clinico-haematological alterations in the infected dogs.
TABLE OF CONTENTS
TITLE PAGE i
APPROVAL PAGE ii
DEDICATION iii
ACKNOWLEDGEMENT iv
LIST OF FIGURES v
LIST OF TABLES vi
LIST OF PLATES vii
TABLE OF CONTENTS viii
ABSTRACT xii
CHAPTER ONE 1
1.0 INTRODUCTION 1
CHAPTER TWO 4
2.0 LITERATURE REVIEW 4
2.1.0 African animal trypanosomosis 4
2.1.1 Aetiology 4
2.1.2 Transmission 4
2.1.3 Life cycle of the parasite 5
2.1.4 Pathogenesis and pathological manifestations 6
2.1.5 Clinical manifestations 10
2.1.6 Immunity in trypanosomosis 11
2.1.7 Immunosuppression in trypanosomosis 13
2.1.8 Haematology 15
2.2.0 ANCYLOSTOMA CANINUM 17
2.2.1 Aetiology 17
2.2.2 Life cycle of Ancylostoma caninum 18
2.2.3 Clinical signs and pathogenicity of Ancylostoma caninum 19
2.2.4 Immunity in helminth infections 20
2.2.5 Haematology 23
CHAPTER THREE 25
3.0 MATERIALS AND METHODS 25
3.1.0 Experimental Animals 25
3.1.1 Experimental design 25
3.1.2 Trypanosome infection 26
3.1.3 Ancylostoma caninum 26
3.1.4 Feacal culture 26
3.1.5 Ancylostoma caninum infection 27
3.1.6 Conjunct Trypanosoma brucei and Ancylostoma caninum infection 27
3.2.0 Detection of parasitaemia 28
3.2.1 Wet mount 28
3.2.2 Buffy coat 28
3.2.3 Giemsa stained thin films 28
3.3 Faecal egg count 29
3.4.0 Haematology 29
3.4.1 Blood collection 29
3.4.2 Packed cell volume 29
3.5 Post mortem examination 30
3.6 Statistical analysis 30
CHAPTER FOUR 31
4.0 RESULTS 31
4.1Course of infection 31
4.1.1 Ancylostoma caninum 31
4.1.2 Trypanosoma brucei 31
4.1.3 Mixed infection (T. brucei and A. caninum) 35
4.2 Faecal Egg Output (EPG) 37
4.3 Haematology 37
4.3.1 Packed cell volume 37
4.3.2 Total white blood cell counts 37
4.3.3 Absolute neutrophil counts 41
4.3.4 Absolute lymphocyte counts 41
4.3.5 Absolute eosinophil counts 41
4.3.6 Absolute monocyte counts 41
4.4 Post mortem findings 46
CHAPTER FIVE 50
5.0 DISCUSSIONS 50
6.0 CONCLUSIONS AND RECOMMENDATIONS 54
REFERENCES 56
APPENDIX 74
INTRODUCTION
The trypanosome is a protozoan parasite transmitted by the bite of a tsetse fly to people and to wild and domestic animals in which it causes trypanosomosis (Maudlin, 2006; ILRAD, 1991).
The disease is widespread across more than a third of African continent infested with the tsetse fly vector (Feldmann, et al., 2005; Torr et al., 2005).
It is one of the most devastating diseases of animals in sub-Sharan Africa with estimated losses due to its direct and indirect consequences running into billions of dollars (Swallow, 1998; Ng’ayo et al., 2005).
Trypanosoma vivax, T. congolense and T. brucei are the most important African animal trypanosome species. Their infections in domestic animals cause anaemia, weight loss and reproductive disorders; infected animals may die if not treated.
Another striking feature of African trypanosomosis is its profound suppression of immune system of the infected
mammalian host (Goodwin, 1970; Goodwin et al., 1972; Rurangirwa et al., 1979; Griffin et al., 1980; ILRAD, 1992).
This impairment of the immune response due to trypanosomosis has given rise to increased susceptibility of
trypanosome-infected animals to other infections (Parkin and Hornby, 1930; Mackenzie et al., 1975; Scott et al., 1977; Nantulya et al., 1982; Ikeme et al., 1984).
REFERENCES
Akpa, P.O., Ezeokonkwo, R. C., Eze, C. A. and Anene, B. M. (2008). Comparative efficacy assessment of pentamidine isethionate and diminazene aceturate in the chemotherapy of Trypanosoma brucei brucei infection in dogs. Veterinary Parasitology 151: 139-149.
Albers, G. A. A., Gray, G. D., Jambre, L. F. Le, Barger, L. A. and Barker, J. S. F. (1990). The effects of Haemonchus contortus infection on haematological parameters in young Merino sheep and its significance for productivity. 50: 99-109.
Anene, B. M., Chime, A. B. and Anika, S. M. (1991). The production performance of imported Friesian cattle under heavy Trypanosoma challenge in a rain forest zone of Nigeria. British Veterinary Journal, 147: 275-282.
Anene, B. M., Chukwu, C. C. and Anika, S. M. (1989a). Immunosuppression of humoral immune response in canine trypanosomiasis. Microbios Letters, 40: 37-46.
Anene B. M., Chukwu, C. C, Chime, A. B. and Anika, S. M. (1989b). Comparative clinical and haematological observation in dogs infected with Trypanosoma brucei and Trypanosoma congolense treated with diminazene aceturate. Zariya Veterinarian 4, 11-18.
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