THE HAEMATOLOGICAL PROFILE FROM NEONATE TO 51 WEEKS

Get Complete Project Material File(s) Now! »

Tsetse-borne pathogens

Trypanosomosis, caused by protozoan parasites of the genus Trypanosoma, has been one of the most important diseases in livestock in sub-Saharan cattle since before colonial times. It remains a serious constraint to economic development in the region (Maudlin 2006). The main vector is tsetse flies, Glossina spp., although other biting flies and mechanical transmission are implicated in the transmission of certain species (Connor & Van den Bossche 2004).
Of the tsetse-transmitted trypanosomes, Trypanosoma congolense, Trypanosoma vivax and Trypanosoma brucei are of particular importance in cattle. Trypanosoma theileri, a stercorarian parasite, is transmitted by tabanid flies. It is regarded as non-pathogenic, but has been associated with disease in certain circumstances (Connor & Van den Bossche 2004). These trypanosomes are blood-borne, with T. congolense confined to the circulatory system of the host. However, T. vivax and T. brucei also invade the host’s tissues (Murray & Dexter 1988).
Anaemia is a well recognized consequence of trypanosomosis. In fact, PCV is used as an indicator for trypanosomosis on a herd-level, even when trypanosomes are not detected by parasitological diagnostics (Van den Bossche, Mudenge, Mubanga & Norval 1999; Van den Bossche & Rowlands 2001b). Murray & Dexter (1988) divided the progression of anaemia intrypanosomosis into two phases. During the first, acute phase of anaemia the PCV falls at the same time that the first wave of parasitaemia develops. Anaemia is indirectly caused by infection through the activation of mononuclear phagocytosis which results in massive erythrophagocytosis. At the same time, trypanosome haemolysins and proteases also induce haemolysis (Murray & Dexter 1988). There is an indication of increased haemopoiesis to compensate for the massive erythrophagocytosis. The second, chronic phase can overlap with the first phase, but is associated with low transient parasitaemias.
Erythrophagocytosis is ongoing but there are now indications of dyshaemopoiesis. The synthesis of red blood cells is insufficient to compensate for the degree of anaemia seen (Dargie, Murray, Murray, Grimshaw & McIntyre 1979; Murray & Dexter 1988). This indicates a degree of bone marrow dysfunction. The affected animal can show either spontaneous recovery, survive this phase with persistent low-grade anaemia or die. The response to treatment during the acute phase is rapid, compared to the chronic phase where treatment is  often ineffective (Urquhart & Holmes 1987). An acute haemorrhagic syndrome has been described in T. vivax (Magona, Walubengo & Odimin 2008b).
Pancytopenia develops in the host during the first wave of the parasitaemia. Apart from anaemia, thrombocytopenia and leukopenia are also constant findings in trypanosomosis (Wellde, Kovatch, Chumo & Wykoff 1978; Murray & Dexter 1988). The decrease in thrombocytes, lymphocytes and neutrophils correlate with the onset, severity and prevalence of trypanosomes in the host’s blood. The development of disseminated intravascular coagulation in end-stage trypanosomosis adds to the loss of thrombocytes and is reflected by generalized petechiae and ecchymoses seen at post mortem examinations (Murray & Dexter 1988).
Immunosuppression in trypanosomosis is also well recognized (Holmes, Mammo, Thomson, Knight, Lucken, Murray, Murray, Jennings & Urquhart 1974; Mackenzie, Boyt, Emslie, ander & Swanepoel 1975; Askonas 1984; Urquhart & Holmes 1987, Uilenberg 1998). Although the host exhibits an active lymphoid response, an immune response to other antigens is almost completely lacking, in particular antigens that stimulate an antibody response (Urquhart & Holmes 1987).

READ  Geographic, political and socio-economic status of Namibia

CHAPTER 1: INTRODUCTION
1. Introduction
2. Literature review .
2.1 Infectious causes of anaemia..
2.2 From infection to disease .
2.3 Interactions between concomitant pathogens.
3. Study objectives.
CHAPTER 2: METHODOLOGY AND MATERIALS
1. Project design
1.1 Study site
1.2 Survey design
2. Monitoring and sampling of calves.
2.1 Recruitment of calves.
2.2 Monitoring .
2.3 Sampling.
3. Diagnostic procedures.
3.1 Sample processing and testing .
3.2 Diagnostic tests..
4. Data analysis ..
4.1 Descriptive statistics.
4.2 Evaluation of diagnostic tests.
4.3 Statistical modelling
CHAPTER 3: EVALUATION OF THE FIELD PERFORMANCE OF FAMACHA© COLOUR CHART IN DETECTING ANAEMIA AND THE PERFORMANCE OF THE SYSMEX AUTOMATED ANALYZER FOR LABORATORY DIAGNOSIS OF ANAEMIA
1. Introduction ..
2. Materials and methods..
2.1 Evaluation of the field performance of the FAMACHA© eye colour chart
2.2 Evaluation of the performance of the Sysmex .
3. Results..
3.1 Evaluation of the field performance of the FAMACHA© .
4. Discussion..
5. Conclusions.
CHAPTER 4: THE HAEMATOLOGICAL PROFILE FROM NEONATE TO 51 WEEKS.
1. Introduction .
2. Materials and methods
2.1 Age-related changes in the haematology of East African short-horn Zebu calves
2.2 “Good” calves – haematology of relatively healthy calves
2.3 The level of anaemia in the population
2.4 Statistical analysis.
3. Results.
3.1 Age-related changes in the haematology of East African short-horn Zebu calves .
3.2 “Good” calves – haematology in relatively healthy calves..
3.3 The level of anaemia in the population
4. Discussion..
4.1 Age-related changes in the haematology of East African short-horn Zebu calves
4.2 “Good” calves – haematology in relatively healthy calves.
4.3 The level of anaemia in the population
5. Conclusion.
CHAPTER 5: THE DISTRIBUTION OF PATHOGENS IN THE POPULATION 
1. Introduction
2. Materials and methods.
2.1 Frequency distribution of pathogens
2.2 Prevalence and cumulative incidences of pathogens
2.3 Prevalence of co-infections 
2.4 Data analysis .
3. Results.
3.1 The frequency distribution of pathogens in the calf population
3.2 The prevalence and cumulative incidences of pathogens
3.3 The level of co-infections of different pathogens in the study population
4. Discussion.
5. Conclusions.
CHAPTER 6: THE PATHOGENIC CAUSES OF ANAEMIA.
CHAPTER 7: THE IMPACT OF CO-INFECTIONS ON THE HAEMATOLOGICAL PROFILE OF CALVES 
CHAPTER 8: GENERAL CONCLUSIONS.
REFERENCES

GET THE COMPLETE PROJECT

Related Posts