This thesis has shown that T. parva infection in R. appendiculatus causes pathology in a proportion of the tick population. These pathologies are characterised by perforated guts, which cause leakage of gut contents into the haemocoel, perforated and malformed Malphighian tubules, damaged salivary glands acini and malformed or missing legs, possibly as a consequence of secondary fungal infection. There is a possibility that T. parva is vulnerable to R. appendiculatus immune mechanisms. The parasite lifecycle has been examined throughout the period of the tick moult, and the results indicate that zygote and kinete forms appear most susceptible to reductive mechanisms. The phenoloxidase cascade is likely to play a role in this process and may be affected in the haemolymph. Very little, if any, research attention has been focused on tick pathology in relation to ECf. However, it is possible that the phenomena described in this thesis could have significant influences on T. parva and R. appendiculatus population dynamics in ECf endemic areas. Further work in this area, particularly on tick transmission from carrier-state infections could make significant contributions to our understanding of, and our ability to successfully manipulate the disease in the field.