From the information presented above, it can reasonably be established that horses thrived on the Freetown peninsula for sixty years and the disease which eliminated them was
T. brucei. This disease was prevalent for at least 15 years although it eventually disappeared, probably before 1900. In addition, clearance of the forest, in three overlapping phases, was carried out prior to and during the outbreak.
From the ecology of the three species of tsetse fly possibly implicated in the outbreak of the disease in Sierra Leone, it can be deduced that deforestation and the consequent regeneration and cultivation led to favourable conditions for the expansion of at least
G. palpalisand G. longipalpis, and possibly also of G. morsitans. Taking into account the information currently available on the inter-relationships between tsetse fly and trypanosome species, it can also be suggested that G. longipalpiswas probably the primary source of the disease but that the disease was sustained, particularly around Freetown itself, by G. palpalisand possibly by other biting flies. That G. longipalpisor even G. morsitansprobably initiated the outbreak makes the eventual disappearance of the disease more understandable since both of these species relied upon regenerated forest and an abundance of game, resources which diminished as agriculture progressed. It is likely that these primary carriers infected horses and cattle moving between the provinces and Freetown, thereby providing the link in spreading the disease to the Colony.
It appears therefore that the removal of the forest led to the outbreak of trypanosomiasis in horses. A different and more rational approach to forestry in Sierra Leone would have avoided this altogether. In fact it is fortunate that the consequences of this indiscriminate deforestation were not more serious since all three tsetse flies in question are carriers of the human sleeping sickness,
T. gambiense. For some reason, however, this species of trypanosome, whilst common in the interior, is not prevalent in the coastal areas of West Africa, though there was in fact, an epidemic of this disease in the 1930s in the Kaiahun area, associated with G. palpalis.
Since the horse is relatively sensitive to tsetse fly and its associated trypanosomes, this animal is a good indicator of the presence of trypanosomiasis. Dr McCoy in his memorandum mentions that horses thrive in the Gambia and at Lagos and that ‘loin disease’ was unknown in these places. He makes no reference, however, to horses in Ghana. The history of the horse in other parts of West Africa may therefore be worth pursuing in this respect.