Meanwhile, other diseases such as venereal diseases and relapsing fever spread in Burao, Hargeysa, and Berbera from 1913 to the 1930s. Dr. Drake-Brockman first diagnosed relapsing fever in 1913. By 1917 the disease was rife in all the towns, particularly Hargeysa. Relapsing fever is a tick-bore disease. It is contained within a relationship between tick and rodent host. When human beings become involved in this relationship they become infected (Hardy, 1993, pp. 967±968). It is a `true famine’ disease, however. It becomes epidemic when “overcrowding, diminished personal hygiene and undernourishment encourage its spread and increase its deadliness”. Hence the disease “rarely occurs except as an epidemic” (Hardy, 1993, p. 968). The disease was new to Somaliland. It was introduced into the country from Ethiopia, during the second decade of the century when many refugees from Ethiopia moved to the country with their livestock, hence introducing the vector of the disease. The disease was later repeatedly introduced through the caravan trade, which became intense from the 1920s onwards and in particular, from 1935±1939. The disease is still endemic in Ethiopia (Hardy, 1993, p. 969). The people were adamant that the source of the disease was foreign. As one report put it, “The natives themselves believe that the Congo floor maggot is the causative agent” (British Parliamentary Papers, 1917, 1918). It was not found in the rural areas. It was, in other words, a disease of the towns. It was prevalent in the mosques and market areas because the mosques were often the place of sleeping for visitors and the market areas were the sites were livestock from Ethiopia was brought for sale (Lovett, 1956). It was overcrowded areas that acted as the nodal points for the spread of the disease. By the 1920s and 1930s, the disease spread to other towns, such as Burao and Odweina. Though a deadly disease, nonetheless, the mortality rate for people was not high. It was estimated at about 0.6% (Edge, 1938). It was, however, a debilitating disease with such symptoms as severe headaches, vomiting, profuse sweating and constipation and made infected people vulnerable to other diseases. Dr. Drake-Brockman first diagnosed the disease (Drake-Brockman, 1914, pp. 4±5). In 1919, for instance, there were 109 relapsing fever cases in Burao. The incidence of the disease fell to 64 cases in 1920. However, in the following year, the number of cases infected with the disease rose again to 113 and then reached epidemic proportions in 1923±1924. The number of cases in the town rose to 500 in 1933; 843 in 1935; 618 in 1936 and 981 in 1937 (Clark, 1937, p. 698). The number of infected cases in Hargeysa and Odweina in those years were also high (Clark, 1937, p.698).
Venereal diseases also spread in the towns and particularly among the `starving pauper element’ from 1910 and onwards. Syphilis was so prevalent among this class that it was feared it might “menace the physique of the next generation” (General Staff, 1925, pp. 36±40). The disease was probably as old as the coastal towns of the northern Somali country, which functioned as the point of contact with the outside world. However, three factors probably limited the spread of the disease into the interior. First, most of the towns were small and the majority was established in the first two decades of the twentieth century. Second, the towns lacked a permanent population. As hitherto pointed out, the population of the towns were seasonal. Third, the sexual more of the people of the interior was extremely conservative. For instance, there were no professional prostitutes in the northern Somali country until the 1930s. Their appearance in Berbera has been noted in a short and popular verse: “Naaga dhaa-dheer/oo dhilooyina/baa dhulkii yimi” (Tall women/who are prostitutes/arrived in the land (Berbera)). One minor poet, who was a pauper, felt jealous about the brisk business of the prostitutes. He said, tongue-in-cheek: “Hadaan siil yar leeyahay/ Berbera kuma sabooleene” (If I had a small pussy/I would not be starving in Berbera). The disease began to spread in the 1920s as the population of the towns and in particular, Berbera increased. The new population consisted mostly of paupers. Women when pushed to the edge of poverty and hunger were not beyond prostituting themselves. Though the disease knows no class boundaries, nonetheless, in the towns it was a disease of the extremely poor and the young.
Furthermore, malaria epidemics were reported in 1931, 1933, 1934, 1935 and 1936 (Colonial Office Report, 1931Colonial Office Report, 1932, 1933, 1934, 1935, 1936). Twelve species of Anopheles had been identified in Somalia in 1965. The main vector of the disease, however, is Anopheles gambiae. There are two transmission seasons for the disease: the gu (March± June) and Dayr (September±December). Dr. Visser stated that the number of infections in the two rainy seasons were not high enough to `build up much immunity’. He added, “The people, therefore, are highly susceptible to epidemic outbreaks” (Visser, 1965). Such epidemics were, however, rare in Somaliland. “Hitherto”, as the 1935 medical report stated, “it has always been assumed that Somaliland has been relatively free from malaria” epidemics (Lee, 1936). The medical staff was not sure why epidemics began to occur frequently in the 1930s. It can be argued, using the insight of students of the disease, that new strains of the disease were introduced into the country. After all, acquired “immunity in malaria is species-specific” (Dunn, 1993, p. 859). Packard argued recently that rainfall is not the only determining factor in the incidence of the disease. Of equal importance was the “number of persons harboring malarial parasites”. Such carriers are needed to infect the mosquito population. “It follows that the incidence of malaria among a human population may be increased by the introduction of a number of infected persons, with or without symptoms, from outside the population, since the increase in carriers raises the likelihood that existing mosquitoes will be infected and that the transmission of parasites to previously uninfected members of the host population will occur” (Packard, 1984, p. 194). The introduction of new strains occurs through new cattle-herding practices, or labor migration, or refugee movements as a result of famines or war, or new settlements, or the cutting of trees and forests. There are, in short, socio-cultural, economic and “human behavioral influences on transmission” of the disease (Prothero, 1965; Packard, 1984, p. 190; Bruce-Chwatt, 1987; Dunn, 1993, p. 862).
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