Study links migration and AIDS. International (Africa).
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The conflict-ridden central African state of Burundi launched a campaign against AIDS as the health minister said 160,000 children were orphans as a result of the disease. "This day can be considered the real beginning of the war against AIDS in our country," said Leonce Ngendakumana National Assembly President. He was opening a workshop designed to develop strategies to combat the spread of HIV, which was attended by UN agencies, aid organizations, and members of the government. Health Minister Juma Kariburyo said 30,000 people had died of AIDS in 2 years in Burundi, which has a population of around 6 million. "We had less than 1% of infection in 1983, but today the urban area figures are more than 20%, and more than 14% in the rural areas," he added. But Jeanne Gapiya, president of a Burundian association for people who are HIV positive, said she feared the true figures could be far higher. Gapiya is HIV positive and has lost her husband, child, brother and sister to AIDS. Minister of Defense Colonel Alfred Nkurunziza told the workshop the disease was rampant within the army. Burundi's Tutsi-dominated army is fighting a bitter civil war against ethnic Hutu rebels. The conflict has caused large refugee movements, which has exacerbated the spread of infectious diseases.
Visceral leishmaniasis appears in the form of notoriously devastating epidemics and as an endemic disease of sporadic nature. In an attempt to understand the nature of this difference and its underlying causes, and to identify possible mechanisms for the instigation of outbreaks, the current status of the characterization of the parasite, its taxonomy, host immunity and genetics, are reviewed with the main focus on eastern Africa, one of the places where the dichotomous epidemiology of the disease is most pronounced. The new molecular tools offer various insights into the understanding of the complex epidemiology of visceral leishmaniasis and the interplay between parasite and host factors. Further insights are also provided on the parts played by demography, genetic history and geography in shaping the overall global portrait of the disease.
An attempt was made to estimate the prevalence of hydatid disease in nomadic pastoralists living in eastern Africa and to identify environmental, cultural and behavioural factors which may influence Echinococcus transmission. 18,565 nomadic pastoralists, from 12 different groups living in the vast, semi-desert regions of Kenya, Sudan, Ethiopia and Tanzania, were screened for hydatid cysts using a portable ultrasound scanner. High prevalences of hydatidosis were recorded among the north-western (5.6%) and north-eastern (2.1%) Turkana of north-west Kenya, the Toposa (3.2%) of southern Sudan, the Nyangatom (2.2%), Hamar (0.5%) and Boran (1.8%) of south-west Ethiopia and northern Kenya and the Maasai (1.0%) of Tanzania. Lower prevalences were recorded amongst the southern (0.3%) and lake dwelling (0.3%) Turkana and the Pokot (0.1%) of Kenya. The disease was not found amongst the Turkana, Samburu, Dassanetch, Gabbra, Somali or Rendille screened on the east side of Lake Turkana. The scanning surveys were well accepted by the people and provided evidence for the need to expand the present hydatid control programme in Turkana to cover the whole hyperendemic focus. Such a programme must contain an educational component for, although most groups recognized hydatid cysts, there was complete lack of knowledge concerning the parasite and its mode of transmission.
African wild dog populations have declined precipitously during the last 100 years in eastern Africa. The possible causes of this decline include a reduction in prey abundance and habitat; disease; and loss of genetic variability accompanied by inbreeding depression. We examined the levels of genetic variability and distinctiveness among populations of African wild dogs using mitochondrial DNA (mtDNA) restriction site and sequence analyses and multivariate analysis of cranial and dental measurements. Our results indicate that the genetic variability of eastern African wild dog populations is comparable to that of southern Africa and similar to levels of variability found in other large canids. Southern and eastern populations of wild dogs show about 1% divergence in mtDNA sequence and form two monophyletic assemblages containing three mtDNA genotypes each. No genotypes are shared between the two regions. With one exception, all wild dogs examined from zoos had southern African genotypes. Morphological analysis supports the distinction of eastern and southern African wild dog populations, and we suggest they should be considered separate subspecies. An eastern African wild dog breeding program should be initiated to ensure preservation of the eastern African form and to slow the loss of genetic variability that, while not yet apparent, will inevitably occur if wild populations continue to decline. Finally, we examined the phylogenetic relationships of wild dogs to other wolf-like canids through analysis of 736 base pairs (bp) of cytochrome b sequence and showed wild dogs to belong to a phylogenetically distinct lineage of the wolf-like canids.
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