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PubMed2000

Diagnosis, management and prevention of the common dyslipidaemias in South Africa--clinical guideline, 2000. South African Medical Association and Lipid and Atherosclerosis Society of Southern Africa Working Group.

The optimum management of dyslipidaemia requires a comprehensive, diagnostic work-up. This, minimally, includes: Characterisation of any hyperlipidaemic disorder present. Identification of additional risk factors so as to assess overall (global) risk of future coronary heart disease (CHD). The global risk is best assessed by a calculation combining the risk factors in the individual. In severe monogenic dyslipidaemias and in patients with confirmed pre-existing CHD the risk is usually high; in most such cases the use of lipid-modifying drugs (LMDs) is indicated. Assessment of psychosocial, economic and educational factors relevant to management. Prevention and cost-effective management of even moderately dyslipidaemic patients require appropriate modification of lifestyle: avoidance of tobacco smoking, participation in regular exercise, and a health-promoting diet. Depending on individual circumstance, vigorous, personalised intervention and expert assistance from dieticians, biokineticists and other health care personnel may determine success. The correct choice of patient for drug treatment is a key therapeutic decision and is best done after full lifestyle modification. Recent evidence confirms that appropriately prescribed LMD therapy can lower morbidity and mortality from CHD as well as all-cause mortality. Patients with the following features are candidates for LMD therapy: have clinical CHD and a low-density lipoprotein cholesterol (LDLC) level > 3.0 mmol/l despite optimum non-pharmacological intervention, or suffer from familial hypercholesterolaemia (FH) or equivalent severe, monogenic disorder, or have a 10-year risk of an acute clinical coronary event of > 20% (or > 30% risk if extrapolated to the age of 60 years) owing to the presence of the hyperlipidaemia alone or in combination with contributory risk factors. The ideal target LDLC concentration is < or = 3 mmol/l, but a reduction of at least 45% should be regarded as a minimum target in severe cases who do not reach this goal. Successful therapy requires on-going attention to compliance, therapeutic response and side-effects, and may necessitate adjustment or reinforcement. Concurrent or contributory conditions, such as smoking, hypertension and diabetes mellitus, must also be treated along with the clinically manifest CHD. Severely hyperlipidaemic, complicated or unresponsive high-risk cases should be referred to an appropriate specialist or lipid clinic. Prevention of CHD in the community should be encouraged through public and professional education, the provision of community facilities for exercise and recreation, and legislation directed at reducing the use of tobacco products and ensuring the appropriate labelling of food products.

Cholestyramine Resin↗
PubMedDate not supplied

[Tuberculosis in tropical Africa. Tuberculosis primary infection: some clinical aspects in tropical Africa].

A review of 140 cases of tuberculous patent primary infections from the hospital of Abidjan University and from an antituberculous unit. The disease begins slowly, general condition is rapidly altered, ventilation troubles are very frequent and so are complications as meningitis and miliary dissemination. In 11,4 p. cent of the cases, measles occurred before the primo-infection. In 38 p. cent of the cases the source of contamination could be identified and in one out of two cases, the mother proved to be responsible for it.

Adolescent↗
PubMed2005

International collaboration, funding and association with burden of disease in randomized controlled trials in Africa.

OBJECTIVE: This study aimed to assess whether randomized controlled trials conducted in Africa with collaborators from outside Africa were more closely associated with health conditions that have a burden of disease that is of specific importance to Africa than with conditions of more general global importance or with conditions important to developed countries. We also assessed whether the source of funding influenced a study's relevance to Africa. METHODS: We compared randomized controlled trials performed in Africa that looked at diseases specifically relevant to Africa (as determined by burden of disease criteria) with trials classified as looking at diseases of global importance or diseases important to developed countries in order to assess differences in collaboration and funding. FINDINGS: Of 520 trials assessed, 347 studied diseases that are specifically important to Africa; 99 studied globally important diseases and 74 studied diseases that are important to developed countries. The strongest independent predictor of whether a study was of specifically African or global importance was the corresponding author's country of origin: African importance was negatively associated with a corresponding author being from South Africa (odds ratio (OR) = 0.04; 95% confidence interval (CI) = 0.02-0.10) but there was little difference between corresponding authors from other African countries and corresponding authors from countries outside Africa. The importance of a study to Africa was independently associated with having more non-African authors (OR per author = 1.31; 95% CI = 1.08-1.58), fewer trial sites (OR per site = 0.69; 95% CI = 0.50-0.96), and reporting of funding (OR = 2.14; 95% CI = 1.15-4.00). Similar patterns were present in the comparisons of trials studying diseases important to Africa versus those studying diseases important to developed countries with stronger associations overall. When funding was reported, private industry funding was negatively associated with African importance compared with global importance (OR = 0.31, P= 0.008 for African importance and OR = 0.51, P= 0.57 for importance for developed countries). CONCLUSION: The relevance to Africa of trials conducted in Africa was not adversely affected by collaboration with non-African researchers but funding from private industry was associated with a decreased emphasis on diseases relevant to Africa.

Africa↗
PubMed2001

Phylogenetic and evolutionary relationships among yellow fever virus isolates in Africa.

Previous studies with a limited number of strains have indicated that there are two genotypes of yellow fever (YF) virus in Africa, one in west Africa and the other in east and central Africa. We have examined the prM/M and a portion of the E protein for a panel of 38 wild strains of YF virus from Africa representing different countries and times of isolation. Examination of the strains revealed a more complex genetic relationship than previously reported. Overall, nucleotide substitutions varied from 0 to 25.8% and amino acid substitutions varied from 0 to 9.1%. Phylogenetic analysis using parsimony and neighbor-joining algorithms identified five distinct genotypes: central/east Africa, east Africa, Angola, west Africa I, and west Africa II. Extensive variation within genotypes was observed. Members of west African genotype II and central/east African genotype differed by 2.8% or less, while west Africa genotype I varied up to 6.8% at the nucleotide level. We speculate that the former two genotypes exist in enzootic transmission cycles, while the latter is genetically more heterogeneous due to regular human epidemics. The nucleotide sequence of the Angola genotype diverged from the others by 15.7 to 23.0% but only 0.4 to 5.6% at the amino acid level, suggesting that this genotype most likely diverged from a progenitor YF virus in east/central Africa many years ago, prior to the separation of the other east/central African strains analyzed in this study, and has evolved independently. These data demonstrate that there are multiple genotypes of YF virus in Africa and suggest independent evolution of YF virus in different areas of Africa.

Africa↗
PubMed2002

Yellow fever in Africa: public health impact and prospects for control in the 21st century.

In the last two decades, yellow fever re-emerged with vehemence to constitute a major public health problem in Africa. The disease has brought untold hardship and indescribable misery among different populations in Africa. It is one of Africa's stumbling blocks to economic and social development. Despite landmark achievements made in the understanding of the epidemiology of yellow fever disease and the availability of a safe and efficacious vaccine, yellow fever remains a major public health problem in both Africa and America where the disease affects annually an estimated 200,000 persons causing an estimated 30,000 deaths. Africa contributes more than 90% of global yellow fever morbidity and mortality. Apart from the severity in morbidity and mortality, which are grossly under reported, successive outbreaks of yellow fever and control measures have disrupted existing health care delivery services, overstretched scarce internal resources, fatigued donor assistance and resulted in gross wastage of vaccines. Recent epidemics of yellow fever in Africa have affected predominantly children under the age of fifteen years. Yellow fever disease can be easily controlled. Two examples from Africa suffice to illustrate this point. Between 1939 and 1952, yellow fever virtually disappeared in parts of Africa, where a systematic mass vaccination programme was in place. More recently, following the 1978-1979 yellow fever epidemic in the Gambia, a mass yellow fever vaccination programme was carried out, with a 97% coverage of the population over 6 months of age. Subsequently, yellow fever vaccination was added to the EPI Programme. The Gambia has since then maintained a coverage of over 80%, without a reported case of yellow fever, despite being surrounded by Senegal which experienced yellow fever outbreaks in 1995 and 1996. The resurgence of yellow fever in Africa and failure to control the disease has resulted from a combination of several factors, including: 1) collapse of health care delivery systems; 2) lack of appreciation of the full impact of yellow fever disease on the social and economic development of the affected communities; 3) insufficient political commitment to yellow fever control by governments of endemic countries; 4) poor or inadequate disease surveillance; 5) inappropriate disease control measures, and 6) preventable poverty coupled with misplaced priorities in resource allocation. Yellow fever can be controlled in Africa within the next 10 years, if African governments seize the initiative for yellow fever control by declaring an uncompromising resolve to control the disease, the governments back up their resolve with an unrelenting commitment and unwavering political will through adequate budgetary allocations for yellow fever control activities, and international organisations, such as WHO, UNICEF, GAVI, etc., provide support and technical leadership and guidance to yellow fever at risk countries. Over a ten-year period, of stage-by-stage mass yellow fever vaccination campaigns, integrated with successful routine immunisation, Africa can bring yellow fever under control. Subsequently, for yellow fever to cease being a public health problem, Africa must maintain at least an annual 80% yellow fever vaccine coverage of children under the age of 1 year, and sustain a reliable disease surveillance system with a responsive disease control programme. This can be achieved at an affordable annual expenditure of less than US$1.00 per person per year, with a reordering of priorities.

Africa↗
PubMed1996

Manifestation and epidemiology of contagious bovine pleuropneumonia in Africa.

Contagious bovine pleuropneumonia (CBPP) is one of the major threats to cattle health and production in Africa. This article reviews the clinical manifestations, lesions and epidemiology of the disease. The clinical manifestations and lesions are typical and are no different in Africa from those seen in other countries. CBPP is a respiratory disease characterised by pneumonia and serofibrinous pleurisy. The usual form of this disease is acute but chronic forms are frequent, particularly in endemic regions. Hyperacute forms, with a high mortality rate, can be seen at the beginning of outbreaks in newly infected regions. The epidemiology of the disease in Africa is dominated by four factors, namely: cattle are the only species affected, there is no reservoir in wild animals, clinical cases or chronic carriers are the usual sources of infection, through direct contact, and cattle movements play a very important role in the maintenance and extension of the disease. CBPP is widespread in Africa and, according to the Office International des Epizooties and to various reports in 1995, the disease is present in 24 countries of tropical Africa. In western Africa, CBPP is mainly enzootic or sporadic but in some countries the incidence is increasing. The situation in Central Africa is not very alarming. However, in eastern and south-eastern Africa, CBPP has become a major issue, placing southern Africa under direct threat. An evaluation of economic losses due to the disease and the cost-benefit ratio of control programmes is indispensable, since such economic assessments are needed before policy-makers decide on programmes of control or eradication. This is an area which needs to be addressed immediately, as the launching of new campaigns, particularly in eastern and southern Africa, is urgently needed.

Africa↗
PubMed1977

Geographical distribution of HBs Ag in Africa.

The incidence of HBs Ag carrier is high in Africa. The HBs Ag subtypes vary in 5 mean areas of the Africa continent. The subtype ayw4(a3) is the most characteristic African subtype, being found with a striking frequency in West Africa (88.8%). In North Africa ayw2(a21) is predominant as in other mediterranean countries. In Saharan area mixed types of HBs Ag are found, intermediary between North and West Africa. In Central Africa y is predominantly associated with w2(a21) or with w4(a3). In east and South Africa ad is largely predominant and the most widespread subtype is adw2(a21). No adr, nor adw4 were found in Africa.

Africa↗
PubMed2004

[Rickettsia africae, the agent of African tick-bite fever: an emerging pathogen in the West Indies and Reunion Island (Indian Ocean)].

Rickettsia africae is the agent of African tick bite fever, an emerging disease transmitted by Amblyomma ticks in sub-Saharan Africa. In 1998, we reported the first documented case of R. africae in the New World, in a patient who had returned from Guadeloupe. In order to confirm the presence of R. africae in the West Indies, entomologic surveys were conducted from 1999 to 2003 to collect Amblyomma, which are considered as potential vectors and reservoirs of the bacteria. Ticks were used as epidemiological tools to detect R. africae by molecular tools and/or cultivate the bacteria in shell-vial cell culture. This paper summarizes the results obtained in the West Indies. R. africae was detected and isolated for the first time in Guadeloupe, and then detected by molecular tools in Martinique and St-Kitts and Nevis. These last results confirm our first hypotheses--that is R. africae is prevalent on all the Caribbean islands where A. variegatum ticks have been introduced from Africa in the 18th and 19th centuries. We also present the results of a study conducted on the Reunion Island, a French island in the Indian Ocean. For the first time there, R. africae was detected in A. variegatum ticks, which were probably introduced from the African mainland or Madagascar with the human colonization during the 17th century Thus, clinicians should be aware that patient presenting in the West Indies or on Reunion Island (or after a trip over there) with fever, eschar (often multiple), regional lymphadenopathy and a rash, might be infected by R. africae.

Animals↗
PubMedDate not supplied

[AIDS in Africa].

While AIDS (Acquired Immunodeficiency Syndrome) certainly represents a worldwide health problem, the attention of many researchers and epidemiologists, besides the WHO itself, has recently focused on Africa for the following reasons: 1) The etiologic agent of AIDS, the Human Immunodeficiency Virus (HIV) (previously named HTLV-III or LAV) is likely to have originated in Africa. Solid evidence has been accumulated that antibodies against HIV were present in African sera collected in the early 1960s. In the same period widespread infection by viruses strictly related to HIV has been documented in primates living in tropical Africa. A second type of HIV (now named HIV-2 and previously known as HTLV-IV or LAV-2) which is responsible for a milder AIDS-related disease, has been subsequently identified in West African inhabitants with its own simian correlate. Although epidemiological evidence for the presence of AIDS in Africa in these early periods is scanty, sporadic cases have retrospectively been identified. 2) Up to 1986, AIDS epidemiology in Africa has been hampered by inconsistency of demographic data, inadequacy of public health services and difficulty of obtaining the necessary laboratory evidence. The few data available (Zaire, Rwanda), suggests an annual incidence in 1983 of 170-800 per million, comparable to higher U.S. and European rates. There is no evidence, however, that African epidemy precedes that of the U.S., for which there is no explanation at present. On the other hand, recent data indicate an alarming acceleration of the African epidemy, that spreads well beyond the risk groups which have been recognized in Western countries. 3) Prevalent infection routes in Africa are not entirely overlapping with Western countries'. Rather than homosexual intercourse (U.S.) and syringe sharing by drug abusers (Italy), most African cases seem to be transmitted by heterosexual promiscuous contacts and, to a lesser extent, by blood derivates and recycled syringes. Insects and tribal rituals have been also suspected as vehicles of infection in Africa; widespread prostitution and inadequate health facilities certainly are. As a consequence, transplacental infection appear much more common than in the West. 4) Clinical aspects of AIDS progression in Africa appear linked to the different spectrum of opportunistic agents present on the continent and to the general hygienic and social conditions prevailing among its people. Rather than generalized lymphoadenopathies and Pneumocystes Carini pneumonia, diarrhoea and extreme weight loss ("Slim disease") represent the most common clinical pattern.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Acquired immunodeficiency syndrome-associated cancers in Sub-Saharan Africa.

Sub-Saharan Africa is considered home to more than 60% of all human immunodeficiency virus (HIV) infected cases, with an estimated adult prevalence of 8.0%. It is stated that this region has contributed more than 90% of childhood deaths related to HIV infection and about 93% of childhood acquired immunodeficiency syndrome (AIDS)-related deaths. Although no country in Africa is spared of the infection, the bulk is seen in East and South Africa, with the highest recorded rates of 20% to 50% in Zimbabwe. On the other hand, West Africa is less affected, while countries in Central Africa have relatively stable infection rates. Although infections, especially tuberculosis, have emerged as the most important HIV/AIDS-associated killers in recent times, AIDS-associated malignancies are increasingly identified in the late stages. As a result of incomplete data from African countries, it is unclear whether the epidemiology and risks of these cancers are the same as observed in the developed countries. Since the advent of AIDS, epidemic Kaposi's sarcoma (KS) has become more common in both sexes in Africa, with a dramatic lowering of the male to female ratio from 19:1 to 1.7:1, especially in East Africa. Although there has been a rising trend of AIDS-associated non-Hodgkin's lymphoma (NHL) worldwide, there is an apparently lower risk in Africa compared with that in the developing world. At present, there is no strong evidence linking increased incidence of invasive cervical cancer to the HIV epidemic; however, some studies have demonstrated an association between HIV and the increased prevalence of human papilloma virus (HPV) and cervical intraepithelial neoplasia (CIN). On the other hand, HIV infection is now established as a risk factor for the development of squamous cell neoplasia of the conjunctiva based on studies from Rwanda, Malawi, and Uganda. Despite the problems and limitations of information from sub-Saharan Africa, interesting trends of HIV/AIDS-related cancers have emerged from comparison of available data. Semin Oncol 28:198-206.

Acquired Immunodeficiency Syndrome↗
PubMed2003

The origin and dispersion of human parasitic diseases in the old world (Africa, Europe and Madagascar).

The ancestors of present-day man (Homo sapiens sapiens) appeared in East Africa some three and a half million years ago (Australopithecs), and then migrated to Europe, Asia, and later to the Americas, thus beginning the differentiation process. The passage from nomadic to sedentary life took place in the Middle East in around 8000 BC. Wars, spontaneous migrations and forced migrations (slave trade) led to enormous mixtures of populations in Europe and Africa and favoured the spread of numerous parasitic diseases with specific strains according to geographic area. The three human plasmodia (Plasmodium falciparum, P. vivax, and P. malariae) were imported from Africa into the Mediterranean region with the first human migrations, but it was the Neolithic revolution (sedentarisation, irrigation, population increase) which brought about actual foci for malaria. The reservoir for Leishmania infantum and L. donovani--the dog--has been domesticated for thousands of years. Wild rodents as reservoirs of L. major have also long been in contact with man and probably were imported from tropical Africa across the Sahara. L. tropica, by contrast, followed the migrations of man, its only reservoir. L. infantum and L. donovani spread with man and his dogs from West Africa. Likewise, for thousands of years, the dog has played an important role in the spread and the endemic character of hydatidosis through sheep (in Europe and North Africa) and dromadary (in the Sahara and North Africa). Schistosoma haematobium and S. mansoni have existed since prehistoric times in populations living in or passing through the Sahara. These populations then transported them to countries of Northern Africa where the specific, intermediary hosts were already present. Madagascar was inhabited by populations of Indonesian origin who imported lymphatic filariosis across the Indian Ocean (possibly of African origin since the Indonesian sailors had spent time on the African coast before reaching Madagascar). Migrants coming from Africa and Arabia brought with them the two African forms of bilharziosis: S. haematobium and S. mansoni.

Africa↗