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  • br Health research consortia in sub Saharan Africa


    Health research consortia in sub-Saharan Africa present a positive outlook for the region through increased scientific capacity. New networks of African–African, African–European, and African–global partnerships provide platforms to advance crucial research domains. Such networks enable junior African researchers to advance their work, and they also poise the region to provide expertise across many health domains. High-income partners also gain by hosting African researchers, increasing international exposure to developing regions, and learning from researchers with few resources. Unfortunately, dissemination of research findings is a constant and major challenge in these partnerships, often because of restricted capacity. Before publication, myriad issues must be addressed, beginning with basic access—even internet connectivity and continuous electricity are problematic in some rural regions. Thus, although partnerships might increase capacity over working in isolation, dissemination challenges remain. Likewise, supervision is a crucially underserved role in African academic institutions. Furthermore, junior academics might have doubts about the quality or relevance of work, and ultimately decide against dissemination. This issue perpetually disrupts research, affecting completion and eventual publication, which exacerbates restrictions in developing regions. Cutting-edge research does not have uniform sustainability, thus partnerships aim to provide guidance from international experts to future African scientific leaders while enhancing local supervision.
    Typhoid fever is a life-threatening systemic disease caused by the bacterium serovar Typhi ( Typhi). Years of focused research have resulted in a detailed, but not complete, understanding of the disease caused by this organism. Diagnostics, host susceptibility, and mth1 pathway responses need further research and investment, but recent technological advances in immunology and high-throughput genomics are providing new insights. Indeed, the burden of typhoid fever might be falling in parts of Asia, and the potential introduction of Vi-polysaccharide-conjugate vaccines could mth1 pathway reduce the burden even more. Other serovars and pathovars also cause invasive disease in human beings, which can be difficult to distinguish clinically from typhoid. Invasive infections with serovars Typhimurium and Enteritidis in young children and also adults living with HIV in parts of sub-Saharan Africa have been reported. However, serovar Paratyphi ( Paratyphi A, the main alternative cause of typhoid-like infections in most of the world, has received little attention. This knowledge gap has the potential to become an Achilles\' heel in the global battle against enteric (typhoid) fever. At the turn of the millennium, Paratyphi A caused about 20% of the global burden of enteric fever. In many areas, hypotonic proportion has steadily increased. In Patan Hospital in Kathmandu, Nepal, standardised surveillance of blood cultures during the past 10 years has shown annual increases in the proportions of individuals with Paratyphi A. More than two-thirds of the culture-confirmed cases of enteric fever are now caused by this serovar. Increases in the proportion of enteric fever cases caused by Paratyphi A have also been reported in India, Pakistan, China, and Cambodia. In some locations, the proportion of enteric fever caused by Paratyphi A is now greater than that caused by Typhi. There is a real threat that Paratyphi A could replace Typhi as the main global cause of enteric fever. Clinicians often believe that Paratyphi A infections are less severe than are those caused by Typhi. However, in the largest comparison to date, no significant differences were shown between disease severity, duration, or outcomes for infection caused by these organisms. Both pathogens are transmitted through the faecal-oral route by ingestion of contaminated food or water. Ingestion is followed by colonisation of the small intestine, invasion of the gastrointestinal mucosal surface, and dissemination throughout the body into the liver, spleen, and bone marrow. Crucially, Typhi and Paratyphi A infect only human beings, and no other serovar entirely mimics the infection in other hosts. Much of the understanding of pathogenesis is derived from the mouse infection model of serovar Typhimurium, which does not adequately replicate human infection. The absence of a suitable animal model has impaired the ability of researchers to develop diagnostic tests that take into account the specific biology of host–pathogen interactions. Researchers, therefore, rely almost solely on specimens collected from patients infected with these pathogens to understand the disease and investigate immunological responses.