Search

During the past four decades, recurrent outbreaks of various arthropod-borne viruses have been reported in Mauritania. This review aims to consolidate the current knowledge on the epidemiology of the major arboviruses circulating in Mauritania. Online databases including PubMed and Web of Science were used to retrieve relevant published studies. The results showed that numerous arboviral outbreaks of variable magnitude occurred in almost all 13 regions of Mauritania, with Rift Valley fever (RVF), Crimean–Congo hemorrhagic fever (CCHF), and dengue (DEN) being the most common infections. Other arboviruses causing yellow fever (YF), chikungunya (CHIK), o’nyong-nyong (ONN), Semliki Forest (SF), West Nile fever (WNF), Bagaza (BAG), Wesselsbron (WSL), and Ngari (NRI) diseases have also been found circulating in humans and/or livestock in Mauritania. The average case fatality rates of CCHF and RVF were 28.7% and 21.1%, respectively. RVF outbreaks have often occurred after unusually heavy rainfalls, while CCHF epidemics have mostly been reported during the dry season. The central and southeastern regions of the country have carried the highest burden of RVF and CCHF. Sheep, cattle, and camels are the main animal reservoirs for the RVF and CCHF viruses. Culex antennatus and Cx. poicilipes mosquitoes and Hyalomma dromedarii, H. rufipes, and Rhipicephalus everesti ticks are the main vectors of these viruses. DEN outbreaks occurred mainly in the urban settings, including in Nouakchott, the capital city, and Aedes aegypti is likely the main mosquito vector. Therefore, there is a need to implement an integrated management strategy for the prevention and control of arboviral diseases based on sensitizing the high-risk occupational groups, such as slaughterhouse workers, shepherds, and butchers for zoonotic diseases, reinforcing vector surveillance and control, introducing rapid point-of-care diagnosis of arboviruses in high-risk areas, and improving the capacities to respond rapidly when the first signs of disease outbreak are identified.

Plasmodium vivax malaria is endemic in Mauritania. Individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency may develop acute hemolytic anemia when exposed to 8-aminoquinoline antimalarial drugs, which are indispensable for a complete cure. The prevalence of G6PD allelic variants was assessed in different ethno-linguistic groups present in Mauritania. A total of 996 blood samples (447 males and 549 females; 499 white Moors and 497 individuals of black African ancestry) were collected from febrile patients in 6 different study sites: Aleg, Atar, Kiffa, Kobeni, Nouakchott, and Rosso. The presence of the African-type G6PD A- (G202A, A376G, A542T, G680T, and T968C mutations) and the Mediterranean-type G6PD B- (C563T) variants was assessed by PCR followed by restriction fragment length polymorphism and/or DNA sequencing. The prevalence of African-type G6PD A- genotype was 3.6% (36/996), with 6.3% (28/447) of hemizygote (A-) males and 1.5% (8/549) of homozygous (A-A-) females. Forty of 549 (7.3%) women were heterozygous (AA-). The following genotypes were observed among hemizygous men and/or homozygous women: A376G/G202A (22/996; 2.2%), A376G/T968C Betica-Selma (12/996; 1.2%), and A376G/A542T Santamaria (2/996; 0.2%). The Mediterranean-type G6PD B- genotype was not observed. The prevalence rates of G6PD A- genotype in male (10/243; 4.1%) and heterozygous female (6/256; 2.3%) white Moors were lower (p < 0.05) than those of males (18/204; 8.8%) and heterozygous females (34/293; 11.6%) of black African ancestry. There were only a few homozygous women among both white Moors (3/256; 1.2%) and those of black African ancestry (5/293; 1.7%). The prevalence of G6PD deficiency in Mauritania was comparable to that of neighboring countries in the Maghreb. Because of the purportedly close ethnic ties between the Mauritanian white Moors and the peoples in the Maghreb, further investigations on the possible existence of the Mediterranean-type allele are required. Moreover, a surveillance system of G6PD phenotype and/or genotype screening is warranted to establish and monitor a population-based prevalence of G6PD deficiency.