Anthropological consideration on prevalence and fitness of β C and β S genotypes in Burkina Faso (a survey in the public schools)
- 3 Downloads
Objective: To study the incidence of hemoglobinopathies (Hb C and Hb S) we have examined 15,367 students, aged 11.4+/-4.64 years (median 11; range 1–26), living in Burkina Faso (12,019 were students of 23 public schools of Ouagadougou and 3348 students of 7 public schools situated in six villages about 12–35 Km from Ouagadougou).
Results: In all schools, we found a prevalence of females (54.2%) over males (45.8%) with a high incidence of Hb AC (19.16%), over Hb AS (8.35%). As expected, the gene frequency of β C in the schools of Ouagadougou was 0.112+/-0.015 and of β S 0.049+/-0.012, and this was similar in village schools (0.128+/-0.010 and 0.049+/-0.09 respectively), irrespective of town latitude. In all groups studied, β S and β C gene frequencies were age dependent since the advantage of HbS carriers in a malarial region is prevalently expressed in the first years of life. In fact, β C gene frequency increases, and β S decreases with age. The Mossi, living mainly in Ouagadougou, show a gene frequency which is similar to the Bissa ethnic groups, where the β C gene frequencies (0.116 and 0.118) are higher than the β S (0.049 and 0.044 respectively). On the contrary in the Peuhl ethnic group β C and β S gene frequencies (0.049 and 0.049) are the same, while in the Yorouba ethnic group immigrated from Nigeria β S gene frequency is higher (0.117) than the β C (0.068), showing that different gene frequencies are found in different ethnic groups.
Conclusion: The difference in β S and β C genes frequencies (0.049 and 0.116) found in comparison with a previously performed study (Labie et al, 1984) in the same region (0.03 for the β S gene and 0.14 for the β C gene), may be due to migration flow of β S genes from the near Sahel region or to changes in life expectancy of children with β C and β S phenotypes. Moreover, the high percentage of SC (1,06%) and SS (0.188%) individuals detected with the present screening, compared with the lower percentages found by Labie et al in 1984, suggest that a modified environment can play an important role in reducing the morbility and lethality of β S genotype. However, even today the number of students affected by HbSC and Hb SS attending the schools remains low. Stricter controls of correlated diseases are necessary to guarantee healthier life conditions.
Key WordsHb C Hb S schools Burkina Faso prevalence fitness
Unable to display preview. Download preview PDF.
- Agarwal A, Guindo A, Cissoko Y, Taylor JG, Coulibaly D, Konè A, Kayentao K, Djinde A, Plowe CV, Doumbo O, Wellems TE, Diallo D, 2000. Hemoglobin C associated with protection from severe malaria in the Dagon of Mali, a West African population with a low prevalence of Hemoglobin S. Blood; 96 (7): 2358–2363.Google Scholar
- Brown AK, Sleeper LA, Miller ST, Pegelow CH, Gill FM, Waclawiw MA. 1994. Reference values and hematologic changes from birth to 5 years in patients with sickle cell disease. Cooperative Study of Sickle Cell Disease. Arch Pediatr Adolesc Med 148(8): 796–804.Google Scholar
- Chippaux JP, Massougbodji A, Castel J, Akogbeto M, Zohoun I, Zohoun T, 1992. Plasmodium falciparum or P. malariae parasitemia in carriers of sickle cell trait in various Benin biotypes. Rev Epidemiol Sante Publique; 40(4): 246–51.Google Scholar
- Friedman MJ, Roth EF, Nagel RL and Trager W. 1979. The role of Hemoglobins C, S, and Nbalt in the inhibition of malaria parasite development in vitro. Am J Trop Med Hyg 28: 777–780.Google Scholar
- Gendrel D, Kombila M, Nardou M, Gendrel C, Djouba F, Martz M, Richard-Lenoble D, 1992. Malaria and hemoglobin S: interactions in African children. Press Med; 23; 21(19): 887–90.Google Scholar
- Hammond, P.B. “The Mossi People.” Columbia Electronic Encyclopedia 1994, Online. 6 April. 2001.Google Scholar
- Kulkarni AG, Jekeme SD 1986. Cord blood screening for haemoglobinopathies in northern Nigeria. Ann Trop Med Parasitol 80(5):549–51.Google Scholar
- Jardin F, Sane M, Cloatre G, Thiam M, Camara P, Pouolin S, M'Baye PS, Klotz F., 1999. Adults with sickle cell anemia in Senegal. Clinical study of 40 homozygote subjects. Med Trop; 59 (3): 271–5.Google Scholar
- Luzzatto L, 1979. Genetics of red cells susceptibility to malaria. Blood; 54: 961–976.Google Scholar
- Ohene-Frempong K, Smith-Whitley K., 1997. Use of hydroxyurea in children with sickle cell disease: what cames next? Semin Hematol; 34 (3 Suppl 3): 30–41.Google Scholar
- Serjeant GR., 1989. Geography and the clinical picture of sickle cell disease. An overview. Ann N Y Acad Sci.; 565:109–19.Google Scholar
- Smith EW and Krevans JR. 1959. Clinical manifestations of hemoglobin C disorders. Bull Johns Hopkins Hosp 104: 17–43.Google Scholar
- Thiam D, Bako R, Seck Fall K, Diakhate L. 1990. In vitro effects of Fagaro xanthoxyloides Lam. on drepanocytic erythrocytes Dakar Med; 35(1): 37–45.Google Scholar
- Wurie AT, Wurie IM, Gevao SM, Robbin-Coker DJ., 1996. The prevalence of sickle cell trait in Sierra Leone. A laboratory profile. West Afr J Med; 15(4): 201–3.Google Scholar