Search

Summary On Aug 25 2020, the Africa Regional Commission for the Certification of Poliomyelitis Eradication declared that the WHO African region had interrupted transmission of all indigenous wild polioviruses. This declaration marks the African region as the fifth of the six WHO regions to celebrate this extraordinary achievement. Following the Yaounde Declaration on Polio Eradication in Africa by heads of state and governments in 1996, Nelson Mandela launched the Kick Polio out of Africa campaign. In this Health Policy paper, we describe the long and turbulent journey to the certification of the interruption of wild poliovirus transmission, focusing on 2016–20, lessons learned, and the strategies and analyses that convinced the Regional Commission that the African region is free of wild polioviruses. This certification of the WHO African region shows the feasibility of polio eradication in countries with chronic insecurity, inaccessible and hard-to-reach populations, and weak health systems. Challenges have been daunting and the sacrifices enormous—dozens of health workers and volunteers have lost their lives in the pursuit of a polio-free Africa.

A paralytic poliomyelitis outbreak occurred in Namibia in 2006, almost exclusively among adults. Nineteen cases were virologically confirmed as due to wild poliovirus type 1 (WPV1), and 26 were classified as polio compatible. Eleven deaths occurred among confirmed and compatible cases (24%). Of the confirmed cases, 97% were aged 15-45 years, 89% were male, and 71% lived in settlement areas in Windhoek. The virus was genetically related to a virus detected in 2005 in Angola, which had been imported earlier from India. The outbreak is likely due to immunity gaps among adults who were inadequately vaccinated during childhood. This outbreak underscores the ongoing risks posed by poliovirus importations, the importance of maintaining strong acute flaccid paralysis surveillance even in adults, and the need to maintain high population immunity to avoid polio outbreaks in the preeradication period and outbreaks due to vaccine-derived polioviruses in the posteradication era.

Measles was virtually eliminated in South Africa following control activities in 1996/7. However, from July 2003 to November 2005, 1676 laboratory-confirmed measles cases were reported in South Africa. We investigated the outbreak's cause and the role of HIV.We traced laboratory-confirmed case-patients residing in the Johannesburg metropolitan (JBM) and O. R. Tambo districts. We interviewed laboratory--or epidemiologically confirmed case-patients or their caregivers to determine vaccination status and, in JBM, HIV status. We calculated vaccine effectiveness using the screening method.Household survey in JBM and O. R. Tambo districts. Outcome measures. Vaccine effectiveness, case-fatality rate, and hospitalisations.In JBM, 109 case-patients were investigated. Of the 57 case-patients eligible for immunisation, 27 (47.4%) were vaccinated. Fourteen (12.8%) case-patients were HIV infected, 46 (42.2%) were HIV uninfected, and 49 (45.0%) had unknown HIV status. Among children aged 12-59 months, vaccine effectiveness was 85% (95% confidence interval (CI): 63, 94) for all children, 63% for HIV infected, 75% for HIV uninfected, and 96% for children with unknown HIV status. (Confidence intervals were not calculated for sub-groups owing to small sample size.) In O. R. Tambo district, 157 case-patients were investigated. Among the 138 case-patients eligible for immunisation, 41 (29.7%) were vaccinated. Vaccine effectiveness was 89% (95% CI 77, 95).The outbreak's primary cause was failure to vaccinate enough of the population to prevent endemic measles transmission. Although vaccine effectiveness might have been lower in HIV-infected than in uninfected children, population vaccine effectiveness remained high.

International audience; Background: Early age at infection with hepatitis B virus (HBV) increases the risk of chronic HBV infection. In addition early age at infection may further increase the risk of persistent viral replication beyond its effect on chronicity. The effects of perinatal and early postnatal transmission on the risk of prolonged hepatitis B e antigenaemia in children with chronic HBV infection are not well documented in Africa. We examine these associations using maternal HBV sero-status and the number of HBV-positive older siblings as proxy measures for perinatal and early postnatal transmission, respectively.Methods: Hepatitis B e antigen (HBeAg)-positive mothers were identified in six population-based HBV sero-surveys conducted in The Gambia between 1986 and 1990. For every HBeAg-positive mother, a hepatitis B surface antigen (HBsAg)-positive HBeAg-negative mother and HBsAg-negative mother were randomly selected from the population surveyed. These mothers and their family members were tested for HBV sero-markers in a subsequent survey conducted between 1991 and 1993.Results: Thirty-eight HBeAg positive mothers and the same number of HBsAg-positive HBeAg-negative mothers and HBsAg-negative mothers participated in the study. Sixty-nine percent of their children also participated. There was a non-significant positive association between HBeAg prevalence in children and the number of HBeAg-positive older siblings (64.1%, 69.2% and 83.3% in children with 0, 1 and ≥2 HBeAg-positive older siblings, respectively). After adjusting for confounders, having an HBeAg-positive mother was a risk factor for HBeAg positivity in children carrying HBsAg (adjusted OR 4.5, 95% CI: 1.0-19.5, p = 0.04), whilst the number of HBeAg-positive older siblings was not.Conclusions: Maternal HBeAg was associated with positive HBeAg in children with chronic HBV infection. This suggests that interrupting mother-to-infant transmission in sub-Saharan Africa might help reduce the burden of liver disease. A timely dose of HBV vaccine within 24 hours of birth, as recommended by WHO, should be implemented in sub-Saharan Africa.