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      Measles

      The Lancet
      Elsevier BV

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          Abstract

          Measles is a highly contagious disease that results from infection with measles virus and is still responsible for more than 100 000 deaths every year, down from more than 2 million deaths annually before the introduction and widespread use of measles vaccine. Measles virus is transmitted by the respiratory route and illness begins with fever, cough, coryza, and conjunctivitis followed by a characteristic rash. Complications of measles affect most organ systems, with pneumonia accounting for most measles-associated morbidity and mortality. The management of patients with measles includes provision of vitamin A. Measles is best prevented through vaccination, and the major reductions in measles incidence and mortality have renewed interest in regional elimination and global eradication. However, urgent efforts are needed to increase stagnating global coverage with two doses of measles vaccine through advocacy, education, and the strengthening of routine immunisation systems. Use of combined measles-rubella vaccines provides an opportunity to eliminate rubella and congenital rubella syndrome. Ongoing research efforts, including the development of point-of-care diagnostics and microneedle patches, will facilitate progress towards measles elimination and eradication.

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          Most cited references89

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          Anticipating the international spread of Zika virus from Brazil.

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            Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality.

            Immunosuppression after measles is known to predispose people to opportunistic infections for a period of several weeks to months. Using population-level data, we show that measles has a more prolonged effect on host resistance, extending over 2 to 3 years. We find that nonmeasles infectious disease mortality in high-income countries is tightly coupled to measles incidence at this lag, in both the pre- and post-vaccine eras. We conclude that long-term immunologic sequelae of measles drive interannual fluctuations in nonmeasles deaths. This is consistent with recent experimental work that attributes the immunosuppressive effects of measles to depletion of B and T lymphocytes. Our data provide an explanation for the long-term benefits of measles vaccination in preventing all-cause infectious disease. By preventing measles-associated immune memory loss, vaccination protects polymicrobial herd immunity.
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              The dynamics of measles in sub-Saharan Africa.

              Although vaccination has almost eliminated measles in parts of the world, the disease remains a major killer in some high birth rate countries of the Sahel. On the basis of measles dynamics for industrialized countries, high birth rate regions should experience regular annual epidemics. Here, however, we show that measles epidemics in Niger are highly episodic, particularly in the capital Niamey. Models demonstrate that this variability arises from powerful seasonality in transmission-generating high amplitude epidemics-within the chaotic domain of deterministic dynamics. In practice, this leads to frequent stochastic fadeouts, interspersed with irregular, large epidemics. A metapopulation model illustrates how increased vaccine coverage, but still below the local elimination threshold, could lead to increasingly variable major outbreaks in highly seasonally forced contexts. Such erratic dynamics emphasize the importance both of control strategies that address build-up of susceptible individuals and efforts to mitigate the impact of large outbreaks when they occur.
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                Author and article information

                Journal
                The Lancet
                The Lancet
                Elsevier BV
                01406736
                December 2017
                December 2017
                : 390
                : 10111
                : 2490-2502
                Article
                10.1016/S0140-6736(17)31463-0
                28673424
                512de5c4-c88c-4072-9b49-ac40df1a9092
                © 2017

                https://www.elsevier.com/tdm/userlicense/1.0/

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