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The research leading to these results has received funding from
the European Research Council (ERC) under the European Union’s
Seventh Framework Programme (FP7/2007–2013)/ERC grant
agreement 279925 and from the U.S. National Science Foundation
under grant 1338832. It is a part of project PP13040 and PE14050
funded by the Korea Polar Research Institute. J. W.C. thanks
J. Mitrovica, and R.F.K. thanks the Leverhulme Trust for additional
support. Numerical models were run at Oxford’s Advanced
Research Computing facility. Bathymetry data are included in the
Figs. S1 to S3
Data Files KR1 and KR2
22 September 2014; accepted 28 January 2015
Reduced vaccination and the risk
of measles and other childhood
Saki Takahashi,1 C. Jessica E. Metcalf,1,2 Matthew J. Ferrari,3 William J. Moss,4
Shaun A. Truelove,4 Andrew J. Tatem,5,6,7 Bryan T. Grenfell,1,6 Justin Lessler4*
The Ebola epidemic in West Africa has caused substantial morbidity and mortality. The
outbreak has also disrupted health care services, including childhood vaccinations,
creating a second public health crisis. We project that after 6 to 18 months of disruptions, a
large connected cluster of children unvaccinated for measles will accumulate across
Guinea, Liberia, and Sierra Leone. This pool of susceptibility increases the expected size of
a regional measles outbreak from 127,000 to 227,000 cases after 18 months, resulting in
2000 to 16,000 additional deaths (comparable to the numbers of Ebola deaths reported
thus far). There is a clear path to avoiding outbreaks of childhood vaccine-preventable
diseases once the threat of Ebola begins to recede: an aggressive regional vaccination
campaign aimed at age groups left unprotected because of health care disruptions.
The current Ebola crisis in West Africa is one of the worst public health disasters in recent memory, having caused more than 21,000 cases and 8400 deaths as of January 2015 and raising the specter of a broader
international crisis (1). However, there are signs
of hope. Evidence shows that the number of cases
is declining in Liberia (2), and sustained trans-
mission has been confined to Guinea, Liberia, and
Sierra Leone, despite several transnational in-
troductions including recent transmission in
Mali. Stopping Ebola would be a triumph for the
global health community and the public health
agencies of the affected countries. But even after
the last Ebola case recovers, the disruptions of
local health systems caused by the outbreak could
lead to a second infectious disease crisis that
could kill as many as, if not more than, the orig-
Through the combination of the World Health
Organization (WHO) Expanded Programme on
Immunization (EPI) and periodic supplemental
immunization campaigns, annual childhood deaths
from vaccine-preventable diseases have dropped
from an estimated 900,000 in 2000 to 400,000
in 2010 (3). Measles is emblematic of this success;
globally, estimated annual measles mortality
has decreased from 499,000 to 102,000 since
2000 (4, 5). The Ebola-affected countries have
been an important part of this achievement:
The three countries reported nearly 93,685
cases of measles in the decade between 1994
and 2003 (despite Sierra Leone not reporting
in 4 years), and only 6937 between 2004 and
2013 (in both periods it is likely that only a
fraction of measles cases were reported to the
WHO) (6). Despite this success, measles susceptibility has been growing in all three countries
in recent years, and each had planned a measles vaccination campaign prior to the Ebola
Measles epidemics often follow humanitarian
crises. Measles is one of the most transmissible
infections, and immunization rates tend to be
lower than for other EPI vaccines, in part because of the older age at which measles vaccine
must be administered [9 months, versus 6 weeks
or younger for the first dose of other vaccines
(7)]. For this reason, explosive measles outbreaks
are often an early result of health system failure.
Outbreaks have followed disruptions due to war
[e.g., the current conflict in Syria (8)], natural
disasters [e.g., the eruptions of Mt. Pinatubo in
1991 (9)], and political crises [e.g., Haiti in the
early 1990s (10)]. The effects are most acute when
measles epidemics are associated with famine
or long-term national instability: A survey of 595
households displaced as a result of the Ethiopian
famine in 2000 found measles to be a contributing cause in 35 of 159 deaths (11), and after
years of instability in the Democratic Republic
of Congo, the country experienced a measles outbreak of 294,455 cases and 5045 deaths between
2010 and 2013 (12).
To understand how Ebola-related health care
disruptions are increasing the risk from measles, we estimated the spatial distribution of unvaccinated children and the measles susceptibility
profile for each country before and after these
disruptions. Geolocated cross-sectional data from
Demographic and Health Surveys (DHS) in Guinea,
Liberia, Sierra Leone, and surrounding countries
were used to estimate vaccine coverage in each
5 km × 5 km grid cell by means of a hierarchical
Bayesian model and spatial smoothing techniques.
These rates were applied to spatially explicit
data on population and birth cohort size to map
the number of children between 9 months and
5 years of age who were unvaccinated against
measles before Ebola-related health care disruptions (Fig. 1A) (13, 14). Forward projections of
the number of unvaccinated children after 6, 12,
and 18 months were generated by reducing the
rate of routine vaccination by 75% for the specified duration (reductions of 25, 50, and 100%
were also considered as a sensitivity analysis). Full
population susceptibility on a national level at
baseline and after 18 months of disruptions were
then estimated by combining these estimates with
the results of models that estimate the immune
profile in each age cohort on the basis of their
1240 13 MARCH 2015 • VOL 347 ISSUE 6227 sciencemag.org SCIENCE
1Department of Ecology and Evolutionary Biology, Princeton
University, Princeton, NJ 08544, USA. 2Woodrow Wilson
School, Princeton University, Princeton, NJ 08544, USA.
3Centre for Infectious Disease Dynamics, Pennsylvania State
University, State College, PA 16801, USA. 4Department of
Epidemiology, Johns Hopkins Bloomberg School of Public
Health, Baltimore, MD 21205, USA. 5Department of
Geography and Environment, University of Southampton,
Southampton SO17 1BJ, UK. 6Fogarty International Center,
National Institutes of Health, Bethesda, MD 20892, USA.
7Flowminder Foundation, 17177 Stockholm, Sweden.
*Corresponding author. E-mail: firstname.lastname@example.org