9 research outputs found
Geographic distribution of virologically-confirmed type 2 cVDPV cases in Egypt between 1988 and 1993.
<p>Individual cases are represented by filled circles of different sizes to show the year of paralysis onset. Population density for Egypt in 1990 is shown by governorate.</p
The distribution of reported cVDPV cases in Egypt (grey bars) is shown on the left hand axis. The estimated number of infections (dotted line) between 1983 (when the initiating infection is estimated to have occurred) and the end of the outbreak is plotted against the right hand axis, and represents a best estimate of the distribution of infections.
<p>The approximation for the number of infections is represented by the area under the curve, and assumes a constant case to infection ratio of 1∶1000, and average case ascertainment of ∼10%.</p
Summary of estimated number of cVDPV infections associated with five small-scale cVDPV outbreaks
<p>Summary of estimated number of cVDPV infections associated with five small-scale cVDPV outbreaks</p
<i>(adapted from </i><i>Fig 1</i><i>; Estivariz et al. 2008 JID 197: 347–354)</i> Geographic distribution of virologically-confirmed and polio-compatible type 1 cVDPV cases on Madura, Indonesia between June and October 2005.
<p>Population density in Madura for 2005 is shown by district</p
Geographic distribution of virologically-confirmed cases (represented by grey circles) and polio compatible cases (represented by filled stars) associated with type 1 cVDPV outbreak in Hispaniola between July 2000 and July 2001.
<p>Environmental samples that were positive for type 1 cVDPV isolates are represented by light grey triangles.</p
Temporal distribution of virologically-confirmed (grey bars) and compatible cVDPV cases (dashed bars) in Madura, plotted against the left axis. The estimated number of infections (dotted lines) between the estimated date of the initiating infection and the end of the outbreak is shown against the right hand axis.
<p>The number and temporal distribution of these infections represents our best estimate, assuming average case ascertainment of 80%, and constant case to infection ratios of 1∶200 (----) or 1∶1000 (- - -). Black arrows indicate the dates of NIDs.</p
Univariable and multivariable analyses of cases (district−6-months where the first AFP case associated with a VDPV2 emergence was detected) vs. controls (district−6-months with no VDPV2 emergence).
<p>Abbreviations: CI, confidence interval; OR, odds ratio; <i>P</i>, p-value. Statistically significant p-values <0.05 are shown in boldface. Borderline significant p-values <0.1 are shown in italics.</p
Illustration of results from the stochastic dynamic mathematical model of VDPV2 emergence and spread.
<p>The model is simulated for 1 year and a population of 10,000 individuals, starting from a VDPV-free equilibrium that includes routine immunisation. OPV2 withdrawal occurs at 6 months (red arrow) and the last tOPV SIA is assumed to occur 4 weeks before this date in agreement with current plans. SIAs are implemented 4 weeks apart. We define the risk of a VDPV2 outbreak after OPV2 withdrawal as the probability of having >200 incident VDPV2 infections during the 6 months following OPV2 cessation. In this illustration, the grey lines represent the number of VDPV infected individuals over time for 20 different simulations of the model assuming 20% routine immunisation coverage and 3 tOPV SIAs with 80% coverage implemented before OPV2 withdrawal.</p
Risk factors for an emergent VDPV2 to establish a circulating lineage associated with >1 case of poliomyelitis in Nigeria.
<p>Serotype-2 population immunity and DTP3 coverage in districts in the 6-month period when the first AFP case associated with each of the 29 independent VDPV2 emergences in Nigeria during 2004−2014 were reported. Red triangles represent isolates that established circulating lineages, whereas blue circles represent single isolates.</p