Spatiotemporal transmission and clustering of enterovirus 71 subgenotype B5 in Taiwan, 2007–2012
International Journal of Infectious Diseases
EV71 infection has been a recognized public health threat in Taiwan since the 1998 large-scale nationwide outbreak. Previous studies reported clusters of EV71 infection shifted northward from south Taiwan in 1999-2005. The EV71 subgenotype B5 was first found in Taiwan in 2007 and phylogenetic analyses showed the circulation of two B5 strains (groups A and B) through 2012. The study objective is to describe the origins and detect clusters of groups A and B B5 strains. Methods & Materials: The
... & Materials: The Sentinel Laboratory Network for Enterovirus Surveillance collects clinical specimens for enterovirus isolation from patients with herpangina or hand, foot, and mouth diseases. We included all patients with laboratory-confirmed EV71 B5 subgenotype infection from October 2007 through December 2012 (n = 1523). Residences of case-patients were geocoded by ArcGIS and analyzed by the space-time permutation model of SaTScan to detect clusters. Results: Descriptive analyses showed that group A B5 infection originated from south Taiwan in October 2007, spread northward to islandwide, and in February 2010, ended in north Taiwan. Group B B5 infection originated from the same terminal county of group A B5 strains in north Taiwan in June 2010, spread along the southwest direction, and subsequently, made their way to east Taiwan. The space-time permutation scan statistics identified 6 clusters of EV71 B5 subgenotype infection; 4 were group A in central (n = 10, radius 3.04 km, p = 0.018), south (n = 5, radius 8.39 km, p = 0.043), and north (n = 9, radius 4.51 km, p = 0.001; n = 7, radius 3.16 km, p = 0.001) Taiwan and 2 were group B in south Taiwan (n = 6, radius 5.38 km, p = 0.001; n = 37, radius 9.91 km, p = 0.001). Conclusion: Transmission of EV71 subgenotype B5 has no consistent spatiotemporal pattern. The southwest seeding and clustering of group B B5 strains in south Taiwan might be the results of increasing population susceptibility due to nonimmuned birth cohorts and waning cross-immunity to prior group A B5 infection. We recommended further studies to identify risk factors for the origins and clusters of EV71 B5 subgenotype. http://dx.