An Explosive Epidemic of DENV-3 in Cairns, Australia

Abstract

From November 2008-May 2009 Cairns Queensland Australia was struck by an explosive epidemic of DENV-3 that exceeded the capacity of highly skilled dengue control team to control it. We describe the environmental, virological and entomological factors associated with this outbreak to better understand the circumstances leading to its occurrence. Patient interviews, serological results and viral sequencing strongly suggest that the imported index case was infected in Kalimantan, Indonesia. A delay in notification of 27 days from importation of the index case until Queensland Health was notified of dengue transmission allowed the virus to amplify and spread unchecked through November 2008. Unseasonably warm weather, with daily mean temperatures exceeding 30°C, occurred in late November and would have shortened the extrinsic incubation period of the virus and enhanced transmission. Analysis of case movements early in the outbreak indicated that the total incubation period was as low as 9–11 days. This was supported by laboratory vector competence studies that found transmission by Aedes aegypti occurred within 5 days post exposure at 28°C. Effective vector competence rates calculated from these transmission studies indicate that early transmission contributed to the explosive dengue transmission observed in this outbreak. Collections from BG sentinel traps and double sticky ovitraps showed that large populations of the vector Ae. aegypti occurred in the transmission areas from November – December 2008. Finally, the seasonal movement of people around the Christmas holiday season enhanced the spread of DENV-3. These results suggest that a strain of DENV-3 with an unusually rapid transmission cycle was able to outpace vector control efforts, especially those reliant upon delayed action control such as lethal ovitraps.

A spatial simulation model for dengue virus infection in urban areas

“…Specifically, while warmer weather and increased human movement had only a small effect on the spread of the virus, a shorter virus strain-specific extrinsic incubation time can explain the observed explosive outbreak of 2008/2009 [7]. In agreement with previous studies, the simulation results presented here highlight the importance of rapid diagnosis of potential index cases and prompt initiation of vector control, as presented above in Figure 9[46].…”

A comparative analysis of three vector-borne diseases across Australia using seasonal and meteorological models

“…For instance, the 2008–9 outbreak involved a strain of dengue with an unusually rapid transmission cycle and also reflected the larger trend of increased overseas travel to dengue-endemic countries. These factors may explain the high severity index of the 2008–9 outbreak, the largest in fifty years in QLD404647. Although the models cannot be used as precise estimates of an outbreak’s scale, they can shed light on the magnitude of an outbreak and highlight potential changes in disease surveillance.…”

Wolbachia-Based Dengue Virus Inhibition Is Not Tissue-Specific in Aedes aegypti

“…The DENV 3 strain used for this experiment was sampled from a patient during an outbreak in Cairns, Australia in 2008/2009 [43]. This strain was selected because it caused one of the largest dengue outbreaks in Australia [43] and because it has been demonstrated to infect both w Mel and Wildtype mosquitoes at a high rate [44].…”

“…This strain was selected because it caused one of the largest dengue outbreaks in Australia [43] and because it has been demonstrated to infect both w Mel and Wildtype mosquitoes at a high rate [44]. Passage 6 of DENV 3 (PFU 10 6 ) was propagated using the protocol by Ye et al ., [45] and stored in single use aliquots of 1mL at -80°C.…”