UC Irvine

This dissertation seeks to untangle how armed conflict exacerbates infectious disease risk through physical, environmental, social, and geographic factors. Across multiple conflict settings, I analyze how conflict intensity impacts cholera and cutaneous leishmaniasis risk in conjunction with relevant environmental factors, as well as suggest an additional tool for measuring conflict's effects on the built environment. I do this by 1) assessing the association between violent conflict events and cholera in Yemen, 2) exploring Earth observation tools for measuring conflict intensity and infrastructure recovery in Yemen and Ukraine, 3) analyzing how environmental and conflict-related factors modify leishmaniasis risk at an ecological scale, and 4) quantifying cutaneous leishmaniasis surveillance gaps in northern Syria. Together, this work provides insights on how armed conflict actively shapes infectious disease dynamics. It also presents a viable tool for measuring conflict intensity and infrastructure damage that is unbound by many of the limitations of traditional tools. In doing so, this dissertation highlights that increases in infectious disease during armed conflict are not naturally occurring or unfortunate collateral damage, but rather the result of intentional human action. These findings have important implications for preparedness, response, and advocacy on behalf of civilians who bear the brunt of conflict.