Dawn M. Nekorchuk

The purpose of this chapter is to demonstrate how Google Earth Engine may be used to support modeling and forecasting of vector-borne infectious diseases such as malaria. In doing so, the chapter will also show how Earth Engine may be used to gather data for subsequent analyses outside of Earth Engine, the results of which can then also be brought back into Earth Engine.

Background: Urbanization generally improves health outcomes of residents and is one of the potential factors that might contribute to reducing malaria transmission. However, the expansion of Anopheles stephensi, an urban malaria vector, poses a threat for malaria control and elimination efforts in Africa. In this paper, malaria trends in urban settings in Ethiopia from 2014 to 2019 are reported with a focus on towns and cities where An. stephensi surveys were conducted. Methods: A retrospective study was conducted to determine malaria trends in urban districts using passive surveillance data collected at health facilities from 2014 to 2019. Data from 25 towns surveyed for An. stephensi were used in malaria trend analysis. Robust linear models were used to identify outliers and impute missing and anomalous data. The seasonal Mann-Kendal test was used to test for monotonic increasing or decreasing trends. Results: A total of 9,468,970 malaria cases were reported between 2014 and 2019 through the Public Health Emergency Management (PHEM) system. Of these, 1.45 million (15.3%) cases were reported from urban settings. The incidence of malaria declined by 62% between 2014 and 2018. In 2019, the incidence increased to 15 per 1000 population from 11 to 1000 in 2018. Both confirmed (microscopy or RDT) Plasmodium falciparum (67%) and Plasmodium vivax (28%) were reported with a higher proportion of P. vivax infections in urban areas. In 2019, An. stephensi was detected in 17 towns where more than 19,804 malaria cases were reported, with most of the cases (56%) being P. falciparum. Trend analysis revealed that malaria cases increased in five towns in Afar and Somali administrative regions, decreased in nine towns, and had no obvious trend in the remaining three towns. Conclusion: The contribution of malaria in urban settings is not negligible in Ethiopia. With the rapid expansion of An. stephensi in the country, the receptivity is likely to be higher for malaria. Although the evidence presented in this study does not demonstrate a direct linkage between An. stephensi detection and an increase in urban malaria throughout the country, An. stephensi might contribute to an increase in malaria unless control measures are implemented as soon as possible. Targeted surveillance and effective response are needed to assess the contribution of this vector to malaria transmission and curb potential outbreaks.

Malaria epidemics can be triggered by fluctuations in temperature and precipitation that influence vector mosquitoes and the malaria parasite. Identifying and monitoring environmental risk factors can thus provide early warning of future outbreaks. Satellite Earth observations provide relevant measurements, but obtaining these data requires substantial expertise, computational resources, and internet bandwidth. To support malaria forecasting in Ethiopia, we developed software for Retrieving Environmental Analytics for Climate and Health (REACH). REACH is a cloud-based application for accessing data on land surface temperature, spectral indices, and precipitation using the Google Earth Engine (GEE) platform. REACH can be implemented using the GEE code editor and JavaScript API, as a standalone web app, or as package with the Python API. Users provide a date range and data for 852 districts in Ethiopia are automatically summarized and downloaded as tables. REACH was successfully used in Ethiopia to support a pilot malaria early warning project in the Amhara region. The software can be extended to new locations and modified to access other environmental datasets through GEE.

Quantitative models describing environmentally-mediated disease transmission rarely focus on the independent contribution of recruitment and the environment on the force of infection driving outbreaks. In this study we attempt to investigate the interaction between external factors and host’s population dynamics in determining the outbreaks of some indirectly transmitted diseases. We first built deterministic and stochastic compartmental models based on anthrax which were parameterized using information from literature and complemented with field observations. Our force of infection function was derived modeling the number of successful transmission encounters as a pure birth process that depends on the pathogen’s dispersion effort. After accounting for individual heterogeneity in pathogen’s dispersion effort, we allowed the force of infection to vary seasonally according to external factors recreating a scenario in which disease transmission increases in response to an environmental variable. Using simulations we demonstrate that anthrax disease dynamics in mid-latitude grasslands is decoupled from hosts population dynamics. When seasonal forcing was ignored, outbreaks matched hosts reproductive events, a scenario that is not realistic in nature. Instead, when allowing the force of infection to vary seasonally, outbreaks were only present in years were environmental variables were appropriate for the outbreaks to develop. We used the stochastic formulation of the force of infection to derive R₀ under scenarios with different assumptions. The derivation of R₀ allowed us to conclude that during epizootic years, pathogen contribution to disease persistence is nearly independent of dispersion. In endemic years, only pathogens with high dispersion significantly prevent disease extinction. Finally, we used our model in a maximum likelihood framework to estimate the parameters that determined a significant anthrax outbreak in Montana in 2008. Our study highlights the importance of the environment in determining anthrax outbreak intensity and could be useful to predict future events that could result in significant wildlife and domestic livestock losses.

The purpose of this study was to assess the objective bioterrorism-related knowledge base and the perceived response readiness of veterinarians in Hawaii to a bioterrorism event, and also to identify variables associated with knowledge-based test performance. An anonymous survey instrument was mailed to all licensed veterinarians residing in Hawaii (N = 229) up to three times during June and July 2004, using numeric identifiers to track non-respondents. The response rate for deliverable surveys was 59% (125 of 212). Only 12% (15 of 123) of respondents reported having had prior training on bioterrorism. Forty-four percent (55 of 125) reported being able to identify a bioterrorism event in animal populations; however, only 17% (21 of 125) felt able to recognize a bioterrorism event in human populations. Only 16% (20 of 123) felt they were able to respond effectively to a bioterrorist attack. Over 90% (106 of 116) expressed their willingness to provide assistance to the state in its response to a bioterrorist event. Veterinarians scored a mean of 70% correct (5.6 out of 8 questions) on the objective knowledge-based questions. Additional bioterrorism preparedness training should be made available, both in the form of continuing educational offerings for practicing veterinarians and as a component of the curriculum in veterinary schools.

Introduction:: Physicians and nurses are integral components of the public health bioterrorism surveillance system. However, most published bioterrorism preparedness surveys focus on gathering information related to selfassessed knowledge or perceived needs and abilities.Objective:: A survey of physicians and nurses in Hawaii was conducted to assess objective knowledge regarding bioterrorism agents and diseases and perceived response readiness for a bioterrorism event.Methods:: During June and July 2004, an anonymous survey was mailed up to three times to a random sample of all licensed physicians and nurses residing in Hawaii.Results:: The response rate was 45% (115 of 255) for physicians and 53% (146 of 278) for nurses. Previous bioterrorism preparedness training associated significantly with knowledge-based test performance in both groups. Only 20% of physicians or nurses had had previous training in bioterrorism preparedness, and 70% expressed willingness to assist the state in the event of a bioterrorist attack.Conclusions:: Additional bioterrorism preparedness training should be made available through continuing education and also should become a component of both medical and nursing school curricula. It is important to provide the knowledge necessary for physicians and nurses to improve their ability to perform in the event of a bioterrorist attack.

Bartonella is a Gram-negative pathogen that is unique among bacteria in being able to induce angioproliferative lesions. Cultured human endothelial cells have provided an in vitro system in which to study the basis of angioproliferation. Previous studies have attributed the organism's ability to induce angioproliferative lesions to direct mitotic stimulation of endothelial cells by these bacteria. Here we show that Bartonella inhibits apoptosis of endothelial cells in vitro , and that its ability to stimulate proliferation of endothelial cells depends to a large extent on its antiapoptotic activity. Bartonella suppresses both early and late events in apoptosis, namely caspase activation and DNA fragmentation, respectively. Its ability to inhibit death of endothelial cells after serum starvation can be recapitulated by media conditioned by bacteria, indicating that direct cell contact is not necessary. Among tested strains, the activity is produced only by Bartonella species that are significant human pathogens and are associated with angioproliferative lesions. We suggest that endothelial cells normally respond to infection by undergoing apoptosis and that Bartonella evolved the antiapoptotic activity to enhance survival of the host cells and therefore itself. We propose that Bartonella 's antiapoptotic mechanism accounts at least in part for its ability to induce vascular proliferation in vivo .