Responding to cholera outbreaks in Somalia in 2017-2019

Background:Somalia reported repeated cholera outbreaks between 2017 and 2019. These outbreaks were attributed to multiple risk factors which made response challenging.Aims:To describe lessons from the preparedness and response to the cholera outbreaks in Somalia between 2017 and 2019.Methods:We reviewed outbreak response reports, surveillance records and preparedness plans for the cholera outbreaks in Somalia from January 2017 to December 2019 and other relevant literature. We present data on cholera-related response indicators including cholera cases and deaths and case fatality rates for the 3 years. Qualitative data were collected from 5 focus group discussions and 10 key informant interviews to identify the interventions, challenges and lessons learnt from the Somali experience.Results:In 2017, a total of 78 701 cholera cases and 1163 related deaths were reported (case fatality rate 1.48%), in 2018, 6448 cholera cases and 45 deaths were reported (case fatality rate 0.70%), while in 2019, some 3089 cases and 4 deaths were reported in Somalia (case fatality rate 0.13%). The protracted conflict, limited access to primary health care, and limited access to safe water and proper sanitation among displaced populations were identified as the main drivers of the repeated cholera outbreaks.Conclusions:Periodic assessment of response to and preparedness for potential epidemics is essential to identify and close gaps within the health systems. Somalia’s experience offers important lessons on preventing and controlling cholera outbreaks for countries experiencing complex humanitarian emergencies.

Tuning the Thromboinflammatory Response to Venous Flow Interruption by the Ectonucleotidase CD39.

Objective- Leukocyte flux contributes to thrombus formation in deep veins under pathological conditions, but mechanisms that inhibit venous thrombosis are incompletely understood. Ectonucleotide di(tri)phosphohydrolase 1 ( ENTPD1 or Cd39), an ectoenzyme that catabolizes extracellular adenine nucleotides, is embedded on the surface of endothelial cells and leukocytes. We hypothesized that under venous stasis conditions, CD39 regulates inflammation at the vein:blood interface in a murine model of deep vein thrombosis. Approach and Results- CD39-null mice developed significantly larger venous thrombi under venous stasis, with more leukocyte recruitment compared with wild-type mice. Gene expression profiling of wild-type and Cd39-null mice revealed 76 differentially expressed inflammatory genes that were significantly upregulated in Cd39-deleted mice after venous thrombosis, and validation experiments confirmed high expression of several key inflammatory mediators. P-selectin, known to have proximal involvement in venous inflammatory and thrombotic events, was upregulated in Cd39-null mice. Inferior vena caval ligation resulted in thrombosis and a corresponding increase in both P-selectin and VWF (von Willebrand Factor) levels which were strikingly higher in mice lacking the Cd39 gene. These mice also manifest an increase in circulating platelet-leukocyte heteroaggregates suggesting heterotypic crosstalk between coagulation and inflammatory systems, which is amplified in the absence of CD39. Conclusions- These data suggest that CD39 mitigates the venous thromboinflammatory response to flow interruption.

Risk mapping of Rinderpest sero-prevalence in Central and Southern Somalia based on spatial and network risk factors.

BACKGROUND: In contrast to most pastoral systems, the Somali livestock production system is oriented towards domestic trade and export with seasonal movement patterns of herds/flocks in search of water and pasture and towards export points. Data from a rinderpest survey and other data sources have been integrated to explore the topology of a contact network of cattle herds based on a spatial proximity criterion and other attributes related to cattle herd dynamics. The objective of the study is to integrate spatial mobility and other attributes with GIS and network approaches in order to develop a predictive spatial model of presence of rinderpest. RESULTS: A spatial logistic regression model was fitted using data for 562 point locations. It includes three statistically significant continuous-scale variables that increase the risk of rinderpest: home range radius, herd density and clustering coefficient of the node of the network whose link was established if the sum of the home ranges of every pair of nodes was equal or greater than the shortest distance between the points. The sensitivity of the model is 85.1% and the specificity 84.6%, correctly classifying 84.7% of the observations. The spatial autocorrelation not accounted for by the model is negligible and visual assessment of a semivariogram of the residuals indicated that there was no undue amount of spatial autocorrelation. The predictive model was applied to a set of 6176 point locations covering the study area. Areas at high risk of having serological evidence of rinderpest are located mainly in the coastal districts of Lower and Middle Juba, the coastal area of Lower Shabele and in the regions of Middle Shabele and Bay. There are also isolated spots of high risk along the border with Kenya and the southern area of the border with Ethiopia. CONCLUSIONS: The identification of point locations and areas with high risk of presence of rinderpest and their spatial visualization as a risk map will be useful for informing the prioritization of disease surveillance and control activities for rinderpest in Somalia. The methodology applied here, involving spatial and network parameters, could also be applied to other diseases and/or species as part of a standardized approach for the design of risk-based surveillance activities in nomadic pastoral settings.