Finally, patients were enrolled with a clinical suspicion of severe infection and we did not screen all medical admissions for sepsis criteria. We therefore may have missed potentially eligible subjects. Subsequent studies should take this into consideration. This study confirms that severe sepsis in a sub-Saharan Africa setting has high mortality amongst both HIV-infected and uninfected adults. Establishment on ART confers significant survival benefit in the HIV positive subset, and the high mortality among patients on ART for less than three months underscores the importance

of vigilant clinical follow-up among this group. Patients at risk of death can be identified using simple, objectively measurable ERK inhibitor manufacturer criteria, which following validation amongst other Enzalutamide nmr populations can be used to standardise multi-site interventional trials of sepsis bundles in resource-poor settings. These will

enable the formulation of appropriate evidenced-based local guidelines and clinical trials for the management of critically ill adults in sub-Saharan Africa. We wish to thank the staff on the medical admissions ward at Queen Elizabeth Central Hospital, and the laboratory staff and data entry team at the Malawi-Liverpool-Wellcome Clinical Research Programme. Finally, we thank patients and guardians for their participation in the study. “
“Dengue fever (DF) is transmitted by mosquito bites that introduce dengue virus (DENV) serotypes 1–4. DF is endemic in tropical and subtropical regions, with at least 50 million new cases arising each year.1 Dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS), the severe forms of DF, affect people in nearly two-thirds of the countries worldwide, particularly

those in Southeast Asia.2 DENV serotype 2 (DENV-2) is a risk factor associated with DSS, whereas DENV-1, DENV-3, and DENV-4 are not.3 Nintedanib (BIBF 1120) Patients who develop DHF initially present symptoms similar to DF patients, but they abruptly develop plasma leakage, which manifests as haemoconcentration, ascites, and pleural effusion, and may result in irreversible DSS during the defeverence stage.4 The pathogenesis of DHF is not fully understood, but an alteration of T helper (Th)1/Th2 immune reaction is thought to be involved.5 Early in DHF, a cascade of cytokines initiates a series of events that lead to a shift from a Th1-type response in mild DF to a Th2-type response resulting in severe DHF.5 Th1/Th2 polarisation is regulated by the induction of interleukin (IL)-10 and IL-12 by monocytes and monocyte-derived dendritic cells (DCs). Moreover, monocytes/macrophages express CD14, a documented DENV receptor; play a critical role in determining the balance of Th1/Th2 responses by modulating IL-12 production.