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Additional file 1: Table S1. Diagnostic ascertainment of the 12 (NIDIAG) target priority infections; Table S2. Case ascertainment of conditions not targeted by the NIDIAG workup; Table S3. STROBE Checklist of items for cross-sectional studies (NIDIAG); Table S4. STARD checklist NIDIAG study.

Many health systems have been severely strained by the ongoing COVID-19 pandemic that has affected hudreds of millions of people and caused millions of deaths across the world. Only resilient health systems are at a position to ensure the well-being of beneficiaries even under stressful conditions. Good health is key to human happiness and well-being, and essential to sustainable development. Healthy populations can reach their full potential, produce and save more, generating wealth for themselves and contributing significantly to the progress and prosperity of their communities. Building health system resilience is thus crucial and should be considered in the efforts to strengthen health systems. Assessing the resilience of a health system may enable key stakeholders to identify weak points and take necessary actions. However, there is so far no common understanding of health system resilience and how it should be assessed. The general objective of this scoping review is to examine how health system resilience can be assessed. More specifically, we will (i) identify the various approaches used or proposed for assessing health system resilience, (ii) describe the conceptual basis supporting these approaches, (iii) summarise their strengths and limitations, and (iv) discuss challenges in the assessment of health system resilience.

Protocol for systematic review on the bacterial causes of childhood pneumonia in children in sub-Saharan Africa.

Protocol for systematic review on the bacterial causes of childhood pneumonia in children in sub-Saharan Africa.

Additional file 1. Meta-analysis forest plots. This file includes detailed methods and forest plots for all meta-analyses conducted, as well as additional information on why meta-analysis could not be conducted for some risk factors.

In resource-limited settings, the scarcity of skilled personnel and adequate laboratory facilities makes the differential diagnosis of fevers complex [1-5]. Febrile illnesses are diagnosed clinically in most rural centers, and both Rapid Diagnostic Tests (RDTs) and clinical algorithms can be valuable aids to health workers and facilitate therapeutic decisions [6,7]. The persistent fever syndrome targeted by NIDIAG is defined as presence of fever for at least one week. The NIDIAG clinical research consortium focused on potentially severe and treatable infections and therefore targeted the following conditions as differential diagnosis of persistent fever: visceral leishmaniasis (VL), human African trypanosomiasis (HAT), enteric (typhoid and paratyphoid) fever, brucellosis, melioidosis, leptospirosis, malaria, tuberculosis, amoebic liver abscess, relapsing fever, HIV/AIDS, rickettsiosis, and other infectious diseases (e.g., pneumonia). From January 2013 to October 2014, a prospective clinical phase III diagnostic accuracy study was conducted in one site in Cambodia, two sites in Nepal, two sites in Democratic Republic of the Congo (DRC), and one site in Sudan (clinicaltrials.gov no. NCT01766830). The study objectives were to (1) determine the prevalence of the target diseases in patients presenting with persistent fever, (2) assess the predictive value of clinical and first-line laboratory features, and (3) assess the diagnostic accuracy of several RDTs for the diagnosis of the different target conditions.

Human T-lymphotropic virus 1 (HTLV-1) is a retrovirus that produces a persistent infection. Two transmission routes (from mother to child and via sexual intercourse) favor familial clustering of HTLV-1. It is yet unknown why most HTLV-1 carriers remain asymptomatic while about 10% of them develop complications. HTLV-1 associated diseases were originally described as sporadic entities, but familial presentations have been reported. To explore what is known about family aggregation of HTLV-1-associated diseases we undertook a systematic review. We aimed at answering whether, when, and where family aggregation of HTLV-1-associated diseases was reported, which relatives were affected and which hypotheses were proposed to explain aggregation. We searched MEDLINE, abstract books of HTLV conferences and reference lists of selected papers. Search terms used referred to HTLV-1 infection, and HTLV-1-associated diseases, and family studies. HTLV-1-associated diseases considered are adult T-cell leukemia/lymphoma (ATLL), HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), HTLV-1-associated uveitis, and infective dermatitis. Seventy-four records reported HTLV-1-associated diseases in more than one member of the same family and were included. Most reports came from HTLV-1-endemic countries, mainly Japan (n = 30) and Brazil (n = 10). These reports described a total of 270 families in which more than one relative had HTLV-1-associated diseases. In most families, different family members suffered from the same disease (n = 223). The diseases most frequently reported were ATLL (115 families) and HAM/TSP (102 families). Most families (n = 144) included two to four affected individuals. The proportion of ATLL patients with family history of ATLL ranged from 2 to 26%. The proportion of HAM/TSP patients with family history of HAM/TSP ranged from 1 to 48%. The predominant cluster types for ATLL were clusters of siblings and parent-child pairs and for HAM/TSP, an affected parent with one or more affected children. The evidence in the literature, although weak, does suggest that HTLV-1-associated diseases sometimes cluster in families. Whether familial transmission of HTLV-1 is the only determining factor, or whether other factors are also involved, needs further research. publishersversion published

Human T-lymphotropic virus 1 (HTLV-1) is the etiologic agent of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Apoptosis is a mechanism of defense elicited by many triggers, including cross-linking of the FAS receptor expressed in viruses-infected cells, and the ligand FASL presented by T-cytotoxic cells. As HAM/TSP has been associated with high levels of proviral load (PVL), we hypothesized that certain genotypes of single-nucleotide polymorphisms (SNPs) associated with a decreased protein expression of FAS and FASL could be risk factors for this disease. Three SNPs: FAS-670A/G (rs1800682), FAS-1377G/A (rs2234767), and FASL-844C/T (rs763110) were analyzed in 73 HAM/TSP patients and 143 HTLV-1 asymptomatic carriers. Ancestry informative markers were used to adjust for ethnicity through a principal component analysis. Gender, age, PVL, and the first three principal components were used as covariates. The FAS/FASL genotype distribution was not associated with HAM/TSP presence (P-> 0.05). The FAS-670 AA genotype was associated with high PVL in comparison to FAS-670 GG in HAM/TSP patients (P = 0.015), while in asymptomatic carriers low levels of PVL were observed (P > 0.05). Our findings suggest that rs1800682, rs2234767, and rs763110 genotypes are not associated with the presence of HAM/TSP, but that the FAS-670 AA genotype can promote higher PVL values in HAM/TSP patients. J. Med. Virol. 89:726-731, 2017. © 2016 Wiley Periodicals, Inc.

Human T-lymphotropic virus 1 (HTLV-1) is a retrovirus that produces a persistent infection. Two transmission routes (from mother to child and via sexual intercourse) favor familial clustering of HTLV-1. It is yet unknown why most HTLV-1 carriers remain asymptomatic while about 10% of them develop complications. HTLV-1 associated diseases were originally described as sporadic entities, but familial presentations have been reported. To explore what is known about family aggregation of HTLV-1-associated diseases we undertook a systematic review. We aimed at answering whether, when, and where family aggregation of HTLV-1-associated diseases was reported, which relatives were affected and which hypotheses were proposed to explain aggregation. We searched MEDLINE, abstract books of HTLV conferences and reference lists of selected papers. Search terms used referred to HTLV-1 infection, and HTLV-1-associated diseases, and family studies. HTLV-1-associated diseases considered are adult T-cell leukemia/lymphoma (ATLL), HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), HTLV-1-associated uveitis, and infective dermatitis. Seventy-four records reported HTLV-1-associated diseases in more than one member of the same family and were included. Most reports came from HTLV-1-endemic countries, mainly Japan (n = 30) and Brazil (n = 10). These reports described a total of 270 families in which more than one relative had HTLV-1-associated diseases. In most families, different family members suffered from the same disease (n = 223). The diseases most frequently reported were ATLL (115 families) and HAM/TSP (102 families). Most families (n = 144) included two to four affected individuals. The proportion of ATLL patients with family history of ATLL ranged from 2 to 26%. The proportion of HAM/TSP patients with family history of HAM/TSP ranged from 1 to 48%. The predominant cluster types for ATLL were clusters of siblings and parent-child pairs and for HAM/TSP, an affected parent with one or more affected children. The evidence in the literature, although weak, does suggest that HTLV-1-associated diseases sometimes cluster in families. Whether familial transmission of HTLV-1 is the only determining factor, or whether other factors are also involved, needs further research.

Additional index case characteristics and their relation to incident tuberculosis among household contacts. (DOCX 18 kb)

Impoverished populations carry a disproportionately high share of the burden of neglected tropical diseases, including dengue. The burden of dengue is high among poor people because they often live in communities where mosquito vectors are abundant, because they use less vector-human barrier methods, and because interventions tend to be less effective in disadvantaged populations. We believe that a better understanding and management of the “causes behind the causes” of dengue would lead to more equitable and more effective control strategies. Two main ideas are worked out. First, we propose targeted interventions in well-defined geographical areas with high risk of dengue transmission. The definition of these high-risk areas should be based on socio-economical, entomological, environmental as well as epidemiological information. Second, there is a need to adapt dengue control tools to local, context-specific factors, in active collaboration with the sectors involved in risk management as well as with the affected communities. Las poblaciones pobres sufren una dimensión desproporcionadamente alta de la carga de enfermedad producida por las enfermedades tropicales desatendidas, dentro de ellas el dengue. La carga de enfermedad por dengue es alta entre los pobres debido a que frecuentemente viven en comunidades donde los vectores son abundantes, porque utilizan menos barreras humano-vectores y, además, por el hecho que las intervenciones suelen ser menos efectivas en estas poblaciones. Consideramos que un mejor entendimiento y manejo de “las causas detrás de las causas” del dengue conducirían a estrategias de control más equitativas y efectivas. En este artículo se desarrollan dos ideas principales: en primer lugar se propone que las intervenciones sean dirigidas a áreas geográficas bien definidas con alto riesgo de transmisión de dengue; dicha definición debería basarse en información socioeconómica, entomológica, ambiental y epidemiológica. En segundo lugar, existe la necesidad de adaptar las herramientas de control de dengue a factores específicos del contexto local, lo cual debe desarrollarse en colaboración activa con los sectores involucrados en el manejo de riesgo, así como con las comunidades afectadas.

The diagnosis of visceral leishmaniasis (VL) in patients with fever and a large spleen relies on showing Leishmania parasites in tissue samples and on serological tests. Parasitological techniques are invasive, require sophisticated laboratories, consume time, or lack accuracy. Recently, rapid diagnostic tests that are easy to perform have become available.

p. 1-11 Submitted by Edileide Reis (leyde-landy@hotmail.com) on 2014-12-03T11:52:55Z No. of bitstreams: 1 Nicolas A. Gillet.pdf: 1059336 bytes, checksum: 232799195c15409c16eb6fad2b1d9470 (MD5) Approved for entry into archive by Delba Rosa (delba@ufba.br) on 2015-06-11T19:05:26Z (GMT) No. of bitstreams: 1 Nicolas A. Gillet.pdf: 1059336 bytes, checksum: 232799195c15409c16eb6fad2b1d9470 (MD5) Made available in DSpace on 2015-06-11T19:05:26Z (GMT). No. of bitstreams: 1 Nicolas A. Gillet.pdf: 1059336 bytes, checksum: 232799195c15409c16eb6fad2b1d9470 (MD5) Previous issue date: 2013 Human T-lymphotropic Virus-1 (HTLV-1) is a retrovirus that persists lifelong by driving clonal proliferation of infected T-cells. HTLV-1 causes a neuroinflammatory disease and adult T-cell leukemia/lymphoma. Strongyloidiasis, a gastrointestinal infection by the helminth Strongyloides stercoralis, and Infective Dermatitis associated with HTLV-1 (IDH), appear to be risk factors for the development of HTLV-1 related diseases. We used high-throughput sequencing to map and quantify the insertion sites of the provirus in order to monitor the clonality of the HTLV-1-infected T-cell population (i.e. the number of distinct clones and abundance of each clone). A newly developed biodiversity estimator called “DivE” was used to estimate the total number of clones in the blood. We found that the major determinant of proviral load in all subjects without leukemia/lymphoma was the total number of HTLV-1-infected clones. Nevertheless, the significantly higher proviral load in patients with strongyloidiasis or IDH was due to an increase in the mean clone abundance, not to an increase in the number of infected clones. These patients appear to be less capable of restricting clone abundance than those with HTLV-1 alone. In patients co-infected with Strongyloides there was an increased degree of oligoclonal expansion and a higher rate of turnover (i.e. appearance and disappearance) of HTLV-1-infected clones. In Strongyloides co-infected patients and those with IDH, proliferation of the most abundant HTLV-1+ T-cell clones is independent of the genomic environment of the provirus, in sharp contrast to patients with HTLV-1 infection alone. This implies that new selection forces are driving oligoclonal proliferation in Strongyloides co-infection and IDH. We conclude that strongyloidiasis and IDH increase the risk of development of HTLV-1-associated diseases by increasing the rate of infection of new clones and the abundance of existing HTLV-1+ clones.

Human T-lymphotropic virus 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) affects approximately 5% of HTLV-1-infected individuals. It is poorly understood why only some infected subjects develop this disease, but host genetic factors may determine susceptibility. The innate immune system may influence disease outcome in HTLV-1-infected subjects because of its role in early immune responses to viral infections. Variation in genes encoding killer cell immunoglobulin-like receptors (KIR) and their human leukocyte antigen (HLA) molecule ligands may affect the risk of HAM/TSP. We performed a two-stage case-control study to examine the distribution of KIR genes and HLA-Cw groups in Peruvian HTLV-1-infected HAM/TSP subjects and asymptomatic carriers. We also tested for epistatic effects between specific KIR genes and HLA-Cw groups. In the first stage, we found several trends towards association with HAM/TSP or proviral load (PVL). However, these results were not replicated in the second stage. In conclusion, this is the first report on KIR gene frequencies in the Peruvian population and may be of significance in hematopoietic stem-cell transplants. Our study did not reveal significant associations between KIR genes and HLA-Cw groups and HAM/TSP or PVL. However, since our study was only powered to detect larger effects, additional studies using larger cohorts are needed.

The coronavirus disease 2019 (COVID-19) outbreak in North, Central, and South America has become the epicenter of the current pandemic. We have suggested previously that the infection rate of this virus might be lower in people living at high altitude (over 2,500 m) compared to that in the lowlands. Based on data from official sources, we performed a new epidemiological analysis of the development of the pandemic in 23 countries on the American continent as of May 23, 2020. Our results confirm our previous finding, further showing that the incidence of COVID-19 on the American continent decreases significantly starting at 1,000 m above sea level (masl). Moreover, epidemiological modeling indicates that the virus transmission rate capacity is lower in the highlands (>1,000 masl) than in the lowlands (HighlightsThere is a negative correlation between altitude and COVID-19 incidence on the American Continent starting from 1,000 m above sea level.The transmission rate of SARS-CoV-2 is lower in the highlands than in the lowlands.The severity of COVID-19 decreases significantly with increased altitude.