Toxoplasma gondii: from animals to humans

Background: Dengue is a growing problem both in its geographical spread and in its intensity, and yet current global distribution remains highly uncertain. Challenges in diagnosis and diagnostic methods as well as highly variable national health systems mean no single data source can reliably estimate the distribution of this disease. As such, there is a lack of agreement on national dengue status among international health organisations. Here we bring together all available information on dengue occurrence using a novel approach to produce an evidence consensus map of the disease range that highlights nations with an uncertain dengue status. Methods/Principal Findings: A baseline methodology was used to assess a range of evidence for each country. In regions where dengue status was uncertain, additional evidence types were included to either clarify dengue status or confirm that it is unknown at this time. An algorithm was developed that assesses evidence quality and consistency, giving each country an evidence consensus score. Using this approach, we were able to generate a contemporary global map of national-level dengue status that assigns a relative measure of certainty and identifies gaps in the available evidence. Conclusion: The map produced here provides a list of 128 countries for which there is good evidence of dengue occurrence, including 36 countries that have previously been classified as dengue-free by the World Health Organization and/or the US Centers for Disease Control. It also identifies disease surveillance needs, which we list in full. The disease extents and limits determined here using evidence consensus, marks the beginning of a five-year study to advance the mapping of dengue virus transmission and disease risk. Completion of this first step has allowed us to produce a preliminary estimate of population at risk with an upper bound of 3.97 billion people. This figure will be refined in future work.

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Refining the global spatial limits of dengue virus transmission by evidence-based consensus

Myasthenia gravis (MG) is an antibody-mediated autoimmune disease of the neuromuscular junction. In approximately 80% of patients, auto-antibodies to the muscle nicotinic acetylcholine receptor (AChR) are present. These antibodies cause loss of AChR numbers and function, and lead to failure of neuromuscular transmission with muscle weakness. The pathogenic mechanisms acting in the 20% of patients with generalized MG who are seronegative for AChR-antibodies (AChR-Ab) have not been elucidated, but there is evidence that they also have an antibody-mediated disorder, with the antibodies directed towards another, previously unidentified muscle-surface-membrane target. Here we show that 70% of AChR-Ab-seronegative MG patients, but not AChR-Ab-seropositive MG patients, have serum auto-antibodies against the muscle-specific receptor tyrosine kinase, MuSK. MuSK mediates the agrin-induced clustering of AChRs during synapse formation, and is also expressed at the mature neuromuscular junction. The MuSK antibodies were specific for the extracellular domains of MuSK expressed in transfected COS7 cells and strongly inhibited MuSK function in cultured myotubes. Our results indicate the involvement of MuSK antibodies in the pathogenesis of AChR-Ab-seronegative MG, thus defining two immunologically distinct forms of the disease. Measurement of MuSK antibodies will substantially aid diagnosis and clinical management.

/pdf/auto-antibodies-to-the-receptor-tyrosine-kinase-musk-in-37z6u6zk9i.pdf

Auto-antibodies to the receptor tyrosine kinase MuSK in patients with myasthenia gravis without acetylcholine receptor antibodies

Crimean-Congo haemorrhagic fever (CCHF) is an often fatal viral infection described in about 30 countries, and it has the most extensive geographic distribution of the medically important tickborne viral diseases, closely approximating the known global distribution of Hyalomma spp ticks. Human beings become infected through tick bites, by crushing infected ticks, after contact with a patient with CCHF during the acute phase of infection, or by contact with blood or tissues from viraemic livestock. Clinical features commonly show a dramatic progression characterised by haemorrhage, myalgia, and fever. The levels of liver enzymes, creatinine phosphokinase, and lactate dehydrogenase are raised, and bleeding markers are prolonged. Infection of the endothelium has a major pathogenic role. Besides direct infection of the endothelium, indirect damage by viral factors or virus-mediated host-derived soluble factors that cause endothelial activations and dysfunction are thought to occur. In diagnosis, enzyme-linked immunoassay and real-time reverse transcriptase PCR are used. Early diagnosis is critical for patient therapy and prevention of potential nosocomial infections. Supportive therapy is the most essential part of case management. Recent studies suggest that ribavirin is effective against CCHF, although definitive studies are not available. Health-care workers have a serious risk of infection, particularly during care of patients with haemorrhages from the nose, mouth, gums, vagina, and injection sites. Simple barrier precautions have been reported to be effective.

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Crimean-Congo haemorrhagic fever

Crimean–Congo hemorrhagic fever

https://horizon.documentation.ird.fr/exl-doc/pleins_textes/pleins_textes_7/b_fdi_51-52/010014577.pdf

Crimean-Congo haemorrhagic fever and Rift Valley fever in south-eastern Mauritania.

General aspects of the 1987 rift valley fever epidemic in Mauritania

An RVF epidemic in southern Mauritania.

This is the last of three papers describing the use of electron microscopy and antigenic tests intended to characterize and place in taxa more than 60 previously unclassified viruses. The first paper describes the viruses we classified as members of the families Arenaviridae, Paramyxoviridae, or Poxviridae. The second paper describes those classified as members of the virus family Bunyaviridae. Another paper, published separately, discusses viruses classified as members of the family Rhabdoviridae. In this paper we report that electron microscopy provided sufficient evidence to provisionally place 14 viruses in the family Reoviridae. By using serologic methods, we placed Minnal virus in the Umatilla serogroup and established new antigenic groups for seven other viruses (Ieri, Picola, Arkonam, Tembe, Fomede, Wongorr, and Gomoka). No antigenic relationships were determined for six other viruses (Andasibe, Itupiranga, Kammavanpettai, Lake Clarendon, Matucare, and Ndelle) provisionally placed in the family Reoviridae.

/pdf/electron-microscopic-and-antigenic-studies-of-57jq3gh82e.pdf

Electron microscopic and antigenic studies of uncharacterized viruses. II. Evidence suggesting the placement of viruses in the family Bunyaviridae.

Dengue 2 and dengue 4 viruses were isolated and re-isolated by inoculation into Aedes pseudoscutellaris continuous cell line (Mos 61) and/or Toxrhynchites brevipalpis. The strain of dengue 2 had been isolated from a patient returning from Casamance (south-western Senegal) and two strains of dengue 4 from patients who lived in Dakar and had not been outside the town in the 15 days before becoming ill. Serological evidence of dengue 4 infection was found in another patient living in Casamance.

J.P. Digoutte

Papers

Crimean-Congo haemorrhagic fever and Rift Valley fever in south-eastern Mauritania.

General aspects of the 1987 rift valley fever epidemic in Mauritania

An RVF epidemic in southern Mauritania.

Electron microscopic and antigenic studies of uncharacterized viruses. II. Evidence suggesting the placement of viruses in the family Bunyaviridae.

Isolation of dengue 2 and dengue 4 viruses from patients in Senegal.