In nature, wild viruses adapted for transmission circulate in many animal species (bats, birds, primates…). Contamination of other animals, including humans, may occur by crossing of the species barrier. Genetic manipulations have been carried out on wild viruses to favor the species jumping and to increase of viral virulence. The aim was to identify the critical genes for pathogenicity. This has been mainly performed on potentially epidemic pathogens, as Myxovirus influenzae of avian flu and coronaviruses of SARS and MERS epidemics. These dangerous experiments were subject to a moratorium in the United States (2014-2017). Three years after the emergence of Covid-19, the origin of du SARS-CoV2 remains a mystery. Covid19 appeared in Wuhan, officially in December 2019, but probably during the autumn 2019. The virus was identified in January 2020. It belongs to the genus Betacoronavirus (subgenus Sarbecovirus). It was at once highly contagious. In addition, the primary isolates were genetically very homogeneous, differing only by two nucleotides without evidence for adaptive mutations. In addition, the Spike protein, a major virulence factor, has a furin site, not found in any other known sarbecovirus. Unlike the SARS and MERS epidemics, no intermediate host has been detected so far. Finally, no other outbreaks were reported at the beginning of the pandemic outside of Wuhan, contrary to what happened with the emergence of SARS (2002) and H7N9 avian influenza (2013). Today, there are two scenarios to explain the emergence of SARS-CoV2. Proponents of the natural origin argue that the bat virus might have directly infected humans, spreading silently at a low level in humans for years, without eliminating the existence of undetected intermediate hosts. This does not explain the origin in Wuhan, far away from the natural virus reservoirs. The furin site would have arisen spontaneously from other coronaviruses. The alternative scenario is that of a laboratory accident after gain-of-function manipulations from a SARS-like virus, or even the occurrence of a human contamination by a natural CoV virus grown on cells in Wuhan. This article is an update to the Quarterly Medical Review (QMR) devoted to the history of modern pandemics. To access this QMR contents, please go here: https://www.sciencedirect.com/journal/la-presse-medicale/vol/51/issue/3.
The COVID-19 pandemic affects the transplant recipients since March 2020. Transplant centers quickly organized themselves to optimize the management of the immunocompromised patients and to progress in the knowledge of this new disease. To this end, a French Registry was created, which includes all solid organ transplant patients who have developed a SARS Cov2 infection. Numerous studies have been carried out using these data to describe this new disease in transplant patients, to characterize its clinical and biological risk factors and to define its prognosis. The 60 days-mortality of transplant patients hospitalized for COVID-19 was evaluated at 23% and renal failure plays a major role in the poor prognosis in addition to the classical risk factors described in the general population. The advent of vaccination has been a great relief but transplanted patients have shown a poor vaccine response keeping them at risk of severe disease even after an adapted vaccination scheme. Specific strategies was proposed in this particularly fragile population like increasing vaccine doses or using anti SARS Cov-2 monoclonal antibodies.
The Covid-19 pandemic appeared in China in December 2019 as a cluster of transmissible pneumonia caused by a new betacoronavirus. On March 11, 2020, the World Health Organization (WHO) declared it a pandemic. Covid-19 is a mild infection in 80% of cases, serious in 15% and critical in 5%. Symptomatic forms include a first phase of flu-like viral invasion, and at times a second phase, dysimmune and inflammatory, with acute respiratory distress syndrome, multiorgan failure and thromboembolic complications. Degree of severity is related to age and comorbidities. SARS-CoV-2 is the third highly pathogenic Betacoronavirus to cross the species barrier. Its genome, an RNA of 29,903 nucleotides, shows strong homogeneity with bat coronaviruses from southern China, but the conditions for its passage in humans have yet to be elucidated. Mutations can give rise to variants of concern (VOC) that are more transmissible and able to evade the host's immune response. Several VOCs have succeeded and replaced one another: Alpha in October 2020, Beta and Gamma in December 2020, Delta in spring 2021 and Omicron in November 2021. The Covid-19 pandemic has evolved in five waves of unequal amplitude and severity, with geographical disparities. Worldwide, it has caused 395,000,000 confirmed cases including 5,700,000 deaths. Epidemiological surveillance applies several indicators (incidence rate, test positivity rate, effective R and occupancy rate of intensive care beds) supplemented by genomic monitoring to detect variants by sequencing. Non-pharmacological measures, particularly face mask wearing, have been effective in preventing the transmission of SARS-CoV-2. Few currently available drugs have proven useful, with the exception of dexamethazone for patients requiring oxygen therapy. Development of SARS-CoV-2 vaccines began early on many platforms. Innovation was brought about by the Pfizer-BioNTech and Moderna messenger RNA vaccines, which claim protective efficacy of 95% and 94.1% respectively, far higher than the 70% minimum set by the WHO. Governments have hesitated between two strategies, mitigation and suppression. The second has been favored in critical periods such as April 2020, when 2.5 billion people throughout the world were confined. Vaccination campaigns got underway at the end of December 2020 and progressed without reaching sufficient herd immunity, leading some nations to consider compulsory vaccination or to require a vaccine or health pass, in order for persons to access different activities. Will the pandemic stop with Omicron and become endemic? This part of the Covid-19 story remains to be told.
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The “Russian flu”, which raged from 1889 to 1894, is considered as the first pandemic of the industrial era for which statistics have been collected. This planetary event started in Turkestan and hit the Russian Empire, before reaching all European countries, the United States of America, and the whole world. Contemporaries were surprised by its high contagiousness as evidenced by attack rates averaging 60% in urban populations, its rapid spread in successive waves circling the globe in a few months by rail and sea, and the tendency of the disease to relapse. Despite its low case-fatality rate (0.10%-0.28%), it is estimated to have caused one million deaths worldwide. On serological grounds, it is generally accepted that the causative agent of Russian influenza was Myxovirus influenzae, the virus identified for all influenza pandemics since the “Spanish flu” of 1918. In light of the Covid-19 pandemic, which has underscored the extraordinary epidemic potential of coronaviruses, this assumption has recently been questioned. Coronaviruses come from wild reservoirs (bats, rodents, birds, …). They induce respiratory symptoms mimicking influenza, possibly leading to respiratory distress with pneumonia. In addition to the Covid-19 pandemic, recent deadly and limited epidemics, such as SARS in 2002 and MERS in 2012, have occurred. Russian influenza presented as an influenza-like syndrome with clinical peculiarities (multivisceral and neurological involvement, skin rash, early iterative relapses), evoking some particularities of Covid-19. Four other coronaviruses circulating in the human population for decades (HCoV-229E, HCoV-NL63, HCoV-OC43, HCoV-HKU1) have been found to be responsible for 15 to 30% of seasonal colds. All of these viruses are of animal origin. Recently, phylogenetic studies have revealed the genetic proximity between a bovine coronavirus BCoV and the human virus HCoV-OC43, indicating that the latter emerged around 1890, at the time of the Russian flu, when an epizootic was raging among cattle throughout Europe. Could the current human virus be the attenuated remnant that appeared after the Russian flu in 1894? Was there a coronavirus pandemic before Covid-19 ?
Trisomy 13 syndrome (Patau syndrome) is a disorder of human chromosomes which occurs in approximately 1 in 10,000-25,000 live-born infants. Trisomy refers to three copies of a chromosome instead of the normal two and in Trisomy 13 there is the presence of an extra #13 chromosome. Approximately 80% of infants with Trisomy 13 syndrome will have a full trisomy (affecting all cells) while the remainder will have a trisomy due to a rearrangement of cells called a translocation (an attachment of all or part of one chromosome to another chromosome) or have mosaicism (two different cell lines in an individual).
L’émergence d’une maladie virale résulte le plus souvent d’un déséquilibre dans l’interaction entre l’agent infectieux, l’hôte et l’environnement. Après une phase d’introduction de la maladie virale dans un territoire ou une population donnée et une fois que les premières chaînes de transmission sont en place, on peut assister à la diffusion de la maladie, voire sa pérennisation si les mesures de contrôle ne sont pas mises en œuvre ou ne sont pas suffisamment efficaces. S’il est difficile d’anticiper la survenue et l’introduction d’une maladie virale émergente, les trois axes suivants de lutte doivent être développés pour en limiter l’impact : (1) anticipation et préparation ; (2) recherche et (3) veille et surveillance. Pour garantir enfin que les mesures prises soient pertinentes au regard des données disponibles et acceptables par la population, il convient de s’appuyer de manière systématique sur une approche multidisciplinaire qui devra être réévaluée de manière dynamique.
Responsiveness to the hepatitis B virus (HBV) vaccination in hemodialysis (HD) patients who had been exposed to the hepatitis E virus (HEV) and persistently generate antibodies against HEV remains unknown. Interferon (IFN)-λ3 positively correlates with the surface HBV antibodies (anti-HBs) in both healthy and HD subjects. We aimed to show whether HD patients differ in circulating IFN-λ3 and vaccine-induced anti-HBs titers concerning natural HEV immunization. HBV/HCV negative HD patients (31 HEV IgG positive, 45 HEV negative), HBV vaccinated and receiving booster doses as needed, had been tested for anti-HBs titers (CMIA) and IFN-λ3 concentrations (ELISA) in the blood collected before a dialysis session. There were no differences in circulating IFN-λ3 and anti-HBs titers between both groups. In responders to the HBV vaccine, there was a positive correlation between plasma IFN-λ3 levels and anti-HBs titers (r = 0.505, adjusted P = 0.01 in HEV exposed subjects; r = 0.523, adjusted P = 0.001 in controls). HEV past infection does not attenuate post-vaccination anti-HBs generation and does not influence a correlation between circulating IFN-λ3 levels and anti-HBs titers.
Environ 5 % des cancers colorectaux (CCR) surviennent dans un contexte de prédisposition héréditaire au cancer. Le syndrome de Lynch est le plus fréquent des syndromes de prédisposition au cancer colorectal et est aussi associé à un sur-risque de développement d’autres cancers (notamment cancer de l’endomètre et cancer de l’ovaire). Il est la conséquence d’une variation génétique constitutionnelle sur un gène faisant partie du système de réparation de l’ADN MisMatch Repair (MMR) : MLH1, MSH2, MSH6ouPMS2 ; ou du gène EPCAM (promoteur du gène MSH2). En cas d’identification d’une mutation prédisposant au syndrome de Lynch, un suivi clinique et la mise en place de mesures de prévention sont recommandés, adaptés au risque estimé de cancer. Des critères cliniques (Amsterdam II et Bethesda) ont été validés afin d’identifier les patients index devant se voir proposer une consultation d’oncogénétique en vue de la mise en œuvre d’une analyse génétique constitutionnelle. Par ailleurs, l’Institut National du Cancer (INCa) recommande que soit réalisé à titre systématique un test tumoral à la recherche de stigmates de défaillance du système MMR en cas de diagnostic d’un CCR avant l’âge de 60 ans ou d’un cancer de l’endomètre avant l’âge de 50 ans ou, quel que soit l’âge si un patient développe une de ces tumeurs dans un contexte d’antécédent personnel ou familial de cancers du spectre du syndrome de Lynch. Dans cette mise au point, nous abordons les modalités de dépistage du syndrome de Lynch (identification du cas index et dépistage familial) et les modalités de surveillance en 2019.
En 2015 en France, la vaccination contre les papillomavirus (HPV) était recommandée entre 11 et 14 ans. Notre étude visait à évaluer les connaissances de parents d’élèves bas-normands sur la pathologie, le dépistage et la vaccination et à mesurer l’impact d’une campagne d’information sur ces aspects et notamment sur les intentions vaccinales. La population correspondait aux parents d’élèves bas-normands en classe de sixième, âgés de 10 ou 11 ans, au cours de l’année scolaire 2015–2016. Les collèges avaient été sélectionnés avec le concours des directions académiques. Les intentions vaccinales avant et après intervention étaient mesurées par un questionnaire distribué aux élèves en avril 2016 et recueilli de mai à juin 2016 par les infirmières scolaires. Au sein des 16 collèges retenus, 1428 questionnaires ont été distribués et 864 recueillis (60,5 %), indifféremment du sexe de l’enfant. Sur 439 collégiennes, 85,9 % n’étaient pas vaccinées contre les HPV. Lorsque la mère était le parent ayant répondu, l’intention vaccinale était plus importante (p < 0,001). Parmi les parents qui avaient pris connaissance de la brochure d’information, 73,7 % l’avaient trouvé utile. Il existait un lien significatif entre les connaissances de l’existence du vaccin contre les HPV et les intentions vaccinales (p < 0,001). Le pourcentage de filles vaccinées était significativement plus élevé après information (10,9 % versus 3,2 %) et on constatait une augmentation significative du pourcentage d’intentions vaccinales après distribution de la brochure (p < 0,001). Le taux de vaccination après information spécifique sur la vaccination contre les HPV était significativement plus élevé. Il semblait exister un impact significativement positif de la campagne d’information réalisée. In 2015, the vaccine against human Papillomavirus (hPV) was recommended in France for children from 11 to 14 years-old. This study assessed the knowledge of parents from Normandy about this vaccine and measured the impact of an information campaign on their intent to have their children vaccinated. Parents from Normandy with children in sixth-grade class, aged 10 to 11, during the 2015–2016 school year were included. The secondary schools were selected in collaboration with academic institutions. The intent to have their child vaccinated was measured with a questionnaire distributed to children in April 2016 and collected from May to June 2016 by school nurses. Among the 16 selected secondary schools, 1428 questionnaires were distributed and 864 (60.5 %) were collected regardless of the gender of the child. Among the 439 girls, 85.9 % were not vaccinated against hPV. The intent to vaccinate was higher when the parent who responded was the mother (P < 0.001). Among the parents who took note of the information booklet, 73.7 % found this information useful. There was a significant association between the knowledge about the vaccine against hPV and the intent to vaccinate (P < 0.001). The percentage of vaccinated girls was significantly higher when their parents were informed (10.9 % versus 3.2 %). We noticed a significant rise of the intent to vaccinate children when information booklets were distributed (P < 0.001). The vaccination rate after specific information about vaccination against hPV was significantly higher. The information campaign has thus a significant positive impact.
La ménopause est associée à une augmentation significative du risque artériel et métabolique. L’hypertension artérielle, fréquente chez la femme ménopausée, est plutôt de type systolique vasculaire. La mesure répétée de la pression artérielle doit être systématique à chaque consultation. Les mesures ambulatoires, en dehors du cabinet médical, doivent être encouragées, le dépistage de l’HTA nocturne étant particulièrement rentable chez la prévention CV chez la femme. L’autodépistage de l’HTA par automesure tensionnelle doit être encouragée à la ménopause. Un traitement anti-hypertenseur sera initié, après une confirmation ambulatoire de l’hypertension artérielle, en association avec une hygiène de vie renforcée, et tiendra compte du niveau global du risque cardiovasculaire. Ll n’y a pas de spécificités thérapeutiques à promouvoir chez la femme hypertendue à l’exception des diurétiques thiazidiques chez la femme ostéoporotique. Chez la femme hypertendue de moins de 60 ans avec symptômes climatériques invalidants, sans antécédent cardiovasculaire artériel ou veineux, le THM peut être proposé dans les 10 ans après le début de la ménopause avec, au préalable, une concertation entre le gynécologue, le cardiologue et le médecin traitant avec une information éclairée sur la balance bénéfice-risque du THM consignée dans le dossier médical. La coopération entre médecins cardiovasculaires, gynécologues et médecins traitants est à promouvoir en France pour optimiser les parcours de soins de ces femmes à risque et améliorer les pratiques professionnelles.
Les critères diagnostiques ont fait l’objet d’une révision récente (2014) autorisant le traitement de certains patients asymptomatiques, sur des critères biologiques et radiologiques.
La simulation interprofessionnelle est une technique pédagogique efficace pour développer les compétences non-techniques en soins critiques et renforcer la collaboration interprofessionnelle des équipes afin d’améliorer la qualité des soins et le devenir du patient.
La nausée est une sensation commune. Elle est ressentie par le sujet comme un état susceptible d’évoluer vers un vomissement. Cependant beaucoup de nausées se maintiennent sans être suivies de vomissements.
L'exposition à un évènement traumatique peut favoriser la survenue de troubles psychiatriques dont le trouble stress post-traumatique (TSPT) mais également des symptômes et/ou pathologies respiratoires, dont l'asthme. Revue systématique de la littérature sur les données concernant l'influence d'un TSPT sur le développement d'un asthme ou l'aggravation d'un asthme préexistant au traumatisme. Medline sur la période 1980–2018 avec pour mots-clés : « PTSD » ou « post-traumatic stress disorder » ou « post-traumatic stress disorder » et « asthme », avec les limites « Title/Abstract » ; les langues retenues étaient l'anglais et le français. Parmi 141 articles, 59 résumés sélectionnés ont donné lieu à une double lecture aboutissant à retenir 14 études. Si le TSPT peut survenir 4 semaines après l'exposition à un traumatisme au cours duquel l'intégrité physique de la personne a été menacée, il peut également se développer plusieurs mois ou années plus tard. Le TSPT est un facteur de risque de développement de l'asthme et peut également aggraver les symptômes d'un asthme préexistant. Il est important de noter que cette relation a été démontrée sur différentes populations, divers traumatismes et quel que soit le genre et/ou l'ethnie. Outre son impact sur le développement de l'asthme, chez les patients asthmatiques, le TSPT peut être responsable d'un mauvais contrôle de l'asthme, de taux plus élevés de recours aux soins (visites au service des urgences et/ou hospitalisation pour asthme) et d'une moindre qualité de vie liée à l'asthme. La présente revue a également suggéré que l'étude de l'association entre le TSPT et l'asthme doit tenir compte des facteurs confondants potentiels, notamment le tabagisme et l'exposition aux poussières (ex : asthme consécutif aux attaques du World Trade Center). Les mécanismes possibles de l'association entre TSPT et asthme sont imparfaitement connus. Plusieurs facteurs incluant le système nerveux, l'axe hypothalamo-hypophyso-surrénalien, la réponse inflammatoire et le système immunitaire pourraient expliquer ce lien. Le TSPT est un facteur de risque de développement de l'asthme et d'aggravation d'un asthme préexistant. Chez les patients asthmatiques, il est donc important de rechercher systématiquement un TSPT survenu après l'évènement traumatique ou préexistant à cet évènement. De plus, lors d'exposition à un évènement traumatique, une attention particulière doit être prêtée aux troubles somatiques dont l'asthme. La majorité des études ayant été menées sur des populations américaines ; il semble important de répliquer les études en population Européenne afin d'apporter de nouveaux éléments de connaissance sur cette association. Exposure to a traumatic event may not only lead to a large variety of mental disorders, such as post-traumatic stress disorder (PTSD) but also respiratory symptoms and/or respiratory diseases, as asthma. Systematic literature review of data on the impact of post-traumatic stress disorder on asthma. Medline, on the period 1980–2018 with the following keywords: "PTSD" or "post-traumatic stress disorder" or "post-traumatic stress disorder" and "asthma", limits "title/abstract"; the selected languages were English or French. Among 141 articles, 23 abstracts have given use to a dual reading to select 14 studies. While PTSD may develop 4 weeks after being exposed to a traumatic event during which the physical integrity of the person has been threatened, it might also develop several months or years later. PTSD has been reported to be a risk factor for asthma and also a factor that might enhance a preexisting asthma. It is also important to note that this relation has been highlighted among several populations, traumatic events and regardless the gender and/or cultural factors. Despite its impact on the development of asthma, in asthmatic patients, PTSD may be responsible for poor asthma control, increased rates of healthcare use (visit in the emergency department and/or hospitalization for asthma) and poor asthma-related quality of life. The study of the association between PTSD and asthma have to take into account some potentially confounding factors, such as smoking status and dust exposure (e.g.: asthma following the terrorist attacks of the World Trade Center). Less is known regarding the potential mechanisms involved in the association between PTSD and asthma. Several factors including the nervous system, the hypothalamo-pituitary-adrenal axis, the inflammatory response and the immune system may explain the association. PTSD is a risk factor for the development of asthma and for the worsening of preexisting asthma. In asthmatic patients, it is of primary importance to systematically screen potential PTSD that might be developed after a traumatic event or a preexisting traumatic condition. Moreover, after exposure to a traumatic event, a special attention needs to be paid to somatic reactions such as asthma. The majority of studies having been conducted on American samples, replicating studies among European samples appears of prime importance in order to add a body of knowledge on the association between somatic and psychiatric conditions.
