24 However, it was later discovered that neutralization of ace2 by recombinant antibodies does not prevent mers-cov infection. 25 Further research identified dipeptyl peptidase 4 ( dpp4 ; also known as CD26 ) as a functional cellular receptor for mers-cov. 23 Unlike other known coronavirus receptors, the enzymatic activity of dpp4 is not required for infection. As would be expected, the amino acid sequence of dpp4 is highly conserved across species and is expressed in the human bronchial epithelium and kidneys. 23 26 Bat dpp4 genes appear to have been subject to a high degree of adaptive evolution as a response to coronavirus infections, so the lineage leading to mers-cov may have circulated in bat populations for a long period of time before being transmitted. 27 Transmission edit On 13 February 2013, the world health Organization stated "the risk of sustained person-to-person transmission appears to be very low." 28 The cells mers-cov infects in the lungs only account for 20 of respiratory epithelial cells, so a large number of virions. Fauci of the national Institutes of health in Bethesda, maryland, stated that as of now mers-cov "does not spread in a sustained person to person way at all.". Fauci stated that there is potential danger in that it is possible for the virus to mutate into a strain that does transmit from person to person.
Virale infecties van het mondslijmvlies gezondheid en wetenschap
19 A second case was found in September 2012, a 49-year-old male living in Qatar presented with similar flu symptoms, and a sequence of the virus was nearly identical to that of the first case. 13 In november 2012, similar cases appeared in Qatar and saudi Arabia. Additional cases were noted, with deaths associated, and rapid research and monitoring of this novel coronavirus began. It is not certain whether the infections are the result of a single zoonotic event with subsequent human-to-human transmission, or if the multiple geographic sites of infection represent multiple zoonotic events from a common unknown source. A study parfum by ziad Memish of riyadh University and colleagues suggests that the virus arose sometime between July 2007 and June 2012, with perhaps as many as 7 separate zoonotic transmissions. Among animal reservoirs, cov has a large genetic diversity yet the samples from patients suggest a similar genome, and therefore common source, though the data are limited. It has been determined through molecular clock analysis, that viruses from the emc/2012 and England/Qatar/2012 date to early 2011 suggesting that these cases are descended from a single zoonotic event. It would appear the mers-cov has been circulating in the human population for greater than one year without detection and suggests independent transmission from an unknown source. 20 21 Tropism edit In humans, the virus has a strong tropism for nonciliated bronchial epithelial cells, and it has been shown to effectively evade the innate immune responses and antagonize interferon (IFN) production in these cells. This tropism is unique in that most respiratory viruses target ciliated cells. 22 23 due to the clinical similarity between mers-cov and sars-cov, it was proposed that they may use the same cellular receptor; the exopeptidase, angiotensin converting enzyme 2 ( ace2 ).
Reference lists were reviewed to retrieve additional relevant information. The expert panel considered the changing epidemiology of hepatitis b infections from surveillance reports, which included follow-up with state health departments to obtain additional information on hcp with acute hepatitis B during reported as having ziekenhuis a positive or unknown Hepb vaccination history. The expert panel reviewed previous recommendations from acip, hicpac, and the. Public health Service; including recommendations defining hcp at risk for occupational exposure, hepb vaccination, and postvaccination serologic testing. The panel also reviewed postexposure prophylaxis ( 1, 5, 9, 11, 13, 15, 16 and results from an electronic survey administered to health-care institutions regarding current practices (see hepatitis b vaccination and Postvaccination Testing among hcp). Various members of the expert panel were consulted to address issues throughout the development of these guidelines. Evidence also was summarized in presentations discussed during expert panel teleconferences.
Hcp protection against hepatitis c virus (hcv human immunodeficiency virus (hiv and other infections also is covered elsewhere ( 1, 11, 14 ). Postvaccination serologic testing and the need for revaccination specific to hcp with immunocompromising conditions (e.g., hcp who are on dialysis, infected with hiv, hematopoietic stem-cell transplant recipients, and receiving chemotherapy) are addressed in separate recommendations ( 15 ). Additional guidance on the management of hcp with chronic hbv infection has been published ( 13 ). A list of frequently used abbreviations is provided ( Box ). New or Updated Information Provided in this guidance This document examines approaches for assessing hbv protection for vaccinated hcp and offers additional guidance for postexposure evaluation and testing of hcp in consideration of: The changing epidemiology of hbv infections in the United States The risk. Methods In 2012, cdc identified and convened subject matter experts in the fields of hbv infection, health-care epidemiology, and evidence-based medicine to form an expert panel to address mechanisms for assessing hbv protection for vaccinated hcp.* The expert panel was comprised of professionals from academic. The expert panel convened 21 teleconferences for deliberations during January 19, 2012January 8, 2013. Materials for teleconference discussion were electronically distributed to members. The expert panel reviewed relevant published literature identified through PubMed searches, citations, and personal files.
Ik heb pijn in mijn mond Thuisarts
Although acute hbv infections have declined substantially since hepb vaccination was introduced in aml the United States, a risk for occupational exposure to hbv persists ( 10 largely from persons with chronic hbv infection. Because vaccine-induced anti-hbs wanes over time, testing hcp for anti-hbs years after vaccination might not distinguish vaccine nonresponders from responders. Pre-exposure assessment of current or past anti-hbs results upon hire or matriculation, followed by one or more additional doses of Hepb vaccine for hcp with anti-hbs 10 mIU/ml, if necessary, helps to ensure that hcp will be protected if they have an exposure to hbv-containing. An expert panel convened by cdc acknowledged that the risk for hbv infection for vaccinated hcp can vary widely by setting and profession, and might be low enough in certain settings that assessment of anti-hbs status and appropriate follow-up can be done at the time. This approach relies on hcp recognizing and reporting blood and body fluid exposures and therefore might be applied on the basis of documented low risk, implementation, and cost considerations. Certain hcp occupations have lower risk for occupational blood and body fluid exposures (e.g., occupations involving counseling versus performing procedures and nontrainees have lower risks for blood and body fluid exposures than trainees. Some settings also will have a lower prevalence of hbv infection in the patient population served than in other settings, which will influence the risk for hcp exposure to hepatitis B surface antigen (HBsAg)-positive blood and body fluids.
All health-care institutions should ensure that hcp receive training to recognize and report exposures, have systems in place to facilitate reporting and postexposure assessment, and have prophylaxis readily accessible for timely administration. This report can guide clinicians, occupational health and student health clinicians, infection-control specialists, hospital and health-care training program administrators, and others in selection of an approach for assessing hbv protection for vaccinated hcp. Hcps are defined as all paid and unpaid persons providing health care, or working or training in health-care settings, who have reasonably anticipated risks for exposure to infectious materials, including blood or body fluids, contaminated medical supplies and equipment, or contaminated environmental surfaces. Hcp might include but are not limited to physicians, nurses, nursing assistants, nurse practitioners, physician assistants, therapists, technicians, emergency medical services personnel, dental personnel, pharmacists, laboratory personnel, autopsy personnel, health-care students and trainees, contractual staff not employed by the health-care facility, and persons not directly. This guidance applies but is not limited to hcp in acute-care hospitals, long-termcare facilities (e.g., nursing homes, skilled nursing facilities, and assisted living facilities physician's offices, dental offices, rehabilitation centers, urgent-care centers, ambulatory surgical centers, dialysis centers, and outpatient clinics, and to persons who provide. Although this guidance pertains to hcp, the same principles might be applicable to persons in other professions with reasonably anticipated risk for blood or body fluid exposure (e.g., public safety workers, embalmers, and crime scene cleanup crews). Recommendations for testing hcp in certain populations at risk for acquisition of hbv infection before matriculation or hire can be found elsewhere and will be reviewed only briefly in this document ( 11 13 ).
Hcp do not recognize all exposures to potentially infectious blood or body fluids ( 2 ) and, even if exposures are recognized, often do not seek postexposure prophylactic management ( 3 ). In serologic studies conducted in the United States during the 1970s, hcp had a prevalence of hbv infection approximately 10 times greater than the general population ( 1 ). In 1983, an estimated 17,000 hbv infections occurred among hcp ( 4 ). Vaccines to prevent hbv became available in the United States in 1981 and were recommended by the Advisory committee on Immunization Practices (acip) for hcp in 1982 ( 5 ). Although a high proportion of healthy vaccine recipients in clinical trials respond to hepatitis B (HepB) vaccination, the proportion of responders can be lower among the general population, particularly among persons with chronic medical conditions ( 6, 7 ).
Acute and chronic hbv infections are rare among hcp who respond to hepb vaccination, but hcp who do not respond to vaccination are thought to remain susceptible. Postvaccination serologic testing for antibody to hepatitis B surface antigen (anti-hbs) identifies vaccine nonresponders and guides the need for revaccination, additional testing for chronic hbv infection, and counseling for hcp who remain susceptible after failing to respond to vaccination. In 1991, acip recommended consideration of postvaccination serologic testing for anti-hbs for hcp at risk for needlestick exposures ( 8 ). In 1997, acip recommended postvaccination serologic testing 12 months after completion of the hepb vaccine series for hcp who have contact with patients or blood and who are at ongoing risk for injuries with sharp instruments or needlesticks ( 9 ). Since 1982 (when Hepb vaccine was recommended for hcp major declines have occurred in reports of acute hepatitis b among hcp ( 10 ). In 2011, acip reaffirmed that unvaccinated and incompletely vaccinated hcp at reasonably anticipated risk for blood or body fluid exposure should receive hepb vaccination before potential exposure, and hcp at high risk for exposure should receive postvaccination serologic testing 12 months after completion of the. This report provides cdc guidance for persons working, training, or volunteering in health-care settings who have documented Hepb vaccination received years before hire or matriculation (e.g., when Hepb vaccination was received as part of routine infant recommended since 1991 or catch-up adolescent recommended since 1995. No postvaccination serologic testing is recommended after routine infant or adolescent Hepb vaccination.
Kleine blaasjes op tong
Immunization of health-care personnel: recommendations of the Advisory committee on Immunization Practices acip. Increasing numbers of hcp antibiotici have received routine hepb vaccination either as infants (recommended since anteflexie 1991) or as catch-up vaccination (recommended since 1995) in adolescence. Hepb vaccination results in protective anti-hbs responses among approximately 95 of healthy-term infants. Certain institutions test vaccinated hcp by measuring anti-hbs upon hire or matriculation, even when anti-hbs testing occurs greater than 2 months after vaccination. This guidance can assist clinicians, occupational health and student health providers, infection-control specialists, hospital and health-care training program administrators, and others in selection of an approach for assessing hbv protection for vaccinated hcp. This report emphasizes the importance of administering Hepb vaccination for all hcp, provides explicit guidance for evaluating hepatitis B protection among previously vaccinated hcp (particularly those who were vaccinated in infancy or adolescence and clarifies recommendations for postexposure management of hcp exposed to blood. Introduction, hepatitis b virus (HBV) has long been recognized as an occupational risk for health-care personnel (hcp including hcp trainees ( 1, 2 ). The virus remains infectious for prolonged periods on environmental surfaces and is transmissible in the absence of visible blood ( 1 ).
Corresponding preparer: Sarah Schillie, md, division of Viral Hepatitis, sites national Center for hiv/aids, viral Hepatitis, std, and tb prevention, cdc. Summary, this report contains cdc guidance that augments the 2011 recommendations of the Advisory committee on Immunization Practices (acip) for evaluating hepatitis B protection among health-care personnel (HCP) and administering post-exposure prophylaxis. Explicit guidance is provided for persons working, training, or volunteering in health-care settings who have documented hepatitis B (HepB) vaccination years before hire or matriculation (e.g., when Hepb vaccination was received as part of routine infant recommended since 1991 or catch-up adolescent recommended since 1995. In the United States, 2,890 cases of acute hepatitis B were reported to cdc in 2011, and an estimated 18,800 new cases of hepatitis b occurred after accounting for underreporting of cases and asymptomatic infection. Although the rate of acute hepatitis b virus (HBV) infections have declined approximately 2011, from.5.9 cases per 100,000 population in the United States, the risk for occupationally acquired hbv among hcp persists, largely from exposures to patients with chronic hbv infection. Acip recommends Hepb vaccination for unvaccinated or incompletely vaccinated hcp with reasonably anticipated risk for blood or body fluid exposure. Acip also recommends that vaccinated hcp receive postvaccination serologic testing (antibody to hepatitis B surface antigen anti-hbs) 12 months after the final dose of vaccine is administered (CDC.
are 99 similar. The genomes can be divided into two clades - a and b - with the majority of cases being caused by clade. Human and camel strains are intermixed suggesting multiple transmission events. Origin edit The first confirmed case was reported in saudi Arabia in 2012. 13 Egyptian virologist. Ali mohamed zaki isolated and identified a previously unknown coronavirus from the man's lungs. Zaki then posted his findings on 24 September 2012 on Promed-mail. 17 19 The isolated cells showed cytopathic effects (cpe in the form of rounding and syncytia formation.
9, mers-cov is one of several viruses identified. Who as a likely cause of a future epidemic. They list it for urgent research and development. 10 11 Contents Virology edit The virus mers-cov is a new member of the beta group of coronavirus, betacoronavirus, lineage. Mers-cov genomes are phylogenetically classified into two clades, clade a and. The earliest cases of mers were of clade a clusters (EMC/2012 and Jordan-N3/2012 and new cases are genetically distinct bestellen (clade B). 12 mers-cov is distinct from sars coronavirus and distinct from the common-cold coronavirus and known endemic human betacoronaviruses hcov-oc43 and hcov-hku1. 13 Until, mers-cov had frequently been referred to as a sars-like virus, 14 or simply the novel coronavirus, and early it was referred to colloquially on messageboards as the "Saudi sars".
Ontsteking in de mond - aandoeningen
This article is about the virus. For the disease, see, middle east respiratory syndrome. The, middle east respiratory syndrome-related coronavirus (. Mers-cov 1 or, emc/2012 hcov-emc/2012 is a novel positive-sense, single-stranded rna virus of the genus, betacoronavirus. Initially called novel coronavirus 2012 or simply novel coronavirus, it was first reported in 2012 after genome sequencing of a virus isolated from sputum samples from a person who fell ill in a 2012 outbreak of a new flu. As of July 2015, mers-cov cases have been reported in over 21 countries, including saudi Arabia, jordan, qatar, Egypt, the United Arab Emirates, kuwait, turkey, occlusive oman, Algeria, bangladesh, Indonesia (none were confirmed austria, 2 the United Kingdom, south Korea, 3 4 the United States,. Thailand, 8 and the Philippines.