Last data update: Jul 01, 2024. (Total: 47134 publications since 2009)
Records 1-30 (of 35 Records) |
Query Trace: Norman L [original query] |
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Intestinal protozoa in returning travellers: a GeoSentinel analysis from 2007 to 2019
Weitzel T , Brown A , Libman M , Perret C , Huits R , Chen L , Leung DT , Leder K , Connor BA , Menéndez MD , Asgeirsson H , Schwartz E , Salvador F , Malvy D , Saio M , Norman FF , Amatya B , Duvignaud A , Vaughan S , Glynn M , Angelo KM . J Travel Med 2024 31 (4) ![]() BACKGROUND: Prolonged diarrhoea is common amongst returning travellers and is often caused by intestinal protozoa. However, the epidemiology of travel-associated illness caused by protozoal pathogens is not well described. METHODS: We analysed records of returning international travellers with illness caused by Giardia duodenalis, Cryptosporidium spp., Cyclospora cayetanensis or Cystoisospora belli, reported to the GeoSentinel Network during January 2007-December 2019. We excluded records of travellers migrating, with an unascertainable exposure country, or from GeoSentinel sites that were not located in high-income countries. RESULTS: There were 2517 cases, 82.3% giardiasis (n = 2072), 11.4% cryptosporidiosis (n = 287), 6.0% cyclosporiasis (n = 150) and 0.3% cystoisosporiasis (n = 8). Overall, most travellers were tourists (64.4%) on long trips (median durations: 18-30 days). Cryptosporidiosis more frequently affected people < 18 years (13.9%) and cyclosporiasis affected people ≥ 40 years (59.4%). Giardiasis was most frequently acquired in South Central Asia (45.8%) and sub-Saharan Africa (22.6%), cryptosporidiosis in sub-Saharan Africa (24.7%) and South-Central Asia (19.5%), cyclosporiasis in South East Asia (31.3%) and Central America (27.3%), and cystoisosporiasis in sub-Saharan Africa (62.5%). Cyclosporiasis cases were reported from countries of uncertain endemicity (e.g. Cambodia) or in countries with no previous evidence of this parasite (e.g. French Guiana). The time from symptom onset to presentation at a GeoSentinel site was the longest amongst travellers with giardiasis (median: 30 days). Over 14% of travellers with cryptosporidiosis were hospitalized. CONCLUSIONS: This analysis provides new insights into the epidemiology and clinical significance of four intestinal protozoa that can cause morbidity in international travellers. These data might help optimize pretravel advice and post-travel management of patients with travel-associated prolonged gastrointestinal illnesses. This analysis reinforces the importance of international travel-related surveillance to identify sentinel cases and areas where protozoal infections might be undetected or underreported. |
Preventing Chronic Disease Collection: From Data to Action: National, state, and local efforts to end menthol and other flavored commercial tobacco product use
Marshall LL , Norman L , Rose SW , Tseng TS . Prev Chronic Dis 2024 21 E39 |
Travel surveillance uncovers dengue virus dynamics and introductions in the Caribbean
Taylor-Salmon E , Hill V , Paul LM , Koch RT , Breban MI , Chaguza C , Sodeinde A , Warren JL , Bunch S , Cano N , Cone M , Eysoldt S , Garcia A , Gilles N , Hagy A , Heberlein L , Jaber R , Kassens E , Colarusso P , Davis A , Baudin S , Rico E , Mejía-Echeverri Á , Scott B , Stanek D , Zimler R , Muñoz-Jordán JL , Santiago GA , Adams LE , Paz-Bailey G , Spillane M , Katebi V , Paulino-Ramírez R , Mueses S , Peguero A , Sánchez N , Norman FF , Galán JC , Huits R , Hamer DH , Vogels CBF , Morrison A , Michael SF , Grubaugh ND . Nat Commun 2024 15 (1) 3508 ![]() ![]() Dengue is the most prevalent mosquito-borne viral disease in humans, and cases are continuing to rise globally. In particular, islands in the Caribbean have experienced more frequent outbreaks, and all four dengue virus (DENV) serotypes have been reported in the region, leading to hyperendemicity and increased rates of severe disease. However, there is significant variability regarding virus surveillance and reporting between islands, making it difficult to obtain an accurate understanding of the epidemiological patterns in the Caribbean. To investigate this, we used travel surveillance and genomic epidemiology to reconstruct outbreak dynamics, DENV serotype turnover, and patterns of spread within the region from 2009-2022. We uncovered two recent DENV-3 introductions from Asia, one of which resulted in a large outbreak in Cuba, which was previously under-reported. We also show that while outbreaks can be synchronized between islands, they are often caused by different serotypes. Our study highlights the importance of surveillance of infected travelers to provide a snapshot of local introductions and transmission in areas with limited local surveillance and suggests that the recent DENV-3 introductions may pose a major public health threat in the region. |
Chikungunya infection in returned travellers: results from the GEOSENTINEL network, 2005-2020
Bierbrier R , Javelle E , Norman FF , Chen LH , Bottieau E , Schwartz E , Leder K , Angelo KM , Stoney R , Libman M , Hamer DH , Huits R , Connor BA , Simon F , Barkati S . J Travel Med 2024 BACKGROUND: Chikungunya is an important travel-related disease because of its rapid geographical expansion and potential for prolonged morbidity. Improved understanding of the epidemiology of travel-related chikungunya infections may influence prevention strategies including education and vaccination. METHODS: We analysed data from travellers with confirmed or probable chikungunya reported to GeoSentinel sites from 2005 to 2020. Confirmed chikungunya was defined as a compatible clinical history plus either virus isolation, positive nucleic acid test, or seroconversion/rising titre in paired sera. Probable chikungunya was defined as a compatible clinical history with a single positive serology result. RESULTS: 1202 travellers (896 confirmed and 306 probable) with chikungunya were included. The median age was 43 years (range 0-91; interquartile range [IQR]: 31-55); 707 (58.8%) travellers were female. Most infections were acquired in the Caribbean (28.8%), Southeast Asia (22.8%), South Central Asia (14.2%) and South America (14.2%). The highest numbers of chikungunya cases reported to GeoSentinel were in 2014 (28.3%), 2015 (14.3%), and 2019 (11.9%). The most frequent reasons for travel were tourism (n = 592; 49.3%) and visiting friends or relatives (n = 334; 27.7%). The median time to presentation to a GeoSentinel site was 23 days (IQR: 7-52) after symptom onset. In travellers with confirmed chikungunya and no other reported illnesses, the most frequently reported symptoms included musculoskeletal symptoms (98.8%), fever/chills/sweats (68.7%), and skin symptoms (35.5%). Among 917 travellers with information available, 296 (32.3%) had a pre-travel consultation. CONCLUSIONS: Chikungunya was acquired by international travellers in almost 100 destinations globally. Vector precautions and vaccination where recommended should be integrated into pretravel visits for travellers going to areas with chikungunya or areas with the potential for transmission.Continued surveillance of travel-related chikungunya may help public health officials and clinicians limit the transmission of this potentially debilitating disease by defining regions where protective measures (e.g. pre-travel vaccination) should be strongly considered. |
Dengue outbreak among travellers returning from Cuba-GeoSentinel Surveillance Network, January-September 2022
Díaz-Menéndez M , Angelo KM , de Miguel Buckley R , Bottieau E , Huits R , Grobusch MP , Gobbi FG , Asgeirsson H , Duvignaud A , Norman FF , Javelle E , Epelboin L , Rothe C , Chappuis F , Martinez GE , Popescu C , Camprubí-Ferrer D , Molina I , Odolini S , Barkati S , Kuhn S , Vaughan S , McCarthy A , Lago M , Libman MD , Hamer DH . J Travel Med 2023 30 (2) Increasing numbers of travellers returning from Cuba with dengue virus infection were reported to the GeoSentinel Network from June to September 2022, reflecting an ongoing local outbreak. This report demonstrates the importance of travellers as sentinels of arboviral outbreaks and highlights the need for early identification of travel-related dengue. |
Comparison of immunodiagnostic assays for the rapid diagnosis of coccidioidomycosis in dogs
Caceres DH , Lindsley MD . J Fungi (Basel) 2022 8 (7) Coccidioidomycosis is a disease caused by the dimorphic fungi Coccidioides spp., which affects humans and a variety of animal species, including domestic dogs. In dogs, accurate diagnosis could provide a substantial improvement on the quality of canine life, as well as an advancement in the mapping of regions endemic for coccidioidomycosis. The purpose of this study was to compare immunodiagnostic assays for anti-Coccidioides antibody (Ab) detection in dogs' serum. Three commercially available immunodiagnostic assays (IMMY(); Norman, OK, USA) were evaluated, including the sna Coccidioides Ab Lateral Flow Assay (LFA), Coccidioides IDCF immunodiffusion assay (IDCF), and the Clarus Coccidioides Ab Enzyme Immunoassay (EIA). Assays were evaluated using 98 dog serum samples: 29 from dogs with coccidioidomycosis, 15 from dogs diagnosed with histoplasmosis, 10 from dogs diagnosed with blastomycosis, and 44 from dogs without a fungal disease. Using specimens from dogs with coccidioidomycosis, the IDCF had an accuracy of 92% (95% confidence interval [95% CI] = 85-96%), the EIA had an accuracy of 91% (95% CI = 83-96%), and the LFA displayed an accuracy of 82% (95% CI = 73-89%). Using Kappa analysis, the agreement between LFA and EIA was 0.59 (95% CI = 0.42-0.75), that between LFA and IDCF was 0.64 (95% CI = 0.48-0.79), and that between EIA and IDCF was 0.79 (95% CI = 0.64-0.90). Most cross-reactions were observed in dogs with histoplasmosis. Compared with EIA and IDCF, the LFA requires substantially less laboratory equipment and infrastructure and rapidly produces results, offering a substantial improvement for the initial screening of coccidioidomycosis in dogs. |
Adapting Survey Data Collection to Respond to the COVID-19 Pandemic: Experiences From a Local Health Department.
Seligson AL , Alroy KA , Sanderson M , Maleki AN , Fernandez S , Aviles A , Dumas SE , Perlman SE , Peebles K , Norman CC , Gwynn RC , Gould LH . Am J Public Health 2021 111 (12) 2176-2185 The New York City (NYC) Department of Health and Mental Hygiene ("Health Department") conducts routine surveys to describe the health of NYC residents. During the COVID-19 pandemic, the Health Department adjusted existing surveys and developed new ones to improve our understanding of the impact of the pandemic on physical health, mental health, and social determinants of health and to incorporate more explicit measures of racial inequities. The longstanding Community Health Survey was adapted in 2020 to ask questions about COVID-19 and recruit respondents for a population-based severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) serosurvey. A new survey panel, Healthy NYC, was launched in June 2020 and is being used to collect data on COVID-19, mental health, and social determinants of health. In addition, 7 Health Opinion Polls were conducted from March 2020 through March 2021 to learn about COVID-19-related knowledge, attitudes, and opinions, including vaccine intentions. We describe the contributions that survey data have made to the emergency response in NYC in ways that address COVID-19 and the profound inequities of the pandemic. (Am J Public Health. 2021;111(12):2176-2185. https://doi.org/10.2105/AJPH.2021.306515). |
Antibodies to SARS-CoV-2 in All of Us Research Program Participants, January 2-March 18, 2020.
Althoff KN , Schlueter DJ , Anton-Culver H , Cherry J , Denny JC , Thomsen I , Karlson EW , Havers FP , Cicek MS , Thibodeau SN , Pinto LA , Lowy D , Malin BA , Ohno-Machado L , Williams C , Goldstein D , Kouame A , Ramirez A , Roman A , Sharpless NE , Gebo KA , Schully SD . Clin Infect Dis 2021 74 (4) 584-590 ![]() BACKGROUND: With limited SARS-CoV-2 testing capacity in the US at the start of the epidemic (January - March), testing was focused on symptomatic patients with a travel history throughout February, obscuring the picture of SARS-CoV-2 seeding and community transmission. We sought to identify individuals with SARS-CoV-2 antibodies in the early weeks of the US epidemic. METHODS: All of Us study participants in all 50 US states provided blood specimens during study visits from January 2 to March 18, 2020. A participant was considered seropositive if they tested positive for SARS-CoV-2 immunoglobulin G (IgG) antibodies on the Abbott Architect SARS-CoV-2 IgG ELISA and the EUROIMMUN SARS-CoV-2 ELISA in a sequential testing algorithm. Sensitivity and specificity of the Abbott and EUROIMMUNE ELISAs and the net sensitivity and specificity of the sequential testing algorithm were estimated with 95% confidence intervals. RESULTS: The estimated sensitivity of Abbott and EUROIMMUN was 100% (107/107 [96.6%, 100%]) and 90.7% (97/107 [83.5%, 95.4%]), respectively. The estimated specificity of Abbott and EUROIMMUN was 99.5% (995/1,000 [98.8%, 99.8%]) and 99.7% (997/1,000 [99.1%, 99.9%), respectively. The net sensitivity and specificity of our sequential testing algorithm was 90.7% (97/107 [83.5%, 95.4%]) and 100.0% (1,000/1,000 [99.6%, 100%]), respectively. Of the 24,079 study participants with blood specimens from January 2 to March 18, 2020, 9 were seropositive, 7 of whom were seropositive prior to the first confirmed case in the states of Illinois, Massachusetts, Wisconsin, Pennsylvania, and Mississippi. CONCLUSIONS: Our findings indicate SARS-CoV-2 infections weeks prior to the first recognized cases in 5 US states. |
Extended delivery of vaccines to the skin improves immune responses.
Joyce JC , Sella HE , Jost H , Mistilis MJ , Esser ES , Pradhan P , Toy R , Collins ML , Rota PA , Roy K , Skountzou I , Compans RW , Oberste MS , Weldon WC , Norman JJ , Prausnitz MR . J Control Release 2019 304 135-145 Vaccines prevent 2-3 million childhood deaths annually; however, low vaccine efficacy and the resulting need for booster doses create gaps in immunization coverage. In this translational study, we explore the benefits of extended release of licensed vaccine antigens into skin to increase immune responses after a single dose in order to design improved vaccine delivery systems. By administering daily intradermal injections of inactivated polio vaccine according to six different delivery profiles, zeroth-order release over 28days resulted in neutralizing antibody titers equivalent to two bolus vaccinations administered one month apart. Vaccinations following this profile also improved immune responses to tetanus toxoid and subunit influenza vaccine but not a live-attenuated viral vaccine, measles vaccine. Finally, using subunit influenza vaccine, we demonstrated that daily vaccination by microneedle patch induced a potent, balanced humoral immunity with an increased memory response compared to bolus vaccination. We conclude that extended presentation of antigen in skin via intradermal injection or microneedle patch can enhance immune responses and reduce the number of vaccine doses, thereby enabling increased vaccination efficacy. |
Cardiovascular risk factors associated with venous thromboembolism
Gregson J , Kaptoge S , Bolton T , Pennells L , Willeit P , Burgess S , Bell S , Sweeting M , Rimm EB , Kabrhel C , Zoller B , Assmann G , Gudnason V , Folsom AR , Arndt V , Fletcher A , Norman PE , Nordestgaard BG , Kitamura A , Mahmoodi BK , Whincup PH , Knuiman M , Salomaa V , Meisinger C , Koenig W , Kavousi M , Volzke H , Cooper JA , Ninomiya T , Casiglia E , Rodriguez B , Ben-Shlomo Y , Despres JP , Simons L , Barrett-Connor E , Bjorkelund C , Notdurfter M , Kromhout D , Price J , Sutherland SE , Sundstrom J , Kauhanen J , Gallacher J , Beulens JWJ , Dankner R , Cooper C , Giampaoli S , Deen JF , Gomez de la Camara A , Kuller LH , Rosengren A , Svensson PJ , Nagel D , Crespo CJ , Brenner H , Albertorio-Diaz JR , Atkins R , Brunner EJ , Shipley M , Njolstad I , Lawlor DA , van der Schouw YT , Selmer RM , Trevisan M , Verschuren WMM , Greenland P , Wassertheil-Smoller S , Lowe GDO , Wood AM , Butterworth AS , Thompson SG , Danesh J , Di Angelantonio E , Meade T . JAMA Cardiol 2019 4 (2) 163-173 Importance: It is uncertain to what extent established cardiovascular risk factors are associated with venous thromboembolism (VTE). Objective: To estimate the associations of major cardiovascular risk factors with VTE, ie, deep vein thrombosis and pulmonary embolism. Design, Setting, and Participants: This study included individual participant data mostly from essentially population-based cohort studies from the Emerging Risk Factors Collaboration (ERFC; 731728 participants; 75 cohorts; years of baseline surveys, February 1960 to June 2008; latest date of follow-up, December 2015) and the UK Biobank (421537 participants; years of baseline surveys, March 2006 to September 2010; latest date of follow-up, February 2016). Participants without cardiovascular disease at baseline were included. Data were analyzed from June 2017 to September 2018. Exposures: A panel of several established cardiovascular risk factors. Main Outcomes and Measures: Hazard ratios (HRs) per 1-SD higher usual risk factor levels (or presence/absence). Incident fatal outcomes in ERFC (VTE, 1041; coronary heart disease [CHD], 25131) and incident fatal/nonfatal outcomes in UK Biobank (VTE, 2321; CHD, 3385). Hazard ratios were adjusted for age, sex, smoking status, diabetes, and body mass index (BMI). Results: Of the 731728 participants from the ERFC, 403396 (55.1%) were female, and the mean (SD) age at the time of the survey was 51.9 (9.0) years; of the 421537 participants from the UK Biobank, 233699 (55.4%) were female, and the mean (SD) age at the time of the survey was 56.4 (8.1) years. Risk factors for VTE included older age (ERFC: HR per decade, 2.67; 95% CI, 2.45-2.91; UK Biobank: HR, 1.81; 95% CI, 1.71-1.92), current smoking (ERFC: HR, 1.38; 95% CI, 1.20-1.58; UK Biobank: HR, 1.23; 95% CI, 1.08-1.40), and BMI (ERFC: HR per 1-SD higher BMI, 1.43; 95% CI, 1.35-1.50; UK Biobank: HR, 1.37; 95% CI, 1.32-1.41). For these factors, there were similar HRs for pulmonary embolism and deep vein thrombosis in UK Biobank (except adiposity was more strongly associated with pulmonary embolism) and similar HRs for unprovoked vs provoked VTE. Apart from adiposity, these risk factors were less strongly associated with VTE than CHD. There were inconsistent associations of VTEs with diabetes and blood pressure across ERFC and UK Biobank, and there was limited ability to study lipid and inflammation markers. Conclusions and Relevance: Older age, smoking, and adiposity were consistently associated with higher VTE risk. |
Notes from the field: Multiple modes of transmission during a Thanksgiving day norovirus outbreak - Tennessee, 2017
Brennan J , Cavallo SJ , Garman K , Lewis K , Irving DJ , Moore C , Thomas L , Hill J , Villegas R , Norman JF , Dunn JR , Schaffner W , Jones TF . MMWR Morb Mortal Wkly Rep 2018 67 (46) 1300-1301 On November 28, 2017, the manager of restaurant A in Tennessee reported receiving 18 complaints from patrons with gastrointestinal illness who had dined there on Thanksgiving Day, November 23, 2017. Tennessee Department of Health officials conducted an investigation to confirm the outbreak, assess exposures, and recommend measures to prevent continued spread. | | On November 23, one patron vomited in a private dining room, and an employee immediately used disinfectant spray labeled as effective against norovirus* to clean the vomitus. After handwashing, the employee served family-style platters of food and cut pecan pie. For the November 23 Thanksgiving Day, restaurant A served 676 patrons a limited menu from 11 a.m. to 8 p.m. The manager provided contact information, seating times, and seating locations for 114 patrons with reservations. All patrons with contact information were telephoned, and a questionnaire was used to assess illness and exposures for anyone living in the household who ate at restaurant A on November 23. Stool specimens were requested from ill patrons. Among the 676 patrons, 137 (20%) were enrolled in a case-control study. |
Multicenter validation of commercial antigenuria reagents to diagnose progressive disseminated histoplasmosis in people living with HIV/AIDS in two Latin American countries
Caceres DH , Samayoa BE , Medina NG , Tobon AM , Guzman BJ , Mercado D , Restrepo A , Chiller T , Arathoon EE , Gomez BL . J Clin Microbiol 2018 56 (6) Histoplasmosis is an important cause of mortality in patients with AIDS, especially in countries with limited access to antiretroviral therapies and diagnostic tests. However, many disseminated infections in Latin America go undiagnosed. A simple, rapid method to detect Histoplasma capsulatum infection in endemic regions would dramatically decrease time to diagnosis and treatment, reducing morbidity and mortality. The aim of this study was to validate a commercial monoclonal Histoplasma galactomannan (HGM) ELISA (Immuno-Mycologics [IMMY], Norman, Oklahoma, USA) in two cohorts of people living with HIV/AIDS (PLHIV). We analyzed urine samples from 589 people (466 from Guatemala and 123 from Colombia), including 546 from PLHIV and 43 from non-PLHIV controls. Sixty-three of these people (35 from Guatemala and 28 from Colombia) had confirmed histoplasmosis by isolation of H. capsulatum Using the standard curve provided by the quantitative commercial test, sensitivity was 98% (95% CI, 95-100) and specificity was 97% (95% CI, 96-99) (cutoff=0.5 ng/mL). Semi-quantitative results, using a calibrator of 12.5 ng/mL of Histoplasma galactomannan to calculate an EIA Index Value (EIV) of the samples, showed a sensitivity of 95% (95% CI, 89-100%) and specificity of 98% (95% CI, 96-99%) (cutoff >/=2.6 EIV). This relatively simple-to-perform commercial antigenuria test showed a high performance, with reproducible results in both countries, suggesting that it can used to detect progressive disseminated histoplasmosis in PLHIV in a wide range of clinical laboratories in countries where histoplasmosis is endemic. |
Major Threat to Malaria Control Programs by Plasmodium falciparum Lacking Histidine-Rich Protein 2, Eritrea.
Berhane A , Anderson K , Mihreteab S , Gresty K , Rogier E , Mohamed S , Hagos F , Embaye G , Chinorumba A , Zehaie A , Dowd S , Waters NC , Gatton ML , Udhayakumar V , Cheng Q , Cunningham J . Emerg Infect Dis 2018 24 (3) 462-470 ![]() ![]() False-negative results for Plasmodium falciparum histidine-rich protein (HRP) 2-based rapid diagnostic tests (RDTs) are increasing in Eritrea. We investigated HRP gene 2/3 (pfhrp2/pfhrp3) status in 50 infected patients at 2 hospitals. We showed that 80.8% (21/26) of patients at Ghindae Hospital and 41.7% (10/24) at Massawa Hospital were infected with pfhrp2-negative parasites and 92.3% (24/26) of patients at Ghindae Hospital and 70.8% (17/24) at Massawa Hospital were infected with pfhrp3-negative parasites. Parasite densities between pfhrp2-positive and pfhrp2-negative patients were comparable. All pfhrp2-negative samples had no detectable HRP2/3 antigen and showed negative results for HRP2-based RDTs. pfhrp2-negative parasites were genetically less diverse and formed 2 clusters with no close relationships to parasites from Peru. These parasites probably emerged independently by selection in Eritrea. High prevalence of pfhrp2-negative parasites caused a high rate of false-negative results for RDTs. Determining prevalence of pfhrp2-negative parasites is urgently needed in neighboring countries to assist case management policies. |
Surgeon General's Reports on Tobacco: A continued legacy of unbiased and rigorous synthesis of the scientific evidence
King BA , Creamer MR , Harrell M , Kelder S , Norman L , Perry CL . Nicotine Tob Res 2017 20 (8) 1033-1036 The author of a recent letter, who declared interests related to the tobacco and electronic cigarette industries, critiqued the objectivity and evidence related to the 2016 US Surgeon General’s Report, E-cigarette Use Among Youth and Young Adults.1 The 2016 report was compiled using a longstanding, peer-reviewed, and comprehensive process to safeguard the scientific rigor and practical relevance of US Surgeon General’s Reports on Tobacco. In this commentary, we describe that process in detail, including specific components that clarify and correct the assertions made in the aforementioned critique. |
Cluster of Neisseria gonorrhoeae isolates with high-level azithromycin resistance and decreased ceftriaxone susceptibility, Hawaii, 2016.
Katz AR , Komeya AY , Kirkcaldy RD , Whelen AC , Soge OO , Papp JR , Kersh EN , Wasserman GM , O'Connor NP , O'Brien PS , Sato DT , Maningas EV , Kunimoto GY , Tomas JE . Clin Infect Dis 2017 65 (6) 918-923 ![]() ![]() Background.: The Centers for Disease Control and Prevention (CDC) currently recommends dual therapy with ceftriaxone and azithromycin for gonorrhea to ensure effective treatment and slow emergence of antimicrobial resistance. Since 2013, the prevalence of reduced azithromycin susceptibility increased in the United States; however, these strains were highly susceptible to cephalosporins. We report on a cluster of N. gonorrhoeae isolates demonstrating high-level azithromycin resistance, several of which also demonstrated decreased ceftriaxone susceptibility. Methods.: Eight N. gonorrhoeae isolates collected from 7 patients on Oahu seen 21 April through 10 May 2016 underwent routine Etest antimicrobial susceptibility testing by Hawaii Department of Health. All demonstrated elevated azithromycin minimum inhibitory concentrations (MICs) >256 mul/mL and elevated ceftriaxone MICs (≥0.125 mug/mL). Isolates were sent to University of Washington and CDC for confirmatory agar dilution testing, and sequence data were sent to CDC for analysis. All patients were interviewed and treated, and when possible, partners were interviewed, tested, and treated. Results.: All isolates had azithromycin MICs >16 microg/mL and 5 had ceftriaxone MICs = 0.125 microg/mL by agar dilution. All isolates were beta-lactamase positive, and were resistant to penicillin, tetracycline, and ciprofloxacin. Genomic analysis revealed genetic relatedness. No patients reported recent travel or antibiotic use and no male patients reported male sex partners. All patients were successfully treated. Conclusions.: This cluster of genetically related gonococcal isolates with decreased ceftriaxone susceptibility and high-level azithromycin resistance may bring the threat of treatment failure in the United States with the current recommended dual therapy one step closer. |
Azithromycin Resistance and Decreased Ceftriaxone Susceptibility in Neisseria gonorrhoeae, Hawaii, USA.
Papp JR , Abrams AJ , Nash E , Katz AR , Kirkcaldy RD , O'Connor NP , O'Brien PS , Harauchi DH , Maningas EV , Soge OO , Kersh EN , Komeya A , Tomas JE , Wasserman GM , Kunimoto GY , Trees DL , Whelen AC . Emerg Infect Dis 2017 23 (5) 830-832 ![]() During 2016, eight Neisseria gonorrhoeae isolates from 7 patients in Hawaii were resistant to azithromycin; 5 had decreased in vitro susceptibility to ceftriaxone. Genomic analysis demonstrated a distinct phylogenetic clade when compared with local contemporary strains. Continued evolution and widespread transmission of these strains might challenge the effectiveness of current therapeutic options. |
The global burden of injury: incidence, mortality, disability-adjusted life years and time trends from the Global Burden of Disease study 2013
Haagsma JA , Graetz N , Bolliger I , Naghavi M , Higashi H , Mullany EC , Abera SF , Abraham JP , Adofo K , Alsharif U , Ameh EA , Ammar W , Antonio CA , Barrero LH , Bekele T , Bose D , Brazinova A , Catala-Lopez F , Dandona L , Dandona R , Dargan PI , De Leo D , Degenhardt L , Derrett S , Dharmaratne SD , Driscoll TR , Duan L , Petrovich Ermakov S , Farzadfar F , Feigin VL , Franklin RC , Gabbe B , Gosselin RA , Hafezi-Nejad N , Hamadeh RR , Hijar M , Hu G , Jayaraman SP , Jiang G , Khader YS , Khan EA , Krishnaswami S , Kulkarni C , Lecky FE , Leung R , Lunevicius R , Lyons RA , Majdan M , Mason-Jones AJ , Matzopoulos R , Meaney PA , Mekonnen W , Miller TR , Mock CN , Norman RE , Orozco R , Polinder S , Pourmalek F , Rahimi-Movaghar V , Refaat A , Rojas-Rueda D , Roy N , Schwebel DC , Shaheen A , Shahraz S , Skirbekk V , Soreide K , Soshnikov S , Stein DJ , Sykes BL , Tabb KM , Temesgen AM , Tenkorang EY , Theadom AM , Tran BX , Vasankari TJ , Vavilala MS , Vlassov VV , Woldeyohannes SM , Yip P , Yonemoto N , Younis MZ , Yu C , Murray CJ , Vos T . Inj Prev 2015 22 (1) 3-18 BACKGROUND: The Global Burden of Diseases (GBD), Injuries, and Risk Factors study used the disability-adjusted life year (DALY) to quantify the burden of diseases, injuries, and risk factors. This paper provides an overview of injury estimates from the 2013 update of GBD, with detailed information on incidence, mortality, DALYs and rates of change from 1990 to 2013 for 26 causes of injury, globally, by region and by country. METHODS: Injury mortality was estimated using the extensive GBD mortality database, corrections for ill-defined cause of death and the cause of death ensemble modelling tool. Morbidity estimation was based on inpatient and outpatient data sets, 26 cause-of-injury and 47 nature-of-injury categories, and seven follow-up studies with patient-reported long-term outcome measures. RESULTS: In 2013, 973 million (uncertainty interval (UI) 942 to 993) people sustained injuries that warranted some type of healthcare and 4.8 million (UI 4.5 to 5.1) people died from injuries. Between 1990 and 2013 the global age-standardised injury DALY rate decreased by 31% (UI 26% to 35%). The rate of decline in DALY rates was significant for 22 cause-of-injury categories, including all the major injuries. CONCLUSIONS: Injuries continue to be an important cause of morbidity and mortality in the developed and developing world. The decline in rates for almost all injuries is so prominent that it warrants a general statement that the world is becoming a safer place to live in. However, the patterns vary widely by cause, age, sex, region and time and there are still large improvements that need to be made. |
Development and Evaluation of Three Real-time PCR Assays for Genotyping and Source Tracking Cryptosporidium in Water.
Li N , Neumann NF , Ruecker N , Alderisio KA , Sturbaum GD , Villegas EN , Chalmers R , Monis P , Feng Y , Xiao L . Appl Environ Microbiol 2015 81 (17) 5845-54 ![]() The occurrence of Cryptosporidium oocysts in drinking source water can present a serious public health risk. To rapidly and effectively assess the source and human-infective potential of Cryptosporidium oocysts in water, sensitive detection and correct identification of oocysts to the species level (genotyping) are essential. In this study, we developed three real-time PCR genotyping assays, two targeting the small subunit (SSU) rRNA gene (18S-LC1 and 18S-LC2 assays) and one targeting the 90 kDa heat shock protein (hsp90) gene (hsp90 assay), and evaluated the sensitivity and Cryptosporidium species detection range of these assays. Using fluorescence resonance energy transfer probes and melt curve analysis, the 18S-LC1 and hsp90 assay could differentiate common human-pathogenic species (C. parvum, C. hominis, and C. meleagridis), while the 18S-LC2 assay was able to differentiate non-pathogenic species (such as C. andersoni) from human-pathogenic ones commonly found in source water. In sensitivity evaluations, the 18S-LC2 and hsp90 genotyping assays could detect as few as one Cryptosporidium oocyst per sample. Thus, the 18S-LC2 and hsp90 genotyping assays might be used in environmental monitoring, whereas the 18S-LC1 genotyping assay could be useful for genotyping Cryptosporidium spp. in clinical specimens or wastewater samples. |
Comparison of whole genome sequences from human and non-human Escherichia coli O26 strains.
Norman KN , Clawson ML , Strockbine NA , Mandrell RE , Johnson R , Ziebell K , Zhao S , Fratamico PM , Stones R , Allard MW , Bono JL . Front Cell Infect Microbiol 2015 5 21 ![]() Shiga toxin-producing Escherichia coli (STEC) O26 is the second leading E. coli serogroup responsible for human illness outbreaks behind E. coli O157:H7. Recent outbreaks have been linked to emerging pathogenic O26:H11 strains harboring stx 2 only. Cattle have been recognized as an important reservoir of O26 strains harboring stx 1; however the reservoir of these emerging stx 2 strains is unknown. The objective of this study was to identify nucleotide polymorphisms in human and cattle-derived strains in order to compare differences in polymorphism derived genotypes and virulence gene profiles between the two host species. Whole genome sequencing was performed on 182 epidemiologically unrelated O26 strains, including 109 human-derived strains and 73 non-human-derived strains. A panel of 289 O26 strains (241 STEC and 48 non-STEC) was subsequently genotyped using a set of 283 polymorphisms identified by whole genome sequencing, resulting in 64 unique genotypes. Phylogenetic analyses identified seven clusters within the O26 strains. The seven clusters did not distinguish between isolates originating from humans or cattle; however, clusters did correspond with particular virulence gene profiles. Human and non-human-derived strains harboring stx 1 clustered separately from strains harboring stx 2, strains harboring eae, and non-STEC strains. Strains harboring stx 2 were more closely related to non-STEC strains and strains harboring eae than to strains harboring stx 1. The finding of human and cattle-derived strains with the same polymorphism derived genotypes and similar virulence gene profiles, provides evidence that similar strains are found in cattle and humans and transmission between the two species may occur. |
Filovirus RefSeq entries: evaluation and selection of filovirus type variants, type sequences, and names.
Kuhn JH , Andersen KG , Bao Y , Bavari S , Becker S , Bennett RS , Bergman NH , Blinkova O , Bradfute S , Brister JR , Bukreyev A , Chandran K , Chepurnov AA , Davey RA , Dietzgen RG , Doggett NA , Dolnik O , Dye JM , Enterlein S , Fenimore PW , Formenty P , Freiberg AN , Garry RF , Garza NL , Gire SK , Gonzalez JP , Griffiths A , Happi CT , Hensley LE , Herbert AS , Hevey MC , Hoenen T , Honko AN , Ignatyev GM , Jahrling PB , Johnson JC , Johnson KM , Kindrachuk J , Klenk HD , Kobinger G , Kochel TJ , Lackemeyer MG , Leroy EM , Lever MS , Muhlberger E , Netesov SV , Olinger GG , Omilabu SA , Palacios G , Panchal RG , Park DJ , Patterson JL , Paweska JT , Peters CJ , Pettitt J , Pitt L , Radoshitzky SR , Ryabchikova EI , Saphire EO , Sabeti PC , Sealfon R , Smither SJ , Sullivan NJ , Swanepoel R , Takada A , Towner JS , van der Groen G , Volchkov VE , Volchkova VA , Wahl-Jensen V , Warren TK , Warfield KL , Weidmann M , Nichol ST . Viruses 2014 6 (9) 3663-82 ![]() Sequence determination of complete or coding-complete genomes of viruses is becoming common practice for supporting the work of epidemiologists, ecologists, virologists, and taxonomists. Sequencing duration and costs are rapidly decreasing, sequencing hardware is under modification for use by non-experts, and software is constantly being improved to simplify sequence data management and analysis. Thus, analysis of virus disease outbreaks on the molecular level is now feasible, including characterization of the evolution of individual virus populations in single patients over time. The increasing accumulation of sequencing data creates a management problem for the curators of commonly used sequence databases and an entry retrieval problem for end users. Therefore, utilizing the data to their fullest potential will require setting nomenclature and annotation standards for virus isolates and associated genomic sequences. The National Center for Biotechnology Information's (NCBI's) RefSeq is a non-redundant, curated database for reference (or type) nucleotide sequence records that supplies source data to numerous other databases. Building on recently proposed templates for filovirus variant naming [<virus name> (<strain>)/<isolation host-suffix>/<country of sampling>/<year of sampling>/<genetic variant designation>-<isolate designation>], we report consensus decisions from a majority of past and currently active filovirus experts on the eight filovirus type variants and isolates to be represented in RefSeq, their final designations, and their associated sequences. |
Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data.
Holmes MV , Dale CE , Zuccolo L , Silverwood RJ , Guo Y , Ye Z , Prieto-Merino D , Dehghan A , Trompet S , Wong A , Cavadino A , Drogan D , Padmanabhan S , Li S , Yesupriya A , Leusink M , Sundstrom J , Hubacek JA , Pikhart H , Swerdlow DI , Panayiotou AG , Borinskaya SA , Finan C , Shah S , Kuchenbaecker KB , Shah T , Engmann J , Folkersen L , Eriksson P , Ricceri F , Melander O , Sacerdote C , Gamble DM , Rayaprolu S , Ross OA , McLachlan S , Vikhireva O , Sluijs I , Scott RA , Adamkova V , Flicker L , Bockxmeer FM , Power C , Marques-Vidal P , Meade T , Marmot MG , Ferro JM , Paulos-Pinheiro S , Humphries SE , Talmud PJ , Mateo Leach I , Verweij N , Linneberg A , Skaaby T , Doevendans PA , Cramer MJ , Harst Pv , Klungel OH , Dowling NF , Dominiczak AF , Kumari M , Nicolaides AN , Weikert C , Boeing H , Ebrahim S , Gaunt TR , Price JF , Lannfelt L , Peasey A , Kubinova R , Pajak A , Malyutina S , Voevoda MI , Tamosiunas A , Maitland-van der Zee AH , Norman PE , Hankey GJ , Bergmann MM , Hofman A , Franco OH , Cooper J , Palmen J , Spiering W , Jong PA , Kuh D , Hardy R , Uitterlinden AG , Ikram MA , Ford I , Hypponen E , Almeida OP , Wareham NJ , Khaw KT , Hamsten A , Husemoen LL , Tjonneland A , Tolstrup JS , Rimm E , Beulens JW , Verschuren WM , Onland-Moret NC , Hofker MH , Wannamethee SG , Whincup PH , Morris R , Vicente AM , Watkins H , Farrall M , Jukema JW , Meschia J , Cupples LA , Sharp SJ , Fornage M , Kooperberg C , LaCroix AZ , Dai JY , Lanktree MB , Siscovick DS , Jorgenson E , Spring B , Coresh J , Li YR , Buxbaum SG , Schreiner PJ , Ellison RC , Tsai MY , Patel SR , Redline S , Johnson AD , Hoogeveen RC , Hakonarson H , Rotter JI , Boerwinkle E , Bakker PI , Kivimaki M , Asselbergs FW , Sattar N , Lawlor DA , Whittaker J , Davey Smith G , Mukamal K , Psaty BM , Wilson JG , Lange LA , Hamidovic A , Hingorani AD , Nordestgaard BG , Bobak M , Leon DA , Langenberg C , Palmer TM , Reiner AP , Keating BJ , Dudbridge F , Casas JP . BMJ 2014 349 g4164 ![]() OBJECTIVE: To use the rs1229984 variant in the alcohol dehydrogenase 1B gene (ADH1B) as an instrument to investigate the causal role of alcohol in cardiovascular disease. DESIGN: Mendelian randomisation meta-analysis of 56 epidemiological studies. PARTICIPANTS: 261 991 individuals of European descent, including 20 259 coronary heart disease cases and 10 164 stroke events. Data were available on ADH1B rs1229984 variant, alcohol phenotypes, and cardiovascular biomarkers. MAIN OUTCOME MEASURES: Odds ratio for coronary heart disease and stroke associated with the ADH1B variant in all individuals and by categories of alcohol consumption. RESULTS: Carriers of the A-allele of ADH1B rs1229984 consumed 17.2% fewer units of alcohol per week (95% confidence interval 15.6% to 18.9%), had a lower prevalence of binge drinking (odds ratio 0.78 (95% CI 0.73 to 0.84)), and had higher abstention (odds ratio 1.27 (1.21 to 1.34)) than non-carriers. Rs1229984 A-allele carriers had lower systolic blood pressure (-0.88 (-1.19 to -0.56) mm Hg), interleukin-6 levels (-5.2% (-7.8 to -2.4%)), waist circumference (-0.3 (-0.6 to -0.1) cm), and body mass index (-0.17 (-0.24 to -0.10) kg/m(2)). Rs1229984 A-allele carriers had lower odds of coronary heart disease (odds ratio 0.90 (0.84 to 0.96)). The protective association of the ADH1B rs1229984 A-allele variant remained the same across all categories of alcohol consumption (P=0.83 for heterogeneity). Although no association of rs1229984 was identified with the combined subtypes of stroke, carriers of the A-allele had lower odds of ischaemic stroke (odds ratio 0.83 (0.72 to 0.95)). CONCLUSIONS: Individuals with a genetic variant associated with non-drinking and lower alcohol consumption had a more favourable cardiovascular profile and a reduced risk of coronary heart disease than those without the genetic variant. This suggests that reduction of alcohol consumption, even for light to moderate drinkers, is beneficial for cardiovascular health. |
Microneedle patches: usability and acceptability for self-vaccination against influenza
Norman JJ , Arya JM , McClain MA , Frew PM , Meltzer MI , Prausnitz MR . Vaccine 2014 32 (16) 1856-62 While therapeutic drugs are routinely self-administered by patients, there is little precedent for self-vaccination. Convenient self-vaccination may expand vaccination coverage and reduce administration costs. Microneedle patches are in development for many vaccines, but no reports exist on usability or acceptability. We hypothesized that naive patients could apply patches and that self-administered patches would improve stated intent to receive an influenza vaccine. We conducted a randomized, repeated measures study with 91 venue-recruited adults. To simulate vaccination, subjects received placebo microneedle patches given three times by self-administration and once by the investigator, as well as an intramuscular injection of saline. Seventy participants inserted patches with thumb pressure alone and the remainder used snap-based devices that closed shut at a certain force. Usability was assessed by skin staining and acceptability was measured with an adaptive-choice analysis. The best usability was seen with the snap device, with users inserting a median value of 93-96% of microneedles over three repetitions. When a self-administered microneedle patch was offered, intent to vaccinate increased from 44% to 65% (CI: 55-74%). The majority of those intending vaccination would prefer to self-vaccinate: 64% (CI: 51-75%). There were no serious adverse events associated with use of microneedle patches. The findings from this initial study indicate that microneedle patches for self-vaccination against influenza are usable and may lead to improved vaccination coverage. |
Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010
Vos Theo , Flaxman Abraham D , Naghavi Mohsen , Lozano Rafael , Michaud Catherine , Ezzati Majid , Shibuya Kenji , Salomon Joshua A , Abdalla Safa , Aboyans Victor , Abraham Jerry , Ackerman Ilana , Aggarwal Rakesh , Ahn Stephanie Y , Ali Mohammed K , Alvarado Miriam , Anderson H Ross , Anderson Laurie M , Andrews Kathryn G , Atkinson Charles , Baddour Larry M , Bahalim Adil N , Barker-Collo Suzanne , Barrero Lope H , Bartels David H , Basanez Maria-Gloria , Baxter Amanda , Bell Michelle L , Benjamin Emelia J , Bennett Derrick , Bernabe Eduardo , Bhalla Kavi , Bhandari Bishal , Bikbov Boris , Bin Abdulhak Aref , Birbeck Gretchen , Black James A , Blencowe Hannah , Blore Jed D , Blyth Fiona , Bolliger Ian , Bonaventure Audrey , Boufous Soufiane , Bourne Rupert , Boussinesq Michel , Braithwaite Tasanee , Brayne Carol , Bridgett Lisa , Brooker Simon , Brooks Peter , Brugha Traolach S , Bryan-Hancock Claire , Bucello Chiara , Buchbinder Rachelle , Buckle Geoffrey , Budke Christine M , Burch Michael , Burney Peter , Burstein Roy , Calabria Bianca , Campbell Benjamin , Canter Charles E , Carabin Helene , Carapetis Jonathan , Carmona Loreto , Cella Claudia , Charlson Fiona , Chen Honglei , Cheng Andrew Tai-Ann , Chou David , Chugh Sumeet S , Coffeng Luc E , Colan Steven D , Colquhoun Samantha , Colson K Ellicott , Condon John , Connor Myles D , Cooper Leslie T , Corriere Matthew , Cortinovis Monica , de Vaccaro Karen Courville , Couser William , Cowie Benjamin C , Criqui Michael H , Cross Marita , Dabhadkar Kaustubh C , Dahiya Manu , Dahodwala Nabila , Damsere-Derry James , Danaei Goodarz , Davis Adrian , De Leo Diego , Degenhardt Louisa , Dellavalle Robert , Delossantos Allyne , Denenberg Julie , Derrett Sarah , Des Jarlais Don C , Dharmaratne Samath D , Dherani Mukesh , Diaz-Torne Cesar , Dolk Helen , Dorsey E Ray , Driscoll Tim , Duber Herbert , Ebel Beth , Edmond Karen , Elbaz Alexis , Ali Suad Eltahir , Erskine Holly , Erwin Patricia J , Espindola Patricia , Ewoigbokhan Stalin E , Farzadfar Farshad , Feigin Valery , Felson David T , Ferrari Alize , Ferri Cleusa P , Fevre Eric M , Finucane Mariel M , Flaxman Seth , Flood Louise , Foreman Kyle , Forouzanfar Mohammad H , Fowkes Francis Gerry R , Franklin Richard , Fransen Marlene , Freeman Michael K , Gabbe Belinda J , Gabriel Sherine E , Gakidou Emmanuela , Ganatra Hammad A , Garcia Bianca , Gaspari Flavio , Gillum Richard F , Gmel Gerhard , Gosselin Richard , Grainger Rebecca , Groeger Justina , Guillemin Francis , Gunnell David , Gupta Ramyani , Haagsma Juanita , Hagan Holly , Halasa Yara A , Hall Wayne , Haring Diana , Haro Josep Maria , Harrison James E , Havmoeller Rasmus , Hay Roderick J , Higashi Hideki , Hill Catherine , Hoen Bruno , Hoffman Howard , Hotez Peter J , Hoy Damian , Huang John J , Ibeanusi Sydney E , Jacobsen Kathryn H , James Spencer L , Jarvis Deborah , Jasrasaria Rashmi , Jayaraman Sudha , Johns Nicole , Jonas Jost B , Karthikeyan Ganesan , Kassebaum Nicholas , Kawakami Norito , Keren Andre , Khoo Jon-Paul , King Charles H , Knowlton Lisa Marie , Kobusingye Olive , Koranteng Adofo , Krishnamurthi Rita , Lalloo Ratilal , Laslett Laura L , Lathlean Tim , Leasher Janet L , Lee Yong Yi , Leigh James , Lim Stephen S , Limb Elizabeth , Lin John Kent , Lipnick Michael , Lipshultz Steven E , Liu Wei , Loane Maria , Ohno Summer Lockett , Lyons Ronan , Ma Jixiang , Mabweijano Jacqueline , MacIntyre Michael F , Malekzadeh Reza , Mallinger Leslie , Manivannan Sivabalan , Marcenes Wagner , March Lyn , Margolis David J , Marks Guy B , Marks Robin , Matsumori Akira , Matzopoulos Richard , Mayosi Bongani M , McAnulty John H , McDermott Mary M , McGill Neil , McGrath John , Medina-Mora Maria Elena , Meltzer Michele , Mensah George A , Merriman Tony R , Meyer Ana-Claire , Miglioli Valeria , Miller Matthew , Miller Ted R , Mitchell Philip B , Mocumbi Ana Olga , Moffitt Terrie E , Mokdad Ali A , Monasta Lorenzo , Montico Marcella , Moradi-Lakeh Maziar , Moran Andrew , Morawska Lidia , Mori Rintaro , Murdoch Michele E , Mwaniki Michael K , Naidoo Kovin , Nair M Nathan , Naldi Luigi , Narayan K M Venkat , Nelson Paul K , Nelson Robert G , Nevitt Michael C , Newton Charles R , Nolte Sandra , Norman Paul , Norman Rosana , O'Donnell Martin , O'Hanlon Simon , Olives Casey , Omer Saad B , Ortblad Katrina , Osborne Richard , Ozgediz Doruk , Page Andrew , Pahari Bishnu , Pandian Jeyaraj Durai , Rivero Andrea Panozo , Patten Scott B , Pearce Neil , Padilla Rogelio Perez , Perez-Ruiz Fernando , Perico Norberto , Pesudovs Konrad , Phillips David , Phillips Michael R , Pierce Kelsey , Pion Sebastien , Polanczyk Guilherme V , Polinder Suzanne , Pope C Arden 3rd , Popova Svetlana , Porrini Esteban , Pourmalek Farshad , Prince Martin , Pullan Rachel L , Ramaiah Kapa D , Ranganathan Dharani , Razavi Homie , Regan Mathilda , Rehm Jurgen T , Rein David B , Remuzzi Guiseppe , Richardson Kathryn , Rivara Frederick P , Roberts Thomas , Robinson Carolyn , De Leon Felipe Rodriguez , Ronfani Luca , Room Robin , Rosenfeld Lisa C , Rushton Lesley , Sacco Ralph L , Saha Sukanta , Sampson Uchechukwu , Sanchez-Riera Lidia , Sanman Ella , Schwebel David C , Scott James Graham , Segui-Gomez Maria , Shahraz Saeid , Shepard Donald S , Shin Hwashin , Shivakoti Rupak , Singh David , Singh Gitanjali M , Singh Jasvinder A , Singleton Jessica , Sleet David A , Sliwa Karen , Smith Emma , Smith Jennifer L , Stapelberg Nicolas J C , Steer Andrew , Steiner Timothy , Stolk Wilma A , Stovner Lars Jacob , Sudfeld Christopher , Syed Sana , Tamburlini Giorgio , Tavakkoli Mohammad , Taylor Hugh R , Taylor Jennifer A , Taylor William J , Thomas Bernadette , Thomson W Murray , Thurston George D , Tleyjeh Imad M , Tonelli Marcello , Towbin Jeffrey A , Truelsen Thomas , Tsilimbaris Miltiadis K , Ubeda Clotilde , Undurraga Eduardo A , van der Werf Marieke J , van Os Jim , Vavilala Monica S , Venketasubramanian N , Wang Mengru , Wang Wenzhi , Watt Kerrianne , Weatherall David J , Weinstock Martin A , Weintraub Robert , Weisskopf Marc G , Weissman Myrna M , White Richard A , Whiteford Harvey , Wiersma Steven T , Wilkinson James D , Williams Hywel C , Williams Sean R M , Witt Emma , Wolfe Frederick , Woolf Anthony D , Wulf Sarah , Yeh Pon-Hsiu , Zaidi Anita K M , Zheng Zhi-Jie , Zonies David , Lopez Alan D , Murray Christopher J L , Global Burden of Disease Study 2010 . Lancet 2013 380 (9859) 2163-96 ![]() BACKGROUND: Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). METHODS: Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. FINDINGS: Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350,000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient -0.37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. INTERPRETATION: Rates of YLDs per 100,000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. FUNDING: Bill & Melinda Gates Foundation. |
A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010
Lim Stephen S , Vos Theo , Flaxman Abraham D , Danaei Goodarz , Shibuya Kenji , Adair-Rohani Heather , Amann Markus , Anderson H Ross , Andrews Kathryn G , Aryee Martin , Atkinson Charles , Bacchus Loraine J , Bahalim Adil N , Balakrishnan Kalpana , Balmes John , Barker-Collo Suzanne , Baxter Amanda , Bell Michelle L , Blore Jed D , Blyth Fiona , Bonner Carissa , Borges Guilherme , Bourne Rupert , Boussinesq Michel , Brauer Michael , Brooks Peter , Bruce Nigel G , Brunekreef Bert , Bryan-Hancock Claire , Bucello Chiara , Buchbinder Rachelle , Bull Fiona , Burnett Richard T , Byers Tim E , Calabria Bianca , Carapetis Jonathan , Carnahan Emily , Chafe Zoe , Charlson Fiona , Chen Honglei , Chen Jian Shen , Cheng Andrew Tai-Ann , Child Jennifer Christine , Cohen Aaron , Colson K Ellicott , Cowie Benjamin C , Darby Sarah , Darling Susan , Davis Adrian , Degenhardt Louisa , Dentener Frank , Des Jarlais Don C , Devries Karen , Dherani Mukesh , Ding Eric L , Dorsey E Ray , Driscoll Tim , Edmond Karen , Ali Suad Eltahir , Engell Rebecca E , Erwin Patricia J , Fahimi Saman , Falder Gail , Farzadfar Farshad , Ferrari Alize , Finucane Mariel M , Flaxman Seth , Fowkes Francis Gerry R , Freedman Greg , Freeman Michael K , Gakidou Emmanuela , Ghosh Santu , Giovannucci Edward , Gmel Gerhard , Graham Kathryn , Grainger Rebecca , Grant Bridget , Gunnell David , Gutierrez Hialy R , Hall Wayne , Hoek Hans W , Hogan Anthony , Hosgood H Dean 3rd , Hoy Damian , Hu Howard , Hubbell Bryan J , Hutchings Sally J , Ibeanusi Sydney E , Jacklyn Gemma L , Jasrasaria Rashmi , Jonas Jost B , Kan Haidong , Kanis John A , Kassebaum Nicholas , Kawakami Norito , Khang Young-Ho , Khatibzadeh Shahab , Khoo Jon-Paul , Kok Cindy , Laden Francine , Lalloo Ratilal , Lan Qing , Lathlean Tim , Leasher Janet L , Leigh James , Li Yang , Lin John Kent , Lipshultz Steven E , London Stephanie , Lozano Rafael , Lu Yuan , Mak Joelle , Malekzadeh Reza , Mallinger Leslie , Marcenes Wagner , March Lyn , Marks Robin , Martin Randall , McGale Paul , McGrath John , Mehta Sumi , Mensah George A , Merriman Tony R , Micha Renata , Michaud Catherine , Mishra Vinod , Hanafiah Khayriyyah Mohd , Mokdad Ali A , Morawska Lidia , Mozaffarian Dariush , Murphy Tasha , Naghavi Mohsen , Neal Bruce , Nelson Paul K , Nolla Joan Miquel , Norman Rosana , Olives Casey , Omer Saad B , Orchard Jessica , Osborne Richard , Ostro Bart , Page Andrew , Pandey Kiran D , Parry Charles D H , Passmore Erin , Patra Jayadeep , Pearce Neil , Pelizzari Pamela M , Petzold Max , Phillips Michael R , Pope Dan , Pope C Arden 3rd , Powles John , Rao Mayuree , Razavi Homie , Rehfuess Eva A , Rehm Jurgen T , Ritz Beate , Rivara Frederick P , Roberts Thomas , Robinson Carolyn , Rodriguez-Portales Jose A , Romieu Isabelle , Room Robin , Rosenfeld Lisa C , Roy Ananya , Rushton Lesley , Salomon Joshua A , Sampson Uchechukwu , Sanchez-Riera Lidia , Sanman Ella , Sapkota Amir , Seedat Soraya , Shi Peilin , Shield Kevin , Shivakoti Rupak , Singh Gitanjali M , Sleet David A , Smith Emma , Smith Kirk R , Stapelberg Nicolas J C , Steenland Kyle , Stockl Heidi , Stovner Lars Jacob , Straif Kurt , Straney Lahn , Thurston George D , Tran Jimmy H , Van Dingenen Rita , van Donkelaar Aaron , Veerman J Lennert , Vijayakumar Lakshmi , Weintraub Robert , Weissman Myrna M , White Richard A , Whiteford Harvey , Wiersma Steven T , Wilkinson James D , Williams Hywel C , Williams Warwick , Wilson Nicholas , Woolf Anthony D , Yip Paul , Zielinski Jan M , Lopez Alan D , Murray Christopher J L , Ezzati Majid , Global Burden of Disease Study 2010 . Lancet 2013 380 (9859) 2224-60 BACKGROUND: Quantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time. METHODS: We estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden. FINDINGS: In 2010, the three leading risk factors for global disease burden were high blood pressure (7.0% [95% uncertainty interval 6.2-7.7] of global DALYs), tobacco smoking including second-hand smoke (6.3% [5.5-7.0]), and alcohol use (5.5% [5.0-5.9]). In 1990, the leading risks were childhood underweight (7.9% [6.8-9.4]), household air pollution from solid fuels (HAP; 7.0% [5.6-8.3]), and tobacco smoking including second-hand smoke (6.1% [5.4-6.8]). Dietary risk factors and physical inactivity collectively accounted for 10.0% (95% UI 9.2-10.8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water and sanitation accounting for 0.9% (0.4-1.6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, most of Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania. INTERPRETATION: Worldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children. FUNDING: Bill & Melinda Gates Foundation. |
Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010
Murray Christopher J L , Vos Theo , Lozano Rafael , Naghavi Mohsen , Flaxman Abraham D , Michaud Catherine , Ezzati Majid , Shibuya Kenji , Salomon Joshua A , Abdalla Safa , Aboyans Victor , Abraham Jerry , Ackerman Ilana , Aggarwal Rakesh , Ahn Stephanie Y , Ali Mohammed K , Alvarado Miriam , Anderson H Ross , Anderson Laurie M , Andrews Kathryn G , Atkinson Charles , Baddour Larry M , Bahalim Adil N , Barker-Collo Suzanne , Barrero Lope H , Bartels David H , Basanez Maria-Gloria , Baxter Amanda , Bell Michelle L , Benjamin Emelia J , Bennett Derrick , Bernabe Eduardo , Bhalla Kavi , Bhandari Bishal , Bikbov Boris , Bin Abdulhak Aref , Birbeck Gretchen , Black James A , Blencowe Hannah , Blore Jed D , Blyth Fiona , Bolliger Ian , Bonaventure Audrey , Boufous Soufiane , Bourne Rupert , Boussinesq Michel , Braithwaite Tasanee , Brayne Carol , Bridgett Lisa , Brooker Simon , Brooks Peter , Brugha Traolach S , Bryan-Hancock Claire , Bucello Chiara , Buchbinder Rachelle , Buckle Geoffrey , Budke Christine M , Burch Michael , Burney Peter , Burstein Roy , Calabria Bianca , Campbell Benjamin , Canter Charles E , Carabin Helene , Carapetis Jonathan , Carmona Loreto , Cella Claudia , Charlson Fiona , Chen Honglei , Cheng Andrew Tai-Ann , Chou David , Chugh Sumeet S , Coffeng Luc E , Colan Steven D , Colquhoun Samantha , Colson K Ellicott , Condon John , Connor Myles D , Cooper Leslie T , Corriere Matthew , Cortinovis Monica , de Vaccaro Karen Courville , Couser William , Cowie Benjamin C , Criqui Michael H , Cross Marita , Dabhadkar Kaustubh C , Dahiya Manu , Dahodwala Nabila , Damsere-Derry James , Danaei Goodarz , Davis Adrian , De Leo Diego , Degenhardt Louisa , Dellavalle Robert , Delossantos Allyne , Denenberg Julie , Derrett Sarah , Des Jarlais Don C , Dharmaratne Samath D , Dherani Mukesh , Diaz-Torne Cesar , Dolk Helen , Dorsey E Ray , Driscoll Tim , Duber Herbert , Ebel Beth , Edmond Karen , Elbaz Alexis , Ali Suad Eltahir , Erskine Holly , Erwin Patricia J , Espindola Patricia , Ewoigbokhan Stalin E , Farzadfar Farshad , Feigin Valery , Felson David T , Ferrari Alize , Ferri Cleusa P , Fevre Eric M , Finucane Mariel M , Flaxman Seth , Flood Louise , Foreman Kyle , Forouzanfar Mohammad H , Fowkes Francis Gerry R , Fransen Marlene , Freeman Michael K , Gabbe Belinda J , Gabriel Sherine E , Gakidou Emmanuela , Ganatra Hammad A , Garcia Bianca , Gaspari Flavio , Gillum Richard F , Gmel Gerhard , Gonzalez-Medina Diego , Gosselin Richard , Grainger Rebecca , Grant Bridget , Groeger Justina , Guillemin Francis , Gunnell David , Gupta Ramyani , Haagsma Juanita , Hagan Holly , Halasa Yara A , Hall Wayne , Haring Diana , Haro Josep Maria , Harrison James E , Havmoeller Rasmus , Hay Roderick J , Higashi Hideki , Hill Catherine , Hoen Bruno , Hoffman Howard , Hotez Peter J , Hoy Damian , Huang John J , Ibeanusi Sydney E , Jacobsen Kathryn H , James Spencer L , Jarvis Deborah , Jasrasaria Rashmi , Jayaraman Sudha , Johns Nicole , Jonas Jost B , Karthikeyan Ganesan , Kassebaum Nicholas , Kawakami Norito , Keren Andre , Khoo Jon-Paul , King Charles H , Knowlton Lisa Marie , Kobusingye Olive , Koranteng Adofo , Krishnamurthi Rita , Laden Francine , Lalloo Ratilal , Laslett Laura L , Lathlean Tim , Leasher Janet L , Lee Yong Yi , Leigh James , Levinson Daphna , Lim Stephen S , Limb Elizabeth , Lin John Kent , Lipnick Michael , Lipshultz Steven E , Liu Wei , Loane Maria , Ohno Summer Lockett , Lyons Ronan , Mabweijano Jacqueline , MacIntyre Michael F , Malekzadeh Reza , Mallinger Leslie , Manivannan Sivabalan , Marcenes Wagner , March Lyn , Margolis David J , Marks Guy B , Marks Robin , Matsumori Akira , Matzopoulos Richard , Mayosi Bongani M , McAnulty John H , McDermott Mary M , McGill Neil , McGrath John , Medina-Mora Maria Elena , Meltzer Michele , Mensah George A , Merriman Tony R , Meyer Ana-Claire , Miglioli Valeria , Miller Matthew , Miller Ted R , Mitchell Philip B , Mock Charles , Mocumbi Ana Olga , Moffitt Terrie E , Mokdad Ali A , Monasta Lorenzo , Montico Marcella , Moradi-Lakeh Maziar , Moran Andrew , Morawska Lidia , Mori Rintaro , Murdoch Michele E , Mwaniki Michael K , Naidoo Kovin , Nair M Nathan , Naldi Luigi , Narayan K M Venkat , Nelson Paul K , Nelson Robert G , Nevitt Michael C , Newton Charles R , Nolte Sandra , Norman Paul , Norman Rosana , O'Donnell Martin , O'Hanlon Simon , Olives Casey , Omer Saad B , Ortblad Katrina , Osborne Richard , Ozgediz Doruk , Page Andrew , Pahari Bishnu , Pandian Jeyaraj Durai , Rivero Andrea Panozo , Patten Scott B , Pearce Neil , Padilla Rogelio Perez , Perez-Ruiz Fernando , Perico Norberto , Pesudovs Konrad , Phillips David , Phillips Michael R , Pierce Kelsey , Pion Sebastien , Polanczyk Guilherme V , Polinder Suzanne , Pope C Arden 3rd , Popova Svetlana , Porrini Esteban , Pourmalek Farshad , Prince Martin , Pullan Rachel L , Ramaiah Kapa D , Ranganathan Dharani , Razavi Homie , Regan Mathilda , Rehm Jurgen T , Rein David B , Remuzzi Guiseppe , Richardson Kathryn , Rivara Frederick P , Roberts Thomas , Robinson Carolyn , De Leon Felipe Rodriguez , Ronfani Luca , Room Robin , Rosenfeld Lisa C , Rushton Lesley , Sacco Ralph L , Saha Sukanta , Sampson Uchechukwu , Sanchez-Riera Lidia , Sanman Ella , Schwebel David C , Scott James Graham , Segui-Gomez Maria , Shahraz Saeid , Shepard Donald S , Shin Hwashin , Shivakoti Rupak , Singh David , Singh Gitanjali M , Singh Jasvinder A , Singleton Jessica , Sleet David A , Sliwa Karen , Smith Emma , Smith Jennifer L , Stapelberg Nicolas J C , Steer Andrew , Steiner Timothy , Stolk Wilma A , Stovner Lars Jacob , Sudfeld Christopher , Syed Sana , Tamburlini Giorgio , Tavakkoli Mohammad , Taylor Hugh R , Taylor Jennifer A , Taylor William J , Thomas Bernadette , Thomson W Murray , Thurston George D , Tleyjeh Imad M , Tonelli Marcello , Towbin Jeffrey A , Truelsen Thomas , Tsilimbaris Miltiadis K , Ubeda Clotilde , Undurraga Eduardo A , van der Werf Marieke J , van Os Jim , Vavilala Monica S , Venketasubramanian N , Wang Mengru , Wang Wenzhi , Watt Kerrianne , Weatherall David J , Weinstock Martin A , Weintraub Robert , Weisskopf Marc G , Weissman Myrna M , White Richard A , Whiteford Harvey , Wiebe Natasha , Wiersma Steven T , Wilkinson James D , Williams Hywel C , Williams Sean R M , Witt Emma , Wolfe Frederick , Woolf Anthony D , Wulf Sarah , Yeh Pon-Hsiu , Zaidi Anita K M , Zheng Zhi-Jie , Zonies David , Lopez Alan D , Global Burden of Disease Study 2010 . Lancet 2013 380 (9859) 2197-223 BACKGROUND: Measuring disease and injury burden in populations requires a composite metric that captures both premature mortality and the prevalence and severity of ill-health. The 1990 Global Burden of Disease study proposed disability-adjusted life years (DALYs) to measure disease burden. No comprehensive update of disease burden worldwide incorporating a systematic reassessment of disease and injury-specific epidemiology has been done since the 1990 study. We aimed to calculate disease burden worldwide and for 21 regions for 1990, 2005, and 2010 with methods to enable meaningful comparisons over time. METHODS: We calculated DALYs as the sum of years of life lost (YLLs) and years lived with disability (YLDs). DALYs were calculated for 291 causes, 20 age groups, both sexes, and for 187 countries, and aggregated to regional and global estimates of disease burden for three points in time with strictly comparable definitions and methods. YLLs were calculated from age-sex-country-time-specific estimates of mortality by cause, with death by standardised lost life expectancy at each age. YLDs were calculated as prevalence of 1160 disabling sequelae, by age, sex, and cause, and weighted by new disability weights for each health state. Neither YLLs nor YLDs were age-weighted or discounted. Uncertainty around cause-specific DALYs was calculated incorporating uncertainty in levels of all-cause mortality, cause-specific mortality, prevalence, and disability weights. FINDINGS: Global DALYs remained stable from 1990 (2.503 billion) to 2010 (2.490 billion). Crude DALYs per 1000 decreased by 23% (472 per 1000 to 361 per 1000). An important shift has occurred in DALY composition with the contribution of deaths and disability among children (younger than 5 years of age) declining from 41% of global DALYs in 1990 to 25% in 2010. YLLs typically account for about half of disease burden in more developed regions (high-income Asia Pacific, western Europe, high-income North America, and Australasia), rising to over 80% of DALYs in sub-Saharan Africa. In 1990, 47% of DALYs worldwide were from communicable, maternal, neonatal, and nutritional disorders, 43% from non-communicable diseases, and 10% from injuries. By 2010, this had shifted to 35%, 54%, and 11%, respectively. Ischaemic heart disease was the leading cause of DALYs worldwide in 2010 (up from fourth rank in 1990, increasing by 29%), followed by lower respiratory infections (top rank in 1990; 44% decline in DALYs), stroke (fifth in 1990; 19% increase), diarrhoeal diseases (second in 1990; 51% decrease), and HIV/AIDS (33rd in 1990; 351% increase). Major depressive disorder increased from 15th to 11th rank (37% increase) and road injury from 12th to 10th rank (34% increase). Substantial heterogeneity exists in rankings of leading causes of disease burden among regions. INTERPRETATION: Global disease burden has continued to shift away from communicable to non-communicable diseases and from premature death to years lived with disability. In sub-Saharan Africa, however, many communicable, maternal, neonatal, and nutritional disorders remain the dominant causes of disease burden. The rising burden from mental and behavioural disorders, musculoskeletal disorders, and diabetes will impose new challenges on health systems. Regional heterogeneity highlights the importance of understanding local burden of disease and setting goals and targets for the post-2015 agenda taking such patterns into account. Because of improved definitions, methods, and data, these results for 1990 and 2010 supersede all previously published Global Burden of Disease results. FUNDING: Bill & Melinda Gates Foundation. |
Association of nucleotide polymorphisms within the O-antigen gene cluster of Escherichia coli O26, O45, O103, O111, O121, and O145 with serogroups and genetic subtypes.
Norman KN , Strockbine NA , Bono JL . Appl Environ Microbiol 2012 78 (18) 6689-703 ![]() Shiga toxin-producing Escherichia coli (STEC) strains are important food-borne pathogens capable of causing hemolytic-uremic syndrome. STEC O157:H7 strains cause the majority of severe disease in the United States; however, there is a growing concern for the amount and severity of illness attributable to non-O157 STEC. Recently, the Food Safety and Inspection Service (FSIS) published the intent to regulate the presence of STEC belonging to serogroups O26, O45, O103, O111, O121, and O145 in nonintact beef products. To ensure the effective control of these bacteria, sensitive and specific tests for their detection will be needed. In this study, we identified single nucleotide polymorphisms (SNPs) in the O-antigen gene cluster that could be used to detect STEC strains of the above-described serogroups. Using comparative DNA sequence analysis, we identified 22 potentially informative SNPs among 164 STEC and non-STEC strains of the above-described serogroups and designed matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) assays to test the STEC allele frequencies in an independent panel of bacterial strains. We found at least one SNP that was specific to each serogroup and also differentiated between STEC and non-STEC strains. Differences in the DNA sequence of the O-antigen gene cluster corresponded well with differences in the virulence gene profiles and provided evidence of different lineages for STEC and non-STEC strains. The SNPs discovered in this study can be used to develop tests that will not only accurately identify O26, O45, O103, O111, O121, and O145 strains but also predict whether strains detected in the above-described serogroups contain Shiga toxin-encoding genes. |
Oral contraceptive formulation and risk of breast cancer
Marchbanks PA , Curtis KM , Mandel MG , Wilson HG , Jeng G , Folger SG , McDonald JA , Daling JR , Bernstein L , Malone KE , Wingo PA , Simon MS , Norman SA , Strom BL , Ursin G , Weiss LK , Burkman RT , Spirtas R . Contraception 2011 85 (4) 342-50 BACKGROUND: While evidence on the association between oral contraceptive (OC) use and breast cancer generally suggests little or no increased risk, the question of whether breast cancer risk varies by OC formulation remains controversial. Few studies have examined this issue because large samples and extensive OC histories are required. STUDY DESIGN: We used data from a multicenter, population-based, case-control investigation. Women aged 35-64 years were interviewed. To explore the association between OC formulation and breast cancer risk, we used conditional logistic regression to derive adjusted odds ratios, and we used likelihood ratio tests for heterogeneity to assess whether breast cancer risk varied by OC formulation. Key OC exposure variables were ever use, current or former use, duration of use and time since last use. To strengthen inferences about specific formulations, we restricted most analyses to the 2282 women with breast cancer and the 2424 women without breast cancer who reported no OC use or exclusive use of one OC. RESULTS: Thirty-eight formulations were reported by the 2674 women who used one OC; most OC formulations were used by only a few women. We conducted multivariable analyses on the 10 formulations that were each used by at least 50 women and conducted supplemental analyses on selected formulations of interest based on recent research. Breast cancer risk did not vary significantly by OC formulation, and no formulation was associated with a significantly increased breast cancer risk. CONCLUSIONS: These results add to the small body of literature on the relationship between OC formulation and breast cancer. Our data are reassuring in that, among women 35-64 years of age, we found no evidence that specific OC formulations increase breast cancer risk. |
Oral contraceptive use and survival in women with invasive breast cancer
Lu Y , Ma H , Malone KE , Norman SA , Sullivan-Halley J , Strom BL , Simon MS , Marchbanks PA , McDonald JA , West DW , Henderson KD , Deapen D , Ursin G , Bernstein L . Cancer Epidemiol Biomarkers Prev 2011 20 (7) 1391-7 BACKGROUND: Oral contraceptives (OC) are widely used in the United States. Although the relation between OC use and breast cancer incidence has been widely studied, the few studies examining associations between OC use prior to breast cancer diagnosis and survival are inconsistent. METHODS: Women with invasive breast cancer participating in the Women's Contraceptive and Reproductive Experiences (CARE) Study, a population-based case-control study (4565 women ages 35-64 years), and the California Teachers Study (CTS) cohort (3929 women ages 28-91 years) were followed for vital status. A total of 1,064 women died in the CARE Study (median follow-up, 8.6 years) and 523 died in the CTS (median follow-up, 6.1 years). Cox proportional hazards regression provided hazard rate ratio estimates [(relative risk, RR)] with 95% confidence intervals (CIs) for risk of death from any cause and from breast cancer. RESULTS: No association was observed for any OC use prior to diagnosis and all-cause mortality [CARE Study: RR = 1.01 (95% CI = 0.86-1.19); CTS: RR = 0.84 (95% CI = 0.67-1.05)]. A decreased risk of all-cause mortality was observed in the CTS among women with more than 10 years of OC use (RR = 0.67, 95% CI = 0.47-0.96); however, no trend of decreasing risk with increasing OC duration was observed (P(trend) = 0.22), and no association was observed in the CARE study. No associations were observed for breast cancer-specific mortality. CONCLUSIONS: OC use is not associated with all-cause or breast cancer-specific mortality among women with invasive breast cancer. IMPACT: These 2 independent studies demonstrated no overall association between OC use and survival among women with breast cancer. Cancer Epidemiol Biomarkers Prev; 20(7); 1391-7. (c)2011 AACR. |
Obesity and survival among black women and white women 35 to 64 years of age at diagnosis with invasive breast cancer
Lu Y , Ma H , Malone KE , Norman SA , Sullivan-Halley J , Strom BL , Marchbanks PA , Spirtas R , Burkman RT , Deapen D , Folger SG , Simon MS , Press MF , McDonald JA , Bernstein L . J Clin Oncol 2011 29 (25) 3358-65 PURPOSE: To evaluate the effect of obesity on survival among black women and white women with invasive breast cancer and to determine whether obesity explains the poorer survival of black women relative to white women. PATIENTS AND METHODS: We observed 4,538 (1,604 black, 2,934 white) women who were 35 to 64 years of age when diagnosed with incident invasive breast cancer between 1994 and 1998. Multivariate Cox regression models were used to examine the effect of body mass index (BMI, in kilograms per square meter) 5 years before diagnosis on risk of death from any cause and from breast cancer. RESULTS: During a median of 8.6 years of follow-up, 1,053 women died (519 black, 534 white), 828 as a result of breast cancer (412 black, 416 white). Black women were more likely to die than white women (multivariate-adjusted relative risk [RR], 1.33; 95% CI, 1.16 to 1.53). Compared with women with BMI of 20 to 24.9 kg/m(2), those who were obese (BMI ≥ 30 kg/m(2)) had a greater risk of all-cause mortality (RR, 1.23; 95% CI, 1.04 to 1.47) and breast cancer-specific mortality (RR, 1.20; 95% CI, 0.99 to 1.46). These associations were observed among white women (all-cause RR, 1.54; 95% CI, 1.21 to 1.96; breast cancer RR, 1.46; 95% CI, 1.11 to 1.92), but not among black women (all-cause RR, 1.03; 95% CI, 0.81 to 1.29; breast cancer RR, 1.02; 95% CI, 0.79 to 1.33). CONCLUSION: Obesity may play an important role in mortality among white but not black patients with breast cancer. It is unlikely that differences in obesity distributions between black women and white women account for the poorer survival of black women. |
Emerging issues in teratology: an introduction
Rasmussen SA , Friedman JM . Am J Med Genet C Semin Med Genet 2011 157 (3) 147-9 Teratology is the study of congenital anomalies and their causes, and interest in teratology has been longstanding, with Egyptian wall paintings depicting children with birth defects over 5,000 years ago [Barrow, 1971]. By definition, teratogenic factors include both non-genetic and genetic factors that increase the risk for birth defects [Fraser, 2010]; however, traditionally, the term “teratogenic” has been used to refer to non-genetic factors that cause birth defects. The study of human teratogenic exposures is a relatively new one, emerging in the past 70 years. Before maternal rubella infection during pregnancy was identified as a cause of birth defects and developmental disabilities in 1941 by an ophthalmologist, Norman Gregg, birth defects were generally believed to be inherited [Gregg, 1991; Webster, 1998]. The uterus was thought to serve as a barrier, protecting the infant from the effects of external factors [Fraser, 2010]. But recognition of maternal rubella syndrome and subsequently, of thalidomide as a cause of birth defects in 1961 by McBride and Lenz [McBride, 1961; Lenz and Knapp, 1962], increased awareness of the effects that non-genetic factors could have on the development of the embryo or fetus. | Much more is now known about teratogenic factors. Understanding these teratogenic exposures is important to geneticists and genetic counselors for several reasons. First, teratogenic conditions need to be included in the differential diagnosis for children and adults presenting to genetics clinic. Clinicians need to ask about potential exposures during pregnancy, be aware of those exposures recognized as causing adverse outcomes, and finally, think beyond what is known, to consider whether an exposure could be the cause of the abnormalities observed in a particular patient. In the past, key observations by astute clinicians have often been critical to the recognition that a particular exposure could be related to an adverse outcome [Carey et al., 2009]. Another reason that geneticists and genetic counselors need to know about teratogenic exposures is that genetic clinicians often serve as a source of information about these exposures. Clinicians who see women during pregnancy are often asked about the safety of a particular medication, and families who have had a child with a birth defect or developmental disability often also ask about whether a particular exposure during their pregnancy might have caused the defects in their child. Finally, identification of non-genetic factors that increase the risk for adverse outcomes can lead to the development of strategies for primary prevention, such as those developed for the prevention of fetal alcohol syndrome, following identification of alcohol as a teratogen [Rasmussen et al., 2009]. |
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