U.S. Preventive Services Task Force: Opportunity for Public Comment

Screening for Bladder Cancer

The U.S. Preventive Services Task Force (USPSTF) is inviting public comment on its draft recommendation statement on screening for bladder cancer. This draft recommendation is an update of the USPSTF 2004 recommendation regarding screening for bladder cancer in adults. To provide comments, please go to
http://www.uspreventiveservicestaskforce.org/tfcomment.htm.
The opportunity to comment on this draft recommendations statement is available until December 28, 2010.

The U.S. Preventive Services Task Force is working to make its recommendations clearer and more useful. This is part of its ongoing effort to keep its work and methods clear to the public it serves.

The USPSTF is a national, independent panel of medical experts that makes recommendations, based on scientific evidence, to primary care doctors and other health care providers about which clinical preventive services they should offer their patients.


Opportunities for Public Comment on Draft U.S. Preventive Services Task Force Recommendation Statements
Draft Recommendation Statements Available for Comment


* Screening for Bladder Cancer
(November 30-December 28, 2010)
U.S. Preventive Services Task Force: Draft Recommendation Statement


The U.S. Preventive Services Task Force (USPSTF) is inviting public comment on its draft Recommendation Statements before they are published. The USPSTF is a national, independent panel of medical experts that makes recommendations, based on scientific evidence, to primary care doctors and other health care providers about which clinical preventive services they should offer their patients.

The USPSTF is taking this new step as part of its ongoing effort to keep its work and methods clear to the public it serves.

Please look at these draft Recommendation Statements and offer your comments on the USPSTF's decisions and how the decisions are communicated. The USPSTF is seeking comments to help make the Recommendation Statements more useful for the primary care provider. All comments will be considered fully as the USPSTF finalizes these recommendations.

How to Comment

Any visitor to this site can comment on any USPSTF draft Recommendation Statements listed here. However, readers should note that the USPSTF writes its recommendations for primary care doctors and other health care providers, using medical and scientific language as appropriate for this audience.

To comment, click on the title of the draft Recommendation Statement at top right. Comments must be received before the comment deadline listed below each title. The comment period for draft Recommendation Statements is 4 weeks.

Once the draft Recommendation Statement is removed from the public comment page, the USPSTF begins considering comments and finalizing the Recommendation Statement. Until the final Recommendation Statement is published, the USPSTF considers the Recommendation Statements on its Web site to be current.

You will receive acknowledgement that your comments have been transmitted. At the present time, the USPSTF can not provide responses to individual comments.

Previous Opportunities for Public Comment
Screening for Testicular Cancer September 21, 2010–October 19, 2010
Ocular Prophylaxis for Gonococcal Ophthalmia Neonatorum August 16, 2010–September 13, 2010
Screening for Osteoporosis July 6, 2010–August 3, 2010

Current as of October 2010

Internet Citation:

Opportunities for Public Comment. U.S. Preventive Services Task Force.
http://www.uspreventiveservicestaskforce.org/tfcomment.htm

U.S. Preventive Services Task Force: Opportunity for Public Comment

Jano ofrece gratuitamente un curso online acreditado sobre el uso clínico de la rifaximina - JANO.es - ELSEVIER

FORMACIÓN
Jano ofrece gratuitamente un curso online acreditado sobre el uso clínico de la rifaximina
Actualidad Ultimas noticias - JANOes
JANO.es · 29 Noviembre 2010 12:35

El objetivo de la formación es mejorar los conocimientos de los profesionales sanitarios en el uso clínico de rifaximina en relación a diversas patologías.

La revista Jano ofrece a sus lectores la posibilidad de realizar un curso online y gratuito sobre el uso de la rifaximina. El objetivo de este curso, acreditado por el Consell Català de Formació Continuada con 1,6 créditos, es mejorar los conocimientos de los profesionales sanitarios en el uso clínico de rifaximina en relación a diversas patologías: encefalopatía hepática, diverticulosis, diverticulitis, sobrecrecimiento bacteriano y síndrome del intestino irritable.
El curso Uso clínico de rifaximina, patrocinado por Bama Geve, está formado por cinco módulos compuestos cada uno de ellos por una parte teórica y un caso clínico. El primer módulo se publicó en la revista Jano Medicina y Humanidades de junio y este mes se ha publicado el de Diverticulitis aguda. El último módulo, dedicado al síndrome del intestino irritable, se publicará en el número de abril de 2011.

La evaluación se realiza a través de la plataforma de formación continuada de Elsevier accediendo a www.rifaximina.elsevierfmc.com. Al finalizar el curso, el alumno tendrá acceso a las respuestas correctas razonadas de los cinco test y a la calificación obtenida. Los que hayan aprobado podrán descargarse automáticamente el diploma correspondiente.

Rifaximina, el primer tratamiento indicado en la encefalopatía hepática registrado en los últimos 30 años, es un antibiótico bactericida, de muy baja absorción intestinal, que actúa sobre microorganismos del aparato digestivo en determinadas infecciones gastrointestinales caracterizadas por su resistencia a otros tratamientos antimicrobianos.

Acceder al curso
RIFAXIMINA

Bama Geve
BAMA-GEVE

Actualidad Ultimas noticias - JANOes - Jano ofrece gratuitamente un curso online acreditado sobre el uso clinico de la rifaximina - JANO.es - ELSEVIER

Pandemic (H1N1) 2009 Virus and Other Respiratory Pathogens | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Co-detection of Pandemic (H1N1) 2009 Virus and Other Respiratory Pathogens

Kassi Koon, Catherine M. Sanders, Comments to Author Jessica Green, Leslie Malone, Holly White, Delineliz Zayas, Rebecca Miller, Stanley Lu, and Jian Han
Author affiliations: HudsonAlpha Institute for Biotechnology, Huntsville, Alabama, USA (K. Koon, C.M. Sanders, J. Han); and Diatherix Laboratories, Huntsville (J. Green, L. Malone, H. White, D. Zayas, R. Miller, S. Lu)

Suggested citation for this article

Abstract
From May through October 2009, a total of 10,624 clinical samples from 23 US states were screened for multiple respiratory pathogen gene targets. Of 3,110 (29.3%) samples positive for pandemic (H1N1) 2009 virus, 28% contained >1 other pathogen, most commonly Staphylococcus aureus (14.7%), Streptococcus pneumoniae (10.2%), and Haemophilus influenzae (3.5%).

For previous and current influenza A pandemics, postmortem studies have established a strong link between secondary bacterial infections and increased deaths (1,2). Numerous respiratory pathogens can be detected from a single sample by using a multiplex molecular method called target-enriched multiplex PCR (3–6). During the 2006 influenza season, this method was used at Vancouver Children and Women's Hospital to study 1,742 patients with acute respiratory infections; >2 pathogens were detected for ≈27% of patients studied (7). We used this method to learn more about infections occurring concurrently with pandemic (H1N1) 2009.

full-text:
Pandemic (H1N1) 2009 Virus and Other Respiratory Pathogens | CDC EID


Suggested Citation for this Article

Koon K, Sanders CM, Green J, Malone L, White H, Zayas D, et al. Co-detection of pandemic (H1N1) 2009 virus and other respiratory pathogens. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1976.htm


DOI: 10.3201/eid1612.091697

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Catherine M. Sanders, HudsonAlpha Institute of Biotechnology–Han Lab, 601 Genome Way, Huntsville, AL 35806, USA; email: csanders@hudsonalpha.com

L. tropica in Golden Jackals and Red Foxes | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Leishmania tropica Infection in Golden Jackals and Red Foxes, Israel

Dalit Talmi-Frank, Noa Kedem-Vaanunu, Roni King, Gila Kahila Bar-Gal, Nir Edery, Charles L. Jaffe, and Gad Baneth Comments to Author
Author affiliations: Hebrew University, Rehovot, Israel (D. Talmi-Frank, N. Kedem-Vaanunu, G. Kahila Bar-Gal, G. Baneth); Israel Nature and Parks Authority, Jerusalem, Israel (R. King); Kimron Veterinary Institute, Bet-Dagan, Israel (N. Edery); and Hebrew University–Hadassah Medical School, Jerusalem (C.L. Jaffe)

Suggested citation for this article

Abstract
During a survey of wild canids, internal transcribed spacer 1 real-time PCR and high-resolution melt analysis identified Leishmania tropica in samples from jackals and foxes. Infection was most prevalent in ear and spleen samples. Jackals and foxes may play a role in the spread of zoonotic L. tropica.

Leishmania tropica is a major cause of cutaneous leishmaniasis in the Old World. Although cutaneous leishmaniasis associated with L. tropica usually is considered an anthroponotic infection (1) in Israel, Jordan, and the Palestinian Authority, it appears to be a zoonosis with a main putative reservoir host, the rock hyrax (Procavia capensis) (2,3). Nevertheless, the possible involvement of other animals in the sylvatic transmission of L. tropica infection is not yet fully understood. L. tropica has been sporadically reported from domestic dogs from human cutaneous leishmaniasis foci in Iran and Morocco (4,5) but not from wild canids. Previous studies of leishmaniasis in wild canids, such as red foxes (Vulpes vulpes) in southern Italy (6) and wolves (Canis lupus) in southwestern Europe (7), found them to be infected with L. infantum. Golden jackals (Canis aureus) infected with L. infantum were reported in Iraq (8) and Kazakhstan (9). A seroepidemiologic study of Leishmania spp. infection in Israel showed that 7.6% of jackals and 5% of foxes tested were seropositive by using L. donovani antigen (10). The aim of this study was to identify and characterize Leishmania spp. infection in wild canids, including jackals, foxes, and wolves, in Israel by using species-specific real-time PCR.

full-text:
L. tropica in Golden Jackals and Red Foxes | CDC EID

Suggested Citation for this Article

Talmi-Frank D, Kedem-Vaanunu N, King R, Bar-Gal GK, Edery N, Jaffe CL, et al. Leishmania tropica infection in golden jackals and red foxes, Israel. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1973.htm


DOI: 10.3201/eid1612.100953

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Gad Baneth, School of Veterinary Medicine, Hebrew University, PO Box 12, Rehovot 76100, Israel; email: baneth@agri.huji.ac.il

Bundibugyo Ebola Virus, Uganda | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Proportion of Deaths and Clinical Features in Bundibugyo Ebola Virus Infection, Uganda

Adam MacNeil, Comments to Author Eileen C. Farnon, Joseph Wamala, Sam Okware, Deborah L. Cannon, Zachary Reed, Jonathan S. Towner, Jordan W. Tappero, Julius Lutwama, Robert Downing, Stuart T. Nichol, Thomas G. Ksiazek, and Pierre E. Rollin
Author affiliations: Centers for Disease Control and Prevention, Atlanta, Georgia, USA (A. MacNeil, E.C. Farnon, D.L. Cannon, Z. Reed, J.S. Towner, S.T. Nichol, T.G. Ksiazek, P.E. Rollin); Ministry of Health, Republic of Uganda, Kampala, Uganda (J. Wamala, S. Okware); Global AIDS Program, Centers for Disease Control and Prevention, Entebbe, Uganda (J.W. Tappero, R. Downing); Uganda Virus Research Institute, Entebbe (J. Lutwama); and University of Texas Medical Branch, Galveston, Texas, USA (T.G. Ksiazek)

Suggested citation for this article

Abstract
The first known Ebola hemorrhagic fever (EHF) outbreak caused by Bundibugyo Ebola virus occurred in Bundibugyo District, Uganda, in 2007. Fifty-six cases of EHF were laboratory confirmed. Although signs and symptoms were largely nonspecific and similar to those of EHF outbreaks caused by Zaire and Sudan Ebola viruses, proportion of deaths among those infected was lower (≈40%).

Ebola hemorrhagic fever (EHF) is a severe disease caused by several species of Ebolavirus (EBOV), in the family Filoviridae. Before 2007, four species of EBOV had been identified; 2 of these, Zaire ebolavirus and Sudan ebolavirus, have caused large human outbreaks in Africa, with proportion of deaths ≈80%–90% and 50%, respectively (1–5). Large outbreaks are associated with person-to-person transmission after the virus is introduced into humans from a zoonotic reservoir. Data suggest that this reservoir may be fruit bats (6,7). During outbreaks of EHF, the virus is commonly transmitted through direct contact with infected persons or their bodily fluids (8–11). The onset of EHF is associated with nonspecific signs and symptoms, including fever, myalgias, headache, abdominal pain, nausea, vomiting, and diarrhea; at later stages of disease, overt hemorrhage has been reported in ≈45% of cases (12).

Bundibugyo District is located in western Uganda, which borders the Democratic Republic of Congo. After reports of a mysterious illness in Bundibugyo District, the presence of a novel, fifth EBOV virus species, Bundibugyo ebolavirus (BEBOV), was identified in diagnostic samples submitted to the Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, USA, in November 2007 (13). In response to detection of EBOV, an international outbreak response was initiated. In this report, we summarize findings of laboratory-confirmed cases of BEBOV infection.

full-text:
Bundibugyo Ebola Virus, Uganda | CDC EID


Suggested Citation for this Article

MacNeil A, Farnon EC, Wamala J, Okware S, Cannon DL, Reed Z, et al. Proportion of deaths and clinical features in Bundibugyo Ebola virus infection, Uganda. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1969.htm

DOI: 10.3201/eid1612.100627

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Adam MacNeil, Centers for Disease Control and Prevention, 1600 Clifton Rd NE, Mailstop G14, Atlanta, GA 30333, USA; email: aho3@cdc.gov

Vaccines: VFC/ACIP-VFC Resolutions

Resolution No. 10/10-2 ADVISORY COMMITTEE ON IMMUNIZATION PRACTICES VACCINES FOR CHILDREN PROGRAM VACCINES TO PREVENT DIPHTHERIA, TETANUS AND PERTUSSIS
The purpose of this resolution is to revise the previous resolution to incorporate new recommendations regarding the interval between Tdap and last dose of Td for children aged 11 through 18 years of age and to update recommendations for certain children between the ages of 7 and 10 years and to streamline the recommendation through the use of links to published documents.

VFC resolution 6/08-3 is repealed and replaced by the following:
http://www.cdc.gov/vaccines/programs/vfc/downloads/resolutions/1010dtap-508.pdf

VFC: The ACIP-VFC Vaccine Resolutions
Vaccines: VFC/ACIP-VFC Resolutions

Brucella ceti Infection in Harbor Porpoise | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Brucella ceti Infection in Harbor Porpoise (Phocoena phocoena)

Thierry P. Jauniaux, Comments to Author Cecile Brenez, David Fretin, Jacques Godfroid, Jan Haelters, Thierry Jacques, Francis Kerckhof, Jan Mast, Michael Sarlet, and Freddy L. Coignoul
Author affiliations: Veterinary College, Liege, Belgium (T.P. Jauniaux, C. Brenez, M. Sarlet, F.L. Coignoul); Royal Belgian Institute of Natural Sciences, Brussels, Belgium (T. Jauniaux, J. Haelters, T. Jacques, F. Kerckhof); Veterinary and Agrochemical Research Centre, Brussels (D. Fretin, J. Mast); and Norwegian School of Veterinary Science, Tromsø, Norway (J. Godfroid)

Suggested citation for this article

Abstract
We describe Brucella sp. infection and associated lesions in a harbor porpoise (Phocoena phocoena) found on the coast of Belgium. The infection was diagnosed by immunohistochemistry, transmission electron microscopy, and bacteriology, and the organism was identified as B. ceti. The infection's location in the porpoise raises questions of abortion and zoonotic risks.

In cetaceans, Brucella spp. infections and related lesions have been found in bottlenose dolphins (Tursiops truncatus) (1), striped dolphins (Stenella coeruleoalba) (2–5), Atlantic white-sided dolphins (Lagenorhynchus acutus) (6,7), common dolphins (Delphinus delphi) (6,8), harbor porpoises (Phocoena phocoena) (6,9), and a minke whale (Balaenoptera acutorostrata) (6). Recently, B. ceti was described as being the cetacean Brucella sp. strain that infects dolphins (10). We report a case of B. ceti infection and associated lesions in a harbor porpoise found on the coast of Belgium in 2008.

full-text:
Brucella ceti Infection in Harbor Porpoise | CDC EID


Suggested Citation for this Article

Jauniaux TP, Brenez C, Fretin D, Godfroid J, Haelters J, Jacques T, et al. Brucella ceti infection in harbor porpoise (Phocoena phocoena). Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1966.htm

DOI: 10.3201/eid1612.101008

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Thierry P. Jauniaux, University of Liege–Veterinary Pathology, Sart Tilman B4, Liege 4000, Belgium; email: t.jauniaux@ulg.ac.be

B. henselae in Skin Biopsy Specimens | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Bartonella henselae in Skin Biopsy Specimens of Patients with Cat-Scratch Disease

Emmanouil Angelakis, Sophie Edouard, Bernard La Scola, and Didier Raoult Comments to Author
Author affiliation: Université de la Méditerranée, Marseille, France

Suggested citation for this article

Abstract
During the past 2 years, we identified live Bartonella henselae in the primary inoculation sites of 3 patients after a cat scratch. Although our data are preliminary, we report that a cutaneous swab of the skin lesion from a patient in the early stage of cat-scratch disease can be useful for diagnosis of the infection.

Bartonella henselae is the main causative agent of cat-scratch disease (CSD). Little is known about the organism's pathogenesis in long-lasting lymphadenopathy, but an immunopathogenesis is assumed (1). B. henselae is infrequently grown from the lymph nodes of humans, and only in a few cases was B. henselae isolated from patients with CSD (2,3). In experiments with mice, B. henselae was eliminated within a few days to 1 week after systemic (intraperitoneal or intravenous) infection (4). Moreover, on the basis of molecular methods, we recently identified that the scalp eschars from 2 patients who were bitten by a tick contained B. henselae (5). In this study, our objective was to determine if B. henselae was present in the papule, which is developed in the scratch line. We report isolation of B. henselae from a swab specimen and the skin biopsy specimens sampled from the skin papule of 3 patients with CSD.

The Study

From January 2007 through February 2010, we tested 92 skin biopsy specimens from patients suspected of having CSD. DNA was extracted by using a QIAamp Tissue Kit (QIAGEN, Valencia, CA, USA) and was used as a template in a previously described real-time reverse transcription–PCR (RT-PCR) specific for a portion of the Bartonella 16S–23S intergenic spacer region and the PAP31 gene for detection of B. henselae (6). B. henselae was identified in 4 skin biopsy specimens (4.3%). For each patient, we received a skin biopsy specimen from the skin papule, a lymph node biopsy specimen, and paired serum samples. For 1 patient, we also received a swab from a skin papule. Immunoglobulin G and M titers were determined by using an immunofluorescent antibody assay (7).

Skin biopsy specimens and the swab were cultured in human embryonic lung fibroblasts by using the centrifugation shell-vial technique (3.7 mL; Sterilin Ltd., Felthan, UK); 12-mm round coverslips seeded with 1 mL of medium containing 50,000 cells and incubated in a 5% CO2 incubator at 37°C for 3 days were used to obtain a confluent monolayer (8). Cultures were surveyed for 4 weeks and detection of bacteria growth was assessed every 7 days on coverslips directly inside the shell vial by using Gimenez and immunofluorescence staining. We obtained a positive culture from 3 patients, and detailed histories are described below (Table).

Patient 1 was a 38-year-old man who had fever (40°C) and asthenia. The patient was a cat owner who had been scratched 8 days before onset of symptoms. Clinical signs were right axillary lymphadenitis and an inflammatory reddish skin lesion on the right hand with epitrochlear adenopathy, which appeared 2 days before he sought treatment. Abdominal ultrasound showed small hepatic abscesses. After the skin biopsy sample was obtained, doxycycline (200 mg/d) was given for 1 week. The patient fully recovered.

Patient 2 was a 17-year-old man with an inflamed red skin lesion on the right foot and epitrochlear adenopathy. The patient reported that he was scratched ≈1 week earlier by his cat and that the skin lesion appeared the day before he sought treatment. Right inguinal lymphadenitis was also identified during examination.

Patient 3 was a 20-year-old man had an inflammatory skin lesion on the left hand. He had a cat scratch 9 days before; the skin papule appeared 1 day before he sought treatment. Left axilliary lymphadenitis was identified during the examination and abdominal ultrasound showed hepatomegaly.

Skin biopsy specimens and lymph nodes from all patients were positive by real-time RT-PCR; patient 2 also had a positive swab specimen. Moreover, all patients had serum samples positive for B. henselae by immunofluorescent antibody assay. We detected gram-negative bacilli (Figure), which were identified as B. henselae by real-time RT-PCR (6), in the cultures of the skin biopsies and swab specimen. Patients 2 and 3 recovered without treatment.

full-text:
B. henselae in Skin Biopsy Specimens | CDC EID


Suggested Citation for this Article

Angelakis E, Edouard S, La Scola B, Raoult D. Bartonella henselae in skin biopsy specimens of patients with cat-scratch disease. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1963.htm


DOI: 10.3201/eid1612.100647

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Didier Raoult, Faculte de Medecine, Unite des Rickettsies, UMR6020, IFR 48, Centre National de Reference Centre Collaborateur OMS, 27 Blvd Jean Moulin, Marseille 13005, France; email: didier.raoult@gmail.fr

Flutracking and Pandemic (H1N1) 2009 | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Online Flutracking Survey of Influenza-like Illness during Pandemic (H1N1) 2009, Australia

Sandra J. Carlson, Craig B. Dalton, David N. Durrheim, Comments to Author and John Fejsa
Author affiliations: Hunter Medical Research Institute, Wallsend, New South Wales, Australia (S.J. Carlson, C.B. Dalton, D.N. Durrheim); Hunter New England Population Health, Newcastle, New South Wales, Australia (S.J. Carlson, C.B. Dalton, D.N. Durrheim, J. Fejsa); and Newcastle University, Newcastle (C.B. Dalton, D.N. Durrheim)

Suggested citation for this article

Abstract
We compared the accuracy of online data obtained from the Flutracking surveillance system during pandemic (H1N1) 2009 in Australia with data from other influenza surveillance systems. Flutracking accurately identified peak influenza activity timing and community influenza-like illness activity and was significantly less biased by treatment-seeking behavior and laboratory testing protocols than other systems.

A variety of surveillance methods were used to monitor the incidence and severity of influenza A pandemic (H1N1) 2009 in Australia. Severity of illness was measured by number of hospitalizations, intensive care unit (ICU) admissions, and deaths. Influenza disease incidence was monitored through laboratory-confirmed cases, general practitioner sentinel surveillance of influenza-like illness (ILI), emergency department visits for ILI, absenteeism data from large employers, and the Flutracking surveillance system (1).

Flutracking is a national weekly online survey of ILI (completed by >8,000 participating community members each week in 2009); it is the only ILI surveillance system that provides comparable data across Australia's states and territories. Flutracking integrates participants' ILI symptom information with their influenza vaccination status (2). Flutracking surveillance has correlated well with other Australian influenza surveillance systems in describing the timing and scale of the 2007 and 2008 seasonal influenza epidemics (3,4). We compared Flutracking data with data from other routine influenza surveillance systems during the 2009 pandemic wave in New South Wales (NSW), Australia's most populous state.

full-text:
Flutracking and Pandemic (H1N1) 2009 | CDC EID


Suggested Citation for this Article

Carlson SJ, Dalton C, Durrheim DN, Fejsa J. Online Flutracking survey of influenza-like illness during pandemic (H1N1) 2009, Australia. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1960.htm

DOI: 10.3201/eid1612.100935

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

David N. Durrheim, Locked Bag 10, Hunter Medical Research Institute, Wallsend, New South Wales 2287, Australia; email: david.durrheim@hnehealth.nsw.gov.au

Wild Chimpanzees and Human Malaria | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Wild Chimpanzees Infected with 5 Plasmodium Species

Marco Kaiser, Anna Löwa, Markus Ulrich, Heinz Ellerbrok, Adeelia S. Goffe, Anja Blasse, Zinta Zommers, Emmanuel Couacy-Hymann, Fred Babweteera, Klaus Zuberbühler, Sonja Metzger, Sebastian Geidel, Christophe Boesch, Thomas R. Gillespie, and Fabian H. Leendertz Comments to Author
Author affiliations: Robert Koch-Institute, Berlin, Germany (M. Kaiser, A. Löwa, H. Ellerbrok, A.S. Goffe, A. Blasse, F.H. Leendertz); GenExpress GmbH, Berlin (M. Kaiser, M. Ulrich); University of Oxford, Tubney Abingdon, UK (A.S. Goffe, Z. Zommers); LANADA/LCPA, Bingerville, Côte d'Ivoire (E. Couacy-Hymann); Budongo Conservation Field Station, Masindi, Uganda (F. Babweteera, K. Zuberbühler); University of St. Andrews, St. Andrews, Scotland, UK (K. Zuberbühler); Max-Planck-Institute for Evolutionary Anthropology, Leipzig, Germany (S. Metzger, S. Geidel, C. Boesch, F.H. Leendertz); and Emory University, Atlanta, Georgia, USA (T.R. Gillespie)

Suggested citation for this article

Abstract
Data are missing on the diversity of Plasmodium spp. infecting apes that live in their natural habitat, with limited possibility of human-mosquito-ape exchange. We surveyed Plasmodium spp. diversity in wild chimpanzees living in an undisturbed tropical rainforest habitat and found 5 species: P. malariae, P. vivax, P. ovale, P. reichenowi, and P. gaboni.

Despite ongoing and, in some regions, escalating morbidity and mortality rates associated with malaria-causing parasites, the evolutionary epidemiology of Plasmodium spp. is not well characterized. Classical studies of the blood pathogens of primates have found protozoa resembling human malaria parasites in chimpanzees and gorillas (1); however, these studies were limited to microscopy, negating conclusions regarding evolutionary relationships between human and ape parasites. Recent studies that used molecular approaches showed that captive and wild chimpanzees (Pan troglodytes) and lowland gorillas (Gorilla gorilla), as well as captive bonobos (Pan paniscus), harbor parasites broadly related to P. falciparum (2–5); wild and captive gorillas and captive bonobos and chimpanzees are sometimes infected with P. falciparum itself (4–6). Further, captive chimpanzees and bonobos have been shown to have malaria parasites related to human P. ovale and P. malariae (6–8); P. vivax has been identified in various monkeys and 1 semiwild chimpanzee (5,9). Recently, P. knowlesi, a simian malaria species, became the fifth human-infecting species (10), highlighting the possibility of transmission of new Plasmodium spp. from wild primates to humans.

full-text:
Wild Chimpanzees and Human Malaria | CDC EID

Suggested Citation for this Article

Kaiser M, Löwa A, Ulrich M, Ellerbrok, Goffe AS, Blasse A, et al. Wild chimpanzees infected with 5 Plasmodium species. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1956.htm

DOI: 10.3201/eid1612.100424

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Fabian H. Leendertz, Robert Koch-Institute, Research Group Emerging Zoonoses, Nordufer 20, 13353, Berlin, Germany; email: leendertzf@rki.de

Hantavirus Pulmonary Syndrome, Maranhão, Brazil | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Hantaviruses and Hantavirus Pulmonary Syndrome, Maranhão, Brazil

Elizabeth S. Travassos da Rosa, Elba R. Sampaio de Lemos, Daniele B. de Almeida Medeiros, Darlene B. Simith, Armando de Souza Pereira, Mauro R. Elkhoury, Wellington S. Mendes,1 José R.B. Vidigal, Renata C. de Oliveira, Paulo S. D'Andrea, Cibele R. Bonvícino, Ana C.R. Cruz, Márcio R.T. Nunes, and Pedro F. da Costa Vasconcelos Comments to Author
Author affiliations: Evandro Chagas Institute, Ananindeua, Brazil (E.S. Travassos da Rosa, D.B. de Almeida Medeiros, D.B. Simith, A. de Souza Pereira, A.C.R. Cruz, M.R.T. Nunes, P.F. da Costa Vasconcelos); Oswaldo Cruz Institute, Rio de Janeiro, Brazil (E.R. Sampaio de Lemos, R.C. de Oliveira, P.S. D'Andrea); Pan American Health Organization, Brasília, Brazil (M.R. Elkhoury); Federal University of Maranhão, São Luís, Brazil (W.S. Mendes); State Health Secretariat, São Luís (J.R.B. Vidigal); National Institute of Cancer, Rio de Janeiro (C.R. Bonvicino); and Pará State University, Belém, Brazil (A.C.R. Cruz, P.F. da Costa Vasconcelos)

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Abstract
To confirm circulation of Anajatuba virus in Maranhão, Brazil, we conducted a serologic survey (immunoglobulin G ELISA) and phylogenetic studies (nucleocapsid gene sequences) of hantaviruses from wild rodents and persons with hantavirus pulmonary syndrome. This virus is transmitted by Oligoryzomys fornesi rodents and is responsible for hantavirus pulmonary syndrome in this region.

Hantaviruses (family Bunyaviridae, genus Hantavirus) cause a viral zoonosis transmitted by rodents belonging to the families Muridae and Cricetidae. Each hantavirus is predominantly associated with a specific rodent species in a specific geographic region. However, infection of other rodent species can occur as a spillover phenomenon (1).

Hantavirus disease has 2 recognized clinical forms, hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome (HPS) (2). The respiratory form of the disease was described in June 1993 during an epidemic of severe respiratory disease caused by Sin Nombre virus in the United States (3). A few months later, 3 HPS cases were identified in 3 siblings in Juquitiba, São Paulo State, Brazil (4). During 1993–2009, a total of 1,246 HPS cases (264 in the Amazon region) were reported in Brazil, and new hantaviruses were identified (Juquitiba virus, Castelo dos Sonhos virus, Araraquara virus, Anajatuba virus, and Rio Mearim (5).

During 2003–2005, an ecoepidemiologic study was conducted in the municipality of Anajatuba, Maranhão, Brazil, to identify reservoirs of hantaviruses after identification of 3 HPS cases (6). Two new hantaviruses, Anajatuba virus and Rio Mearim virus, were isolated from Oligoryzomys fornesi (rice rat) rodents and Holochilus sciureus (marsh rat) rodents, respectively, and genetically characterized (5). To confirm circulation of Anajatuba virus in Maranhão, Brazil, we conducted a serologic survey (immunoglobulin [Ig] G ELISA) and phylogenetic studies (nucleocapsid gene sequences) of hantaviruses obtained from wild rodents and persons with HPS.

full-text:
Hantavirus Pulmonary Syndrome, Maranhão, Brazil | CDC EID

Suggested Citation for this Article

Travassos da Rosa ES, Sampaio de Lemos ER, de Almeida Medeiros DB, Simith DB, de Souza Pereira A, Elkhoury MR, et al. Hantaviruses and hantavirus pulmonary syndrome, Maranhão, Brazil. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1952.htm

DOI: 10.3201/eid1612.100418



1Deceased.

Comments to the Authors

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Pedro F. da Costa Vasconcelos, Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, SVS/MS, Rod. BR 316, Km 07, SNº, Bairro, Levilândia, 66030-000 Belém, Brazil; email: pedrovasconcelos@iec.pa.gov.br

Ocular Thelaziosis in Dogs | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Ocular Thelaziosis in Dogs, France

Perrine Ruytoor, Eric Déan, Olivier Pennant, Philippe Dorchies, René Chermette, Domenico Otranto, and Jacques Guillot Comments to Author
Author affiliations: École Nationale Vétérinaire d'Alfort, ANSES, UPEC, Maisons-Alfort, France (P. Ruytoor, R. Chermette, J. Guillot); Clinique Vétérinaire, Lognes, France (E. Déan); Clinique Vétérinaire, Vergt, France (O. Pennant); É́cole Nationale Vétérinaire de Toulouse, Toulouse, France (P. Dorchies); and University of Bari, Bari, Italy (D. Otranto)

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Abstract
During 2005–2008, veterinary practitioners reported ocular infection by Thelazia spp. nematodes in 115 dogs and 2 cats in southwestern France. Most cases were detected in Dordogne, particularly in 3 counties with numerous strawberry farms, which may favor development of the fruit fly vector. Animal thelaziosis may lead to emergence of human cases.

Thelazia spp. (Spirurida, Thelaziidae) nematodes live in the conjunctival sac of warm-blooded vertebrates. These nematodes are responsible for epiphora, conjunctivitis, keratitis, and corneal ulcers (1–3). Thelazia spp. nematodes are transmitted by different species of flies feeding from the lacrimal secretions of the definitive hosts. Among the 10 species, T. californiensis and T. callipaeda parasitize carnivores and sometimes humans. T. californiensis is confined to the western United States and has never been reported in Europe (1). T. callipaeda, the "oriental eye worm," is common in the former Soviet republics and in India, Thailand, People's Republic of China, and Japan (2), where it causes infections in humans, dogs, and cats (3). Wild mammals, such as foxes and lagomorphs, are reservoir hosts for the nematodes. During the past decade T. callipaeda infection was proven to be widespread among dogs and cats from northern (Aosta valley) to southern (Basilicata region) Italy (4). In Ticino, a region of southern Switzerland, a retrospective study identified 106 T. callipaeda–positive dogs and 5 positive cats during 2005–2007 (5). Recently, the first autochthonous case of thelaziosis in a dog was described in southern Germany (6). Locally transmitted cases of thelaziosis were first reported in 4 dogs and 1 cat that lived or spent time in the department of Dordogne in southwestern France (7).

full-text:
Ocular Thelaziosis in Dogs | CDC EID


Suggested Citation for this Article

Ruytoor P, Déan E, Pennant O, Dorchies P, Chermette R, Otranto D, et al. Ocular thelaziosis in dogs, France. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1943.htm

DOI: 10.3201/eid1612.100872

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Jacques Guillot, Service de Parasitologie, École Nationale Vétérinaire d'Alfort, 7 ave du Général de Gaulle, 94704 Maisons-Alfort, France; email: jguillot@vet-alfort.fr

M. tuberculosis in Asian Elephants, Thailand | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Mycobacterium tuberculosis Infection of Domesticated Asian Elephants, Thailand

Taweepoke Angkawanish, Worawidh Wajjwalku, Comments to Author Anucha Sirimalaisuwan, Sittidet Mahasawangkul, Thattawan Kaewsakhorn, Kittikorn Boonsri, and Victor P.M.G. Rutten
Author affiliations: National Elephant Institute, Forest Industry Organization, Lampang, Thailand (T. Angkawanish, S. Mahasawangkul); Kasetsart University, Nakhonpathom, Thailand (W. Wajjwalku); Chiang Mai University, Chiang Mai, Thailand (A. Sirimalaisuwan, T. Kaewsakhorn, K. Boonsri); Utrecht University, Utrecht, the Netherlands (T. Angkawanish, V.P.M.G. Rutten); and University of Pretoria, Onderstepoort, South Africa (V.P.M.G. Rutten)

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Abstract
Four Asian elephants were confirmed to be infected with Mycobacterium tuberculosis by bacterial culture, other diagnostic procedures, and sequencing of 16S–23S rDNA internal transcribed spacer region, 16S rRNA, and gyrase B gene sequences. Genotyping showed that the infectious agents originated from 4 sources in Thailand. To identify infections, a combination of diagnostic assays is essential.

During the past 2 decades, infections of captive African and Asian elephants with Mycobacterium bovis and M. tuberculosis have been diagnosed worldwide (1–4). Transmission of these infections to other mammals and veterinary personnel has also been observed (5). To date, M. tuberculosis infection has not been reported in elephants in Thailand. Four elephants referred to the National Elephant Institute (NEI) Hospital during 2005–2008, three of which showed signs of weakness and chronic weight loss, and 1 showed serous nasal discharge. Tuberculosis was confirmed by using conventional and molecular diagnostic assays.

full-text:
M. tuberculosis in Asian Elephants, Thailand | CDC EID


Suggested Citation for this Article

Angkawanish T, Wajjwalku W, Sirimalaisuwan A, Mahasawangkul S, Kaewsakhorn T, Boonsri K, et al. Mycobacterium tuberculosis infection of domesticated Asian elephants, Thailand. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1949.htm

DOI: 10.3201/eid1612.100862

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Worawidh Wajjwalku, Faculty of Veterinary Medicine, Kasetsart University, Nakhonpathom, Thailand; email: fvetwww@yahoo.com

African Swine Fever Virus, Northwestern Iran | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Emergence of African Swine Fever Virus, Northwestern Iran

Pooneh Rahimi, Amir Sohrabi, Javad Ashrafihelan, Rosita Edalat, Mehran Alamdari, Mohammadhossein Masoudi, Saied Mostofi, and Kayhan Azadmanesh Comments to Author
Author affiliations: Pasteur Institute of Iran, Tehran, Iran (P. Rahimi, A. Sohrabi, R. Edalat, K. Azadmanesh); University of Tabriz, Tabriz, Iran (J. Ashrafihelan); and Veterinary Organization, Tabriz (M. Alamdari, M. Masoudi, S. Mostofi)

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Abstract
In 2008, African swine fever was introduced into Georgia, after which it spread to neighboring Armenia, Azerbaijan, and the Russian Federation. That same year, PCR and sequence analysis identified African swine fever virus in samples from 3 dead female wild boars in northwestern Iran. Wild boars may serve as a reservoir.

African swine fever (ASF) is a notifiable, highly contagious, lethal, hemorrhagic disease in domestic pigs (1,2). ASF virus (ASFV) (International Committee on Taxonomy of Viruses database no. 00.002.0.01.001), an enveloped double-stranded DNA virus, is the only known DNA arbovirus (3). Maintenance and transmission of ASFV involves cycling of virus between soft ticks of the genus Ornithodoros and wild pigs (warthogs, bush pigs, and giant forest boars) (1,2). The virus can also be acquired through ingestion of contaminated feed.

The syndrome caused by ASFV in pigs was initially described in Kenya and later in most other African countries (1,4). In Africa, it causes a long-term, persistent infection in warthogs and bush pigs (2,3,5). Clinical diagnosis of ASF is difficult because signs of ASF and other hemorrhagic diseases are similar and because virulence varies among ASFV isolates (1,2,5,6).

In June 2007, ASFV was identified in the Caucasus region, including Georgia, Russian Federation, and Armenia (2). Diagnosis near the port of Poti, Georgia, was based on clinical findings, and virus identification was later confirmed by laboratory investigations. ASFV might have been introduced into Georgia by ships carrying contaminated pork or pork products from other countries. After entering Georgia, the virus extended into Armenia in August 2007. The probable route of virus entry into Armenia was movement of infected pigs and wild boars across the border (7). By the end of 2007, an outbreak had occurred in Yerevan and Ararat, after which 1 additional case occurred in February 2008.

In December 2007, the Russian Federation reported its first ASF outbreak since the 1970s. The virus may have entered through neighboring Georgia (7,8). In January 2008, presence of ASF was officially confirmed in northwest Azerbaijan, ≈180 km east of the Georgia border (village of Nic). Because most residents of Nic keep pigs in backyard smallholdings, ASFV may have entered Nic in contaminated pork (or pork products) or in infected wild boars (7,8).

In December 2008 and January 2009, ASFV spread to wild boars in northwestern Iran. As in Georgia, initial diagnosis was based on clinical signs and postmortem examinations. Virus identification was subsequently confirmed by laboratory investigations.


full-text:
African Swine Fever Virus, Northwestern Iran | CDC EID


Suggested Citation for this Article

Rahimi P, Sohrabi A, Ashrafihelan J, Edalat R, Alamdari M, Masoudi M, et al. Emergence of African swine fever virus, northwestern Iran. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited].
http://www.cdc.gov/EID/content/16/12/1946.htm

DOI: 10.3201/eid1612.100378

Comments to the Authors

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Kayhan Azadmanesh, Department of Virology, Pasteur Institute of Iran, PO Box 1316942551, 12th Farvardin St, Pasteur Ave, Tehran, Iran; email: azadmanesh@pasteur.ac.ir

Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus, CME Activity | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
MEDSCAPE CME ACTIVITY
Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus, South Korea

Medscape, LLC is pleased to provide online continuing medical education (CME) for this journal article, allowing clinicians the opportunity to earn CME credit. This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Medscape, LLC and Emerging Infectious Diseases. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians. Medscape, LLC designates this educational activity for a maximum of 0.25 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity. All other clinicians completing this activity will be issued a certificate of participation. To participate in this journal CME activity: (1) review the learning objectives and author disclosures; (2) study the education content; (3) take the post-test and/or complete the evaluation at www.medscapecme.com/journal/eid; (4) view/print certificate.

Learning Objectives

Upon completion of this activity, participants will be able to:

* Describe the pattern and characteristics of resistance seen with antiviral agents in pandemic (H1N1) 2009 in South Korea.

Medscape CME Editor [Contact us at eideditor@cdc.gov]

Thomas J. Gryczan, MS, Technical Writer/Editor, Emerging Infectious Diseases. Disclosure: Thomas J. Gryczan, MS, has disclosed no relevant financial relationships.
Medscape CME Author

Desiree Lie, MD, MSEd, Clinical Professor; Director of Research and Faculty Development, Department of Family Medicine, University of California, Irvine at Orange. Disclosure: Désirée Lie, MD, MSEd, has disclosed the following relevant financial relationship: served as a nonproduct speaker for "Topics in Health" for Merck Speaker Services.
Authors

Disclosures: Hwajung Yi, PhD; Joo-Yeon Lee, PhD; Eun-Hye Hong, BS; Mi-Seon Kim, BS; Donghyok Kwon, MS; Jang-Hoon Choi, MS; Woo-Young Choi, PhD; Ki-Soon Kim, PhD; Jong-Koo Lee, MD; Hee-Bok Oh, PhD; and Chun Kang, MS, have disclosed no relevant financial relationships.

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Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus, CME Activity | CDC EID





EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Dispatch
Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus, South Korea

Hwajung Yi, Joo-Yeon Lee, Eun-Hye Hong, Mi-Seon Kim, Donghyok Kwon, Jang-Hoon Choi, Woo-Young Choi, Ki-Soon Kim, Jong-Koo Lee, Hee-Bok Oh, and Chun Kang Comments to Author
Author affiliation: Korea Centers for Disease Control and Prevention, Seoul, South Korea

Suggested citation for this article

Abstract
To identify oseltamivir resistance, we analyzed neuraminidase H275Y mutations in samples from 10 patients infected with pandemic (H1N1) 2009 virus in South Korea who had influenza that was refractory to antiviral treatment with this drug. A neuraminidase I117M mutation that might influence oseltamivir susceptibility was detected in sequential specimens from 1 patient.

Since April 2009, pandemic (H1N1) 2009 has spread worldwide and caused the first influenza pandemic of the 21st century. Pandemic (H1N1) 2009 virus initially showed resistance to amantadine but susceptibility to oseltamivir (1). Thereafter, 285 cases of oseltamivir-resistant pandemic viral infection were reported worldwide on April 14, 2010 (2). However, information is limited about oseltamivir-resistant pandemic influenza in South Korea. Monitoring of community circulation of oseltamivir-resistant viruses has not yet detected any evidence of oseltamivir resistance in South Korea. To identify these viruses, we conducted specific surveillance of antiviral drug–resistant infection in patients whose illness did not resolve after antiviral treatment.

The Study

The study was reviewed and approved by ethics committees of relevant institutions and hospitals. After patients provided informed consent, we obtained >150 clinical specimens from patients in various hospitals in South Korea. Respiratory specimens (>60% nasopharyngeal swab specimens) were obtained during October 2009–January 2010 from patients whose illness had been clinically refractory to antiviral treatment since October 2009.

Viral RNAs were isolated from specimens of 10 patients (Table 1) by using the QIAamp viral RNA Mini Kit (QIAGEN, Crawley, UK). PCR products of the neuraminidase (NA) and matrix 2 (M2) genes were generated by reverse transcription–PCR with primers for NA (forward: 5′-AAATTAACGGGCAATTCCTCTCT-3′; reverse: 5′-CCGAAAATCCCACTGCATATGTAT-3′) and M2 (forward: 5′-CTAGCTCCAGTGCTGGTCTGA-3′; reverse: 5′-CTCAGGCACTCCTTCCGTAGA-3′). DNA sequences of NA and M2 reverse transcription–PCR products were analyzed by using the Big-Dye Terminator Sequencing Reaction Kit and an ABI 3700 DNA analyzer (Applied Biosystems, Foster City, CA, USA). A total of 58 NA sequences and 52 M2 sequences were obtained and analyzed by using the sequence analysis tool in the Influenza Sequences and Epitopes Database for detecting oseltamivir-resistance mutations (3).

Ten patients were detected who had oseltamivir-resistant pandemic (H1N1) 2009 virus with the H275Y substitution in viral NA (Table 2). Oseltamivir resistance was associated with oseltamivir treatment on the basis of H275Y changes from the oseltamivir-sensitive genotypes to oseltamivir-resistant genotypes of viral NA in consecutive samples from the same patient. Furthermore, a novel NA (I117M) substitution that may be associated with oseltamivir resistance (4,5) was detected in specimens from 1 patient (patient G) who had myelodysplasia and received oseltamivir and peramivir (Tables 1, 2).

In addition, we cultured viral isolates from clinical specimens (patients A and C) and evaluated antiviral susceptibility by measuring the dose of oseltamivir and zanamivir required for 50% inhibition (IC50) of NA activity. One isolate of pandemic (H1N1) 2009 virus with an oseltamivir-sensitive genotype (H275 in its NA) was susceptible to oseltamivir (IC50 1.18 nmol/L) and zanamivir (IC50 0.42 nmol/L). Viral isolates from patients A and C with an oseltamivir-resistant genotype (Y275 in NA) were resistant only to oseltamivir (IC50 713.2 nmol/L and 359.4 nmol/L, respectively). Susceptibility to zanamivir was not altered whether NA contained Y275 or H275 (IC50 0.13 nmol/L and 0.78 nmol/L, respectively).

Patients with oseltamivir-resistant pandemic (H1N1) 2009 were treated during hospitalization with oseltamivir alone or with a combination of other antiviral drugs (Table 2). Active surveillance that evaluated spread of oseltamivir-resistant viral infections among hospital staff, family members, and other patients who had contacted with or cared for the patients showed no evidence of virus transmission in the hospitals

full-text:
Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus | CDC EID


Suggested Citation for this Article

Y Hi, Lee J-Y, Hong E-H, Kim M-S, Kwon D, Choi J-H, et al. Oseltamivir-resistant pandemic (H1N1) 2009 virus, South Korea. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1938.htm

DOI: 10.3201/eid1612.100600

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Chun Kang, Division of Influenza Viruses, Center for Infectious Diseases, National Institute of Health, Korea Centers for Disease Control and Prevention, Nokbeon-dong, Eunpyeong-gu, Seoul, 122–701, South Korea; email:ckang@nih.go.kr

Pandemic Influenza on Troop Ship, 1918 | CDC EID

EID Journal Home > Volume 16, Number 12–December 2010
Volume 16, Number 12–December 2010
Historical Review
Mortality Risk Factors for Pandemic Influenza on New Zealand Troop Ship, 1918

Jennifer A. Summers, Comments to Author Nick Wilson, Michael G. Baker, and G. Dennis Shanks
Author affiliations: University of Otago, Wellington, New Zealand (J.A. Summers, N. Wilson, M.G. Baker); and Australian Army Malaria Institute, Enoggera, Queensland, Australia (G.D. Shanks)

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Abstract
We describe the epidemiology and risk factors for death in an outbreak of pandemic influenza on a troop ship. Mortality and descriptive data for military personnel on His Majesty's New Zealand Transport troop ship Tahiti in July 1918 were analyzed, along with archival information. Mortality risk was increased among persons 25–34 years of age. Accommodations in cabins rather than sleeping in hammocks in other areas were also associated with increased mortality risk (rate ratio 4.28, 95% confidence interval 2.69–6.81). Assignment to a particular military unit, the field artillery (probably housed in cabins), also made a significant difference (adjusted odds ratio in logistic regression 3.04, 95% confidence interval 1.59–5.82). There were no significant differences by assigned rurality (rural residence) or socioeconomic status. Results suggest that the virulent nature of the 1918 influenza strain, a crowded environment, and inadequate isolation measures contributed to the high influenza mortality rate onboard this ship.

To plan and prepare appropriately for future influenza pandemics, public health authorities need to better understand the epidemiology of previous pandemics. Much remains obscure about the epidemiology of the influenza pandemic of 1918–19, the spread of which depended on the transportation of large numbers of troops during World War I.

Pandemic influenza outbreaks among closed military populations are problematic and sometimes show high mortality rates. Reports on this topic have been published. These include descriptions of 1918 pandemic outbreaks in U.S. and Australian troop and civilian ships in 1918–19 (1–5), descriptions of 1918 pandemic outbreaks in military camps in the United States, the United Kingdom, and New Zealand (2,3,6–8), and more recent influenza outbreaks onboard naval and civilian ships (9–12).

Some studies have investigated specific risk factors for death from the 1918 pandemic. Evidence has shown that lower socioeconomic status increased mortality risk (13,14) and that young adults, for as-yet-unexplained reasons, had disproportionately higher mortality rates (13–16). Rural living versus urban living is another risk factor that has been investigated and has showed conflicting results (17–20). Lower mortality rates were observed among seasoned troops (>6 months experience) compared with newly recruited troops, possibly because of previous exposure to respiratory pathogens in seasoned troops (8,21,22).

The purpose of this study was to examine the 1918 outbreak on His Majesty's New Zealand Transport (HMNZT) Tahiti (Figure 1) and to identify mortality risk factors among persons onboard. During and after World War I, HMNZT Tahiti made numerous trips, transporting reinforcements and supplies from New Zealand to Europe, and bringing home New Zealand troops (Figure 2). On July 10, 1918, HMNZT Tahiti departed New Zealand with the 40th Reinforcements, a unit that consisted largely of infantry replacements. The voyage across the Indian Ocean and around the Cape of Good Hope was uneventful. HMNZT Tahiti was to join a convoy in Freetown, Sierra Leone, before heading to England. Upon reaching Freetown, reports of disease ashore resulted in all ships in the convoy being quarantined at port (7,25). However, a conference was attended by captains and wireless operators from every ship in the convoy onboard the His Majesty's Ship Mantua. The Mantua had experienced an influenza outbreak onboard 2 days after leaving the United Kingdom on August 1, 1918, and is thought to have been responsible for bringing the second wave of the 1918 pandemic to western Africa from England (5,26).

HMNZT Tahiti left Freetown on August 26, 1918, as part of the convoy after being resupplied by local workers (who were another possible source of infection with the new pandemic influenza strain). On the day of sailing, influenza case-patients began to be admitted to the onboard hospital. Over the next few weeks of the voyage, influenza developed in >1,000 of the 1,217 persons onboard (25). By the time HMNZT Tahiti reached Plymouth, England, on September 10, 1918, a total of 68 men had died onboard the ship (23,27). Eight other men and 1 nurse who had been on the ship died of influenza in England. HMNZT Tahiti, the worst affected ship in the convoy, was referred to as the death ship, and a Court of Inquiry was held to investigate this outbreak.

Historical Context and Mortality Data

Historical information was obtained from the official report of the outbreak held in Wellington from Archives New Zealand (27), the Inquiry Report from the Transport Epidemic Committee to the House of Representatives of New Zealand, dated December 9, 1918, and the written account of Colonel E.J. O'Neill as officer commanding the 40th Reinforcements (25). Individualized data on all military personnel on the July 1918 sailing of HMNZT Tahiti recorded in the Cenotaph database were obtained from the Auckland War Memorial Museum (28). An electronic dataset (Roll-of-Honor) covering all deaths among New Zealand military personnel during World War I was obtained from Peter Dennis (Australian Defence Force Academy, University of New South Wales, Canberra, Australian Capital Territory). The Roll-of-Honor and Cenotaph databases were matched to identify persons onboard HMNZT Tahiti whose death from the disease had been listed. The precise cause of death was only reported in the Cenotaph database for 3 of 77 case-patients and was recorded as influenza or pneumonia. One death recorded as a drowning was included because a recently published study showed that the drowning occurred when a febrile soldier aboard HMNZT Tahiti threw himself into the sea (29).

full-text (large):
Pandemic Influenza on Troop Ship, 1918 | CDC EID


Suggested Citation for this Article

Summers JA, Wilson N, Baker MG, Shanks GD. Mortality risk factors for pandemic influenza on New Zealand troop ship, 1918. Emerg Infect Dis [serial on the Internet]. 2010 Dec [date cited]. http://www.cdc.gov/EID/content/16/12/1931.htm

DOI: 10.3201/eid1612.100429

Comments to the Authors

Please use the form below to submit correspondence to the authors or contact them at the following address:

Jennifer A. Summers, Department of Public Health, University of Otago, Box 7343, Wellington South, Wellington 5011, New Zealand; email: jenn.summers@gmail.com

NIAID Media Availability: Landmark Discoveries Characterize NIH HIV/AIDS Research in 2010

FOR IMMEDIATE RELEASE
Monday, Nov. 29, 2010

NIAID MEDIA AVAILABILITY
Landmark Discoveries Characterize NIH HIV/AIDS Research in 2010

WHAT:
On World AIDS Day, December 1st, the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, reflects on encouraging milestones from the past year in HIV/AIDS research that are advancing us toward controlling and ultimately ending the pandemic.

* Pre-exposure prophylaxis (PrEP) proves effective at reducing the risk of HIV acquisition among men who have sex with men: As published Nov. 23 in the New England Journal of Medicine online, the NIAID-sponsored study known as iPrEx found that a daily dose of an oral antiretroviral drug approved to treat HIV infection reduced the risk of HIV acquisition among men who have sex with men by 44 percent. Even higher rates of effectiveness, up to 73 percent, were found among study participants who adhered most closely to the daily drug regimen. NIAID and The Gates Foundation co-funded the iPrEx study. Additional and continued research is needed to determine whether PrEP will be similarly effective at preventing HIV infection in other at-risk populations.

* Vaginal microbicide prevents HIV infection: For the first time in nearly 15 years of research, scientists discovered a vaginal microbicide gel that gives women a level of protection against HIV infection. The CAPRISA 004 study, conducted by the Centre for the AIDS Programme of Research in South Africa (CAPRISA), found that the use of a microbicide gel containing a 1 percent concentration of the antiretroviral drug tenofovir resulted in 39 percent fewer HIV infections compared with a placebo gel. NIAID was among the organizations that provided substantial support and resources to establish the infrastructure and training for CAPRISA. Ongoing and future clinical trials will build on these study results with the goal of bringing a safe and effective microbicide to the general public.

* Antibody discoveries propel HIV vaccine research: In the past year, researchers have discovered at least eight antibodies that can stop a wide range of HIV strains from infecting human cells in the laboratory. For instance, a team led by NIAID scientists discovered two human antibodies that can block more than 90 percent of known global HIV strains from infecting human cells, and demonstrated how one of these disease-fighting proteins accomplishes this feat. Learning the structure of the new antibodies and where they bind to the virus is helping equip scientists with the tools to design a vaccine that could stimulate healthy people to make some of the antibodies as protection against HIV infection.

* New hope for people co-infected with HIV and tuberculosis (TB): The Cambodia-based study known as CAMELIA demonstrated that the survival of untreated, HIV-infected adults with very weak immune systems and newly diagnosed TB can be prolonged by starting antiretroviral therapy two weeks after beginning TB treatment, rather than waiting eight weeks, as had been standard. This finding is valuable because beginning treatment for HIV in some highly immunocompromised individuals paradoxically can worsen the symptoms of co-infections such as TB, yet waiting too long to start antiretroviral therapy can lead to death. TB accounted for nearly a quarter of the 2 million HIV-related deaths worldwide in 2008. NIAID and the French National Agency for Research on AIDS and Viral Hepatitis co-funded the CAMELIA study.

WHO:
Anthony S. Fauci, M.D., NIAID director; Carl Dieffenbach, Ph.D., director of the NIAID Division of AIDS; and Gary J. Nabel, M.D., Ph.D., director of the NIAID Vaccine Research Center, are available for comment.

CONTACT:
To schedule interviews, please contact Laura Sivitz Leifman, 301-402-1663, niaidnews@niaid.nih.gov.

NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at www.niaid.nih.gov.

The National Institutes of Health (NIH)—The Nation's Medical Research Agency—includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIAID Media Availability: Landmark Discoveries Characterize NIH HIV/AIDS Research in 2010

Proposed Cigarette Product Warning Labels

FDA Announces Proposal for New Cigarette Health Warnings

On November 10, HHS and FDA announced a proposal to require new and prominent health warnings on all cigarette packages, cartons, and advertisements. The inclusion of larger and more noticeable graphic health warnings will clearly convey the negative health consequences of smoking to educate all Americans about the health risks of cigarettes. The public is being encouraged to comment directly on these proposed warnings and to help FDA choose the graphic health warnings required by law for use on cigarette packages, cartons, and advertisements. The submitted comments will be officially considered in the final warnings that will be issued by June 22, 2011.

Proposed Cigarette Product Warning Labels


Overview
The Family Smoking Prevention and Tobacco Control Act (Tobacco Control Act) requires that cigarette packages and advertisements have larger and more visible graphic health warnings.

FDA issued a proposed rule, Required Warnings for Cigarette Packages and Advertisements, proposing to modify the required warnings that appear on cigarette packages and in cigarette advertisements. These new required warnings would consist of nine new textual warning statements accompanied by color graphics depicting the negative health consequences of smoking.

Timeline for Final Regulations
The Tobacco Control Act requires FDA to issue final regulations requiring these color graphics by June 22, 2011. It also specifies that the requirement for the new health warnings on cigarette packages and advertisements will take effect 15 months after issuance of this final rule.

FULL-TEXT:
Proposed Cigarette Product Warning Labels

Trials use technology to help young adults achieve healthy weights, November 29, 2010 News Release - National Institutes of Health (NIH)

Monday, November 29, 2010
Contact:
NHLBI Communications Office
NHLBI_news@nhlbi.nih.gov
301-496-4236

Trials use technology to help young adults achieve healthy weights

Seven NIH-funded trials seek participants to use Web, cell phones, social networking

To engage young adults in protecting their future heart health, the National Institutes of Health's National Heart, Lung, and Blood Institute (NHLBI) has funded seven clinical trials that combine behavioral weight management programs with technologies such as text messaging, online social networking, and Bluetooth-enabled scales. Several of the trials have begun seeking participants.

"These studies have the potential to teach us about successfully engaging young adults in achieving a healthy weight at a critical time in their lives," said Susan B. Shurin, M.D., acting director of the NHLBI. "Learning effective strategies for weight management further empowers young adults to protect their future heart health. These studies are designed to provide evidence to help us guide young adults toward approaches that work and allow them to choose the options that work best for them."

The Early Adult Reduction of Weight through Lifestyle Intervention (EARLY) Trials seek to prevent weight gain and promote weight loss among young adults, defined as ages 18-35, through healthy eating and physical activity. The trials are receiving a total of $36 million over five years and are partially supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

"We expect the use of technology will help us reach young adults at risk of weight gain and inspire them to stay at a healthy weight," said trials steering committee chair Leslie Lytle, Ph.D., who is leading a trial that features Web-based social networking among community college students.

Previous NHLBI research has shown that people aged 18-49 gain an average of 1-2 pounds each year, with the largest weight gain of 3 pounds per year occurring in 20-29-year-olds. Such weight gain can lead to high blood pressure, high blood cholesterol, diabetes, and other risk factors for cardiovascular disease. Few studies have examined how to effectively engage this high-risk age group in achieving and maintaining a healthy weight.

The following individual trials will help reach young adults aged 18-35:

* Treating Adults at Risk for Weight Gain with Interactive Technology (TARGIT) at the University of Tennessee, Memphis, will use the iPod Touch, webinars, and podcasts to deliver a behavioral weight loss intervention to young adults who are trying to quit smoking. Delivered in conjunction with an effective tobacco quit line, TARGIT will be the first combined tobacco cessation-weight management program targeted to young adults. There will be 330 participants. ClinicalTrials.gov ID: NCT01199185. Participant contact: (901) 448-8400 or www.targitstudy.org
* Innovative Approaches for Diet, Exercise, and Activity (IDEA) at the University of Pittsburgh will test how a weight loss intervention enhanced with text message reminders and wearable exercise monitors improves weight loss as compared to a standard intervention. There will be 480 young adult participants. ClinicalTrials.gov ID: NCT01131871. Participant contact: (412) 488-4184 or www.idea.pitt.edu
* eMoms Roc: Electronically Mediated Weight Interventions for Pregnant and Postpartum Women at Cornell University/University of Rochester, N.Y., will test Internet-based programs to promote the health of pregnant and postpartum women. These e-interventions will focus on diet, physical activity, weight, and other issues of interest to childbearing women. The 3,500 participants will be ethnically and socioeconomically diverse women in their first 20 weeks of pregnancy. eMoms Roc is co-funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development. Participant contact: http://www.emomsroc.org/
* Choosing Healthy Options in College Environments and Settings (CHOICES) at the University of Minnesota, Minneapolis, will test a for-credit course that includes Web-based social networking to prevent unhealthy weight gain in 440 student participants attending two-year community colleges. ClinicalTrials.gov ID: NCT01134783. Participant contact: (612) 624-2374 or Megan Treziok (trezi003@umn.edu)
* Cell Phone Intervention for You (CITY) at Duke University, Durham, N.C., will test two weight loss approaches against a control in a total of 360 participants. In one approach, participants will use cell phones for self-monitoring and social networking. In the other, they use cell phones for self-monitoring only and also receive personal coaching. ClinicalTrials.gov ID: NCT01092364. Participant contact: (919) 681-CITY (2489) or www.dukecitystudy.org
* Social/Mobile Approaches to Reducing Weight (SMART) at the University of California, San Diego, will test a behavioral intervention that uses mobile phones, Facebook, and the Web. The goal is to help 380 overweight or obese university student participants lose weight. ClinicalTrials.gov ID: NCT01200459. Participant contact: smartinfo@ucsd.edu
* Study of Novel Approaches for Prevention (SNAP) at Brown University/Miriam Hospital will test a Web-based weight management intervention against a control in 600 young adult participants. The goal is to help participants self-regulate their weight by either making large changes in their eating and exercise habits to lose weight, or making small changes to prevent or reverse weight gain. ClinicalTrials.gov ID: NCT01183689. Participant contact: www.snapstudy.org

The trial teams have completed initial research on the best ways to recruit young adults and keep them active in the proposed trials. Some have now begun to recruit participants for the two-year, randomized, controlled clinical trials. All seven trials are expected to start enrollment by spring 2011. Although each trial is slightly different and will be conducted at a single institution, the teams are using a set of common measures and questionnaires so they can better compare their findings when the trials are complete.

"Comparing findings and pooling data from all seven studies will maximize what the research community learns about developing strategies to address weight control among young adults," said Catherine Loria, Ph.D., a nutritional epidemiologist in the NHLBI's Division of Cardiovascular Sciences.

People interested in participating in one of the trials are encouraged to contact each site directly. More information can be found at www.clinicaltrials.gov.

To schedule an interview with an NHLBI spokesperson, contact the NHLBI Communications Office at 301-496-4236 or nhlbi_news@nhlbi.nih.gov.

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases, and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases, information on NHLBI’s role in the American Recovery and Reinvestment Act, and other materials are available online at www.nhlbi.nih.gov.

The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute's Web site at http://www.nichd.nih.gov.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

Resources:

* Early Adult Reduction of Weight through Lifestyle Intervention (EARLY) Trials: http://www.earlytrials.org
* Coronary Artery Risk Development in Young Adults (CARDIA): https://biolincc.nhlbi.nih.gov/studies/cardia/
* What Are Overweight and Obesity?: http://www.nhlbi.nih.gov/health/dci/Diseases/obe/obe_whatare.html

Trials use technology to help young adults achieve healthy weights, November 29, 2010 News Release - National Institutes of Health (NIH)

Scientists Find Way to Partially Reverse Aging in Mice: MedlinePlus

Scientists Find Way to Partially Reverse Aging in Mice
Impact on people is unclear at this early stage of research, study author says

URL of this page: http://www.nlm.nih.gov/medlineplus/news/fullstory_106051.html (*this news item will not be available after 02/27/2011)

By Robert Preidt
Monday, November 29, 2010
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SUNDAY, Nov. 28 (HealthDay News) -- U.S. scientists say they have partially reversed age-related degeneration in mice, leading to new brain and testes growth, improved fertility and the return of lost cognitive function, or thinking skills.

The advance in aging science was achieved by working with telomerase genes in the mice, said the team at the Dana-Farber Cancer Institute in Boston.

The researchers developed mice with a controllable telomerase gene. (Telomerase is an enzyme that helps maintain telomeres -- the protective "caps" on the ends of chromosomes.) As people age, low levels of telomerase lead to progressive erosion and shortening of the telomeres, resulting in physical and mental decline, the study authors explained in a news release from the institute.

Creating mice with a controllable telomerase switch enabled the scientists to create prematurely aged mice. The switch also enabled the team to determine that reactivating telomerase in the mice could restore telomeres and reduce the signs and symptoms of aging.

In addition, the mice did not show signs of cancer -- a key concern because cancer cells can use telomerase to make themselves virtually immortal. Researchers noted that this is an important area of study for future investigation.

In the future, it may be possible to use this approach to treat people with conditions such as rare genetic premature aging syndromes, in which shortened telomeres play an important role, said study senior author Dr. Ronald A. DePinho, director of Dana-Farber's Belfer Institute of Applied Cancer Science.

"Whether this would impact on normal aging is a more difficult question," he said in the news release. "But it is notable that telomere loss is associated with age-associated disorders and thus restoration of telomeres could alleviate such decline."

DePinho also said the study may lead to new directions for regenerative medicine because the findings suggest that dormant adult stem cells in extremely aged tissues remain viable and can be reactivated to repair tissue damage.

"If you can remove the underlying damage and stresses that drive the aging process and cause stem cells to go into growth arrest, you may be able to recruit them back into a regenerative response to rejuvenate tissues and maintain health in the aged," he said in the release.

The study was released online in advance of publication in an upcoming print issue of the journal Nature.

SOURCE: Dana-Farber Cancer Institute, news release, Nov. 28, 2010
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Scientists Find Way to Partially Reverse Aging in Mice: MedlinePlus

Type 1 Diabetes Death Rate is Falling, But Not Fast Enough: MedlinePlus

Type 1 Diabetes Death Rate is Falling, But Not Fast Enough
Average rate is still 7 times higher in people with the disease vs those without it, study finds

URL of this page: http://www.nlm.nih.gov/medlineplus/news/fullstory_106027.html (*this news item will not be available after 02/24/2011)

Friday, November 26, 2010
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FRIDAY, Nov. 26 (HealthDay News) Death rates have dropped significantly in people with type 1 diabetes, according to a new study.

Researchers also found that people diagnosed in the late 1970s have an even lower mortality rate compared with those diagnosed in the 1960s.

"The encouraging thing is that, given good [diabetes] control, you can have a near-normal life expectancy," said the study's senior author, Dr. Trevor J. Orchard, a professor of epidemiology, medicine and pediatrics in the Graduate School of Public Health at the University of Pittsburgh, Penn.

But, the research also found that mortality rates for people with type 1 still remain significantly higher than for the general population -- seven times higher, in fact. And some groups, such as women, continue to have disproportionately higher mortality rates: women with type 1 diabetes are 13 times more likely to die than are their female counterparts without the disease.

Results of the study are published in the December issue of Diabetes Care.

Type 1 diabetes is an autoimmune disease that causes the body's immune system to mistakenly attack the body's insulin-producing cells. As a result, people with type 1 diabetes make little or no insulin, and must rely on lifelong insulin replacement either through injections or tiny catheter attached to an insulin pump. Insulin is a hormone that allows the body to use blood sugar.

Insulin replacement therapy isn't as effective as naturally-produced insulin, however. People with type 1 diabetes often have blood sugar levels that are too high or too low, because it's difficult to predict exactly how much insulin you'll need. When blood sugar levels are too high due to too little insulin, it causes damage that can lead to long term complications, such as an increased risk of kidney failure and heart disease. On the other hand, if you have too much insulin, blood sugar levels can drop dangerously low, potentially leading to coma or death.

These factors are why type 1 diabetes has long been associated with a significantly increased risk of death, and a shortened life expectancy.

However, numerous improvements have been made in type 1 diabetes management during the past 30 years, including the advent of blood glucose monitors, insulin pumps, newer insulins, better medications to prevent complications and most recently continuous glucose monitors.

To assess whether or not these advances have had any effect on life expectancy, Orchard, along with his student, Aaron Secrest, and their colleagues, reviewed data from a type 1 diabetes registry from Allegheny County, Pennsylvania. The registry contained information on almost 1,100 people under the age of 18 at the time they were diagnosed with type 1 diabetes.

The children were sorted into three groups based on the year of their diagnosis: 1965 to 1969, 1970 to 1974 and 1975 to 1979. As of January 2008, 279 of the study participants had died, a death rate that is 7 times higher than would be expected in the general population.

When the researchers broke the mortality rate down by the time of diagnosis, they found that those diagnosed later had a much improved mortality rate. The group diagnosed in the 1960s had a 9.3 times higher mortality rate than the general population, while the early 1970s group had a 7.5 times higher mortality than the general population. For the late 1970s group, mortality had dropped to 5.6 times higher than the general population.

The mortality rate in women with type 1 diabetes remained significantly higher, however, at 13 times the rate expected in women in the general population.

In addition, blacks with diabetes had a significantly lower 30-year survival rate than their white counterparts -- 57 percent versus 83 percent, according to the study.

Although Orchard said it isn't clear why women and blacks have higher-than-expected mortality, Barbara Araneo, director of complications therapies at the Juvenile Diabetes Research Foundation, said that both discrepancies have been found in other research, and that one theory is that blacks may have a greater genetic susceptibility to heart disease or high blood pressure. And, for women, she said previous research has shown that, "women with diabetes lose their innate protection against [heart disease], similar to the loss sustained in postmenopausal phases of life." But, she said, it's not clear how diabetes causes this loss.

The overall message of the study, however, is a positive one.

"The outcome of this study shows that diabetes care has improved in many ways over the last couple of decades, and as a result people with diabetes are living longer now," said Araneo, adding, "Managing and taking good care of your diabetes is the surest way to reduce the risk of developing complications later in life."

"What we're seeing now is incredibly encouraging, but it's not necessarily the full story yet," said Orchard, who noted that improvements in diabetes care should continue to lower mortality rates in people with type 1 diabetes.

SOURCES: Trevor J. Orchard, M.B.B.C.H, professor, epidemiology, medicine and pediatrics, Graduate School of Public Health, University of Pittsburgh, Penn.; Barbara Araneo, Ph.D., director, complications therapies, Juvenile Diabetes Research Foundation; December 2010 Diabetes Care
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Type 1 Diabetes Death Rate is Falling, But Not Fast Enough: MedlinePlus