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Katie Greenland,
Jane Whelan,
Ewout Fanoy,
Marjon Borgert,
Koen Hulshof,
Kioe-Bing Yap, Corien Swaan,
Tjibbe Donker,
Rob van Binnendijk,
Hester de Melker,
Susan Hahné
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ABSTRACT: We investigated a mumps outbreak within a highly vaccinated university student population in the Netherlands by conducting a retrospective cohort study among members of university societies in Delft, Leiden and Utrecht. We used an online questionnaire asking for demographic information, potential behavioural risk factors for mumps and the occurrence of mumps. Vaccine status from the national vaccination register was used. Overall, 989 students participated (20% response rate). Registered vaccination status was available for 776 individuals, of whom 760 (98%) had been vaccinated at least once and 729 (94%) at least twice. The mumps attack rate (AR) was 13.2% (95%CI 11.1-15.5%). Attending a large student party, being unvaccinated and living with more than 15 housemates were independently associated with mumps ((RR 42 (95%CI 10.1-172.4); 3.1 (95%CI 1.7-5.6) and 1.8 (95%CI 1.1-3.1), respectively). The adjusted VE estimate for two doses of MMR was 68% (95%CI 41-82%). We did not identify additional risk factors for mumps among party attendees. The most likely cause of this outbreak was intense social mixing during the party and the dense communal living environment of the students. High coverage of MMR vaccination in childhood did not prevent an outbreak of mumps in this student population.
Vaccine 05/2012; 30(31):4676-80. · 3.77 Impact Factor
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Emerging Infectious Diseases 01/2012; 18(1):191-3. · 6.79 Impact Factor
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Adam Meijer,
Marcel Jonges,
Floor Abbink,
Wim Ang,
Janko van Beek,
Matthias Beersma,
Peter Bloembergen,
Charles Boucher,
Eric Claas,
Gé Donker, [......],
Annelies Riezebos-Brilman,
Martin Schutten,
Fré Sebens,
Foekje Stelma, Corien Swaan,
Aura Timen,
Annemarie van 't Veen,
Erhard van der Vries,
Margreet te Wierik,
Marion Koopmans
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ABSTRACT: Enhanced surveillance of infections due to the pandemic A(H1N1) influenza virus, which included monitoring for antiviral resistance, was carried out in the Netherlands from late April 2009 through late May 2010. More than 1100 instances of infection with the pandemic A(H1N1) influenza virus from 2009 and 2010 [A(H1N1) 2009] distributed across this period were analyzed. Of these, 19 cases of oseltamivir-resistant virus harboring the H275Y mutation in the neuraminidase (NA) were detected. The mean 50% inhibitory concentration (IC50) levels for oseltamivir- and zanamivir-susceptible A(H1N1) 2009 viruses were 1.4-fold and 2-fold, respectively, lower than for the seasonal A(H1N1) influenza viruses from 2007/2008; for oseltamivir-resistant A(H1N1) 2009 virus the IC50 was 2.9-fold lower. Eighteen of the 19 patients with oseltamivir-resistant virus showed prolonged shedding of the virus and developed resistance while on oseltamivir therapy. Sixteen of these 18 patients had an immunodeficiency, of whom 11 had a hematologic disorder. The two other patients had another underlying disease. Six of the patients who had an underlying disease died; of these, five had received cytostatic or immunosuppressive therapy. No indications for onward transmission of resistant viruses were found. This study showed that the main association for the emergence of cases of oseltamivir-resistant A(H1N1) 2009 virus was receiving antiviral therapy and having drug-induced immunosuppression or an hematologic disorder. Except for a single case of a resistant virus not linked to oseltamivir therapy, the absence of detection of resistant variants in community specimens and in specimens from contacts of cases with resistant virus suggested that the spread of resistant A(H1N1) 2009 virus was limited. Containment may have been the cumulative result of impaired NA function, successful isolation of the patients, and prophylactic measures to limit exposure.
Antiviral research 07/2011; 92(1):81-9. · 3.61 Impact Factor
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ABSTRACT: To the Editor: From June 1 through October 16, 2008, an outbreak of 99 reported measles cases occurred in the Netherlands (1). This outbreak was the largest measles outbreak in the Netherlands since 1999-2000, when >/=3,200 cases, including 3 deaths, were reported (2).
Emerging Infectious Diseases 03/2010; 16(3):567-9. · 6.79 Impact Factor
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Michiel van Boven,
Tjibbe Donker,
Mariken van der Lubben,
Rianne B van Gageldonk-Lafeber,
Dennis E te Beest,
Marion Koopmans,
Adam Meijer,
Aura Timen, Corien Swaan,
Anton Dalhuijsen,
Susan Hahné,
Anneke van den Hoek,
Peter Teunis,
Marianne A B van der Sande,
Jacco Wallinga
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ABSTRACT: Despite impressive advances in our understanding of the biology of novel influenza A(H1N1) virus, little is as yet known about its transmission efficiency in close contact places such as households, schools, and workplaces. These are widely believed to be key in supporting propagating spread, and it is therefore of importance to assess the transmission levels of the virus in such settings.
We estimate the transmissibility of novel influenza A(H1N1) in 47 households in the Netherlands using stochastic epidemic models. All households contained a laboratory confirmed index case, and antiviral drugs (oseltamivir) were given to both the index case and other households members within 24 hours after detection of the index case. Among the 109 household contacts there were 9 secondary infections in 7 households. The overall estimated secondary attack rate is low (0.075, 95%CI: 0.037-0.13). There is statistical evidence indicating that older persons are less susceptible to infection than younger persons (relative susceptibility of older persons: 0.11, 95%CI: 0.024-0.43. Notably, the secondary attack rate from an older to a younger person is 0.35 (95%CI: 0.14-0.61) when using an age classification of <or=12 versus >12 years, and 0.28 (95%CI: 0.12-0.50) when using an age classification of <or=18 versus >18 years.
Our results indicate that the overall household transmission levels of novel influenza A(H1N1) in antiviral-treated households were low in the early stage of the epidemic. The relatively high rate of adult-to-child transmission indicates that control measures focused on this transmission route will be most effective in minimizing the total number of infections.
PLoS ONE 01/2010; 5(7):e11442. · 4.09 Impact Factor
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Grace M S Tjon,
Roel A Coutinho,
Anneke van den Hoek,
Sylvia Esman,
Clementine J Wijkmans,
Christian J P A Hoebe,
Bert Wolters, Corien Swaan,
Ronald B Geskus,
Nicole Dukers,
Sylvia M Bruisten
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ABSTRACT: The duration and level of virus excretion in blood and faeces of patients with hepatitis A virus (HAV) infection were studied in relation to levels of alanine aminotransferase (ALT), disease severity and HAV genotype. Clinical data, blood and faeces were collected from 27 patients with acute hepatitis A (median age: 33 years) for a maximum of 26 weeks. Single blood donations from 55 other patients with acute HAV (median age: 32 years) were also used. Virus loads were quantified by competitive nested RT-PCR. HAV was excreted in faeces for a median period of 81 days after disease onset, with 50% of patients still excreting high levels at Day 36 (2 x 10(6) - 2 x 10(8) copies/ml faeces suspension). Viraemia was detected, but not quantifiable, for a median period of 42 days. In the first 10 days of illness, higher ALT levels were correlated with higher viraemia levels. Comparison of patients infected with genotype 1a with those infected with type 1b did not differ significantly in terms of the duration of HAV excretion or jaundice. In conclusion, faecal excretion of HAV is at a high titre in the first month, perhaps making patients infectious for a longer period than assumed currently. Blood banks should be aware that viraemia may be present for more than 1 month, and genotype did not affect the duration of virus excretion or jaundice.
Journal of Medical Virology 12/2006; 78(11):1398-405. · 2.82 Impact Factor
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Grace M.S. Tjon,
Roel A. Coutinho,
Anneke van den Hoek,
Sylvia Esman,
Clementine J. Wijkmans,
Christian J.P.A. Hoebe,
Bert Wolters, Corien Swaan,
Ronald B. Geskus,
Nicole Dukers,
Sylvia M. Bruisten
[show abstract]
[hide abstract]
ABSTRACT: The duration and level of virus excretion in blood and faeces of patients with hepatitis A virus (HAV) infection were studied in relation to levels of alanine aminotransferase (ALT), disease severity and HAV genotype. Clinical data, blood and faeces were collected from 27 patients with acute hepatitis A (median age: 33 years) for a maximum of 26 weeks. Single blood donations from 55 other patients with acute HAV (median age: 32 years) were also used. Virus loads were quantified by competitive nested RT-PCR. HAV was excreted in faeces for a median period of 81 days after disease onset, with 50% of patients still excreting high levels at Day 36 (2 × 106–2 × 108 copies/ml faeces suspension). Viraemia was detected, but not quantifiable, for a median period of 42 days. In the first 10 days of illness, higher ALT levels were correlated with higher viraemia levels. Comparison of patients infected with genotype 1a with those infected with type 1b did not differ significantly in terms of the duration of HAV excretion or jaundice. In conclusion, faecal excretion of HAV is at a high titre in the first month, perhaps making patients infectious for a longer period than assumed currently. Blood banks should be aware that viraemia may be present for more than 1 month, and genotype did not affect the duration of virus excretion or jaundice. J. Med. Virol. 78:1398–1405, 2006. © 2006 Wiley-Liss, Inc.
Journal of Medical Virology 10/2006; 78(11):1398 - 1405. · 2.82 Impact Factor
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Grace M S Tjon,
Roel A Coutinho,
Anneke van den Hoek,
Sylvia Esman,
Clementine J Wijkmans,
Christian J P A Hoebe,
Bert Wolters, Corien Swaan,
Ronald B Geskus,
Nicole H T M Dukers,
Sylvia M Bruisten
[show abstract]
[hide abstract]
ABSTRACT: The duration and level of virus excretion in blood and faeces of patients with hepatitis A virus (HAV) infection were studied in relation to levels of alanine aminotransferase (ALT), disease severity and HAV genotype. Clinical data, blood and faeces were collected from 27 patients with acute hepatitis A (median age: 33 years) for a maximum of 26 weeks. Single blood donations from 55 other patients with acute HAV (median age: 32 years) were also used. Virus loads were quantified by competitive nested RT-PCR. HAV was excreted in faeces for a median period of 81 days after disease onset, with 50% of patients still excreting high levels at Day 36 (2 x 10(6) - 2 x 10(8) copies/ml faeces suspension). Viraemia was detected, but not quantifiable, for a median period of 42 days. In the first 10 days of illness, higher ALT levels were correlated with higher viraemia levels. Comparison of patients infected with genotype 1a with those infected with type 1b did not differ significantly in terms of the duration of HAV excretion or jaundice. In conclusion, faecal excretion of HAV is at a high titre in the first month, perhaps making patients infectious for a longer period than assumed currently. Blood banks should be aware that viraemia may be present for more than 1 month, and genotype did not affect the duration of virus excretion or jaundice.
