A Organização Mundial da Saúde (OMS) decreta em 10/08/2010 o início da fase pós-pandêmica do vírus Influenza Pandêmica (H1N1) 2009

MINISTÉRIO DA SAÚDE

SECRETARIA DE VIGILÂNCIA EM SAÚDE

DEPARTAMENTO DE VIGILÂNCIA EPIDEMIOLÓGICA

COORDENAÇÃO GERAL DE DOENÇAS TRANSMISSÍVEIS

COORDENAÇÃO DE VIGILÂNCIA DAS DOENÇAS DE TRANSMISSÃO RESPIRATÓRIAS E  IMUNOPREVENÍVEIS

SCS, Quadra 04, Edifício Principal, 2º andar – CEP: 70.304-000

(61) 3213-8092/8097/8098

NOTA TÉCNICA N.º 15/2010/COVER/CGDT/DEVEP/SVS/MS

Assunto: A Organização Mundial da Saúde (OMS) decreta em 10/08/2010 o início da fase pós-pandêmica do vírus Influenza Pandêmica (H1N1) 2009.

1. Nessa terça-feira, 10 de agosto de 2010, a Organização Mundial da Saúde (OMS) anunciou o início da fase pós-pandêmica da gripe H1N1 (Figura abaixo). Isso significa que o vírus continua circulando no mundo, mas junto com outros vírus sazonais (da gripe comum) e em intensidade diferente entre os países. Alguns países, como a Índia e Nova Zelândia, ainda tem apresentado epidemia pela gripe H1N1. De acordo com a OMS, o monitoramento epidemiológico mostrou que o vírus H1N1 não sofreu mutação para formas mais letais, a resistência ao antiviral fosfato de oseltamivir não se desenvolveu de forma importante e a vacina se mostrou uma medida eficaz para proteger a população.

Fonte: http://www.who.int/en/. Acesso em 10/08/2010.

2. Essas evidências contribuíram para a decisão de mudar o nível de alerta para fase pós-pandêmica. No entanto, a OMS alerta que, mesmo com a mudança de nível, o monitoramento e as ações preventivas devem continuar, especialmente em relação aos grupos mais vulneráveis para desenvolver formas graves da doença, como gestantes, portadores de doenças crônicas e crianças menores de dois anos. "A vigilância contínua é extremamente importante", orientou a diretora-geral da OMS, Margareth Chan, que ressaltou a importância da vacinação no enfrentamento da pandemia.

3. O Ministro da Saúde, José Gomes Temporão, reforça as recomendações da OMS e destaca a vacinação recorde realizada no Brasil. “Fizemos um imenso esforço conjunto e conseguimos vacinar, em apenas três meses, 88 milhões de pessoas. Isso nos permite ter todos os índices de gripe em queda e a demanda por atendimento médico por doenças respiratórias está menor que o esperado para esta época do ano”, afirma o ministro. Ele ressalta, no entanto, que é necessário continuar monitorando a circulação do vírus e manter os cuidados típicos do período do inverno, como os hábitos de higiene.

4. A análise dos indicadores qualitativos informados à OMS revela, além da queda de demanda por atendimento médico, que o Brasil apresenta, atualmente, uma intensidade baixa a moderada na proporção de pessoas com doenças respiratórias agudas.

5. No Brasil, no ano epidemiológico de 2009, foram confirmados 46.100 casos e 2.051 óbitos por influenza pandêmica. De 1º de janeiro a 31 de julho de 2010, foram confirmados 95 óbitos e 753 casos de influenza pandêmica em pacientes hospitalizados e, desde o mês de março, observa-se uma redução no número dos casos graves e óbitos pela influenza pandêmica em todo o país. Essas informações mostram que ações adequadas de vigilância, como a estratégia de vacinação desenvolvida, resultam positivamente para o controle da doença. No entanto, seguindo orientações da OMS, o Ministério da Saúde manterá, junto com os estados e os municípios, o monitoramento da gripe H1N1.

6. Mesmo com estes resultados positivos, é importante que as ações de controle e prevenção no país não sejam minimizadas, somente sejam adequadas para a nova fase. Portanto, a população deve continuar adotando hábitos de higiene (como lavar as mãos freqüentemente e usar lenços descartáveis ao tossir e espirrar) e ter atenção especial com crianças, gestantes, portadores de doenças crônicas (como cardiopatias, diabetes, nefropatias e outras) e idosos. Ao surgirem sinais de gripe ou resfriado, como febre, tosse, dor de cabeça e nas articulações, as pessoas não devem tomar remédios por conta própria (pois eles podem mascarar sintomas e dificultar o diagnóstico) e devem procurar o serviço de saúde mais próximo.

7. Em relação à rotina de vigilância de influenza, as secretarias estaduais e municipais de saúde devem priorizar:

a) O monitoramento de eventos incomuns;

b) A investigação de casos graves individuais ou em situações de surto;

c) O monitorando das infecções respiratórias agudas e vírus circulantes;

d) A manutenção e atualização dos fluxos de informações.

8. Para maiores esclarecimentos, a área técnica nacional de influenza se coloca a disposição através do correio eletrônico gripe@saude.gov.br.

Brasília, 11 de agosto de 2010.


Recebido por e-mail de Marcelo M. Pinto

Debates aquecem evento da FIOCRUZ

Primeiro dia do Seminário As relações da Saúde Pública com a Imprensa – o caso da Influenza A (H1N1) foi marcado por reflexões e participação do público

              

“A mídia vendia o medo”, disse o chefe da Assessoria de Comunicação do Ministério da Saúde, Marcier Trombiere, no início da oficina Por dentro do Ministério da Saúde: a estratégia de comunicação do MS sobre a Influenza A (H1N1). Durante a apresentação, o assessor mostrou ao público como é feita a comunicação de emergência e quais estratégias o Ministério adotou a partir do alerta da doença. “O objetivo do planejamento era passar informações para a população de maneira clara, sem amedrontar. A medida era de prevenção, mas não foi o que aconteceu”, complementou.

Marcier falou ainda sobre a importância do debate. “Estes eventos nos proporcionam a oportunidade de compartilhar experiências fundamentais para receber novas informações. O momento é de reflexão dos profissionais após as tensões. É hora de avaliar nossas responsabilidades”.

Já a chefe de redação do Núcleo de Comunicação da Secretaria de Vigilância em Saúde do MS, Beth Almeida, falou sobre a atuação do Núcleo e a articulação com as secretarias estaduais durante a crise. Segundo Beth, o alerta sobre a pandemia veio do Centro de informações Estratégicas em Vigilância Sanitária (CIEVS) e o NUCOM deveria preparar as assessorias de imprensa para fornecer informações precisas. “A responsabilidade do jornalista deve ser a mesma do médico”, comparou. E acrescentou: “Um dos princípios para da comunicação de risco é anunciar rápido e com transparência. A pandemia H1N1 foi a primeira que ocorreu em uma época com tantas ferramentas de comunicação disponíveis, pois a propagação da notícia foi muito mais fácil”.

O Seminário As relações da Saúde Pública com a Imprensa – o caso da Influenza A (H1N1), promovido pela FIOCRUZ Brasília, foi iniciado ontem, 25 de agosto, e contou com a presença de instituições como Ministério da Saúde, Secretaria de Saúde do DF, Sindicato dos Jornalistas, Fiocruz e os editores da TV Record e do Correio Braziliense.

A assessora de comunicação da Prefeitura de Sorocaba, Evenize Batista, veio à Brasília só para participar do Seminário. “Vim para buscar mais informações e avaliações sobre o trabalho da imprensa neste caso. Acho evidente a falta de preparo da mídia para lidar com assuntos relativos à saúde. Estou ansiosa pelo debate final”.

O jornalista e pesquisador da Associação de Laboratórios de Estudos Avançados em Jornalismo (LABJORN) da Unicamp, Marcel Silva, comentou sobre suas expectativas em relação aos debates. “O jornalista tem que ver o mundo fora da redação. A mídia está cada vez mais industrializada e sem reflexão. Quando se trata de saúde pública, deve-se ter cuidado, pois o alarde das notícias sobrecarregou os atendimentos nos sistemas de saúde. Os jornais não fizeram um planejamento como os gestores fizeram”, criticou.

O coordenador de atendimento e produção da assessoria de imprensa do MS, Rodrigo Hilário, fez uma perspectiva histórica dos cenários da crise, encerrando o primeiro dia do Seminário. “Temos que tratar a saúde da população com responsabilidade. O trabalho do jornalista reflete na vida das pessoas comuns, que não tem conhecimento aprofundado. Temos sempre que pensar no efeito que o nosso trabalho para estas pessoas, pois elas são o objetivo final do nosso trabalho”, concluiu.

Debates e mesas redondas

A programação do segundo dia de Seminário conta com a realização das mesas redondas Mídia e Saúde: os desafios, mitos e verdades sobre a Influenza A (H1N1) e Saúde Pública e Imprensa: interdependência e balanço da atuação.

O Seminário As relações da Saúde Pública com a Imprensa – o caso da Influenza A (H1N1) está sendo transmitido ao vivo pela internet, por meio de parceria com o Ministério da Saúde. O acesso é feito pelo site www.saude.gov.br/emtemporeal. Além de assistir ao debate, o internauta poderá enviar perguntas via internet, que são respondidas ao vivo pelos palestrantes.

Confira a programação completa no site http://www.fiocruzbrasilia.fiocruz.br.

Enviado  por e-mail por Paulo Abílio Lisboa

Novel Swine Influenza Virus Reassortants in Pigs, China

Emerging Infectious Diseases

Volume 16, Number 7–July 2010

Yuhai Bi,¹ Guanghua Fu,¹ Jing Chen,¹ Jinshan Peng, Yipeng Sun, Jingjing Wang, Juan Pu, Yi Zhang, Huijie Gao, Guangpeng Ma, Fulin Tian, Ian H. Brown, and Jinhua Liu 

Author affiliations: China Agricultural University, Beijing, People's Republic of China (Y. Bi, G. Fu, J. Chen, J. Peng, Y. Sun, J. Wang, J. Pu, Y. Zhang, H. Gao, J. Liu); Shandong Animal Disease Control Center, Jinan, People's Republic of China (J. Chen, F. Tian, J. Liu); Veterinary Laboratories Agency–Weybridge, Addlestone, Surrey, UK (I.H. Brown); China Rural Technology Development Center, Beijing (G. Ma); and Chongwen Animal Health Inspection Institute, Beijing (J. Peng)

Suggested citation for this article

Abstract

During swine influenza virus surveillance in pigs in China during 2006–2009, we isolated subtypes H1N1, H1N2, and H3N2 and found novel reassortment between contemporary swine and avian panzootic viruses. These reassortment events raise concern about generation of novel viruses in pigs, which could have pandemic potential.

Genetic characterization of pandemic (H1N1) 2009 virus has indicated that it may have derived from swine (1,2). However, because of the lack of systematic swine influenza surveillance, the generation pathway of the novel virus is uncertain. Therefore, we attempted to obtain more information about swine influenza viruses isolated from pigs.

The Study

During December 2006–February 2009 in the People's Republic of China, 3,546 samples from 3 main swine industry provinces—Fujian (765 samples), Guangdong (1,276 samples), and Shandong (1,505 samples)—were collected for influenza surveillance. Nasal and tracheal swab samples were collected from apparently healthy domestic pigs at abattoirs. Virus isolation and identification were performed as described (3). Of 29 strains of influenza A virus obtained, 19 were subtype H1N1, 1 subtype H1N2, and 9 subtype H3N2. Subtype H1N2 was isolated from diseased pigs in Guangdong Province in 2006; the others were isolated from healthy pigs. Isolation rates for subtypes H1N1 and H3N2 were 0.54% and 0.25%, respectively, indicating that subtype H1N1 viruses were predominant in the sampled pig population.

To determine genetic and antigenic characteristics, we conducted phylogenetic and antigenic analysis of all isolates. Cross–hemagglutination-inhibition showed that the subtype H3N2 viruses could be divided into 2 distinct antigenic groups (Appendix Table 1). Viruses of subtype H1 (swine/Shandong/101/2008, swine/Shandong/327/2008, and swine/Shandong/275/2009) reacted well with antiserum to the European avian-like swine virus, swine/FJ/204/2007, but not with antiserum to classical swine (H1N1) virus, swine/Guangdong/1/2005. The other 6 subtype H1N1 isolates reacted strongly with antiserum to swine/Guangdong/1/2005 (Appendix Table 1; Appendix Table 2), indicating that the antigenicity of the subtype H1N1 viruses could also be divided into 2 distinct antigenic groups. Subtype H1N2 virus (swine/Guangdong/1222/2006) had low reactivity with swine/Guangdong/1/2005 and swine/Fujian/204/2007 (Appendix Table 2), indicating that the antigenicity of subtype H1N2 isolate differed from that of classical and European avian-like swine viruses.

Phylogenetic analysis showed that the H3 hemagglutinin (HA) tree separated into avian and human lineages (Technical Appendix [ 1,054 KB, 11 pages], panel A), implying that at least 2 independent H3 sublineages of virus prevail in pigs in China. Neuraminidase (NA) genes of the 9 subtype H3N2 and 1 subtype H1N2 isolates were located in distinct lineages (Technical Appendix [ 1,054 KB, 11 pages], panel B). A cluster was formed by 4 strains of H3N2—swine/Fujian/43/2007, swine/Guangdong/811/2006, swine/Shandong/106/2007, and swine/Shandong/133/2007—and the cluster grouped with Eurasian avian (H9N2) viruses. Four H3N2 strains—swine/Guangdong/211/2006, swine/Guangdong/423/2006, swine/Guangdong/223/2006, and swine/Guangdong/968/2006—were located in the intermediate human sublineage represented by A/Beijing/39/75 (H3N2). One subtype H3N2 isolate, swine/Guangdong/7/2006, grouped closely with A/Moscow/10/99 (H3N2), and the subtype H1N2 isolate swine/Guangdong/1222/2006 shared close similarities with North American swine triple reassortant viruses (Technical Appendix [ 1,054 KB, 11 pages], panel B). These findings showed that viruses of avian, intermediate human, and recent human N2 sublineages were prevalent in pigs in China.

Phylogenic analysis of subtype H1 HA showed that the 9 subtype H1N1 isolates were located in either the classical or European avian-like swine lineages (Technical Appendix [ 1,054 KB, 11 pages], panel C). Swine/Guangdong/1222/2006, together with subtype H1N2 isolates from Hong Kong and subtype H1N2 strains from Guangxi, have a sister-like relationship with those of pandemic (H1N1) 2009 virus (Technical Appendix [ 1,054 KB, 11 pages], panel C). Consistent with characteristics of HA genes, NA genes of the 6 influenza (H1N1) strains isolated belong to classical swine lineages (Technical Appendix [ 1,054 KB, 11 pages], panel D). The other 3 isolates—swine/Shandong/101/2008, swine/Shandong/275/2008, and swine/Shandong/327/2008—together with pandemic (H1N1) 2009 virus, were located in the European avian-like swine group.

The polymerase acidic protein (PA) gene of swine/Guangdong/7/2006 (H3N2) was closely related to that of duck/Guangdong/12/2000 (H5N1) (Technical Appendix [ 1,054 KB, 11 pages], panel G), and other internal genes of swine/Guangdong/7/2006 were located in the recent human subtype H3N2 lineages (Technical Appendix [ 1,054 KB, 11 pages], panels E, F, and H–J). The matrix (M) gene of the 3 isolates—swine/Guangdong/211/2006 (H3N2), swine/Guangdong/223/2006 (H3N2), and swine/Guangdong/423/2006 (H3N2)—grouped in classical swine lineage (Technical Appendix [ 1,054 KB, 11 pages], panel I), and other internal genes were located in intermediate human subtype H3N2 lineage (Technical Appendix [ 1,054 KB, 11 pages], panels E–H and J). Except for the fact that the PA gene of swine/Guangdong/968/2006 and NA gene of swine/Guangdong/811/2006 are of the Eurasian H9N2 avian virus lineage (Technical Appendix [ 1,054 KB, 11 pages], panels B and G), the other internal genes are located in the same lineages with the 3 viruses swine/Guangdong/211/2006, swine/Guangdong/223/2006, and swine/Guangdong/423/2006 (Technical Appendix [ 1,054 KB, 11 pages], panels E–J). The polymerase basic protein 1 (PB1), PA, NP, and nonstructural (NS) genes of swine/Shandong/106/2007 (H3N2) and swine/Shandong/133/2007 (H3N2) belong to the Eurasian avian lineage grouping with the H9N2 viruses (Technical Appendix [ 1,054 KB, 11 pages], panels F–H and J). The PB2 and M genes of the 2 isolates group in human subtype H1N1 lineage (Technical Appendix [ 1,054 KB, 11 pages], panels E and I). The PA and M genes of swine/Fujian/43/2007 (H3N2) belong to recent human-like H3N2 virus lineages (Technical Appendix [ 1,054 KB, 11 pages], panels G and I); the NS gene originates from European avian-like virus (Technical Appendix [ 1,054 KB, 11 pages], panel J), and the PB2, PB1, and NP genes were located in the Eurasian avian lineages with subtype H9N2 viruses (Technical Appendix [ 1,054 KB, 11 pages], panels E, F, and H). Except for the M gene, all other internal genes of swine/Guangdong/1222/2006 have a sister-like relationship with those of pandemic (H1N1) 2009 virus (Technical Appendix [ 1,054 KB, 11 pages], panels E–J). The PB1 gene of swine/Shandong/275/2008 was an exception, grouping with Eurasian avian subtype H9N2 virus (Technical Appendix [ 1,054 KB, 11 pages], panel F). All 6 internal genes of the 3 Shandong isolates were located in the European avian-like lineages (Technical Appendix [ 1,054 KB, 11 pages], panel E–J). All 8 genes of the 6 subtype H1N1 Guangdong isolates formed 1 cluster and belonged to classical swine lineages (Technical Appendix [ 1,054 KB, 11 pages], panels C–J), indicating that none of these viruses were recent reassortants (Table).

Conclusions

Influenza A subtypes H1N1, H1N2, and H3N2 viruses co-circulate in China. Genetic analysis showed that the single subtype H1N2 virus and all subtype H3N2 viruses examined were either double- or triple-reassortant viruses, which have been rarely documented in China. Finding a gene fragment ostensibly of highly pathogenic avian influenza (H5N1) virus in a subtype H3N2 virus implies that subtype H5N1 viruses may be able to contribute genes to virus pathogenic processes in pigs. Moreover, European avian-like swine (H1N1) virus undergoes reassortment with avian (H9N2) viruses.

Some researchers have hypothesized that pigs may serve as hosts for genetic reassortment between human and avian influenza viruses (4). Our results show that subtypes H3N2 and H1N2 and 1 European avian-like swine (H1N1) virus were all derived from relatively recent reassortment events. The gene fragments of the subtype H3N2 viruses comprised those of human subtype H3N2 (A/Victoria/75-like and A/Moscow/99-like) and the strains H1N1 classical swine, Eurasian H5N1, and H9N2 avian. Infection of pigs with avian H5N1 and H9N2 viruses in China has been reported, and swine H1 and H3 viruses appear widely established in the pig population in China and elsewhere in Southeast Asia (5–9). These findings raise more questions about the generation of novel viruses, which may have zoonotic potential, in pigs.

Pandemic (H1N1) 2009 virus probably resulted from reassortment of recent North American influenza subtypes H3N2 and/or H1N2 swine viruses with Eurasian avian-like swine viruses (2). The current situation, therefore, presents continued risk for further reassortment of swine influenza virus in pig populations and continued spread of pandemic (H1N1) 2009 virus to pigs worldwide. Systematic influenza virus surveillance in pigs is needed in China.

Acknowledgments

We thank Shu Yuelong for providing the inactivated antigen and serum.

The study was supported by the National Natural Scientific Foundation (30950002, 30901072), National Key Technologies R&D Program (2006BAD06A01, 2010BAD04B01), National Basic Research Program (973) (2005CB523003), 863 program (2006AA10A205), and the Program for Cheung Kong Scholars and Innovative Research Team in University of China (No. IRT0866). J.H.L. was also funded by the Taishan Scholar Foundation.

Dr Bi is a PhD student at the College of Veterinary Medicine, China Agricultural University, and has research interests in the epidemiology and pathogenic mechanism of influenza virus and paramyxovirus.

References

1. Garten RJ, Davis CT, Russell CA, Shu B, Lindstrom S, Balish A, et al. Antigenic and genetic characteristics of swine-origin 2009 A(H1N1) influenza viruses circulating in humans. Science. 2009;325:197–201. PubMed DOI
2. Smith GJ, Vijaykrishna D, Bahl J, Lycett SJ, Worobey M, Pybus OG, et al. Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic. Nature. 2009;459:1122–5. PubMedDOI
3. Liu J, Bi Y, Qin K, Fu G, Yang J, Peng J, et al. Emergence of European avian influenza virus–like H1N1 swine influenza A viruses in China. J Clin Microbiol. 2009;47:2643–6. PubMed DOI
4. Ito T, Couceiro JN, Kelm S, Baum LG, Krauss S, Castrucci MR, et al. Molecular basis for the generation in pigs of influenza A viruses with pandemic potential. J Virol. 1998;72:7367–73.
5. Wen NX, Wu DM, Song YH, Zhou MH, Huang XQ, Liang HH. Isolation and identification of type A swine influenza virus. Progress in Veterinary Medicine. 2008;29:53–5.
6. Yu H, Zhang GH, Hua RH, Zhang Q, Liu TQ, Liao M, et al. Isolation and genetic analysis of human origin H1N1 and H3N2 influenza viruses from pigs in China. Biochem Biophys Res Commun. 2007;356:91–6. PubMed DOI
7. Chen YJ, Li HY, Shen ZY, Chen HL, Yu KZ, Bi YZ, et al. Molecular evolution of hemagglutinin gene of H1N1 subtype swine influenza viruses isolated from the mainland of China. Chin J Prev Vet Med. 2005;27:13–7.
8. Guo YJ, Webster RG, Zhuge YH. Swine (H1N1) viruses isolated from pigs in China and studies on the origin of isolates. Chinese Journal of Experimental and Clinical Virology. 1992;6:347–52.
9. Yu H, Hua RH, Zhang Q, Liu TQ, Liu HL, Li GX, et al. Genetic evolution of swine influenza A (H3N2) viruses in China from 1970 to 2006. J Clin Microbiol. 2008;46:1067–75. PubMed DOI

Tables

Table. Genetic origin of swine influenza viruses

Appendix Table 1. Antigenic characterization of influenza (H3N2) viruses isolated from pigs

Appendix Table 2. Antigenic characterization of influenza subtype H1 viruses isolated from pigs

Suggested Citation for this Article

Bi Y, Fu G, Chen J, Peng J, Sun Y, Wang J, et al. Novel swine influenza virus reassortants in pigs, China. Emerg Infect Dis [serial on the Internet]. 2010 Jul [date cited]. http://www.cdc.gov/EID/content/16/7/1162.htm

DOI: 10.3201/eid1607.091881

Pandemic (H1N1) 2009 - update 98

Weekly update

30 April 2010 -- As of 25th of April, worldwide more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 17919 deaths.

WHO is actively monitoring the progress of the pandemic through frequent consultations with the WHO Regional Offices and Member States and through monitoring of multiple sources of information.

Situation update:

The current situation is largely unchanged since the last update. The most active areas of transmission of pandemic influenza H1N1 virus continue to be parts of West and Central Africa with some focal areas of activity in South and Southeast Asia. Pandemic influenza activity H1N1 remains low in much of the temperate areas of both the northern and southern hemispheres. Seasonal influenza type B virus is the predominant influenza virus, though also at low levels of circulation, across East Asia, Northern and Eastern Europe. Influenza type B viruses have also been detected in Central Africa and this week in West Africa. Seasonal influenza H3N2 viruses have continued to be detected in South and Southeast Asia, as well as sporadically in some countries of West and Central Africa, and Eastern Europe.

In Sub-Saharan Africa, data from a limited number of countries suggests that active transmission of pandemic influenza H1N1 virus is declining across West and West-central Africa. Ghana is reporting moderate amounts of pandemic virus (16 % of all clinical specimens tested were positive for pandemic influenza) but smaller numbers of cases continue to be detected in Senegal, Niger and Cameroon. In East Africa, influenza activity has returned to low levels. Only Rwanda has detected small numbers of pandemic virus in the past week. In addition, a few seasonal influenza H3N2 viruses are seen in Ghana. Influenza type B has been increasingly detected in the area, notably in Ghana and Cameroon.

In East Asia, pandemic influenza H1N1 virus circulation is now sporadic. In China, Mongolia, and Republic of Korea most influenza like illness cases continued to be primarily due to seasonal influenza type B viruses. In China and Mongolia influenza detections have continued to decline compared to previous recent weeks. The Republic of Korea reported increasing levels of respiratory disease activity associated with increasing detections of seasonal influenza type B in respiratory specimens over five consecutive weeks. Of note, small numbers of pandemic influenza H1N1, seasonal H3N2 and H1N1 viruses continued to be sporadically detected in some countries of the region.

In Southeast Asia, overall levels of influenza activity were low. Although the predominant influenza virus circulating was still pandemic influenza H1N1, there was co-circulation of seasonal influenza type B and, to a lesser extent, H3N2 viruses in several countries including Singapore, Cambodia, Indonesia and Thailand. Malaysia has reported increasing levels of respiratory diseases activity associated with pandemic influenza H1N1 laboratory confirmed cases. Media sources have also reported school closures in the country. In Singapore, influenza-like-illness levels are still below the seasonal epidemic threshold but have increased compared to previous week.

In South Asia, Bangladesh reported an increase in respiratory diseases activity associated with increasing numbers of pandemic influenza H1N1 laboratory confirmed cases since beginning of April. India reported pandemic influenza activity in the states of Maharashtra and recently Karnataka. Levels of respiratory diseases activity in both of these countries appear much less intense than in the initial wave of transmission which occurred late 2009. Although pandemic influenza is the predominant virus circulating in the region, seasonal influenza type B viruses continued to be detected in Iran and Bangladesh.

In the tropical zone of the Americas, limited data suggested that pandemic influenza H1N1 activity remains low but with a few localized areas of transmission. Jamaica, Panama and Guatemala, reported increasing trends in respiratory disease activity. In Cuba, all provinces reported an increase in numbers of acute respiratory diseases cases in the last two weeks, mainly from the city of Havana. In Peru, the number of pneumonia cases in children under 5 years of age in Lima has been increasing since six consecutive weeks and remained above the epidemic threshold. However, the extent to which these pneumonia cases have been due to pandemic influenza H1N1 virus is not known. Notably, respiratory syncitial virus (RSV) has been reported to be circulating in the area.

In the temperate zone of the Northern Hemisphere, overall pandemic influenza H1N1 activity remained low. In United States, the proportion of outpatient visits for influenza-like illness was below the national baseline. No influenza B is reported by countries of North America. In Europe, pandemic influenza activity is at very low intensity in all countries. The overall proportion of sentinel respiratory samples testing positive for influenza remained stable at about 4.5%. For the current week, the total number of sentinel influenza B detections continued to exceed that of influenza A, mainly due to viral detections from Eastern Europe: Central, Siberian, Far Eastern regions of the Russian Federation and Kazakhstan.

In the temperate countries of the Southern Hemisphere, influenza-like illness activity remained low and at the levels experienced at the same time in previous years. Australia has continued to report sporadic detections of pandemic influenza H1N1, seasonal influenza B and H3N2 viruses in low numbers in recent weeks.

The Global Influenza Surveillance Network (GISN) continues monitoring the global circulation of influenza viruses, including pandemic, seasonal and other influenza viruses infecting, or with the potential to infect, humans including seasonal influenza. For more information on virological surveillance and antiviral resistance please see the weekly virology update (Virological surveillance data, below).

Weekly update (Virological surveillance data)

The cumulative total for reports of antiviral resistant isolates of pandemic (H1N1) 2009 virus remains at 285. There have been no new cases reported since the situation update on 16 April 2010. 

28 April 2010 -- For this reporting week (15-28 April 2010), no additional cases of oseltamivir resistant pandemic influenza A (H1N1) 2009 viruses have been reported. The cumulative total remains at 285 so far. All but one of these have the H275Y substitution and are assumed to remain sensitive to zanamivir.

*Countries in temperate regions are defined as those north of the Tropic of Cancer or south of the Tropic of Capricorn, while countries in tropical regions are defined as those between these two latitudes. 

**Abbreviations: influenza-like-illness (ILI), acute respiratory infection (ARI), and severe acute respiratory infection (SARI)

WHO Clinical Management Guidelines for Human infection with Pandemic (H1N1), 2009: 

WHO Guidelines for Pharmacological Management of Pandemic (H1N1) 2009 Influenza and other Influenza Viruses: 

MAP OF INFLUENZA ACTIVITY AND VIRUS SUBTYPES (WEEK 15: 11 APRIL - 17 APRIL 2010)

Map of influenza activity and virus subtypes [png 230kb]

Description: Displayed data reflect the most recent data reported to Flunet (www.who.int/FluNet), WHO regional offices or on Ministry of health websites in the last 2 weeks. The percent of specimens tested positive for influenza includes all specimens tested positive for seasonal or pandemic influenza. The pie charts show the distribution of virus subtypes among all specimens that were tested positive for influenza. The available country data were joined in larger geographical areas with similar influenza transmission patterns to be able to give an overview (http://www.who.int/csr/disease/swineflu/transmission_zones/en)

Qualitative indicators (Week 29 to Week 15: 13 July 2009 - 17 April 2010)

The qualitative indicators monitor: the global geographic spread of influenza, trends in acute respiratory diseases, the intensity of respiratory disease activity, and the impact of the pandemic on health-care services.

Human infection with pandemic (H1N1) 2009 virus: updated interim WHO guidance on global surveillance 

The maps below display information on the qualitative indicators reported. Information is available for approximately 60 countries each week. Implementation of this monitoring system is ongoing and completeness of reporting is expected to increase over time.

List of definitions of qualitative indicators

Geographic spread of influenza activity

Map timeline

Trend of respiratory diseases activity compared to the previous week

Map timeline

Intensity of acute respiratory diseases in the population

Map timeline

Impact on health care services

Map timeline

Laboratory-confirmed cases of pandemic (H1N1) 2009 as officially reported to WHO by States Parties to the IHR (2005) as of 25th of April 2010

Map of affected countries and deaths

The countries and overseas territories/communities that have newly reported their first pandemic (H1N1) 2009 confirmed cases since the last web update (No. 97): none.

The countries and overseas territories/communities that have newly reported their first deaths among pandemic (H1N1) 2009 confirmed cases since the last web update (No. 97): none.

Region	Deaths*
WHO Regional Office for Africa (AFRO)	168
WHO Regional Office for the Americas (AMRO)	At least 8316
WHO Regional Office for the Eastern Mediterranean (EMRO) **	1019
WHO Regional Office for Europe (EURO)	At least 4835
WHO Regional Office for South-East Asia (SEARO)	1773
WHO Regional Office for the Western Pacific (WPRO)	1808
Total*	At least 17919

*The reported number of fatal cases is an under representation of the actual numbers as many deaths are never tested or recognized as influenza related.
**No update since 7 March 2010

Risk for Transmission of Pandemic (H1N1) 2009 Virus by Blood Transfusion

Chieko Matsumoto,  Rieko Sobata, Shigeharu Uchida, Takao Hidaka, Syunya Momose, Satoru Hino, Masahiro Satake, and Kenji Tadokoro

Author affiliation: Japanese Red Cross Society Blood Service Headquarters, Tokyo, Japan

Suggested citation for this article

To the Editor: Influenza A pandemic (H1N1) 2009 virus emerged in early 2009 in Mexico and has since spread worldwide. In Japan, the first outbreak of the novel influenza was reported in May 2009 (1) and became pandemic in November. Although no cases of transfusion-transmitted influenza have been published, evidence exists of brief viremia before onset of symptoms (2,3). The possibility of transmission of this virus through transfusion of donated blood is of concern. The Japanese Red Cross Blood Centers have intercepted blood products with accompanying postdonation information indicating possible pandemic (H1N1) 2009 infection and attempted to identify the viral genome in those products by using nucleic acid amplification technology (NAT).

Figure

Figure. Number of blood donations from persons for whom pandemic (H1N1) 2009 infection was diagnosed postdonation and time between donation and diagnosis, by donor age, Japan.

During June–November 2009, blood samples were collected from plasma and erythrocyte products that had been processed from donations; postdonation information indicated diagnosis of pandemic (H1N1) 2009 infection soon after donation. Viral RNA was extracted from plasma samples and erythrocyte fractions by using a QIAamp Virus Biorobot MDx kit (QIAGEN, Valencia, CA, USA) and a High Pure Viral Nucleic Acid Large Volume kit (Roche Diagnostics, Indianapolis, IN, USA), respectively. RNA samples were subjected to real-time reverse transcription–PCR (RT-PCR) of hemagglutinin (HA) and matrix (M) genes of influenza A by using PRISM 7900 (Applied Biosystems, Foster City, CA, USA). The RT-PCR of HA was specific for pandemic (H1N1) 2009 virus, whereas the RT-PCR of M was designed to detect both pandemic (H1N1) 2009 and seasonal influenza A viruses. The sequences of probes and primers were synthesized according to the protocols developed by the Japanese National Institute of Infectious Diseases (4). Either 200 μL of a plasma sample or 100 μL of packed erythrocytes was used for each test, and the test was performed 2× for each gene in each sample. Before the investigation using donated blood samples, the sensitivity of the NAT system was checked by spiking experiments. Viral particles of pandemic (H1N1) 2009 virus (A/California/04/2009 [H1N1]), donated by the National Institute of Infectious Diseases, were spiked into plasma and erythrocyte samples from healthy volunteers. Viral RNA was detected in the plasma samples spiked with viral particles corresponding to 300 genome equivalents/mL and in the packed erythrocyte samples spiked with viral particles corresponding to 3,000 genome equivalents/mL.

NAT was conducted by using 96 plasma and 67 erythrocyte samples obtained from 96 blood donors who had symptoms of influenza within 7 days postdonation. For 20 donors, pandemic (H1N1) 2009 was diagnosed within 1 day postdonation and, for another 20, within 2 days postdonation (Figure). Pandemic (H1N1) 2009 virus was not found in any of the samples tested, but it was consistently detected in the external positive control. These results suggest that the viremia with pandemic (H1N1) 2009 virus, if any, is very low and can be missed by current NAT or that the viremic period is too brief to identify viremia. Although the risk for transmission of pandemic influenza by transfusion seems to be low, further investigation is needed to elucidate this risk.

References

1. Shimada T, Gu Y, Kamiya H, Komiya N, Odaira F, Sunagawa T, et al. Epidemiology of influenza A (H1N1)v virus infection in Japan, May–June 2009. Euro Surveill. 2009;14:pii:19244.
2. Likos AM, Kelvin DJ, Cameron CM, Rowe T, Kuehnert MJ, Norris PJ. Influenza viremia and the potential for blood-borne transmission. Transfusion. 2007;47:1080–8. PubMed DOI
3. Khakpour M, Saidai A, Naficy K. Proved viraemia in Asian influenza (Hong Kong variant) during incubation period. BMJ. 1969;4:208–9. PubMed DOI
4. Kageyama T. H1N1 novel influenza. In: Pathogen detection manual (version 1) [in Japanese]. Tokyo: National Institute of Infectious Diseases; 2009.

Figure

Figure. Number of blood donations from persons for whom pandemic (H1N1) 2009 infection was diagnosed postdonation and time between donation and diagnosis, by donor age, Japan.

Suggested Citation for this Article

Matsumoto C, Sobata R, Uchida S, Hidaka T, Momose S, Hino S, et al. Risk for transmission of pandemic (H1N1) 2009 virus by blood transfusion [letter]. Emerg Infect Dis [serial on the Internet]. 2010 Apr [date cited]. http://www.cdc.gov/EID/content/16/4/722.htm

DOI: 10.3201/eid1604.091795

Pandemic (H1N1) 2009 Infection in Swine Herds, Manitoba, Canada

Tim Pasma  and Tomy Joseph
Author affiliation: Manitoba Agriculture, Food and Rural Initiatives, Winnipeg, Manitoba, Canada

Suggested citation for this article

Abstract
In Manitoba, Canada, several swine herds were infected by pandemic (H1N1) 2009 virus in the summer of 2009. Results of several investigations concluded that outbreaks of infection with this virus are similar in duration to outbreaks of infections with swine influenza viruses A (H1N1) and A (H3N2).

On April 21, 2009, the US Centers for Disease Control and Prevention announced the finding of a novel strain of influenza virus A (H1N1), now known as pandemic (H1N1) 2009 virus, in 2 children in southern California (1). By June 11, this virus had spread so quickly and extensively among humans that the World Health Organization declared a phase 6 pandemic (2). The disease in humans is a self-limiting, uncomplicated respiratory illness with fever; however, severe disease and deaths have occurred (3). Clinical signs in humans are generally mild and include fever, slight cough, sneezing, and nasal discharge. Vomiting and diarrhea also have been reported in up to 38% of cases (3).

Pandemic (H1N1) 2009 virus also has affected swine. On May 2, 2009, the virus was isolated from a swine herd in Alberta, Canada (4). The disease in swine has been reported as mild in field and experimental conditions. Clinical signs in pigs include fever, slight cough, sneezing, and nasal discharge. Diarrhea was also reported in experimentally infected pigs; however, this symptom may have been secondary to the influenza infection (5). In experimental infection of pigs, clinical signs peaked on days 4–5 postinfection (5).

In Manitoba, Canada, pandemic (H1N1) 2009 virus was first detected in a swine herd on June 30, 2009. During the following months, more outbreaks in Manitoba were reported in farrowing, nursery, and finishing herds. Our study aimed to determine the length of time that virus was shed in swine herds after a field outbreak of pandemic (H1N1) 2009.

The Study

We studied 5 herds in which pandemic (H1N1) 2009 was diagnosed. We collected information about the production type and number of animals housed in the barn, influenza vaccination status of the herd, date of influenza-like illness in any barn employees before the outbreak, date of the outbreak as determined by onset of clinical signs, and sampling date and number of positive swabs. In each herd, 32 nasal swabs were taken from randomly selected pigs as soon as possible after diagnosis. The procedure was repeated every 7 days until all the samples tested showed negative results.

Nasal swabbing was performed by using a polyester swab with a plastic handle that was placed in a viral transport medium (Starswab Multitrans Collection & Transport System; Starplex Scientific Inc, Etobicoke, Ontario, Canada). The swabs were refrigerated and submitted to the Veterinary Services Diagnostic Laboratory at Manitoba Agriculture, Food and Rural Initiatives (Winnipeg, Manitoba, Canada). Samples were tested by using a generic real-time PCR specific for the genomic RNA segment 7 (matrix gene) of the influenza A virus provided by the National Centre for Foreign Animal Disease (Winnipeg, Manitoba, Canada) (3) and an H1 differential PCR (6) provided by the National Microbiology Laboratory (Winnipeg, Manitoba, Canada).

We tested 5 herds (herds A–E) in which pandemic (H1N1) 2009 virus was diagnosed (Table). Herds A, B, and D were finishing herds, herd C was a nursery herd, and herd E was a farrowing herd. Herd sizes ranged from 850 to 4,100 pigs. For herds C and D, human illness 16–92 days before the outbreak was reported. The owners of herds A and B reported that they received pigs from a previously infected herd. For persons in contact with herd E, no ill persons were reported, and no pigs from previously affected herds were received before the outbreak. Pigs in herd E were vaccinated for swine influenza A (H1N1) and (H3N2) viruses with an autogenous vaccine.

Clinical signs in pigs were reported to be mild, with no deaths. However, herd D, co-infected with porcine reproductive and respiratory syndrome virus, Mycoplasma hyopneumoniae, and porcine circovirus, reported a 1% outbreak-associated death rate. No vomiting or diarrhea was reported in any pigs infected with the virus.

Nasal swabbing of the pigs demonstrated that pandemic (H1N1) 2009 virus was no longer detected in swine 10–20 days after clinical signs appeared. When tested again the week before slaughter (day 67), herd B showed no evidence of virus shedding.

Conclusions

We demonstrated that field infections of pandemic (H1N1) 2009 in swine are similar in duration to infections with other swine influenza viruses. In the herds studied, the virus caused mild illness identical to the clinical signs typical of swine influenza (7). Sampling by nasal swab indicated that pandemic (H1N1) 2009 virus sheds for up to 20 days after clinical signs appear. Our findings support the laboratory work of Lange et al., who established that pigs experimentally infected with this strain intermittently shed the virus 6–11 days postinfection and ceased excretion by day 11 (5). Shedding of the circulating strains of swine influenza in nasal secretions stops by 5–7 days postinfection (7–9). Our study also indicates that autogenous vaccine prepared with circulating H1N1 subtype may not protect pigs from pandemic (H1N1) 2009 infection.

Our study has several limitations. Other swine viruses, such as porcine reproductive and respiratory syndrome virus, may interfere with the detection of swine influenza viruses from nasal swabs (8), and we did not test for other viruses. In addition, the virus can be difficult to diagnose in nursery pigs because of maternal antibodies and low levels of exposure (8), which may have affected the samples from the nursery herd. The small sample size and the unknown sensitivity of the PCR in this specific application also limit the findings of our study.

The swine herds we studied quickly cleared the virus after infection. This study supports the recommendations developed by the Canadian Food Inspection Agency (10) and the World Organisation for Animal Health (OIE) (11). These guidelines state that pigs infected with pandemic (H1N1) 2009 virus should be managed similarly to herds infected with any swine influenza virus. On the basis of our study findings, restrictions of trade or slaughter of pigs as a public health intervention are irrational actions.

Only 10 countries have reported pandemic (H1N1) 2009 infection in commercial swine to the OIE (12). Whether pandemic (H1N1) 2009 will become established in swine populations worldwide remains to be seen. All countries should implement vigilant surveillance for, and monitor for changes in the structure and behavior of, the virus.

Acknowledgments

We thank Linda Duffy, Cherry McCormick, Cheryl Sachvie, Cherie Scammell-Chandler, and Tracy Scammell-LaFleur for their assistance in processing samples.

Dr Pasma is a veterinarian with Animal Health and Welfare, Chief Veterinary Office/Food Safety Knowledge Centre, Manitoba Agriculture, Food and Rural Initiatives, Winnipeg, Manitoba, Canada. His research interest is in the epidemiology of swine influenza.

Dr Joseph is a virologist with Veterinary Diagnostic Services Laboratory, Livestock Knowledge Centre, Manitoba Agriculture, Food and Rural Initiatives, Winnipeg. His research interests include diagnostic virology and the molecular basis of pathogenesis of avian and swine influenza viruses.

References

1. Centers for Disease Control and Prevention. Swine influenza A (H1N1) infection in two children—southern California, March–April 2009. MMWR Morb Mortal Wkly Rep. 2009;58:400–2.
2. World Health Organization. Global alert and response. Current WHO phase of pandemic alert [cited 29 Jan 2010]. http://www.who.int/csr/disease/avian_influenza/phase/en
3. Novel Swine-Origin Influenza A (H1N1) Virus Investigation Team, Dawood FS, Jain S, Finelli L, Shaw MW, Lindstrom S, et al. Emergence of a novel swine-origin influenza A (H1N1) virus in humans. N Engl J Med. 2009;360:2605–15. PubMed DOI
4. Howden KJ, Brockhoff EJ, Caya FD, McLeod LJ, Lavoie M, Ing JD, et al. An investigation into human pandemic influenza virus (H1N1) 2009 on an Alberta swine farm. Can Vet J. 2009;50:1153–61.
5. Lange E, Kalthoff D, Blohm U, Teifke JP, Breithaupt A, Maresch C, et al. Pathogenesis and transmission of the novel swine-origin influenza virus A/H1N1 after experimental infection of pigs. J Gen Virol. 2009;90:2119–23. PubMed DOI
6. Leblanc JJ, Li Y, Bastien N, Forward KR, Davidson RJ, Hatchette TF. Switching gears for an influenza pandemic: validation of a duplex RT-PCR for simultaneous detection and confirmation of pandemic (H1N1) 2009. J Clin Microbiol. 2009;47:3805–13. PubMed
7. Olsen CW, Brown IH, Easterday BC, Van Reeth K. Swine influenza. In: Straw BE, Zimmerman JJ, D'Allaire S, Taylor DJ, editors. Diseases of swine. 9th ed. Ames (IA): Blackwell Publishing; 2006. p. 469–82.
8. Gillespie TG. Diagnosing endemic swine influenza virus in nursery pigs using cross-sectional serologic profiling. Swine Health and Production. 1999;7:81–3.
9. Janke BH. Diagnosis of swine influenza. Swine Health and Production. 2000;8:79–84.
10. Canadian Food Inspection Agency. News release. Management of pandemic H1N1 in swine herds [cited 2009 Oct 5]. http://www.inspection.gc.ca/english/corpaffr/newcom/2009/20090724e.shtml
11. World Organisation for Animal Health. Press releases. Pandemic (H1N1) 2009: the OIE reiterates its recommendations to animal health authorities worldwide [cited 2009 Oct 5].http://www.oie.int/eng/press/en_090713.htm
12. World Organisation for Animal Health. WAHID interface. Weekly disease information [cited 2009 Dec 3]. http://www.oie.int/wahis/public.php?page=weekly_report_index&admin=0

Table

Table. Findings from study of 5 tested swine herds in which pandemic (H1N1) 2009 was diagnosed, Manitoba, Canada, 2009