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Severe Influenza Illness Reported

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arirish View Drop Down
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    Posted: February 01 2016 at 10:48am
Flu Season Begins: Severe Influenza Illness Reported

CDC urges rapid antiviral treatment of very ill and high risk suspect influenza patients without waiting for testing


Summary
Influenza activity is increasing across the country and CDC has received reports of severe influenza illness. Clinicians are reminded to treat suspected influenza in high-risk outpatients, those with progressive disease, and all hospitalized patients with antiviral medications as soon as possible, regardless of negative rapid influenza diagnostic test (RIDT) results and without waiting for RT-PCR testing results. Early antiviral treatment works best, but treatment may offer benefit when started up to 4-5 days after symptom onset in hospitalized patients. Early antiviral treatment can reduce influenza morbidity and mortality.

Since October 2015, CDC has detected co-circulation of influenza A(H3N2), A(H1N1)pdm09, and influenza B viruses. However, H1N1pdm09 viruses have predominated in recent weeks. CDC has received recent reports of severe respiratory illness among young- to middle-aged adults with H1N1pdm09 virus infection, some of whom required intensive care unit (ICU) admission; fatalities have been reported. Some of these patients reportedly tested negative for influenza by RIDT; their influenza diagnosis was made later with molecular assays. Most of these patients were reportedly unvaccinated. H1N1pdm09 virus infection in the past has caused severe illness in some children and young- and middle-aged adults. Clinicians should continue efforts to vaccinate patients this season for as long as influenza viruses are circulating, and promptly start antiviral treatment of severely ill and high-risk patients if influenza is suspected or confirmed.


http://emergency.cdc.gov/han/han00387.asp
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Post Options Post Options   Thanks (0) Thanks(0)   Quote FluMom Quote  Post ReplyReply Direct Link To This Post Posted: February 01 2016 at 7:59pm
My doc did not wait or test when I had the flu. He gave me Tamiflu and I still ended up in hospital with pneumonia within a week. I was out of work for 5 weeks and I thought I was going to die!

This flu is nasty.
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Post Options Post Options   Thanks (0) Thanks(0)   Quote hachiban08 Quote  Post ReplyReply Direct Link To This Post Posted: February 01 2016 at 8:53pm
My friend currently has pneumonia for the first time in her life. I have had a scratchy throat the past three days, coughing all day/night, with post nasal drip I can occasionally feel.
Be prepared! It may be time....^_^v
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Post Options Post Options   Thanks (0) Thanks(0)   Quote arirish Quote  Post ReplyReply Direct Link To This Post Posted: February 02 2016 at 9:37am
CDC releases alert on seasonal flu, warns of severe cases

The CDC today issued a Health Alert Network (HAN) advisory that warns of severe flu cases and recommends how to prevent unnecessary outbreaks.

Although the pneumonia and influenza mortality rate of week 3 (ending Jan 23, as the CDC noted on Jan 30) was below the epidemic thresholds in both the 122 Cities Mortality Reporting System and the NCHS Mortality Surveillance System, the rate of flu reports is increasing, particularly those caused by 2009 H1N1.

According to the CDC, 2009 H1N1, which is now a seasonal strain, has caused severe respiratory illness leading to hospitalization and some fatalities in patients.

The f CDC recommends that anyone 6 months or older should still receive the flu vaccine as soon as possible for protection yet this season. All US flu vaccines protect against H1N1, H3N2, and influenza B viruses.

In addition, antiviral drugs are strongly recommended for high-risk patients, such as those who are hospitalized, under the age of 2, over the age of 65, and have other factors that put them at risk, the agency said. Antiviral treatment should also be given to high-risk patients even if they are just suspected of having influenza, preferably within 48 hours of symptom onset, the CDC added.

The advisory also cautions clinicians that rapid influenza diagnostic tests may yield false-negatives, so antiviral therapy should not be withheld based on results from these tests.

This is the first time since December 2014 that the CDC has issued a HAN over flu. At that point a drifted H3N2 strain was circulating and was eventually associated with decreased vaccine effectiveness and a more severe flu season.


http://www.cidrap.umn.edu/news-perspective/2016/02/news-scan-feb-01-2016

http://emergency.cdc.gov/han/han00387.asp

http://www.cdc.gov/flu/weekly/index.htm
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Post Options Post Options   Thanks (0) Thanks(0)   Quote arirish Quote  Post ReplyReply Direct Link To This Post Posted: February 04 2016 at 12:22pm
Eurosurveillance, Volume 21, Issue 5, 04 February 2016

Rapid communication


Emergence of influenza A(H1N1)pdm09 genogroup 6B and drug resistant virus, India, January to May 2015


M Parida 1 , PK Dash 1 , JS Kumar 1 , G Joshi 1 , K Tandel 1 , S Sharma 1 , A Srivastava 1 , A Agarwal 1 , A Saha 1 , S Saraswat 1 , D Karothia 1 , V Malviya


To investigate the aetiology of the 2015 A(H1N1)pdm09 influenza outbreak in India, 1,083 nasopharyngeal swabs from suspect patients were screened for influenza A(H1N1)pdm09 in the state of Madhya Pradesh. Of 412 positive specimens, six were further characterised by phylogenetic analysis of haemagglutinin (HA) sequences revealing that they belonged to genogroup 6B. A new mutation (E164G) was observed in HA2 of two sequences. Neuraminidase genes in two of 12 isolates from fatal cases on prior oseltamivir treatment harboured the H275Y mutation.

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An epidemic of influenza A(H1N1)pdm09, affecting over 39,000 persons and causing more than 2,500 deaths occurred in India in 2015 [1]. We show that genotype 6B strains forming two sub-lineages circulated during the outbreak. Comparison of the sequences of six outbreak strains recovered in this work, to other published genotype 6B sequences, also reveals a unique combination of previously-reported mutations in the haemagglutinin (HA) gene. Two of the six sequences additionally display a E164G mutation in HA2, which has not been reported to date, moreover a N129D mutation in HA1 is observed for two sequences derived from patients with severe disease. Among strains analysed from 12 fatal cases on prior oseltamivir treatment, two harbour the H275Y mutation in the neuraminidase (NA) gene, which confers resistance to this antiviral.


Description of the study


Sampling and testing for influenza A(H1N1)pdm09

A total of 1,083 acute phase nasopharyngeal swab specimens from patients suspected of influenza (as prior defined [2]), were referred by 13 district health authorities of Madhya Pradesh, India between 29 January and 7 May 2015. Upon specimen collection, the travel history, treatment status, and symptoms of the patients were recorded in addition to age, sex and place of residence. The samples were handled in a designated biosafety level (BSL) 3 laboratory and viral RNA was extracted using QIAamp viral RNA mini kit (Qiagen). The RNA samples were screened by World Health Organization (WHO)–Centers for Disease Control and Prevention (CDC) approved quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) for influenza A(H1N1)pdm09 [3].


Molecular analyses of the strains

Six clinical samples testing positive for influenza A(H1N1)pdm09 by qRT-PCR were selected based on patients’ disease severity category A (n=2; A/India/DRDE_GWL897/2015 and A/India/DRDE GWL721/2015), B (n=2; A/India/DRDE_GWL703/2015, A/India/DRDE_GWL989/2015), and C (n=2; A/India/DRDE GWL719/2015 and A/India/DRDE_GWL812/2015) as previously described [2], and used for direct nucleotide (nt) sequencing of the haemagglutinin (HA) gene. A phylogenetic analysis was performed by comparing with nt sequence of 45 globally diverse influenza A(H1N1)pdm09 viruses retrieved from GenBank (as further shown in the phylogenetic tree) and the Global Initiative on Sharing Avian Influenza Data (GISAID) (Table 1). The phylogenetic tree in this analysis was constructed with maximum likelihood and bootstrap analysis of 1,000 replicates using Mega 5.03 software [4]. Further the amino acid substitutions were marked at the major branches for better clarity.




Influenza A(H1N1)pdm09 HA amino-acid sequences were inferred from the genetic sequences obtained in this study, and the protein structures were modelled using Modeller software and compared to prototype A/California/07/2009 through Discovery studio client 4.1.

The qRT-PCR positive samples from 12 fatal cases, all on prior oseltamivir therapy, were also tested for a mutation (H275Y) conferring resistance to this antiviral by PCR–restriction fragment length polymorphism (RFLP) analysis of the NA gene [5]. Of these 12 cases, one (with corresponding sample: A/India/DRDE GWL719/2015) also belonged to the group of six patients, from whom the HA gene was sequenced. The PCR–RFLP positive samples were further confirmed through nt sequencing of the target sites of the NA gene.


Results of screening for influenza A(H1N1)pdm09

A total of 1,083 patients, including 525 males, were screened for influenza A(H1N1)pdm09 by qRT-PCR. The age range of these patients varied from 0 to 90 years-old, with age groups between 21 and 30 year-old (n=284) as well as between 31 and 40 year-old (n=179) representing 26% and 17% of the total respectively (Table 2). Of the 1,083 clinical samples tested, 412 (38%) were found positive for influenza A(H1N1)pdm09 virus. Similar to patients screened, most of those testing positive were from young age groups, with 21 to 30 years-old (n=104; 25%) representing the majority, followed by 31 to 40 year-olds (n=69; 17%). The positivity rate among the different age groups varied from 25 to 59% (Table 2). The female to male sex ratio of PCR positive patients was found to be 1.20:1.


The clinical features of PCR confirmed patients revealed presence of cough (n=378; 92%), fever >38°C (n=350; 85%), sore throat (n=331; 80%), shortness of breath (n=271; 66%) and catarrh (n=253; 61%).


Molecular characteristics of outbreak strains

HA sequences from six samples of influenza A(H1N1)pdm09-positive patients in this study were recovered and deposited in National Center for Biotechnology Information (NCBI)-GenBank under the accession numbers KT867219, KT867220, KT867221, KT867222, KT867223 and KT867224. The HA open reading frame was found to be 1,701 nt in length.

Phylogenetic analysis of the six sequences, together with geographically diverse global influenza A(H1N1)pdm09 viral sequences, including sequences recovered in India in previous years, revealed that the six sequences clustered with genogroup 6B sequences. Sequences from India in 2014 also belonged to this genogroup (e.g. A/India/159/2014, A/India/6427/2014 and A/India/5964/2014). Moreover, within this genogroup, two distinct lineages could be observed

Four study sequences (A/India/DRDE GWL703/2015, A/India/DRDE GWL721/2015, A/India/DRDE GWL897/2015 and A/India/DRDE GWL989/2015), which were derived from patients with disease severity categorised as A and B, were found grouped into one lineage (lineage 1) of genogroup 6B. Lineage 1 additionally included some Indian sequences (A/India/159/2014 and A/India/6427/2014) from 2014. The two remainder study sequences (A/India/DRDE GWL719/2015 and A/India/DRDE GWL812/2015), both originating from category C patients, segregated into the other genogroup 6B lineage (lineage 2). A 2014 Indian sequence (A/India/5964/2014) also belonged to lineage 2. The two lineages differed by an amino acid substitution at position 84 in HA1, whereby lineage 1 sequences had an N and lineage 2 sequences an S.

No clear difference was observed between 2015 and 2014 Indian sequences included in the analysis, except that 2015 strains in lineage 2 (A/India/DRDE GWL719/2015 and A/India/DRDE GWL812/2015) encoded a N129D mutation in HA1 (HA1 numbering system).

The comparative analysis of inferred peptide-sequences confirmed that the 2015 Indian viruses harboured the signature amino acid substitutions of genogroup 6B (D97N, K163Q, S185T, S203T, A256T and K283E) [6,7].

In addition to the six substitutions defining genotype 6B, all HA-sequenced viruses in this study presented five mutations compared to prototype A/California/07/2009, namely, P83S, I321V in HA1, as well as E47K, S124N, and E172K in HA2 (Figure 2). Further to these total 11 mutations, N129D was found in HA1 sequences of two specimens (A/India/DRDE GWL719/2015 and A/India/DRDE GWL812/2015) from patients with severe disease (both category C including one fatal case). Also, E164G was found in HA2 of A/India/DRDE GWL721/2015 and A/India/DRDE GWL812/2015.


A thorough in silico analysis revealed that all of the 11 mutations common to the 2015 Indian sequences studied here, have been reported in different strains of influenza A(H1N1)pdm09 virus isolated from various parts of the world in the past [8-10]. However, to date, no single strain was reported to possess all these 11 mutations together, except the Indian 2015 strains sequenced in this study. Moreover, the E164G mutation found in HA2 of A/India/DRDE GWL812 and A/India/DRDE GWL721 has not previously been reported.

Modelling reveals that mutations are found in the head, stalk and tail region of HA protein but the majority were found in the head region which covers the major antigenic binding region. The HA2 E172K mutation showed distinct structural changes in the tail region compared to the influenza A(H1N1)pdm09 virus prototype [11].

Two influenza A(H1N1)pdm09 strains from 12 fatal cases were found to possess H275Y oseltamivir resistance mutation.


Discussion

Influenza A viruses have been responsible for four influenza pandemics in last century viz., Spanish influenza (H1N1) in 1918, Asian influenza (H2N2) in 1957, Hong Kong influenza (H3N2) in 1968 and pandemic influenza (H1N1) in 2009, which was caused by influenza A(H1N1)pdm09. During the 2009 pandemic period (2009–2010), India was affected with around 50,000 cases and a case fatality of 6% [12]. After the end of the 2009 pandemic, the virus continued to circulate at low level in the population, and during the period from 2011 to 2014 the circulation of the virus declined [13]. From January to May 2015 however, over 39,000 persons in India were affected by a new epidemic of influenza A(H1N1)pdm09, with more than 2,500 deaths [1]. The outbreak spread across 22 of the 29 states in the country, making it the largest since 2009. This sudden re-emergence and wide spread simultaneous reporting of influenza A(H1N1)pdm09 along with higher number of hospitalisations and deaths was a major public health concern.

By further characterising the strains infecting patients positive for influenza A(H1N1)pdm09 through HA phylogeny, this study finds that sequences of genogroup 6B were circulating during the 2015 epidemic. The genogroup 6B was found to evolve from a Russian isolate (A/Moscow-Oblast/CRIE-08/2013) and is since then circulating in many parts of the world. However, this is the first report from India regarding circulation of genogroup 6B, coinciding with a large scale outbreak [1].

Researchers from Massachusetts Institute of Technology (MIT) have recently reported mutations D225N, and T200A in a 2014 Indian strain (A/India/6427/2014, which also clusters with genogroup 6B sequences in the phylogenetic tree Figure 1) making the virus more infectious [14]. Although we did not find these two mutations in our study, all the sequences that we characterised harboured five mutations (P83S, I321V in HA1, as well as E47K, S124N, and E172K in HA2), which although previously described, have not been reported in combination. Moreover, two isolates from patients with severe disease harboured a N129D mutation in HA1 and two isolates had a mutation in HA2, E164G, that has not been observed to date. These unique features of the viruses found here may have played a role in shaping the large scale epidemic with cases of severe disease. On the other hand, the 2015 epidemic in India may be attributed to lack of immunity among an immune-naïve population. It is also noteworthy that seasonal influenza vaccination is not very common in India.

Some limitations of the study include that the samples were only tested for influenza A(H1N1)pdm09 virus, whereby only 38% of samples tested were positive. Therefore, co-circulation of other influenza subtypes or types could not be ruled out. Moreover the sequence analysis was conducted with only few positive samples that did not cover other gene segments than the HA and NA genes.

The influenza A(H1N1)pdm09 virus represents a quadruple reassortment of two swine, one human, and one avian strain of influenza virus [15]. The largest proportion of genes comes from swine influenza viruses (30.6% from North American swine strains, 17.5% from Eurasian swine strains), followed by North American avian strains (34.4%) and human influenza strains (17.5%). It will be interesting to investigate the involvement of any gene reassortment in the 2015 outbreak in India through complete genome sequencing.

Two of 12 strains from fatal cases were found to harbour a mutation conferring resistance to oseltamivir. Learning more about the 2015 strains circulating in India could help public health officials determine treatment options and inform on vaccines for the next influenza season, which is likely to include currently circulating strains [16].

Our findings show the importance of systematic molecular surveillance to provide insight into strains circulating during influenza epidemics.

for complete article including charts and graphs see:http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=21366
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Post Options Post Options   Thanks (0) Thanks(0)   Quote Dutch Josh Quote  Post ReplyReply Direct Link To This Post Posted: February 09 2016 at 6:17am
http://ecdc.europa.eu/en/press/news/_layouts/forms/News_DispForm.aspx?ID=1354&List=8db7286c-fe2d-476c-9133-18ff4cb1b568&Source=http%3A%2F%2Fecdc.europa.eu%2Fen%2FPages%2Fhome.aspx

The composition of influenza vaccines in the southern hemisphere in 2015 and in the northern hemisphere in 2015–16 were identical and thus provide an indication of how effective vaccination could be in Europe. Estimates of vaccine effectiveness in New Zealand are encouraging, with an overall effectiveness against hospitalisations of 50%.

For Europe, the vaccine effectiveness is expected to be lower than in the 2015 season in New Zealand. Europe is seeing a higher prevalence of B/Victoria virus circulating, which is not included in the widely used trivalent vaccine, and it is unclear if the emergence of a new genetic subgroup of A(H1N1) virus might compromise vaccine effectiveness.

Que sera, sera, Whatever will be, will be, The future is not ours to see, Que sera, sera !
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http://www.influenza.spb.ru/en/influenza_surveillance_system_in_russia/epidemic_situation/

Russia is reporting mutations in the H1N1 flu-virus. The vaccine used in Europe is becoming a mismatch both for the B-flu (expected to become more prevalent further in the season) and mutations in the H1N1-virus. 

From their report:

Antigenic characterization

Totally 108 influenza A(H1N1)pdm09, 2 influenza A(H3N2) and 5 influenza B viruses were characterizated antigenically in two NICs of Russia since the beginning of the season. According to St.Petersburg NIC data 6  influenza A(H1N1)pdm09 strains were related closely to influenza A/California/07/09 virus. Most of 102 influenza A(H1N1)pdm09 viruses investigated in Moscow NIC were similar to vaccine A/California/07/09 virus however 10 of them had decreased up to 1/16 titer in interaction with antiserum to this virus. Two A(H3N2) strains were similar to influenza A/Hong-Kong/5738/2014 virus, with antiserum to influenza A/Switzerland/9715293/2013 they reacted up to 1/4 - 1/8 of homological titer in HI. All investigated 5 influenza B viruses belonged to Victorian limeage and were similar to influenza B/Brisbane/60/2008 reference strain reacting with antiserum to this virus up to 1/4 - 1/8 of homological titer in HI.

Genetic characterization55 investigated influenza A(H1N1)pdm09 virus strains were A/South Africa/3626/2013-like. All viruses bear clade 6B specific mutations in HA (S84N, S162+N and I216T) and formed new genetic group according to phylogenetic analysis. Two A(H1N1)pdm09 sequences obtained directly from autopsy sample showed the presence of additional mutation D222G in HA1.

Que sera, sera, Whatever will be, will be, The future is not ours to see, Que sera, sera !
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