PREVENTION

Instructions


First, get a flu shot. Before each flu season, the influenza vaccine is created by companies that are designated by the US government. The vaccine is then distributed all across the United States, and priority is given to people who are older and those who are sick and those who are hospitalized. If you are one of those people, please make sure to get your flu shot.


Second, stay healthy and take your vitamins. Exercising, not smoking, eating healthy, and taking multivitamins will keep your immune system healthy and make it harder for the influenza virus to infect you.


Third, wash your hands and stay away from sick people. This cannot be overstated. Washing your hands is the best way to keep from getting many infections, and staying away from sick people is also important. This means staying away from public places where you might be exposed to the influenza virus.

LINK: http://www.ehow.com/how_5177082_prevent-influenza-virus.html

A Community Cluster of Oseltamivir-Resistant Cases of 2009 H1N1 Influenza

To the Editor: Oseltamivir-resistant infection with the 2009 pandemic influenza A (H1N1) virus has so far been described only rarely and is conferred by the H275Y substitution in the neuraminidase enzyme.1 Only 3 of the 32 patients with oseltamivir-resistantinfection reported on as of this writing were not receiving oseltamivir when the resistant viruses were detected, and ongoingcommunity transmission has not yet been shown.1 However, the emergence of oseltamivir-resistant 2009 H1N1 influenza remains a grave concern, since widespread oseltamivir resistance has been observed in seasonal H1N1. This resistance was unrelated to selective drug pressure, and the H275Y substitution did not appear to reduce transmissibility or severity.2,3 We report on a cluster of seven cases of oseltamivir-resistant 2009 H1N1 infection in Vietnam.
In July 2009, during a 42-hour journey, 10 students socialized together in the same train carriage. None of the students knew each other before the journey, none had contact with a person with suspected influenza in the week before the trip, none weresymptomatic during the journey, and none were previously or currently receiving oseltamivir. Fever developed in four of the students within 12 hours after arrival and in two more students within 48 hours after arrival (Fig. 1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). An additional case was identified in a traveler in a different carriage (Patient G). Nasal swabs, throat swabs, or both from all seven persons were positive for 2009 H1N1 RNA when tested with reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assays, and viruses were successfully cultured from specimens obtained from three of the persons. The H275Y substitution was detected retrospectively in diagnostic specimens obtained from all seven subjects before any oseltamivir treatment. The concentrations of oseltamivir carboxylate required for a 50% inhibition ofneuraminidase activity of the isolated viruses in a fluorometric neuraminidase-inhibition assay were 323.6, 429.5, and 889.2 nM; these concentrations confirmed resistance4 (see the Supplementary Appendix).
Six patients were admitted to a hospital for isolation, one patient was isolated at home, and all were treated with oseltamivir phosphate at a dose of 75 mg twice daily (Fig. 1 in the Supplementary Appendix), since resistance testing had not yet been performed. All patients recovered uneventfully, although one patient (Patient F), with the highest 50% inhibitory concentration, continued to test positive on RT-PCR until day 9, despite receiving oseltamivir from the day of the onset of illness. An extensive public health investigation did not identify additional patients or the index patient.
In this cluster, infection developed in at least 6 of the 10 people who were probably exposed to the index patient; this shows that resistant 2009 H1N1 viruses are transmissible and can replicate and cause illness in healthy people in the absence of selective drug pressure. Ongoing transmission from the cluster was not detected, but the tracing of all contacts was not possible, so ongoing transmission cannot be ruled out. However, only three other resistant cases have been detected in Vietnam as of this writing, and all were due to selection of resistant viruses during treatment rather than person-to-person transmission. Although data are limited, it is likely that the detected levels of oseltamivir resistance are clinically relevant.5 The loss of oseltamivir as a treatment option for severe 2009 H1N1 infection could have profound consequences. To minimize this risk, the use of oseltamivir should be restricted to prophylaxis and treatment in high-risk persons or the treatment of people with severe or deteriorating illness, antiviral stockpiles should be diversified and optimal dosages and combination therapies should be urgently studied. Close monitoring and reporting of resistance to neuraminidase inhibitors are essential.

Le Quynh Mai, M.D., Ph.D.
National Institute of Hygiene and Epidemiology
Hanoi, Vietnam

Heiman F.L. Wertheim, M.D., Ph.D.
Oxford University Clinical Research Unit
Hanoi, Vietnam

Tran Nhu Duong, M.D., Ph.D.
National Institute of Hygiene and Epidemiology
Hanoi, Vietnam

H. Rogier van Doorn, M.D., Ph.D.
Oxford University Clinical Research Unit
Ho Chi Minh City, Vietnam

Nguyen Tran Hien, M.D., Ph.D.
National Institute of Hygiene and Epidemiology
Hanoi, Vietnam

Peter Horby, M.B., B.S., F.F.P.H.
Oxford University Clinical Research Unit
Hanoi, Vietnam
peter.horby@gmail.com

for the Vietnam H1N1 Investigation Team
Supported by grants from the Wellcome Trust United Kingdom (081613/Z/06/Z and 077078/Z/05/Z, to Drs. Wertheim, van Doorn, and Horby) and the South East Asia Infectious Disease Clinical Research Network (N01-A0-50042, to Drs. Wertheim, van Doorn, and Horby).
Financial and other disclosures provided by the authors are available with the full text of this letter at NEJM.org.
This letter (10.1056/NEJMc0910448) was published on December 9, 2009, at NEJM.org.
References
1. Oseltamivir-resistant pandemic (H1N1) 2009 influenza virus, October 2009. Wkly Epidemiol Rec 2009;84:453-459. [Medline]
2. Moscona A. Global transmission of oseltamivir-resistant influenza. N Engl J Med 2009;360:953-956. [Free Full Text]
3. Cianco B, Meerhoff T, Kramarz P, et al. Oseltamivir-resistant influenza A(H1N1) viruses detected in Europe during season 2007-8 had epidemiological and clinical characteristics similar to co-circulating susceptible A(H1N1) viruses. Euro Surveill 2009;14:pii=19412-pii=19412.
4. Wetherall NT, Trivedi T, Zeller J, et al. Evaluation of neuraminidase enzyme assays using different substrates to measure susceptibility of influenza virus clinical isolates to neuraminidase inhibitors: report of the Neuraminidase Inhibitor Susceptibility Network. J Clin Microbiol 2003;41:742-750. [Free Full Text]
5. Wattanagoon Y, Stepniewska K, Lindegårdh N, et al. Pharmacokinetics of high-dose oseltamivir in healthy volunteers. Antimicrob Agents Chemother 2009;53:945-952. [Free Full Text]

LINK: http://content.nejm.org/cgi/content/full/362/1/86-a

EPIDEMIOLOGY

Seasonal variations

Influenza reaches peak prevalence in winter, and because the Northern and Southern Hemispheres have winter at different times of the year, there are actually two different flu seasons each year. This is why the World Health Organization (assisted by the National Influenza Centers) makes recommendations for two different vaccine formulations every year; one for the Northern, and one for the Southern Hemisphere.
A long-standing puzzle has been why outbreaks of the flu occur seasonally rather than uniformly throughout the year. One possible explanation is that, because people are indoors more often during the winter, they are in close contact more often, and this promotes transmission from person to person. Increased travel due to the Northern Hemisphere winter holiday season may also play a role. Another factor is that cold temperatures lead to drier air, which may dehydrate mucus, preventing the body from effectively expelling virus particles. The virus also survives longer on surfaces at colder temperatures and aerosol transmission of the virus is highest in cold environments (less than 5 °C) with low relative humidity. Indeed, the lower air humidity in winter seems to be the main cause of seasonal influenza transmission in temperate regions.
However, seasonal changes in infection rates also occur in tropical regions, and in some countries these peaks of infection are seen mainly during the rainy season. Seasonal changes in contact rates from school terms, which are a major factor in other childhood diseasessuch as measles and pertussis, may also play a role in the flu. A combination of these small seasonal effects may be amplified by dynamical resonance with the endogenous disease cycles. H5N1 exhibits seasonality in both humans and birds.
An alternative hypothesis to explain seasonality in influenza infections is an effect of vitamin D levels on immunity to the virus. This idea was first proposed by Robert Edgar Hope-Simpson in 1965. He proposed that the cause of influenza epidemics during winter may be connected to seasonal fluctuations of vitamin D, which is produced in the skin under the influence of solar (or artificial) UV radiation. This could explain why influenza occurs mostly in winter and during the tropical rainy season, when people stay indoors, away from the sun, and their vitamin D levels fall.

Pandemic Influenza Vaccine Policy — Considering the Early Evidence

EDITORIAL

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Influenza Editorial


LINK: http://content.nejm.org/cgi/content/full/361/25/e59

The Emotional Epidemiology of H1N1 Influenza Vaccination

PERSPECTIVES

Danielle Ofri, M.D., Ph.D.

Last spring, when 2009 H1N1 influenza first came to our attention, my patients were in a panic. Our clinic was flooded with callsand walk-in patients, all with the same question: "When will there be a vaccine?"
It was all so new then, and we didn't have an answer. That lack of answer seemed to fuel anxiety to a fever pitch. A substantialcohort of my patients continued calling, almost on a weekly basis, to ask about the vaccine.
These, of course, were the same patients who routinely refused the seasonal flu vaccine. Each year we'd go through the same drill: I'd offer them the flu shot. I'd explain the clinical reasoning behind this recommendation. I'd strongly encourage vaccination.
"No, thanks," they'd say. "The vaccine makes me sick." Or "My brother had a bad reaction." Or, simply, "I don't do flu shots."
The irony was painful. No matter how often I trotted out the statistics of 30,000 to 40,000 annual deaths from influenza, the patients would not be moved. So when they demanded the H1N1 vaccine last spring, I reminded them of their reluctance over the seasonal flu shot. "Oh, that's different," they said.
Six months have passed. Flu season is now here. After repeated delays, H1N1 vaccine finally arrived in our clinic earlier this month to the uniform relief of the medical staff. But my formerly desperate patients were now leery. "It's not tested," they said. "Everyone knows there are problems with the vaccine." "I'm not putting that in my body."
I was unprepared for this response, but maybe I shouldn't have been. For weeks now, in the schoolyard of my children's elementary school, other parents had been sidling up to me, seemingly in need of validation. "You're not giving your kids that swine flu shot, are you?" they'd say, their tone nervous, if a bit derisive.
How to explain this dramatic shift in 6 short months? It certainly isn't related to logic or facts, since few new medical data became available during this period. It seems to reflect a sort of psychological contagion of myth and suspicion.
Just as there are patterns of infection, there seem to be patterns of emotional reaction ("emotional epidemiology") associated with new illnesses. When 2009 H1N1 influenza was first detected, it fit a classic pattern that Priscilla Wald recently outlined in her book Contagious1: It was novel and mysterious; it emerged from a teeming third-world city, and it was now making its insidious — and seemingly unstoppable — way toward the "civilized" world.
This is the story line for most headline-grabbing illnesses — HIV, Ebola virus, SARS, typhoid. These diseases capture our imagination and ignite our fears in ways that more prosaic illnesses do not. These dramatic stakes lend themselves quite naturally to thriller books and movies; Dustin Hoffman hasn't starred in any blockbusters about emphysema or dysentery.
When the inoculum of dramatic illness is first introduced into society, the public psyche rapidly becomes infected. Almost like an IgE-mediated histamine release, there is an immediate flooding of fear, even if the illness — like Ebola — is infinitely less likely to cause death than, say, a run-in with the Second Avenue bus. This immediate fear of the unknown was what had all my patients demanding the as-yet-unproduced H1N1 vaccine last spring.
As the novel disease establishes itself within society, a certain amount of emotional tolerance is created. H1N1 infection waxed and waned over the summer, and my patients grew less anxious. There was, of course, no medical basis for this decreased vigilance. Unusual risk groups and atypical seasonality should, in fact, have raised concern. By late summer, the perceived mysteriousness of H1N1 had receded, and the number of messages on my clinic phone followed suit.
But emotional epidemiology does not remain static. As autumn rolled around, I sensed a peeved expectation from my patients that this swine flu problem should have been solved already. The fact that it wasn't "solved," that the medical profession seemed somehow to be dithering, created an uneasy void. Not knowing whether to succumb to panic or to indifference, patients instead grew suspicious.
No amount of rational explanation — about the natural variety of influenza strains, about the simple issue of outbreak timing that necessitated a separate H1N1 vaccine — could allay this wariness.
Similarly, reassuring fellow parents that I was indeed vaccinating my own children did little to ease their apprehension. When the New York City public school system offered free vaccinations for both students and families, there was an abysmally poor turnout. Less than one quarter of the consent forms sent home in kids' backpacks were returned.
The dramatic shift in public sentiment over the course of this H1N1 epidemic is both fascinating and frustrating. It is clear that there is a distinct emotional epidemiology and that it bears only a faint connection to the actual disease epidemiology of the virus.
We cannot combat H1N1 influenza merely by ensuring adequate supplies of vaccine and oseltamivir. Unless the medical profession confronts the emotional epidemiology of H1N1 with a full-court press, we run the risk of an uncontrollable epidemic.
There is no doubt that we are far behind the curve in terms of public relations. Our science has not been dithering at all, but our articulation of that science has often seemed that way, from the unfortunate initial appellation of swine flu to our inability to clarify distinctions between vaccine-production issues and clinical-risk issues. Suspicion has its own contagion, and we have not been aggressive enough in countering it.
Every practicing clinician is, to some degree, an armchair epidemiologist. We register patterns of disease as they play out among our patients. We are also keen detectives of emotional epidemiology, though we often aren't aware of this as such. Keeping tabs on the emotional epidemiology as well as the disease epidemiology, and treating both with equal urgency, are the essential clinical tools for this influenza season.
Financial and other disclosures provided by the author are available with the full text of this article at NEJM.org.

Source Information
From New York University School of Medicine and Bellevue Hospital, New York.

This article (10.1056/NEJMp0911047) was published on November 25, 2009, at NEJM.org. LINK http://content.nejm.org/cgi/content/full/NEJMp0911047

References
1. Wald P. Contagious: cultures, carriers, and the outbreak narrative. Durham, NC: Duke University Press, 2008.

2009 H1N1 ACIP Vaccination Recommendations

LISTEN AUDIO



In this podcast, Dr. Tony Fiore discusses who should be vaccinated against 2009 H1N1 flu during the 2009-2010 season. He explains the target groups for vaccination, and how these groups differ from those recommended for seasonal flu vaccination. Created: 9/2/2009 by Coordinating Center for Infectious Diseases, National Center for Immunization and Respiratory Diseases, Influenza Division (CCID/NCIRD/ID). Date Released: 9/2/2009. Series Name: CDC Featured Podcasts.

CASE REPORT - 11 JUNE 2010

Pandemic (H1N1) 2009

Weekly update

11 June 2010 -- As of 6 June, worldwide more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18156 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:
Active but declining transmission of pandemic influenza virus persists in limited areas of the tropics, particularly in Southeast Asia and the Caribbean. As countries of the temperate southern hemisphere enter winter, only sporadic influenza activity has been detected so far, except in Chile and Uruguay, both of which have recently reported small numbers of pandemic influenza virus detections. Although seasonal influenza B viruses have been the predominant type of influenza virus circulating worldwide since the end of February 2010, there have been increasing but low level detections of seasonal influenza H3N2 viruses, particularly in South America and in East Africa.
In the tropics of the Americas, overall pandemic influenza activity is low, however, both seasonal influenza H3N2 and type B viruses are actively circulating in parts of tropical South America. Active but declining transmission of pandemic influenza virus continues to be detected primarily in Cuba. Since early 2010, pandemic influenza virus has circulated at low levels in Costa Rica. Sporadic detections of pandemic influenza virus continue to be reported in Brazil. During the most recent reporting week (last week of May 2010), both Brazil and Venezuela reported regional spread of influenza activity associated with an increasing trend of respiratory diseases. In Venezuela, recent influenza activity (which began during early May 2010) has been predominantly due to circulating seasonal influenza A viruses. In Bolivia, circulation of seasonal influenza viruses, predominantly type B, was observed between March and May 2010 and now appears to be subsiding.
In Asia overall pandemic influenza virus transmission remains low, except in parts of tropical South and Southeast Asia, particularly Singapore, Malaysia, and Bangladesh. In Singapore, overall levels of ARI remained slightly below the epidemic threshold and the proportion of respiratory samples testing positive for pandemic influenza virus increased slightly to 34%. In Malaysia, limited data suggests that pandemic influenza virus transmission has begun to decline since plateauing during May 2010. In Bangladesh, there has been stable persistent low level co-circulation of pandemic and seasonal influenza B viruses since March 2010. Sporadic detections of pandemic influenza virus continued to be reported across other parts of Asia. In East Asia, overall influenza activity remains low, however, seasonal influenza B viruses continue to circulate at low and declining levels.
In Sub-Saharan Africa, pandemic influenza virus continued to circulate at low levels in parts of West Africa, most notably in Ghana. During the most recent reporting week, 13% of all respiratory samples tested positive for pandemic influenza virus in Ghana. Small but significant numbers of seasonal H3N2 viruses have been detected in Kenya and Tanzania since late May 2010.
Overall, in the temperate regions of the northern hemisphere, pandemic influenza viruses have been detected only sporadically during the past month. In the temperate southern hemisphere, only two countries, Chile and Uruguay, have recently reported small numbers of pandemic influenza virus detections. In Chile, there was low level geographically limited circulation of pandemic influenza virus during May 2010; 3.4% of respiratory samples tested positive for pandemic influenza virus during the last week of May 2010. Of note, in Uruguay, 11 (44%) of 25 samples tested positive for pandemic influenza during the most recent reporting week (the last week of May 2010); however, the corresponding intensity of respiratory diseases in the population is not yet known. Other respiratory viruses, most notably RSV, are known to be circulating in Chile and Argentina. There have been no recent detections of pandemic influenza virus in South Africa. In New Zealand and Australia, overall levels of ILI remain low; only sporadic detections of seasonal and pandemic influenza viruses have been recently reported in Australia.
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).