CIDRAP: MRSA Pneumonia Suspected In Calvert County Flu Cluster

 

Clumps of methicillin-resistant Staphylococcus aureus – Credit CDC PHIL

# 6210

 

 

Although we haven’t seen any official updates since late yesterday afternoon, reports have been trickling in through various media outlets suggesting that the fatal flu cluster in Lusby, Md.  involved the seasonal H3N2 virus and an aggressive form of MRSA pneumonia.

 

Lisa Schnirring of CIDRAP News  brings us up to date this evening with this report.  Follow the link to read her report in its entirety.

 

 

MRSA pneumonia suspected in fatal flu cluster

Lisa Schnirring Staff Writer

Mar 8, 2012 (CIDRAP News) – Another family member linked to a fatal flu cluster in Calvert County, Md., has been hospitalized, as suspicion grew that an aggressive drug-resistant form of pneumonia may have played a role in the severe illnesses, according to media reports.

 

Maryland and Calvert County health officials didn't report any new details about the cases, but the Washington Post reported yesterday that the sister of the 81-year-old woman who died has been hospitalized at MedStar Washington Hospital Center with fever but no other flu symptoms.

(Continue . . . )

 

 

Tissues taken during autopsies from two of the victims have reportedly been sent to the CDC for further analysis, which can take a day or two to complete.

»» Read More

Vietnam:`New’ H3N2 Swine Flu Virus Reported

 

UPDATED: 1500hrs

Henry Niman has posted this afternoon that after further review, he believes this report to be a badly translated repost of a story from December on 10 Cases in the United States we already knew about. 

Today’s story is ambiguous enough to make that a plausible explanation.   Unless and until we can get some confirmation of this story I would advise that you view the following report with caution.

 

# 6131

 

 

This morning Editor & Senior Moderator Tetano on FluTrackers has picked up a series of news articles coming out of Vietnam talking about 10 human cases of infection by a `new’ H3N2 swine flu virus.

 

Two of these articles are machine translated from Vietnamese, and are therefore a bit garbled, but the third is an English Language report from the VOV (Voice of Vietnam). 

 

Assuming the major points of today’s report are correct (not always a given), there is not enough information provided to know how this virus compares to the A/H3N2v virus which has been detected in a handful of cases in the United States (see CDC Releases Updated H3N2v Interim Guidance).

 

Keeping the usual caveats in mind regarding early media reports, here is the story from the Voice of Vietnam.

 

 

New strain of swine flu detected

Updated : 5:16 PM, 09/02/2012

(VOV) - The Heath Ministry has quoted sources from the Ho Chi Minh City Pasteur Institute confirming that a new kind of porcine flu virus, A/H3N1, has appeared, apparently a combination of the pig-related A/H1N1 and A/H3N2 flu viruses.

 

The medical sector has monitored 10 patients infected with the A/H3N2 virus with porcine origin, and found that three of them had not had direct contact with any diseased pigs.

 

Therefore, the sector has not ruled out the possibility of a mutation in the A/H3N2 strain which could lead to transmission between humans, instead of strictly from pigs to humans as previously.

 

However, the situation has not reached an alarming level because the virus has not changed much; it has low toxicity and has shown no sign of drug resistance.

 

Flu vaccines are able to cope with small changes in this kind of virus, said Le Hoang San, Vice Director of the HCMC Pasteur Institute.

 

 

Swine are highly susceptible to the influenza virus, and are capable of serving as `mixing vessels’, allowing them to reassort into new hybrid strains.

 

Reassortment happens when two different influenza viruses co-infect the same host, swap genetic material, and produce a hybrid virus. 

 

That is essentially what happened in 2009, when the H1N1 swine flu virus emerged after bouncing around swine herds for a decade or more, picking up genetic changes along the way.

 

And not surprisingly, this recently emergent `humanized’  H1N1 virus has re-entered the swine population and is once again mixing and matching with other circulating swine flu viruses.

 

As a result we now have a Swine H3N2 virus that has reassorted with the 2009 pandemic H1N1 virus, producing a new hybrid that has – in a limited fashion – begun to emerge into the human population.

 

The article above calls the Vietnamese strain a `combination of the pig-related A/H1N1 and A/H3N2 flu viruses’ – which if we take literally – suggests a different reassortment than the one we’ve seen in the United States.

 

 

As stories in the media often gloss over or confuse crucial scientific details we really need to wait for a more definitive report before we can talk about the origin, genetic makeup, and potential of this new virus.

 

For now, this is simply something new to keep an eye on in the ever changing and always surprising world of influenza.

 

Update:  In a conversation with Sharon Sanders of FluTrackers this morning, she pointed out that this article refers to this new reassortant virus as H3N1 (once) and H3N2 (twice).

I took the first mention (H3N1) as a likely misprint, but until we can get some clarification, I don’t think we can say with any confidence exactly which strain this new virus is.

»» Read More

New England Seal Deaths Tied to H3N8 Flu Virus

 

 

# 6022

 

We’ve a follow up from NOAA today on the mysterious deaths of seals along the New England coastline earlier this fall.  In early November I reported (see NOAA: New England Dead Seals Test Positive For Flu) that initial tests indicated an influenza A virus, but more testing was needed to determine the exact strain.

In the past, we’ve seen rare and isolated influenza infections resulting in seal deaths from the H7N7 and H4N5 avian flu viruses.

 

Today we learn that the viral culprit in this latest incident is a variant of the H3N8 avian flu strain, versions of which are known to also infect horses and dogs.

 

My thanks to @JustinNOAA for the link to this news release.

 

 

Science team identifies influenza virus subtype that infected five dead seals

Risk to humans and pets low; tests continue

PDF/Print version

Harbor Seals (Credit NOAA)

A virus similar to one found in birds but never before in harbor seals was the cause of five of 162 recent deaths of the animals  in New England, according to a group of federal agencies and private partners.

 

This Influenza A virus subtype, H3N8, appears to have a low risk of transmission to humans. Experts continue to analyze this virus, and any findings of public health significance will be immediately released. The virus is not the infamous H5N1  virus that caused a global pandemic in 2007, or the H1N1 virus from 2009.

 

Any member of the public who sees a seal in distress is reminded to:

• Stay at least 150 feet away
• Keep dogs leashed and away from seals
• Call NOAA Fisheries Service's stranding hotline at 1-866-755-NOAA (6622)

“The work that NOAA and its partners have done to help identify and confirm the virus strain H3N8 in these animals has been an important first step in the investigation into this event,” said Dr. Teri Rowles, lead veterinarian and coordinator of the Marine Mammal Health and Stranding Program for NOAA Fisheries Service. “We are now conducting tests on additional animals to learn more about the role this virus may have played in the die-off and to better understand the virus itself.”

 

Experts believe that Influenza A virus caused a bacterial pneumonia which was responsible for the death of the five seals. Most terrestrial animals infected with the previously known H3N8 virus suffered upper respiratory infections, and most recovered.

 

"This H3N8 virus is usually associated with wild birds, and a separate group of H3N8 infects horses and dogs,” said Dr. Hon Ip, of the USGS’s National Wildlife Health Center. "This is the first time that a virus which is similar to the H3N8 avian influenza virus has been associated with a large scale mortality in marine mammals."

(Continue . . . )

»» Read More

Hong Kong: Swine Influenza Surveillance

 

 

# 5965

 

 

According to the FAO, the world produces somewhere on the order of 100 million tonnes of pork every year, and that number is expected to increase by another 20% by 2020.

 

By then, roughly half of the world’s pork supply will come from China (cite).

 

Swine are highly susceptible to the influenza virus, and are capable of serving as `mixing vessels’, allowing them to reassort into new hybrid strains.

 

Reassortment happens when two different influenza viruses co-infect the same host, swap genetic material, and produce a hybrid virus. 

 

That is essentially what happened in 2009, when the H1N1 swine flu virus emerged after bouncing around swine herds for a decade or more, picking up genetic changes along the way.

 

And not surprisingly, this recently emergent `humanized’  H1N1 virus has re-entered the swine population and is once again mixing and matching with other circulating swine flu viruses.

 

In recent months we’ve been following reports of a handful of sporadic human infections across three states (Indiana, Pennsylvania, Maine) by a swine H3N2 virus that has reassorted with – and borrowed the M gene segment from – the pandemic H1N1 virus.

 

So far, the number of cases is small, and the CDC states there is no evidence that this emerging hybrid virus is spreading in an efficient or sustained manner. But the concern is, that over time it might evolve into a more human-adapted virus.

 

For some recent coverage of these trH3N2 cases, you may wish to revisit:

 

CDC Update On trH3N2 Swine Infections

Maine Confirms A 2nd trH3N2 Case

CDC Update On trH3N2 Cases

A 5th trH3N2 SOIV Report

CDC Update On Recent Novel Swine Flu Cases

MMWR: Swine-Origin Influenza A (H3N2) Virus Infection in Two Children

 

Given the potential for the creation and emergence of novel influenza viruses, surprisingly little testing and surveillance of pigs takes place around the world. 

 

Even in the U.S. some hog farmers are reluctant to allow their herds to be tested (see Swine Flu: Don’t Test, Don’t Tell) out of fears that the discovery of a new swine flu virus would depress pork sales.

 

As might be expected, Hong Kong - which was the first battleground for the H5N1 bird flu virus in 1996, and which had to deal with SARS in 2003 – has a very aggressive surveillance system.

 

Today the HKSAR government has released the latest results from their ongoing slaughterhouse surveillance program conducted by the University of Hong Kong.

 

Between August and mid-October 1,000 pigs were tested, and while no `human H1N1’ viruses were detected,  15 reassorted H3N2 viruses with (unspecified) genetic contributions from the 2009 H1N1 virus were discovered.

 

First, some excerpts from the press release, then I’ll return with a little more.

 

FEHD releases results of regular influenza virus surveillance in pigs from August to October

 

Hong Kong (HKSAR) - The Centre for Food Safety (CFS) of the Food and Environmental Hygiene Department (FEHD) today (November 16) announced results of the regular influenza virus surveillance programme on pigs conducted by the University of Hong Kong (HKU) for August to mid October at the Sheung Shui Slaughterhouse.

 

Among some 1 000 samples tested, no human swine influenza virus (pandemic H1N1) was detected. However, 15 samples were found to contain a virus that was essentially a swine influenza H3N2 virus but had picked up some genes of human swine influenza virus. The same virus was also found in the last round of surveillance programme for May to July.

 

The HKU expert in charge of the surveillance programme,professor JSM Peiris, reiterated that this swine influenza H3N2 virus, which carried the genes of the human swine influenza virus, is unlikely cause any major human health risk or problems in food safety.

 

Under the regular influenza virus surveillance programme for pigs, the CFS has been helping HKU researchers to collect blood and tracheal and nasal swabs from pigs at the Sheung Shui Slaughterhouse twice a month to monitor influenza virus activity in pigs.

 

"CFS will continue to monitor reports of the HKU surveillance programme and make announcements on a regular basis. Results will be announced immediately if there are significant public health impacts," the spokesman said.

(Continue . . .)

 

 

While this report describes these reassorted swine H3N2 viruses as having `picked up some genes of human swine influenza virus’, it provides no further details. 

 

It would be of interest to see just how closely related these reassorted viruses are to the trH3N2 isolates that have recently been detected in the United States over the past few months.

 

Hopefully we’ll get a more specific description of these H3N2 reassortants over time.

 

For now, and until such time that these reassortants evolve to become more easily transmissible among humans, they pose a relatively low public health threat.

 

While it is always possible that the next pandemic will emerge from the wild, the odds say it will come from a farm – where large numbers of animals intermingle, swap viruses, and come in daily contact with humans.

 

Which is why increasing our surveillance of livestock for zoonotic diseases must become a priority.

 

Over the past 5 years, we’ve revisited the subject of influenza reassortment dozens of times.   For more on this topic, you may wish to visit:

 

Virology Journal: Receptor Cells In Minor Poultry Species

mBio: A/H1N1 Potential For Mutation

Study: The Continuing Evolution Of Avian H9N2

EID Journal: Co-Infection By Influenza Strains

EID Journal: Swine Flu Reassortants In Pigs

If You’ve Seen One Triple Reassortant Swine Flu Virus . . .

 

And as always, if you have not already read it, I highly recommend Helen Branswell’s Scientific American article called Flu Factories.

»» Read More

An Influenza Double Whammy

 

 

 

# 5936

 

 

Although we’ve seen this sort of thing a few times before, the news yesterday that researchers in Cambodia detected two patients with dual influenza infections (back in 2009) has made quite a splash in the media overnight.

 

Some of the headlines include:

 

It's Possible to Come Down With Two Flu Viruses at Once Yahoo! 

Cambodians infected with both swine, seasonal flu The Straits Times

Global flu watch: Report of rare flu coinfection in Southeast Asia hot... PhysOrg.com

 

Like the influenza virus itself, the UK papers tend to go for the throat with their headlines:

 

Britain On Alert For New Super-flu Daily and Sunday Express

Deadly strain of super-flu 'could spread to Britain within 24 hours' Daily Mail

 

 

Before these hyperbolic headlines entice anyone to head down to the bunker, the study on which these stories are based found no `super flu’.

 

In fact, while researchers detected a relatively rare dual infection of seasonal H3N2 and the new pandemic H1N1 virus in a pair of Cambodian patients, in neither case did they find a reassortant virus.

 

The point is, this is the sort of set up that could have produced a new, potentially dangerous hybrid virus.

 

First stop, the study which appears in the American Journal of Tropical Medicine & Hygiene, then we’ll come back and look at the potential ramifications of dual influenza infections.

 

Dual Infection of Novel Influenza Viruses A/H1N1 and A/H3N2 in a Cluster of Cambodian Patients

Christopher A. Myers, Matthew R. Kasper, Chadwick Y. Yasuda, Chin Savuth, David J. Spiro, Rebecca Halpin, Dennis J. Faix, Robert Coon, Shannon D. Putnam, Thomas F. Wierzba and Patrick J. Blair

 

 

The details are behind a pay wall, but as the authors point out in their abstract:

 

This incident confirms dual influenza virus infections and highlights the risk of zoonotic and seasonal influenza viruses to coinfect and possibly, reassort where they cocirculate.

 

 

Earlier this year you may recall we saw a similar co-infection in Canada that actually led to the creation of a unique hybrid reassorted virus (see Webinar: pH1N1 – H3N2 A Novel Influenza Reassortment).

 

In this case, the patient was a 16-month old boy from the Greater Toronto Area who was admitted briefly to a local hospital for respiratory and gastrointestinal symptoms in January of 2011.

 

The child was sent home, and recovered without incident, and no other family members or contacts reported flu-like symptoms.

 

It wasn’t until later, when viral cultures showed a hybrid (reassorted) H1N1-H3N2 virus, did scientists realize that something unusual had occurred.

 

Details of this event were presented in an online webinar on June 16th of this year. 

 

From the abstract:

 

pH1N1 – H3N2: A Novel Influenza Virus Reassortment

Presenter:

Dr. Jonathan Gubbay- Medical Microbiologist, OAHPP

Abstract

Dr. Jonathan Gubbay, medical microbiologist at the Toronto Public Health Laboratory, will present on a new influenza virus that has been discovered by the Ontario Agency for Health Protection and Promotion (OAHPP). It is the first Canadian confirmed finding of a patient with a coinfection of seasonal H3N2 and pH1N1 followed by reassortment.

(Continue . . .)

 

A little more than a year ago, in EID Journal: Co-Infection By Influenza Strains, I wrote about a study in New Zealand during the opening months of the 2009 pandemic that discovered at least 11 co-infections (out of 1,044 samples tested) with the older seasonal H1N1 virus and the newly emergent pandemic H1N1 virus.

 

Pandemic (H1N1) 2009 and Seasonal Influenza A (H1N1) Co-infection, New Zealand, 2009

Matthew Peacey , Richard J. Hall, Stephanie Sonnberg, Mariette Ducatez, Shevaun Paine, Mackenzie Nicol, Jacqui C. Ralston, Don Bandaranayake, Virginia Hope, Richard J. Webby, and Sue Huang

 

 

The authors state that the rate of co-infection could actually be higher, since samples were not checked for any other flu strains such as H3N2 and influenza B.

 

And going back even further, Maryn McKenna wrote – in an article for CIDRAP News – of an Indonesian teen who was found to have been co-infected with an avian (H5N1) and a human (H3N2) influenza strain.

 

Avian, human flu coinfection reported in Indonesian teen

Maryn McKenna Contributing Writer

Mar 17, 2008 – ATLANTA (CIDRAP News) – An Indonesian teenager has been brought forward as a case of simultaneous infection with seasonal and avian strains of influenza—a possibility that health planners have long warned could give rise to a pandemic flu strain.

(Continue . . . )

 

In the Indonesian and New Zealand cases above, no reassortant viruses were detected. Still, this research suggests that humans, like swine, could be `mixing vessels’ for influenza. 

 

While gene swapping is possible under a co-infection scenario, it isn’t by any means assured.

 

And even should a reassortment take place, the resulting virus might not prove biologically `fit’, or if it is `fit’, any worse than either of its parental strains.

 

However, the potential for creating a devastating novel flu strain cannot be discounted.

 

Last August, in Professor Peter Doherty On Bird Flu, we looked at his worries on the possibility that the H5N1 virus might one day swap genes (reassort) with the H1N1 virus and produce an easily transmitted, highly virulent flu strain.

 

And in September we saw research (see Study: Reassorted H1N1-H5N1 Produced Virulent Strain) where a laboratory-created reassortant virus with genes taken from the H5N1 and H1N1 virus produced a highly transmissible and virulent strain.

 

Of course, while the world was waiting for bird flu, in 2009 a reassorted Swine flu virus unexpectedly sparked a global pandemic. We were fortunate that it wasn’t any more severe than it was, but it illustrates that there are many ways a pandemic can evolve.

 

 

In addition to the various clades of human flu strains ( both pdmH1N1 & H3N2) now circulating, and a growing constellation of avian flu strains (H5N1, H9N2, H7N7, etc), we continue to see rare sporadic human infections by reassorted swine viruses as well (Maine Confirms A 2nd trH3N2 Case).

 

Further evidence that nature’s laboratory is open 24/7, and that influenza viruses are constantly mutating and reassorting, looking for an evolutionary advantage.

 

While most of these reassortant viruses are doomed to end up in the evolutionary dustbin, failing to thrive and compete with other viruses, it only takes one fit, virulent, and easily transmissible virus to spark a global pandemic.

 

And that is something that might emerge tomorrow, next month, or perhaps not until years from now.  

 

But history as history has us shown over and over:

 

Pandemics happen.  Count on it.

»» Read More

Pennsylvania DOH: Updated FAQ On The Novel Swine Flu Cluster

 

 

 

# 5818

 

 

The Pennsylvania Department of Health has updated their FAQ sheet (Q & A: Novel Influenza A Virus) on the recent detections of a reassorted H3N2 swine flu virus in three children who attended a county fair in mid-August.

 

It is still very early in the epidemiological investigation of these cases, and there are a lot of questions yet to be answered.

 

Prime among those is whether this virus has the potential to spread efficiently in humans.

 

For now, evidence of sustained human transmission has not been found.  Of course, the CDC is still investigating, and that could change if more cases show up.

 

But it is important to note, that even if a few more cases were to show up over the next few weeks, that wouldn’t necessarily mean that we are faced with an epidemic or pandemic situation. 

 

For that to happen the virus would need to be adapted well enough to human physiology to have an R₀ number (basic reproductive number) sufficient to sustain an outbreak.

 

The R₀  number signifies the average number of secondary infections caused by one infectious person entering a totally susceptible population. 

 

If less than 1.0, outbreaks are likely to sputter and die out.  If greater than 1.0, the outbreak is more capable of spreading. 

 

And as we’ve seen with roughly 20 other reported novel swine infections since 2005, and with a significant number of H5, H7, and H9 avian flu infections, it is possible to have limited outbreaks of a novel flu virus without it sparking an epidemic.

 

We’ll need to wait for more epidemiological evidence before we can know whether this particular virus has `legs’. If it is spreading efficiently (and that’s still a big `if’), we ought to see evidence of that fairly soon.

 

It is also possible that if this virus isn’t ready for prime time right now, that through further reassortment or mutation, it could become better adapted down the road. The only constant with influenza viruses is change.

 

So this situation deserves ongoing surveillance.

 

But regardless of this virus’s fate, the risks of seeing another novel pandemic virus emerge sometime in the future from either the farm or the wild are genuine.

 

 

A few recent blogs on this possibility include:

 

Professor Peter Doherty On Bird Flu

Two Reassortment Studies To Ponder

Hong Kong: Influenza Surveillance In Pigs

The (Swine) Influenza Reassortment Puzzle

 

 

The CDC’s investigation into these recent novel flu cases in Pennsylvania continues, and hopefully we’ll know more shortly.

 

Below are some excerpts from yesterday’s (9/6/11) updated Health Department FAQ. 

 

 

Questions & Answers: Novel Influenza A Virus

 
About the Flu Virus/Current Vaccination 

• 

What is this novel influenza A virus? 
Influenza A viruses occur in many animals, including humans, swine (pigs) and wild birds.This particular virus is unique from other previous H3N2 human infections in that it also contains a genetic piece of the 2009 H1N1 virus.

  
• Is it possible for humans to transmit it to other humans?  
Currently, it does not appear the virus is spreading from person‐to‐person.  However, we will continue to learn ore as our investigation into this new virus continues.  

•

How serious is this virus?  
We currently know of three cases of this novel influenza virus. One patient has recovered and the other two are recovering. Our investigation will continue to focus on the seriousness of the virus.  Based on what we know about other types of flu, illness can range from very mild symptoms to death in particularly susceptible populations (like older people, young children and those with certain medical conditions).

 

•  What does this mean for this year’s flu vaccines? Will the current vaccine cover both seasonal flu and this new strain of flu?  
The 2011‐2012 vaccine is the same as last year, covering two strains of influenza A pandemic H1N1 and a H3N2 strain that has been circulating for a few years now) as well as a strain of influenza B.  It is too early to tell whether or not this new strain will even need vaccination.  

<SNIP>

Should we be concerned that a flu pandemic is pending?  

A pandemic is a global outbreak of disease.  A flu pandemic happens when a new strain of the flu virus appears for which people have little or no immunity. As a result, it spreads easily from person to person around the world, causing widespread illness and death.

 

Currently, we don’t have any evidence to support that this novel influenza A virus will lead to a pandemic, as we haven’t yet been able to prove that it is being transmitted from human to human.

 

As with any new influenza A virus, public health officials  are working to learn more about the source of this particular strain and to determine how/if it can be spread from person to person. 

»» Read More

M Is For Mutation

 

 

 

# 5812

 

 

I usually try to avoid using the word `Mutant’ or `Mutation’ in my blog titles about flu because, strictly speaking . . .

 

All influenza viruses are the product of mutation.

 

Flu viruses are inherently unstable (in particularly, influenza A), and are constantly evolving and changing. Mutating. Which explains why scientists must adjust the flu vaccine nearly every year.

 

Of course, the media loves the word `Mutation’ – I suspect because it conjures up vivid images in the minds of their readers. And to the public, mutations are almost universally perceived as `bad’. 

 

Earlier this week we saw a plethora of `Mutant’ headlines, including:

 

New bird flu virus mutation threatens Vietnam -Thanh Nien Daily

No vaccine yet for mutant bird flu ...  - The Straits Times

Mutant Bird-Flu Strain Spreads in Asia - The Daily Beast

Mutant bird flu strain in Asia prompts call for scrutiny - MSNBC

 

 

While the emergence of this (relatively) new strain of H5N1 is a big story, so far we’ve seen no evidence to suggest that this `mutation’ poses any greater threat to humans than do any of the other dozen or so clades of the bird flu virus.

 

But that isn’t the sort of lede that sells newspapers.

 

Since the `M’ word seems to be on the lips of many people this week, today seems like a good day to go over how influenza viruses mutate.

 

Don’t worry. 

 

I’ll keep this layman simple, mostly so I – a non-scientist - can understand it.  Real scientists, however, may wish to avert their eyes.

 

The genetic sequence of the influenza virus can be represented by a chain of letters identifying the hundreds of amino acids that make up the viral genome.

 

A tiny sub-section of that chain might have an amino acid sequence that looks something like:

 

MKAILVVMLYTFATA

 

As the virus inhabits a cell, and begins to replicate, it makes thousands of copies of itself which then burst out of the cell after a few hours and go on to infect other cells.

 

Those cells, in turn, make copies that go forth to infect more cells and repeat the process.

 

But being a single-strand RNA virus, the influenza virus tends to be sloppy in making copies of itself. As it replicates millions of times, tiny errors sometimes creep in. If in the process of making copies it mixes up just a single amino acid, we can end up with a mutated virus.

 

MKAILVVMLYTFATA

MKAILVVMLYTFATA

MKAIFVVMLYTFATA      -  Voila! A mutation

MKAIFVVMLYTFATA

MKAIFVVMLYTFATA

 

Above, I’ve swapped out the amino acid leucine (L) at position 5 for phenylalanine (F), simulating a replication error.

Assuming the result is a `biologically fit’ and competitive virus (most aren’t), then it may go on to infect other cells, and conceivably, other hosts.

 

Of course, that doesn’t mean it will make the virus more dangerous.  A mutation can make the virus less virulent or less transmissible.

 

Or it may simply have no effect at all.

 

These small mutations in the virus are called drift, and over time the flu virus can accumulate enough changes so that last year’s vaccine is no longer effective.

 

And that is essentially the story behind this new 2.3.2.1 clade of the H5N1 virus. Enough antigenic changes have accumulated in its genome to allow it to evade the poultry vaccines currently in use.

 

Of course, mutations like these are also capable of bringing about other changes, including antiviral resistance, or perhaps increasing the virulence or transmissibility of the virus.

 

So while not necessarily alarming, this week’s bird flu news is certainly worthy of our attention.

 

Bigger changes in the influenza virus generally come about through a process known as reassortment or shift.

 

Reassorted viruses can result when two different flu strains inhabit the same host (human or otherwise) at the same time. Under the right conditions, they can swap one or more gene segments and produce a hybrid virus.

 

 

While far less common than drift, shift can produce dramatic changes in how a virus behaves, and has been responsible for the creation of pandemic viruses in the past. 

 

Again this week, we’ve received news of a pair of `reassortant’ swine H3N2 flu viruses detected in children from two different states (see MMWR: Swine-Origin Influenza A (H3N2) Virus Infection in Two Children).

 

For those of us who were covering the earliest reports of a novel swine flu outbreak in April of 2009, this week’s report admittedly has a tinge of deja flu.

 

But it is important to remember that over the past 5 years (excluding the 2009 H1N1 virus) nearly 2 dozen similar novel swine flu viruses have been detected across the country. It is also probable that a number of other novel infections have escaped notice – yet so far none has been shown to spread efficiently from human-to-human.

 

That could change, of course - as each reassortant is  a new roll of the genetic dice - and so the CDC quite understandably is encouraging enhanced local flu surveillance, and would mount a vigorous response if more cases were to start to appear. 

 

Flu viruses have been quietly mutating and reassorting for thousands of years, but only rarely does that result in a pandemic strain. The vast majority of these mutations end up in evolution’s dustbin.

 

Even though we don’t always know what they signify, today we have the surveillance tools that enable us to watch some of these genetic changes when they start to appear.

 

 

And while that means we are likely to hear about a lot of potential viral threats that never materialize, it also means we may get some invaluable advance warning about the next pandemic virus before it strikes. 

»» Read More

Webinar: pH1N1 – H3N2 A Novel Influenza Reassortment

 

 

# 5622

 

Last week we got word of the first detection of a reassortment between the (formerly) pandemic H1N1 virus and a seasonal H3N2 influenza virus, which was announced by researchers in Toronto, Canada.

 

The case involved a  16-month-old boy from the Greater Toronto Area was admitted briefly to a local hospital for respiratory and gastrointestinal symptoms last January.

 

The child was sent home, and recovered without incident, and no other family members or contacts reported flu-like symptoms.

 

It wasn’t until later, when viral cultures showed a hybrid (reassorted) H1N1-H3N2 virus, did scientists realize that something unusual had occurred.

 

It is known that influenza viruses – if they co-infect the same host simultaneously – have the ability to swap genetic segments and form a hybrid.

 

This sort of reassortment can occur in any host; human, porcine, or avian.  

Most of the time, these reassortments are evolutionary dead ends. They are either biologically unfit, or unable to compete with their better adapted parental strains, and fail to reproduce and thrive.

 

On exceedingly rare occasions, they can produce a competitive new virus - and as we saw in 2009 - spark a global pandemic.

 

Since both of the contributor viruses in this case are already widely circulating strains, concerns over this particular reassortment becoming a serious public health threat are slim.

 

But it does highlight the fact that reassortments can, and do, occur. And the importance of enhanced surveillance if we hope to detect the next pandemic flu threat early.

 

You can read a few more details on this case in the following Canadian Press article from last Friday.

 

New flu virus emerges after child co-infected with H1N1, H3N2; vaccine protective

By Sheryl Ubelacker, Health Reporter, The Canadian Press

 

 

On Thursday of next week (June 16th) a free webinar and Teleconference is planned as part of the OAHPP (Ontario Agency for Health Protection and Promotion) Grand Rounds that will provide the latest information and perhaps some additional insight on this reassorted virus.

 

Registration is Free and Easy on the Eventbrite website. 

 

The details from the webinar announcement follow:

 

OAHPP Rounds: pH1N1 – H3N2: A Novel Influenza Virus Reassortment

Thursday, June 16, 2011 from 12:00 PM - 1:00 PM (ET)

Toronto Ont.,

 

Presenter:

Dr. Jonathan Gubbay- Medical Microbiologist, OAHPP

Discussant:

Dr. Natasha Crowcroft- Director, Surveillance and Epidemiology, OAHPP

Abstract

Dr. Jonathan Gubbay, medical microbiologist at the Toronto Public Health Laboratory, will present on a new influenza virus that has been discovered by the Ontario Agency for Health Protection and Promotion (OAHPP). It is the first Canadian confirmed finding of a patient with a coinfection of seasonal H3N2 and pH1N1 followed by reassortment. To the best of our knowledge, this is the first case ever reported globally. The sample was submitted to OAHPP laboratories and testing identified co-infection and reassortment of the two viruses. These results were validated by National Microbiology Laboratory in Winnipeg.

 

The new virus is a hybrid of two viruses currently circulating in humans, both of which are covered by the current seasonal influenza vaccine (the H3N2 virus and the H1N1 virus). There have been no reports of additional cases or human-to-human transmission. Dr. Gubbay will be discussing the above case as well as molecular changes within the seasonal H3N2 influenza that have been seen this season.

 

Dr. Natasha Crowcroft will be the discussant, commenting on the public health significance of this finding.

 

I’ve already registered, and will make every attempt to attend via the webinar. 

»» Read More

EID Journal: H1N1 Reassortment Possibilities

 

 

# 5255

 

 

The only constant about flu viruses is that they are always changing. Among the world’s viruses, influenza are some of the most adept at reinventing themselves in order to get around mankind’s acquired immunity.  

 

Since influenza strains spread amazingly well, herd immunity can build rapidly.  Without the ability to evade this immunity, influenza viruses would soon run out of susceptible hosts.

 

The two methods that influenza viruses use to evolve are antigenic drift (small mutations, sometimes single amino acid substitutions) and antigenic shift (large, often dramatic changes due to viral reassortment).

 

Drift happens slowly, and incrementally, and is the reason why the flu vaccine must be updated and changed every year or two.  

 

Shift, or reassortment, happens abruptly when two different influenza viruses co-infect the same host and swap genetic material.

 

 

Influenza A viruses have 8 gene segments (PB2, PB1, PA, HA, NP, NA, M1, M2, NS1, NS2).

 

Which means that any two compatible influenza viruses could conceivably – and under the right conditions – generate more than 250 different combinations by swapping one or more of their 8 (potentially) interchangeable gene segments.

 

The key words being “under the right conditions”.

 

If it were easy, or a common occurrence, we’d be up to our hip boots in new, reassorted viruses all the time.

 

But it happens often enough that we recognize it as a real threat.   Shift is how new pandemic strains are born, and it was precisely the mechanism that created the 2009 `swine’ flu strain.

 

Which brings us to a new study, which appears today in the CDC’s EID Journal, that looks at the potential for the 2009 H1N1 virus to reassort with other currently circulating flu viruses and create a more virulent flu strain.

 

You’ll, no doubt, recognize some of the authors of this paper, notably Ab Osterhaus and Ron Fouchier. I’ve reproduced the link, and the abstract (slightly reformatted for readability) below.

 

Volume 17, Number 2–February 2011

Research

Possible Increased Pathogenicity of Pandemic (H1N1) 2009 Influenza Virus upon Reassortment

 

Eefje J.A. Schrauwen, Sander Herfst, Salin Chutinimitkul, Theo M. Bestebroer, Guus F. Rimmelzwaan, Albert D.M.E. Osterhaus, Thijs Kuiken, and Ron A.M. Fouchier

Abstract

Since emergence of the pandemic (H1N1) 2009 virus in April 2009, three influenza A viruses—seasonal (H3N2), seasonal (H1N1), and pandemic (H1N1) 2009—have circulated in humans. Genetic reassortment between these viruses could result in enhanced pathogenicity.

 

We compared 4 reassortant viruses with favorable in vitro replication properties with the wild-type pandemic (H1N1) 2009 virus with respect to replication kinetics in vitro and pathogenicity and transmission in ferrets.

 

Pandemic (H1N1) 2009 viruses containing basic polymerase 2 alone or in combination with acidic polymerase of seasonal (H1N1) virus were attenuated in ferrets.

 

In contrast, pandemic (H1N1) 2009 with neuraminidase of seasonal (H3N2) virus resulted in increased virus replication and more severe pulmonary lesions.

 

The data show that pandemic (H1N1) 2009 virus has the potential to reassort with seasonal influenza viruses, which may result in increased pathogenicity while it maintains the capacity of transmission through aerosols or respiratory droplets.

 

 

Since you could wait a very long time indeed for reassortments like these to occur naturally - in order to study them – man made flu viruses must be created in the laboratory using reverse genetics.

 

To simplify matters, these researchers only looked at four laboratory generated reassortments out hundreds of possible combinations, selecting those that replicated well in vitro. 

 

While some of these hybrid viruses were weaker that the original 2009 H1N1 virus, reassortants incorporating the NA (neuraminidase) gene from the seasonal H3N2 virus proved more pathogenic (at least in ferrets).

 

All of these tested reassortants retained `biological fitness’ and could be transmitted among ferrets through aerosol or respiratory droplets.

 

The authors state:

 

We conclude that the pandemic (H1N1) 2009 virus has the potential to reassort with seasonal influenza virus A (H1N1) and influenza virus A (H3N2) and that such reassortment events could result in viruses with increased pathogenicity in ferrets.

 

Although increased pathogenicity in ferrets cannot be extrapolated directly to increased pathogenicity in humans, ferrets are susceptible to natural infection and respiratory disease and lung pathology develop in a manner similar to that in humans infected with seasonal, avian, or pandemic influenza viruses.

 

 

Follow the above link to read about how the tests were conducted, some of the limitations on these sorts of experiments, and additional details on the results.

 

If all of this sound vaguely familiar, last November we saw another study (see  mBio: A/H1N1 Potential For Mutation) that looked at the potential for the 2009 H1N1 virus to become more pathogenic through the more common process; antigenic `drift’.

Their conclusion read, in part:

We report that the emergence of an A/H1N1 pandemic strain of higher virulence is possible and that, despite their lack of detection thus far in humans, viable seasonal/pandemic virus reassortants can be generated.

 

 

While both of these studies point to the potential for the 2009 H1N1 virus to either drift or shift to a more virulent strain, when – or even if – that might ever happen is impossible to say.

 

But they do serve as reminders of how quickly flu strains can change, and of the pressing need to increase our global surveillance capabilities so that we can spot these emerging strains as early as possible.

»» Read More

Flu Viruses: Jostling For Position

 

 

 

# 5237

 

 

Like the UK and most of Europe, Hong Kong is reporting a strong return of the 2009 H1N1 `swine’ flu this year, in stark contrast to the H3N2 dominated flu season being experienced here in the US and Canada.

 

In fact, when you look at the latest global flu surveillance figures from the World Health Organization, you’ll find major differences in the predominate viruses currently circulating across Asia, Australia, and Europe.

 

 

• In Russia, it is primarily influenza B.  
• In China, it’s H1N1, followed by H3N2, and then influenza B. 
• In western Europe, mostly H1N1, followed by influenza B, and with very low levels of H3N2

 

Today, Hong Kong’s CHP (Centre for Health Protection) issued a statement on their recent spike in influenza cases, attributing roughly 3/4ths of all influenza cases to the H1N1 virus.

 

 

Hong Kong enters influenza peak season

The Centre for Health Protection (CHP) of the Department of Health today (January 17) called on the public to maintain vigilance against seasonal influenza as latest surveillance data showed that Hong Kong has entered the winter influenza peak season.

The Public Health Laboratory Centre (PHLC) of the CHP has detected increases in the number of influenza isolations recently. A total of 149 influenza detections were recorded last week (ending January 15, 2011) compared with 26, 47 and 77 in the weeks ending December 25, 2010, January 1 and January 8, 2011 respectively. The number of influenza-like illness outbreaks occurring in institutions and schools also increased from three in the week ending January 8 to 17 in the week ending January 15.

 

The majority (76%) of influenza viruses isolated in the recent two weeks were influenza A (H1N1) 2009 (i.e. human swine influenza), followed by influenza A (H3N2) (12%) and influenza B (12%).

 

The number of other respiratory viral infections detected by PHLC, including Respiratory Syncytial Virus (RSV), parainfluenza virus and adenovirus, have also increased.

(Continue . . . )

 

 

For the first three-quarters of the 20th century, the world apparently only had to contend with one influenza A strain at a time.   In fact, that was believed to be the normal scheme of things.

One A strain ruled until a new strain emerged to supplant it.  

 

We assume that’s what happened in 1918 with the H1N1 `Spanish flu’ (`assume’ because we lack the ability to determine what viruses circulated prior to 1918), in 1957 when the H2N2 `Asian’ flu replaced H1N1, and again in 1968 with the H3N2 `Hong Kong’ flu replacing H2N2. 

 

It wasn’t until 1976, when the H1N1 virus suddenly reappeared after an absence of 20 years (sparking an epidemic mostly in children), that we saw two influenza A viruses co-exist each year, bumping shoulders, jostling for position, and playing a viral version of king-of-the-mountain.

 

 

Since then, some years H3N2 dominated, and some years it was the H1N1 virus. We’ve had two B strains (Yamagata & Victoria) co-circulating since the 1980s as well.

 

When the novel H1N1 virus emerged in 2009, it seemed to have the potential to supplant both of these previously circulating influenza A viruses. 

 

And for a time, it appeared that it had. Reports of the old `seasonal H1N1’ and H3N2 viruses had all but vanished a year ago.  

 

Starting last spring, however, we began to see an increase in H3N2 cases globally, and this fall, in the Western Hemisphere, it has been the dominant strain.

 

While exceedingly rare, we occasionally still see an old seasonal H1N1 virus as well, as was recently reported in Canada by GISN. There obviously remains some small reservoir of hosts keeping that strain on life support.

 

Midway through our convoluted flu season here in the Northern Hemisphere, one can’t help but wonder what surprises lay ahead when the flu moves south of the equator in a few more months.

 

Stay tuned.   It’s bound to be interesting.

»» Read More

CDC: Statement On Swine H3N2 Influenza

 

 

# 5051

 

 

Over the past 72 hours there has been quite a bit of speculation on the internet regarding 2 recent cases of H3N2 swine influenza contracted by people in different states.  

 

Long time readers of this blog know that while rare, we occasionally will see a novel swine influenza virus jump to humans.

 

Although the 2009 swine flu pandemic was an exception, most of the time this turns out to be a one-off dead-end transmission, and goes no further. 

 

 

Which is why – while I was aware of these cases two days ago - with scant details available, I opted to wait until we could get something more reliable than simple conjecture before mentioning them in this blog.  

 

One case was reported in a line item in  this week’s MMWR as a novel H3N2 infection in Pennsylvania, although little else was provided.

 

Today, the CDC has released a comprehensive statement which I am reproducing below.

 

Read the whole statement - but for those who prefer the condensed version - I’ve extracted the main points (underscores mine), which are:

 

Dates of illness onset in the two patients are more than six weeks apart and the viruses from the two patients have some genetic differences, confirming that these two cases are not linked.

 

Ongoing investigations in both states have not shown any evidence of community transmission of these viruses. The most likely scenario at this point is that these are two isolated cases of human infection with swine influenza viruses that, while very rare, do occur from time to time

 

 

 

 

November 12, 2010

Reports of Human Infections with Swine Origin Influenza A (H3N2)

The November 12, 2010 FluView reports two human infections with swine origin influenza A (H3N2) viruses in the United States. Test samples from two patients submitted by Wisconsin and Pennsylvania have been confirmed at CDC as positive for swine origin triple-reassortant (tr) H3N2 influenza viruses—viruses that normally infect pigs. While human infection with swine influenza viruses is rare, it can occur. This is most likely to occur when people are in close proximity to infected pigs, such as in pig barns and livestock exhibits housing pigs at fairs. Both of the patients with confirmed trH3N2 infection reported in FluView were in the vicinity of live pigs. Dates of illness onset in the two patients are more than six weeks apart and the viruses from the two patients have some genetic differences, confirming that these two cases are not linked. Ongoing investigations in both states have not shown any evidence of community transmission of these viruses. The most likely scenario at this point is that these are two isolated cases of human infection with swine influenza viruses that, while very rare, do occur from time to time. Both patients have fully recovered from their illnesses; however, these two cases do underscore the importance of human and animal surveillance for influenza.

 

These two cases reported in FluView bring the total number of human infections with swine origin influenza viruses reported to CDC since 2005 to 18. Previously, three of these reports had been swine origin A (H3N2) viruses. The Pennsylvania and Wisconsin cases bring the number of reports swine origin A (H3N2) infections in humans in the United States to five. The viruses identified in Pennsylvania and Wisconsin are similar to viruses that infected a patient in Iowa in September 2009, a patient in Kansas in August 2009 and a patient in Minnesota in May 2010.

 

Swine Influenza (swine flu) is a respiratory disease of pigs caused by type A influenza viruses that regularly causes outbreaks of influenza in pigs. Swine flu viruses cause high levels of illness and low death rates in pigs. Swine influenza viruses may circulate among swine throughout the year, but most outbreaks occur during the late fall and winter months similar to outbreaks in humans. There are four main influenza type A virus subtypes that have been isolated in pigs: H1N1, H1N2, H3N2, and H3N1. Most flu viruses circulating in pigs are referred to as "triple-reassortant" viruses because these flu viruses contain genes from human, swine and avian influenza viruses.

 

Most commonly, cases of human infection with swine-origin influenza viruses occur in people with direct exposure to pigs. The patient in Pennsylvania lives in an area where live pigs are farmed and the patient in Wisconsin became sick two days after attending a state fair where pigs were exhibited. It's important to note that swine influenza viruses are not transmitted to humans by food. You can not get swine influenza from eating pork or pork products. Eating properly handled and cooked pork and pork products is safe.

 

In the past, CDC received reports of approximately one human infection with a swine influenza virus every one to two years, but in the past few years, about three cases have been reported per year. Increased reporting of human infections with swine influenza could be the result of increased influenza testing capacity and capabilities in public health laboratories.

 

These trH3N2 viruses are different from the 2009 H1N1 virus that has been circulating in the United States since late April 2009. They are also different from human seasonal influenza A (H3N2) viruses that typically circulate among people during the flu season. Swine trH3N2 viruses commonly circulate in pigs in North America, but rarely infect humans. These viruses are different from the swine classical H1N1 or swine trH1N1 influenza viruses that also circulate in pigs in North America because they have H3N2 surface antigens. Tr H3N2 viruses first emerged in North American swine herds in the late 1990s. The H3 and N2 genes which first emerged in swine flu viruses originated from human seasonal H3N2 influenza viruses that circulated globally among humans in the late 1990s.

 

Although the vast majority of instances of human infection with animal influenza viruses do not result in human to human transmission, each case should be fully investigated to be sure that such viruses are not spreading among humans and to limit further exposure of humans to infected animals if infected animals are identified. Surveillance for both seasonal and novel influenza viruses is conducted by the CDC and its state and local health partners year round.

 

For more information about swine influenza, visit http://www.cdc.gov/flu/swineflu/

»» Read More

Global Influenza Report: Week 42

 

 

 

# 5042

 

 

With the end of the declared pandemic, the World Health Organization has dropped back to providing a global flu update to once every 2 weeks. 

 

This report – current as of week 42 – was released on Nov 8th.

 

H3N2 continues to be the predominant player around the world, and in most countries, is overshadowing the 2009 H1N1 strain. 

 

Influenza B is circulating as well, and is particularly prevalent in the southern hemisphere as a late-season strain.

 

Some excerpts, but follow the link to read the whole thing.

 

Description: Displayed data reflect the most recent information reported to 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 all influenza subtypes. The pie charts show the distribution of virus subtypes among all specimens that were tested positive for influenza.

 

 

Influenza - Update 120

8 November 2010 - Summary:

Worldwide, overall influenza activity remained low, except in parts of the tropics, most notably in Southeast Asia, and to a lesser extent in the tropical areas of the Americas. After late winter and springtime influenza epidemics in several countries of the temperate southern hemisphere, influenza activity has returned to near or below baseline in most places.

 

Notably, however, a recent post-season rise in cases has been noted across parts of southern Africa associated with localized outbreaks of influenza H1N1 (2009) virus.

Seasonal influenza A(H3N2) viruses continued to be the predominant circulating type or subtype of influenza viruses worldwide, however, in addition, in many countries there has been co-circulation of seasonal influenza B viruses and to a lesser extent, influenza H1N1 (2009) viruses. The latter has been recently predominant in a limited number of countries, including in India.

 

Virological surveillance

The WHO Global Influenza Surveillance Network is constantly monitoring the evolution of influenza viruses. Like other influenza viruses, the influenza H1N1 (2009) viruses have being undergoing genetic evolution. Since their emergence, variants having substitutions at residues 125/142, 222 and/or 374/391 in the haemagglutinin gene have been detected. Recently other genetic mutations have also been reported.

However, antigenic characterization to date has shown that all these viruses are not antigenically distinguishable from the vaccine virus A/California/7/2009.

FluNet reports

During weeks 41 to 42 (10 -23 October, 2010), National Influenza Centres (NICs) from 31 countries reported data to FluNet*. A total of 1,749 specimens were reported as positive for influenza viruses, 1,512 (86.4%) were typed as influenza A and 237 (13.6%) as influenza B. Of the sub-typed influenza A viruses reported, 15.6% were influenza H1N1(2009) and 84.0 % were influenza A(H3N2).

 

 

The number of countries, regions, and territories reporting since the height of the pandemic has dropped by nearly 2/3rds, but the following gives some indication of the relative distribution of virus strains reported in the northern hemisphere since mid-summer.

 

 

As you can see, H3N2 (light blue) has been the predominate strain identified in the northern hemisphere since early August, while the 2009 H1N1 strain (yellow) has declined.

 

Past performance is no guarantee of future results, but the upward trend in the H3N2 virus over the past few months has some observers concerned that we may see a tough flu season ahead. 

 

Years where H3N2 dominates tend to be more severe than years where H1N1 is the major strain in circulation.

 

The good news is, it isn’t too late to get your flu shot.

 

This year’s shot provides coverage for both the 2009 H1N1 and and the Perth H3N2 strains, along with a B strain.

»» Read More

H3N2 Fatalities In Japan

 

 

 

# 5035

 

In 1968 a new influenza strain – H3N2 – was identified in Hong Kong and quickly spread around the world as the third (and mildest) influenza pandemic of the 20th century. 

 

H3N2 supplanted the H2N2 virus that had been around since the previous pandemic in 1957. It was dubbed the Hong Kong Flu, and until 1977, was to be the only influenza A strain in circulation.

 

H1N1 returned in 1977 under mysterious circumstances, as the Russian Flu (many believe it escaped from a Russian lab).

 

From 1977 till 2009 these two viruses co-circulated around the world, each drifting, mutating, and evolving gradually over time.

 

 

Some years H1N1 would be the main strain seen, while other years it would be the descendents of the Hong Kong Flu.  Years where H3N2 made up the bulk of influenza A infections tended to produce worse flu seasons and a greater number of fatalities, especially among the elderly.

 

At roughly the same time that the 2009 H1N1 virus appeared – a new, mutated strain of H3N2 appeared as well.   It was overshadowed, and outpaced by the novel H1N1 virus, and for awhile it looked as if it might not survive alongside swine flu.

 

But H3N2 hung on, and has been showing up in increasing numbers around the world over the past few months. 

 

This mutated `Perth’ strain of the H3n2 virus has changed sufficiently to make older vaccinations, and previous exposures, less likely to provide immunity.

 

The good news is that it is covered in this year’s flu vaccine.

 

While flu activity remains low around the world, we are starting to see reports of outbreaks – including this one from Japan - where a half dozen patients died in one hospital from the H3N2 virus in less than a week.

Their ages ranged from 60 to 90, and they are among several dozen who have been sickened.  Hospital staff and patients are both reportedly experiencing flu symptoms.

 

Although the AP and others picked up on this story yesterday, FluTrackers  created a thread with translations of the original Japanese press reports early Saturday morning (Hat Tip Makoto), and has updated the story since then. 

 

You can read them here.  The latest update gives this timeline.

 

25 patients and 8 staffs are suffering from influenza now

29 Oct., vaccinated against the flu
31 Oct., a man died(eighties)
2 Nov., 2 men died(sixties, nineties) a woman died(seventies)
4 Nov., a woman died(eighties)
5 Nov., a man died(eighties)

asahi.com

 

The short time span between vaccination and outbreak could simply mean that the vaccine did not have time (typically 2-3 wks) to convey any protective antibodies to the recipients (many of whom were elderly, and less likely to mount a robust immune response, anyway).

 

An alternative theory is being bandied about the Internet that somehow the vaccine contributed to this outbreak or the fatality rate. 

 

Since correlation doesn’t necessarily imply causation, until we see evidence considerably more substantial than just a short gap between the vaccinations and the outbreak, these sorts of theories while interesting, remain highly speculative.

 

 

On the face of it,  this would seem to be an unusually severe outbreak - suggestive of perhaps a change or drift in the virus. 

 

Again, a possibility.

 

But there is a lot we don’t know about this story yet, including information on any pre-existing conditions these fatal cases may have had. 

 

There may simply be less to this story than it at first appears.  It will likely take a few days to get answers.

 

Obviously we will await any word of sequence analysis of this strain, and an investigation into any potential link to the administration of the flu vaccine, with considerable interest.

 

In the meantime, with flu season on its way and likely to feature this drifted H3N2 virus, getting vaccinated now – while you still have time to build immunity –  still (until proven otherwise) remains your best option to avoid the flu this year.

»» Read More

CDC: FluView & Global Flu Activity

 

 

# 5006

 

 

The 2010-11 influenza season hasn’t ramped up yet in the northern hemisphere, and so there is still time to get a flu shot and start building antibodies before you are apt to be exposed.

 

This year - in addition to the likely return of H1N1 - we’ve a new (Perth) strain of the H3N2 virus against which many are likely to have only limited immunity.

 

When H3 viruses dominate – unlike their H1N1 cousins – they generally produce more severe flu seasons and often impact senior citizens harshly.

 

Internationally, we are seeing a good deal of H3N2 around the world, and in some areas it is the dominant strain.  

 

First a look at the latest International flu report (note: this data is from weeks 38-39), then this week’s FluView report from the CDC.

 

The RED slices of the pie chart indicated H3N2, while ORANGE indicates H1N1.   Yellow is Untyped influenza A.

 

 

Influenza activity in most areas of the southern hemisphere peaked several weeks ago, and is now on the decline.

 

 

Seasonal Flu: International Situation Update

October 20, 2010, 11:00 AM ET

Global Flu Activity Update, October 19, 2010

The following summary of key influenza-related updates was created from regional World Health Organization (WHO) reports, country reports, CDC field staff updates, and other sources. Updates are listed by region and focus on data collected during epidemiologic weeks 37 through 40 (September 12 – October 9, 2010). Northern Temperate

Europe

In week 40, influenza activity intensity was low in all reporting European countries (20 countries), according to the European Centre for Disease Prevention and Control. Nineteen countries collected sentinel respiratory specimens in week 40, and 2 out of 161 specimens (1.2%) were influenza-positive.

Canada

ILI consultation rates in weeks 38 and 40 are at baseline levels and below the level reported in 2009, according to the Public Health Agency of Canada.

 

 

You can access the current, and historical Fluview  influenza activity reports at this link with weekly reports going back more than a decade.

 

 

2010-2011 Influenza Season Week 41 ending October 16, 2010

All data are preliminary and may change as more reports are received.

Synopsis:

During week 41 (October 10-16, 2010), influenza activity remained low in the United States.

• Ninety-two (3.6%) specimens tested by U.S. World Health Organization (WHO) and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories and reported to CDC/Influenza Division were positive for influenza.
• The proportion of deaths attributed to pneumonia and influenza (P&I) was below the epidemic threshold.
• No influenza-associated pediatric deaths were reported.
• The proportion of outpatient visits for influenza-like illness (ILI) was below the national baseline. All 10 regions reported ILI below region-specific baseline levels and all 49 states with sufficient data experienced minimal ILI activity.
• Geographic spread of influenza in the District of Columbia, Puerto Rico, and 24 states was assessed as sporadic, Guam and 26 states reported no influenza activity and the U.S. Virgin Islands did not report.

Pneumonia and Influenza (P&I) Mortality Surveillance

During week 41, 6.5% of all deaths reported through the 122-Cities Mortality Reporting System were due to P&I. This percentage was below the epidemic threshold of 6.6% for week 41.

»» Read More