Wednesday, July 18, 2018

Sci Rpts: Genetic Characterization & Pathogenic Potential Of Avian H10 Viruses


Among avian flu viruses, subtypes H5 and H7 - due to their 20 year history of producing high human mortality -  tend to garner the bulk of our attention. That said, there are a number of other `second tier' avian viruses that pose a zoonotic threat.
Best known, and discussed often in this blog due to its ability to easily reassort with other viruses, is LPAI H9N2 (see recent overview).
Although the true number of human infections is unknown, at least 3 dozen have been identified over the past 20 years (see FluTrackers Global Cumulative H9N2 Partial Case List 1998-2017).
H9N2 is regarded as having at least some pandemic potential (see CDC IRAT SCORE), and several candidate vaccines have been developed over the years.
But also, in 2013 we saw a woman was hospitalized with mild pneumonia from H6N1 in Taiwan. The following year, in the EID Journal: Seropositivity For H6 Influenza Viruses In China, researchers reported a low - but significant - level of H6 antibodies,  particularly among live bird handlers.

While in 2004 the first known human H10 infections (see Avian Influenza Virus A (H10N7) Circulating among Humans in Egypt) were reported, followed in 2012 by a limited outbreak among workers at a chicken farm in Australia (see in EID Journal: Human Infection With H10N7 Avian Influenza).
Most of these avian flu infections were mild or asymptomatic, and self limiting. Often only producing conjunctivitis or mild flu-like symptoms.
But in late 2013 a new H10N8 virus emerged in Mainland China (see Lancet: Clinical & Epidemiological Characteristics Of A Fatal H10N8 Case) infecting three people, killing at least two.

With both H10N8 and H10N7 now shown capable of infecting humans - albeit with widely varying degrees of severity - H10 is now viewed as deserving of more research and respect.
Yesterday, Scientific Reports published the following characterization report on a number of H10 reassortants (H10N1, H10N6, H10N7 & H10N9) found to be circulating in live poultry markets in Bangladesh.
It's a long, detailed, report and you'll want to read it in its entirety.  First the abstract, then I'll return with a couple of snippets from the body of the study.

Genetic characterization and pathogenic potential of H10 avian influenza viruses isolated from live poultry markets in Bangladesh
Rabeh El-Shesheny,John Franks, Bindumadhav M. Marathe, M. Kamrul Hasan, Mohammed M. Feeroz, Scott Krauss, Peter Vogel, Pamela McKenzie, Richard J. Webby & Robert G. Webster

Scientific Reportsvolume 8, Article number: 10693 (2018) | Download Citation


Fatal human cases of avian-origin H10N8 influenza virus infections have raised concern about their potential for human-to-human transmission. H10 subtype avian influenza viruses (AIVs) have been isolated from wild and domestic aquatic birds across Eurasia and North America.

We isolated eight H10 AIVs (four H10N7, two H10N9, one H10N1, and one H10N6) from live poultry markets in Bangladesh. Genetic analyses demonstrated that all eight isolates belong to the Eurasian lineage.

HA phylogenetic and antigenic analyses indicated that two antigenically distinct groups of H10 AIVs are circulating in Bangladeshi live poultry markets.
We evaluated the virulence of four representative H10 AIV strains in DBA/2J mice and found that they replicated efficiently in mice without prior adaptation. Moreover, H10N6 and H10N1 AIVs caused high mortality with systemic dissemination.

These results indicate that H10 AIVs pose a potential threat to human health and the mechanisms of their transmissibility should be elucidated.
        (Continue  . . . . )

In the discussion section of the study, the authors (which include both Webby & Webster from St. Jude Children’s Research Hospital) point out the risks of the co-circulation of H9N2 viruses in Bangladesh.

As we've discussed previously (see The Lancet: H9N2’s Role In Evolution Of Novel Avian Influenzas), these ubiquitous (in Asia and increasingly in the Middle East) LPAI viruses have lent their internal genes to some of the most dangerous avian viruses in the wild.
The H9N2 AIV is endemic in Bangladesh21,44,45,46 and has acquired mammalian host–specific mutations in its internal genes, which have been shown to facilitate transmission from avian species to humans44. H9N2 AIVs are significant donors of genetic material to emerging zoonotic viruses such as H5Nx, H7N9, and H10N8 AIVs posing an enormous threat to both human health and poultry industry. The wide circulation of H9N2 AIVs in Bangladeshi LPMs affords H9N2 with more opportunities for reassortment with other AIV subtypes, such as H10 AIVs. 
While the number of reported H10 infected humans has been small, due to a lack of surveillance and testing, it is likely that those numbers under represent reality. 
In 2014's BMC: H10N8 Antibodies In Animal Workers – Guangdong Province, China, we saw evidence suggesting that people may have been infected with the H10N8 virus in China before the first  case was recognized. 
As the following snippet indicates, a similar serological study published in 2010 showed evidence of H10 infection among American turkey farmers.

Transmission of H10 AIVs to humans has resulted in some fatal cases, and serologic evidence indicates that H10 AIVs were previously transmitted among turkey farmers in the United States47.
This should raise concern about the potential for human-to-human transmission of H10 AIVs. Evaluation of the biologic properties of H10 and other subtypes of AIVs circulating in LPMs is essential for understanding the emergence and evolution of these viruses and to reduce their potential pandemic threat to public health.

While we often hear (for good reason) that the H7N9 virus is the top pandemic contender in the wild, the same was being said about H5N1 until an upstart swine-origin H1N1 virus came out of left field and sparked the 2009 pandemic.

Which is why we need to constantly look beyond the obvious pandemic threats, if we hope to have a head's up over what comes down the pike next.

Denmark: HPAI H5N6 Reported In Dead Eider


Although news about HPAI H5N6 in Europe has been pretty much absent for the past couple of months (see latest DEFRA report), and the warmth of summer usually helps to suppress bird flu, we've a new report of the discovery of HPAI H5N6 in a wild bird in Denmark, north of Lolland.
This is the first HPAI detection in Denmark since mid-April - although LPAI H5 was reported in early May - and the 30th positive finding in wild birds of 2018.
This from Denmark's Veterinary and Food Administration, after which, I return with a bit more.

Avian influenza - current situation

There are 16 July detected highly pathogenic bird flu in a dead wild bird found Smålandshavet north of Lolland.

wild birds

Discovery of bird flu in wild birds

National Veterinary Institute have 16 July 2018 identified highly pathogenic avian influenza type H5N6 in a dead eider. Eider was found with several other dead birds Smålandshavet north of Lolland.
It is the first time since mid-April that gathered a dead wild bird in nature, which turns out to be infected with highly pathogenic avian influenza. The total number of cases this year has now reached 30. 
Previously, it has been especially sea eagles and buzzards, which are found to be infected, but the infection is also found in other species of birds such as crows, gulls, swans and one cormorant. The findings are gradually made many places in Denmark, including in North Jutland, Zealand, Lolland, Falster, Funen, Bornholm and Als.

The first findings of highly pathogenic avian influenza H5N6 was done in early March in an eagle found near Slagelse. For details about findings see map of Denmark here .

Sporadic finds of bird flu is not surprising, but usually it is rare to find highly pathogenic bird flu in mid summer. There have been no reports of human infection with the avian influenza virus type.
While H5N6  hasn't sparked the kind of large scale avian epizootic we saw over the winter of 2016-17 with H5N8 - both viruses have shown unusual persistence, and an expanded host range - in wild birds.
And that is a fairly recent change.
A 2015 study (see PNAS: The Enigma Of Disappearing HPAI H5 In North American Migratory Waterfowl) - conducted after the 2014-15 North American HPAI H5 epizootic - concluded that while migratory waterfowl can briefly carry HPAI H5, they were not a good long-term reservoir for highly pathogenic avian flu viruses.
HPAI viruses appeared to burn out fairly quickly in aquatic waterfowl populations - likely due to their long standing immunity to LPAI viruses - and would therefore have to be reintroduced periodically.
That changed in the fall of 2016 when H5N8 returned to Europe and brought with it a number of genetic and behavioral changes attributed to a reassortment event that likely took place sometime in the spring of 2016 (see EID Journal: Reassorted HPAI H5N8 Clade - Germany 2016).
Last summer we saw scattered reports of H5N8 across much of Europe, with the UK's DEFRA Warning Of A `Constant Risk' From Avian Flu in early  September.
While far less pronounced this summer, we've been watching widespread and persistent HPAI H5N8 outbreaks in Russia and Bulgaria the past few months.

Although the finding of HPAI H5N6 in a dead Eider (even in July) is far from earth shattering, it is a reminder that - despite the inhospitable summer season - some remnants of the HPAI H5N6 virus continue to circulate in European wild birds as well.

Tuesday, July 17, 2018

Nipah Transmission In Kerala Outbreak

Credit CDC


The Nipah virus, first identified in 1999 after hundreds of abattoir workers in Malaysia and Singapore were infected by pigs carrying the virus (see MMWR Update: Outbreak of Nipah Virus -- Malaysia and Singapore, 1999), has been on our watch list for nearly two decades.
Carried asymptomatically by fruit bats that range across South East Asia and the Indian Ocean region - Nipah, (and its Australian cousin Hendra) - can occasionally spill over into humans, horses, pigs, and presumably other mammals. 

While outbreaks of Nipah since 1999 have been relatively small, widely scattered, and mostly reported out of Bangladesh - last May the Indian Government announced their third NiV outbreak since 2001, with the last one in 2007.
Human-to-human transmission - primarily in households and in hospital settings - has been frequently reported with the Nipah virus, but is generally described as `limited'.
Last night CIDRAP News carried a brief report (see Nipah outbreak report details hospital transmission patterns) on the apparently robust human-to-human transmission of the virus in this 19-person outbreak. 
News Scan for Jul 16, 2018

Nipah outbreak report details hospital transmission patterns

A report summing up all the investigation findings in India's Nipah virus outbreak says 17 of 19 patients appear to have contracted the virus from the index patient, a 26-year-old man, Press Trust of India (PTI) reported yesterday, citing findings released by health officials from Kerala state.

The people exposed to the first patient included 3 family members, 4 people at the first hospital that treated him, and 10 at a medical college hospital where he was taken for a computed tomography scan. One patient was infected by another patient at the first hospital.

People infected at the first hospital included the man's sister, who helped care for him. Though the man was at the second hospital for only 1 day, he passed the virus to 10 people.
(Continue . . . )

The good news in all of this is that most of the H-2-H transmission appears to be from the index patient to others, while only one secondary transmission (patient to patient) was documented.
As we've discussed previously (see Two MERS-CoV Hospital Super Spreading Studies), some patients shed more virus than others, and are therefore more able to infect others. 
Additionally, the index patient in an outbreak isn't usually identified as being highly infectious right away, so initial infection control procedures may be lax.  Once additional cases show up, they tend to be isolated more quickly, limiting their ability to further spread the virus.

The concern is, that the Nipah virus already has two of the three qualities we look for in an emerging pandemic threat.  It can jump fairly easily to humans, and it has a very high (75%) mortality rate. 
All it lacks is the ability to transmit H-2-H efficiently, and in a sustained manner.  And like MERS-CoV, and Ebola, and (to a lesser extent) Avian flu, it is part way there.
In the 2013 paper The pandemic potential of Nipah virus by Stephen P. Luby, the author writes (bolding mine):
Characteristics of Nipah virus that increase its risk of becoming a global pandemic include: humans are already susceptible; many strains are capable of limited person-to-person transmission; as an RNA virus, it has an exceptionally high rate of mutation: and that if a human-adapted strain were to infect communities in South Asia, high population densities and global interconnectedness would rapidly spread the infection.
Two weeks ago, in IJID: Enhancing Preparation For Large Nipah Outbreaks Beyond Bangladesh, we looked at a new open-access article that appeared in the International Journal of Infectious Diseases, that discussed the potential of the Nipah virus producing a large urban epidemic, similar to what we saw in West Africa with Ebola in 2014.

And the Nipah virus is on the short list of select agents considered to have significant bio-terrorism applications (see National Academy Of Sciences: Biodefense in the Age of Synthetic Biology).

While novel influenza - because of its mutability, transmissibility, and impressive track record  - remains the pandemic threat that keeps most scientists up at night, it is far from the only threat.
The next pandemic could also come from a bat coronavirus, a mutation in the Monkeypox virus, an exotic hemorrhagic fever, or from something completely out of left field. 
All reasons why pandemic preparedness needs to become a year-round national priority, not just something we think about during severe flu seasons or during the centenary of a particularly bad global epidemic.

For more on the challenges posed by the next pandemic, you may wish to revisit:

The Challenge Of Promoting Pandemic Preparedness

Pandemic Unpreparedness Revisited
Smithsonian Livestream: “The Next Pandemic: Are We Prepared?"
World Bank: World Ill-Prepared For A Pandemic

Monday, July 16, 2018

Legionella Cases Rising


Forty-two summers ago the world was anxiously waiting to see whether a recently discovered novel H1N1 flu virus - detected among soldiers the previous winter at Fort Dix, N.J. - would return as a pandemic.  
As a young paramedic, I played a very minor role in our county health department's response, which you can read about in Deja Flu, All Over Again.
Although the dreaded swine flu pandemic never manifested, the summer of 1976 is notable for the outbreak of a - then unidentified illness - among attendees of an American Legion bicentennial celebration held at the Bellevue-Stratford Hotel in Philadelphia.

Within days of returning home from the convention, more than 180 people would fall ill with (often) severe flu-like symptoms, and at least 29 died.  Notified by a doctor who saw multiple patients fall ill after attending the convention, the CDC launched an investigation. 
Pandemic influenza was ruled out fairly quickly, and four months later a CDC lab would identify the culprit as an aquatic gram-negative bacterium - subsequently dubbed Legionella pneumophila - which could cause mild to severe pneumonia.
Legionella wasn't new of course, just finally isolated and identified. Its discovery led to retrospective identification of previous outbreaks, including an earlier outbreak at the same Philadelphia hotel (see The Lancet 1974 outbreak of Legionnaires' Disease diagnosed in 1977).
A milder version of Legionnaires' Disease, known as Pontiac Fever, was also identified following the 1976 Legionnaire's outbreak. 
We now know that the Legionella bacteria grow readily in older, or poorly maintained, (usually warm) fresh water sources and can be aerosolized by air conditioners and cooling systems, hot tubs, fountains, and even shower heads.

 Although many are able to fight off the infection, and remain asymptomatic or only mildly ill, those who are over 50, are former or current smokers, or who have a weakened immune system are the most likely to develop pneumonia. 
And although the cause isn't known, as the chart at the top of this blog indicates, the number of identified cases has quadrupled since the year 2000.  While a lot of this may be due to better testing and surveillance, there may be other factors at work as well. 
You may recall that during the summer and fall of 2015, NYC saw no fewer than 3 outbreaks of this bacterial pneumonia - including one that resulted in 138 cases and 16 deaths - all linked to a single cooling tower in the South Bronx.
The CDC estimates that between 8,000 and 18,000 Americans are hospitalized with Legionnaire's Disease each year.  As many people who contract this type of bacterial infection experience only minor symptoms, this is likely an under count of the total affected.

Last week the State of Michigan published the following press release on a recent spike in local cases.
CONTACT: Lynn Sutfin, 517-241-2112

LANSING, Mich. – The Michigan Department of Health and Human Services (MDHHS) is coordinating with local health departments across the state to investigate cases of legionellosis this summer. To date in 2018, there have been 135 confirmed cases of legionellosis reported in 33 counties compared to 107 confirmed cases during the same timeframe in 2017. 

Confirmed cases include 24 in the City of Detroit, 19 in Macomb County, 16 in Oakland County, 11 in Wayne County and 10 in Genesee County. Twenty-four cases have been confirmed statewide since July 1, and another 13 cases are pending confirmation.

This increase corresponds with national increases in legionellosis. Legionellosis is most common in the summer and early fall when warming, stagnant waters present the best environment for bacterial growth in water systems.

MDHHS and local health departments are working to inform healthcare providers of the increase in cases and share information regarding testing and treatment. Legionellosis is a respiratory infection caused by Legionella bacteria. Legionnaires’ disease is an infection with symptoms that include fever, cough and pneumonia. A milder form of legionellosis, Pontiac fever, is an influenza-like illness without pneumonia that resolves on its own. 

Legionella bacteria are found naturally in fresh water lakes and streams but can also be found in man-made water systems. Potable water systems, cooling towers, whirlpool spas and decorative fountains offer common environments for bacterial growth and transmission if they are not cleaned and maintained properly. Warm water, stagnation and low disinfectant levels are conditions that support growth in these water systems.

Transmission to people occurs when mist or vapor containing the bacteria is inhaled. Legionellosis does not spread person to person. Risk factors for exposure to Legionella bacteria include:
  • Recent travel with an overnight stay.
  • Recent stay in a healthcare facility.
  • Exposure to hot tubs.
  • Exposure to settings where the plumbing has had recent repairs or maintenance work.
Most healthy individuals do not become infected after exposure to Legionella. Individuals at a higher risk of getting sick include the following:
  • People over age 50.
  • Current or former smokers.
  • People with chronic lung disease.
  • People with weakened immune systems from diseases, such as cancer, diabetes or liver or kidney failure.
  • People who take immunosuppressant drugs.
Individuals with any concerns about Legionnaires’ disease or exposure to the Legionella bacteria should talk to their healthcare provider. MDHHS and local health departments will continue to monitor cases and provide updates to the public. More information on Legionella and Legionnaires’ disease can be found on the Centers for Disease Control and Prevention website.

Despite the statement above, saying that `Legionellosis does not spread person to person', in 2016 in NEJM: Probable Person-to-Person Transmission Of Legionnaires’ Disease, we saw an epidemiological investigation following the 2014 outbreak in Portugal that strongly suggests that - while very rare - it is possible.

The CDC's Fast Facts on Legionella now states:
In general, people do not spread Legionnaires’ disease to other people. However, this may be possible under rare circumstances. 
Legionella is just one of many causes of Community Acquired Pneumonia (CAP), which combined cause roughly 1 million hospitalizations, and about 50,000 deaths, each year in the United States. 

Somewhat surprisingly, the causative agent in more than half of all CAP cases is never identified, although viral infections appear to out-number bacterial infections by roughly 2:1.

In 2010, the CDC began their EPIC Study (Etiology Of Pneumonia In the Community) – which they describe as a:
. . .  prospective, multicenter, population-based, active surveillance study; systematic enrollment and comprehensive diagnostic methods were used. The main objective of the EPIC study was to determine the burden of pneumonia hospitalizations in U.S. children and adults as well as to identify viruses and bacteria associated with these hospitalizations.
We looked at the results in 2015's The CDC’s EPIC CA-Pneumonia Study, but briefly they found:
  • one or more viruses in 530 (23%) cases
  • bacteria in 247 (11%) cases
  • bacterial and viral pathogens in 59 (3%) cases
  • and a fungal or mycobacterial pathogen in 17 (1%) of cases
The most commonly detected pathogens were:
  • Human rhinovirus (in 9% of patients)
  • Influenza virus (in 6%)
  • and Streptococcus pneumoniae (in 5%).

Whether the increase in Legionella the past twenty years is a product of better lab testing, an older society more prone to infection, or aging infrastructures which are more likely to grow and aerosolize the bacteria, is up for for debate.
In all likelihood, all play some part.
There are things you can do to help protect yourself, however.  You should talk to your doctor about pneumococcal vaccines, as they can significantly reduce your risk of developing pneumonia from the covered strains. (note: Legionella isn't among those strains covered by the vaccine).

Beyond vaccines, the CDC recommends:

Protect Your Health with These Healthy Living Practices

Try to stay away from sick people. If you are sick, stay away from others as much as possible to keep from getting them sick. You can also help prevent respiratory infections by:
  • Washing your hands regularly
  • Cleaning surfaces that are touched a lot
  • Coughing or sneezing into a tissue or into your elbow or sleeve
  • Limiting contact with cigarette smoke
  • Managing and preventing conditions like diabetes

Sunday, July 15, 2018

Post-Disaster Sequelae

Three Major Disasters In Just Over 30 Days


The NEJM has published a special report (see below) that attempts to calculate  the death toll in the wake of Hurricane Maria last September. As everyone knows by now, most of the inhabitants were without electricity, potable water, and cellular service for months.

Other long duration post-storm challenges included a badly damaged infrastructure and severely compromised supply chain, making it difficult to obtain food, prescription medicines, medical care, and police or rescue services. 
Extrapolating the results of a survey of 3299 randomly selected households, they estimated 4645 excess deaths occurred in first 100 days following the storm. 
I've excerpted the abstract, but you'll want to follow the link to read the report in its entirety.   After which, I'll have more.

Mortality in Puerto Rico after Hurricane Maria
Nishant Kishore, M.P.H., Domingo Marqués, Ph.D., Ayesha Mahmud, Ph.D., Mathew V. Kiang, M.P.H., Irmary Rodriguez, B.A., Arlan Fuller, J.D., M.A., Peggy Ebner, B.A., Cecilia Sorensen, M.D., Fabio Racy, M.D., Jay Lemery, M.D., Leslie Maas, M.H.S., Jennifer Leaning, M.D., S.M.H., Rafael A. Irizarry, Ph.D., Satchit Balsari, M.D., M.P.H., and Caroline O. Buckee, D.Phil.



Quantifying the effect of natural disasters on society is critical for recovery of public health services and infrastructure. The death toll can be difficult to assess in the aftermath of a major disaster. In September 2017, Hurricane Maria caused massive infrastructural damage to Puerto Rico, but its effect on mortality remains contentious. The official death count is 64.

Using a representative, stratified sample, we surveyed 3299 randomly chosen households across Puerto Rico to produce an independent estimate of all-cause mortality after the hurricane. Respondents were asked about displacement, infrastructure loss, and causes of death. We calculated excess deaths by comparing our estimated post-hurricane mortality rate with official rates for the same period in 2016. 


From the survey data, we estimated a mortality rate of 14.3 deaths (95% confidence interval [CI], 9.8 to 18.9) per 1000 persons from September 20 through December 31, 2017. This rate yielded a total of 4645 excess deaths during this period (95% CI, 793 to 8498), equivalent to a 62% increase in the mortality rate as compared with the same period in 2016. However, this number is likely to be an underestimate because of survivor bias. The mortality rate remained high through the end of December 2017, and one third of the deaths were attributed to delayed or interrupted health care. Hurricane-related migration was substantial.


This household-based survey suggests that the number of excess deaths related to Hurricane Maria in Puerto Rico is more than 70 times the official estimate. (Funded by the Harvard T.H. Chan School of Public Health and others.)
Not being a statistician, I'm not going to try to analyze their methods or results, I'll only toss in my 2 cents that this estimate is likely still an undercount.  And these numbers are only calculated through December 31st, 2017.
The challenges of responding to any major disaster are enormous, and coming - as this one did - as the third major U.S. disaster in just over a month (preceded by Hurricanes Harvey in Texas & Irma in Florida), resources were already badly strained.
Add in that the hurricane struck an island nearly 1000 miles from the mainland,  whose long neglected infrastructure was already in bad shape - and you have all the necessary plot points for a bad disaster movie.  Except this was no movie.

As a first responder in the 1970s, we had a radio code that - quite frankly - we heard far too often.  It varies by municipality, but where I worked it was 10-89; No Units Available. 
It meant that every ambulance, and every rescue unit, was tied up. No units were available to respond. And the next emergency call might go unanswered for 10, 20, maybe 30 minutes or longer. 
For months after the storm - whether it be restoration of utilities, delivery of food and medicine, or availability of medical care -  much of Puerto Rico was in 10-89 status. And as a result, a lot of people died.
The debate over what could have been done differently will continue, but I can tell you, for a first responder there is no hell quite like not being able to respond when you know you are desperately needed and lives are at stake. 
The question is, was this a fluke? A once-in-a-lifetime disaster that no one could have anticipated, or reasonably prepared for?   Or are we deluding ourselves by believing `it can't happen here (again)'.

Since - until last year - the United States had been in a 10+ year major hurricane drought, the idea of 3 major storms hitting the U.S. in quick succession seemed unlikely.  
But in 2005, we saw a modern record of 28 Atlantic named storms, 7 of which were of major (Cat 3+) intensity.  Nine storms had impact on the United States, although three - Katrina, Rita, and Wilma - were particularly destructive. 
The previous year (2004) also saw 9 U.S. land falling storms, and while not as destructive, no fewer than 5 named storms crossed over Florida, four of which were major hurricanes.


So the potential for seeing multiple major hurricanes strike in short order - even in the same state - is certainly there.
As bad as these disaster were, they pale in comparison to the 2010 earthquake in Haiti, which probably killed more than 200,000 people.  Or the estimated quarter of a million people who died from the 2004 Indian ocean tsunami, or the tens of thousands who perished from the 2011 Tōhoku earthquake and tsunami in Japan.
But all of these disaster areas have something in common.

It may take weeks, months, or even years before life returns to normal, and the actual loss in terms of mortality, morbidity and permanent disability, PTSD, homes and belongings, businesses, jobs and life savings, and continuity of a community are never fully tallied or appreciated.
We've looked at some of these after effects in the past.
There are always the usual post-disaster accidents; drownings, carbon monoxide poisoning from using charcoal or generators indoors. Falls from roofs or ladders from clearing debris, or chain saw accidents. And even skin infections and food poisoning from contaminated waters (see After The Storm Passes).

Heat (or cold) related deaths may occur when the power is out for extended periods (see MMWR: Heat-Related Deaths During an Extreme Heat Event), and people who rely on oxygen concentrators at home could find themselves in a life threatening situation.
But some after effects may be harder to link to a disaster.
In March of 2009, in a study led by Dr. Anand Irimpen (Associate Professor of clinical medicine at Tulane), it was disclosed that residents of New Orleans saw a 300% increase in heart attacks in the first 2 years after hurricane Katrina.
A follow up, published in 2014 (see Tulane University: Post-Katrina Heart Attack Rates - Revisited), once again found the impact of Katrina on cardiac health remained pronounced.
Also in 2014, in Post-Disaster Stress Cardiomyopathy: A Broken-Hearted Malady, we looked at a rare condition known as Takotsubo cardiomyopathy – or stress induced cardiomyopathy which is often linked to extreme grief or stress, as might be experienced following a disaster.
Also known as broken heart syndrome, this acute ballooning of the heart ventricles is a well-recognized cause of acute heart failure and dangerous cardiac arrhythmias. 
While often hidden from view, the psychological impact of a disaster can be enormous and ongoing. In 2011, in Post Disaster Stress & Suicide Rates, we looked at the impact of disaster-related PTSD (Post Traumatic Stress Disorder). 

This has been recognized as such a pressing problem that the  World Health Organization released a comprehensive Guidelines For Post-Trauma Mental Health Care book on the treatment of PTSD, acute stress, and bereavement in 2013.

Our list of post-disaster sequelae is long, and far from complete.  But it does provide us with an idea of just how much is at risk when a major disaster strikes.

Another CAT 5 storm will strike a populated area of the United States, a major earthquake (M7.0+) will hit a major metropolitan area, and the world will see another severe pandemic.  
It's just a matter of time.  
And when that happens - no matter how well prepared we think we are - we'll wish we had done more.  As a nation, as a community, and as individuals.
The lesson of hurricane Maria is that back-to-back disasters can quickly overwhelm local, state, and federal relief efforts and that failed or damaged infrastructure can prevent needed help or supplies from reaching the victims for days, weeks, or even months. 
While I can't control what FEMA or my state is able to do in response to the next disaster, I do have a say in what I can do.

Living in hurricane country, I've made it a point to have a disaster plan, a disaster buddy, a bug-out destination, and the things I would need to survive without electricity, running water, open grocery stores or pharmacies for a week or longer. 
As long-time readers of this blog already know, I was forced to put all of that into action last year with Hurricane Irma (see A Post Irma Update).
While none of this guarantees me a good outcome when the next disaster strikes, it does better my odds.  And it also allows me to be in a position to help others, either directly, or by not taking immediate assistance from local relief efforts so that it can go to someone else.

For more on the long-term impacts of disasters, and how to prepare for them, you may wish to revisit:
All Disaster Responses Are Local
Supply Chain Of Fools (Revisited)
Little Preps Mean A Lot
In An Emergency, Who Has Your Back?
When 72 Hours Isn’t Enough

Friday, July 13, 2018

From H5N1 to HxNy: Overview Of Human Infection with AI in The Western Pacific Region - WHO


Until the mid-1990s, avian influenza viruses were thought to pose only a very limited threat to human health, and the few novel human infections that had been detected, had generally been mild. 
That notion abruptly changed in 1997 when 18 people contracted H5N1 in Hong Kong, and six of them died. 
A massive campaign of poultry eradication bought a 5 year respite, but in 2003 two members of a family turned up in Hong Kong with the virus after visiting Fujian Province, China (see WHO H5N1 timeline). A third family member had died on the Mainland, but no tests were taken.

From this sputtering and uncertain beginning (see chart above), H5N1 began to spread - at first across Southeast Asia (Vietnam, Laos, Cambodia, Thailand) - and within a couple of years, into Europe, Africa, and the Middle East. 
For several years Indonesia and Vietnam were the world's hot spots for human infection, but eventually that focus would shift to Egypt. 
Along the way, the virus was also changing, diversifying into new clades and subclades. The H5N1 virus circulating in Indonesia was genetically distinct from the H5N1 found in China, or that spreading in Egypt. 

For the first decade, H5N1 stood pretty much alone at the top of our avian flu worry list, albeit with some second tier viruses (H7N7, H5N2, H9N2, etc.) in the wings. In 2013, H7N9 - a worthy contender to H5N1 - emerged in China, and has (at least for now) replaced H5N1 as our biggest concern.
But it wasn't alone.
Several other HPAI viruses, able to infect humans - all originating from China - would emerge in 2013 and 2014; H10N8 and H5N6. Earlier this year, we saw the first known human infection with H7N4 (see UK PHE Guidance & Risk Assessment On Human H7N4 In China).

While novel flu viruses can emerge from anywhere on the globe, Eastern China has an impressive record of spawning new subtypes (see Viral Reassortants: Rocking The Cradle Of Influenza). 
This week the World Health Organization has published a review of human infections with avian flu viruses in the Western Pacific over the past 15 years.
It's a long and informative read, and discusses in frank terms some of the challenges in getting accurate data, and the likelihood of seeing additional novel viruses emerge from this region in the future.

I've only excerpted the abstract and some comments from the Conclusions. Follow the link to read it in its entirety. 

From H5N1 to HxNy: An epidemiologic overview of human infections with avian influenza in the Western Pacific Region, 2003–2017

Sarah Hamid,a Yuzo Arima,b Erica Dueger,a,f Frank Konings,a Leila Bell,a Chin-Kei Lee,c Dapeng Luo,d Satoko Otsu,e Babatunde Olowokure,a Ailan Lia and WPRO Health Emergencies Programme Teama

a WHO Regional Office for the Western Pacific.
b National Institute of Infectious Diseases, Japan.
c WHO Country Office China.
d WHO Country Office Lao People's Democratic Republic.
e WHO Country Office Viet Nam.
f Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA, USA.


Since the first confirmed human infection with avian influenza A(H5N1) virus was reported in Hong Kong SAR (China) in 1997, sporadic zoonotic avian influenza viruses causing human illness have been identified globally with the World Health Organization (WHO) Western Pacific Region as a hotspot. A resurgence of A(H5N1) occurred in humans and animals in November 2003.

Between November 2003 and September 2017, WHO received reports of 1838 human infections with avian influenza viruses A(H5N1), A(H5N6), A(H6N1), A(H7N9), A(H9N2) and A(H10N8) in the Western Pacific Region. Most of the infections were with A(H7N9) (n = 1562, 85%) and A(H5N1) (n = 238, 13%) viruses, and most (n = 1583, 86%) were reported from December through April. In poultry and wild birds, A(H5N1) and A(H5N6) subtypes were the most widely distributed, with outbreaks reported from 10 and eight countries and areas, respectively.

Regional analyses of human infections with avian influenza subtypes revealed distinct epidemiologic patterns that varied across countries, age and time. Such epidemiologic patterns may not be apparent from aggregated global summaries or country reports; regional assessment can offer additional insight that can inform risk assessment and response efforts. As infected animals and contaminated environments are the primary source of human infections, regional analyses that bring together human and animal surveillance data are an important basis for exposure and transmission risk assessment and public health action. Combining sustained event-based surveillance with enhanced collaboration between public health, veterinary (domestic and wildlife) and environmental sectors will provide a basis to inform joint risk assessment and coordinated response activities.



Despite these limitations, disseminating regional analyses can improve Member States' situational awareness, knowledge of the epidemiology in neighbouring countries as well as of the broader regional perspective, and risk assessment and response efforts.
This analysis specifically demonstrates the usefulness of combining multiple sources of surveillance data for better informed risk assessments, including those based on the WHO Tool for Influenza Pandemic Risk Assessment.57 Moreover, using multiple sources of information helps to assess potential surveillance biases, thereby improving decision-making.

Further sporadic human infections with avian influenza viruses are likely to occur. Although A(H5N1) incidence may have declined, A(H7N9) virus has emerged, and other avian influenza viruses have been detected in recent years.

In China, country of the origin of recently identified avian influenza virus strains, the poultry industry has expanded greatly in the past two decades.58 In many areas, the close proximity of humans and animals increases the risk of human exposure to zoonotic influenza viruses.3 As infected animals or contaminated environments are the primary sources for human infection, risk assessments should incorporate a One Health approach and gather information from all relevant sectors. Continued surveillance at the human–animal interface is imperative for all avian influenza viruses.

Every sporadic human infection provides a virus with an opportunity to change its genetic makeup, increasing the possibility of an influenza virus with pandemic potential to arise.

Strengthened communication and collaboration between animal and human health sectors at subnational, national, regional and global levels are necessary to monitor the dynamics of influenza virus activity. An APSED approach that aligns with One Health initiatives combining sustained event-based surveillance with enhanced collaboration between the human, animal (domestic and wildlife) and environmental sectors will provide a basis to inform joint risk assessment and coordinate response capacities.
       (Continue . . . )

Hamid S, Arima Y, Dueger E, Konings F, Bell L, Lee CK, et al. From H5N1 to HxNy: An epidemiologic overview of human infections with avian influenza in the Western Pacific Region, 2003–2017. Western Pac Surveill Response J. 2018 Jul;9(2). doi:10.5365/wpsar.2018.9.2.001