Vietnam Reports A Possible Change In The H5N1 Virus

Photo Credit – FAO

 

# 6536

 

Overnight, the Vietnamese media has been carrying reports of a supposed recent change in the H5N1 virus, but before we get to that, a little background.

 

Just over a year ago (see FAO Warns On Bird Flu) concerns were raised in southeast Asia over the spread of a new clade of the H5N1 virus  (2.3.2.1) that effectively evaded the poultry vaccine currently in use. 

 

This 2.3.2.1 clade wasn’t really new, having been detected in China for several years.  But in 2010-2011 it had begun to spread widely.

 

It was characterized last September (see WHO Report : Antigenic & Genetic Characteristics of H5N1 & H9N2 Viruses) as having appeared in wild birds and poultry in Bangladesh, China, Hong Kong SAR, India, Japan, the Republic of Korea, Myanmar, and Vietnam.

 

While the press briefly had a field day over this new strain the CDC , the OIE, and the World Health Organization  quickly reminded us that while the bird flu threat remains, there was no evidence at the time to suggest that this new strain is any more transmissible to – and among – humans than the earlier strains.

 

The World Health Organization’s report from October of 2011, Updated unified nomenclature system for the highly pathogenic H5N1 avian influenza viruses, identifies and updates the known clades of the H5N1 virus that have emerged since the detection of the A/goose/Guangdong/1996 H5N1 virus strain back in the mid 1990s.

 

As you can see, the virus has evolved from one strain into a complex family of similar, but genetically distinct clades of H5N1.  Some less successful clades have died out along the way, but many co-circulate around the globe.

 

(click to load larger image)

 

All of which means we are not watching just one H5N1 virus strain, we are watching at least 20 genetically separate clades of the virus, with many minor variants of each clade thrown in the mix.

 

Or to put it another way, H5N1 – like all flu strains – is a constantly moving target, continually evolving, looking for an evolutionary advantage. 

 

All of which serves as prelude to this morning’s report:

 

Overnight the Vietnamese media has carried numerous stories indicating some sort of change has been detected clade 2.3.2.1 of the H5N1 virus. My thanks go to Treyfish and Shiloh of FluTrackers for finding, and posting a number of these (English language & translated) reports in this thread.

 

Rather than deal with a kludgy machine translation, we’ll go with the Voice of Vietnam’s (VOV) English Language story.

 

Updated : 5:25 PM, 05/09/2012

New highly toxic avian flu virus spreads to Vietnam

 

A new strain of avian flu virus that was found in China two months ago has appeared in Vietnam, health experts have confirmed.

 

The new strain, 2.3.2.1 C, which has been detected through epidemic investigations, is highly toxic and therefore extremely deadly, Diep Kinh Tan, Deputy Minister of Agriculture and Rural Development, said at a meeting on September 4 to review the epidemic situation.

 

The 2.3.2.1 C strain has recently spread to Vietnam and is now present in affected areas in seven provinces and cities, namely Haiphong, Ha Tinh, Ninh Binh, Nam Dinh, Bac Kan, Thanh Hoa and Quang Ngai, said Hoang Van Nam, head of the Department of Animal Health (DoAH).

 

As the new strain is different from the A/H5N1 virus, the ministry is to conduct experiments and tests to confirm if the vaccines that are being used to combat A/H5N1 are also effective against the new strain.

 

If the existing medication is ineffective, studies on new vaccines against the new strain should be conducted soon, Tan said, adding that he has asked the DoAH to isolate the virus for this purpose.

 

(Continue . . . )

 

 

Media reports such as this one are always a little dicey, since they contain very little in the way of hard scientific evidence. Hopefully we’ll get a clarification from the FAO, or an official statement from the Vietnamese government at some point.

 

What is apparent from this, and other reporting out of Vietnam, is that the H5N1 situation there continues to be fluid, and that concerns over the continual evolution and spread of the virus run high.

 

Although we continue to see isolated human infections around the world, and the virus continues to evolve (see H5N1: An Increasingly Complex Family Tree), for now H5N1 is primarily a threat to poultry.

 

The concern, of course, is that over time that could change.

 

And so the world remains at Pre-pandemic Phase III on the H5N1 virus, and we continue to watch for signs that the virus is adapting better to humans.

Toxoplasmosis: Some Intriguing Para-Cites

Credit CDC

 

# 6535

 

 

If you gauge a pathogen’s success by how many people it infects, then Toxoplasmosis gondii must surely rank as a superstar among parasites. Somewhere between 1/3rd and 1/2 of all humans on the planet are incidental hosts to this remarkable parasite – most without apparent signs of illness.

 

While Toxoplasmosis, the disease caused by T. gondii , is usually comprised of minor and short-lived flu-like symptoms, that is not to say that infection is always trivial.

 

There are serious health risks with T. gondii, particularly to fetuses exposed from freshly infected mothers during the first trimester, and to those with compromised immune systems (including organ transplant recipients and persons with HIV).

 

The CDC lists Toxoplasmosis as one of five  Neglected Parasitic Infections (others include Chagas Disease, Cysticercosis, Toxocariasis, & Trichomoniasis) needing more more attention by public health officials.

 

And there’s even a fascinating, albeit controversial, debate over whether T. gondii infection can subtly influence an individual’s (or an entire society’s) psychological leanings.  

 

But more on that later.

 

First, the Advisory Committee on the Microbiological Safety of Food (ACMSF) has provided the UK’s Food Standards Agency with a 70-page report on T. gondii in the food supply, and states that too little is known about the risks and recommends further study of the issue.

 

While hard numbers are difficult to derive, they estimate roughly 350,000 people become infected with T. gondii each year in the UK, of which 80%-90% will be asymptomatic. 

 

The FSA says they will review this report, and issue a response in the near future.  First a link to the report, followed by the FSA press release, after which I’ll return with more.

 

Further studies on toxoplasma needed

A risk profile on toxoplasma in the food chain by the Advisory Committee on the Microbiological Safety of Food (ACMSF) has recommended that further studies are needed to establish the importance of foodborne routes of infection and identify the highest risks. The suggested studies include work to assess the prevalence of toxoplasma in UK livestock and in food.

(Continue . . . )

 

 

While still considered, for the most part, a relatively benign infection in humans, there is a growing body evidence that suggests T. gondii may exert a greater influence on our lives and health than previously thought.

 

So today, a bit of a review of this ever-so-clever pathogen.

 

While many mammals (including man) can harbor T. gondii – the definitive host is the feline  – which is only animal that can promote the sexual reproductive part of the parasite’s life cycle.

 

The resultant oocyst is shed in cat feces and can infect the soil -from where it can go on to infect a wide variety of animals – but outside of feline hosts is unable to complete its life cycle.

 

T. gondii, however, has developed unique methods of getting itself back into cats, where it can reproduce.  

 

Mice, traditionally a mainstay of feline cuisine, lose their fear of the scent of cats after the parasite invades their brains. Absent their normal survival instincts, they are more likely to become dinner, and thereby return the parasite to its primary host.

 

 

While cats, mice, and birds make up the primary circle of infection for T. gondii, humans and other mammals are often infected as well.  The CDC lists four main methods of transmission.

 

• Foodborne
• Animal-to-human (zoonotic)
• Mother-to-child (congenital)
• Rare instances (transplants, blood transfusions)

 

As far as its prevalence is concerned, the CDC states:

 

In the United States it is estimated that 22.5% of the population 12 years and older have been infected with Toxoplasma. In various places throughout the world, it has been shown that up to 95% of some populations have been infected with Toxoplasma. Infection is often highest in areas of the world that have hot, humid climates and lower altitudes.

 

Before you make plans to exile your cat to a new home, Cornell University’s College of Veterinary Medicine advises:

 

Can I "catch" toxoplasmosis from my cat?

Because cats only shed the organism for a few days in their entire life, the chance of human exposure is small. Owning a cat does not mean you will be infected with the disease. It is unlikely that you would be exposed to the parasite by touching an infected cat, because cats usually do not carry the parasite on their fur. It is also unlikely that you can become infected through cat bites or scratches. In addition, cats kept indoors that do not hunt prey or are not fed raw meat are not likely to be infected with T. gondii.

In the United States, people are much more likely to become infected through eating raw meat and unwashed fruits and vegetables than from handling cat feces.

 

The aberrant psychological behavior in infected mice is pretty well documented, and that has led some researchers to wonder whether toxoplasmosis infections can affect human personality traits as well.

In recent years toxoplasmosis has been tenuously linked to increased rates of suicide, some cases of schizophrenia, and even the rate of traffic accidents.

 

The caveat being, that (repeat after me): correlation does not automatically imply causation.

 

A few cites:

 

Toxoplasma gondii seropositivity and suicide rates in women.

Ling VJ, Lester D, Mortensen PB, Langenberg PW, Postolache TT.

Toxoplasma Infection Increases Risk of Schizophrenia, Study Suggests

Release Date: 01/16/2008

Findings from what is believed to be the largest comparison of blood samples collected from healthy individuals and people with schizophrenia suggest that infection with the common Toxoplasma gondii parasite, carried by cats and farm animals, may increase the risk of schizophrenia.

Increased risk of traffic accidents in subjects with latent toxoplasmosis: a retrospective case-control study

Jaroslav Flegr, Jan Havlícek, Petr Kodym, Marek Malý, and Zbyněk Smahel

Conclusion

The subjects with latent toxoplasmosis have significantly increased risk of traffic accidents than the noninfected subjects. Relative risk of traffic accidents decreases with the duration of infection. These results suggest that 'asymptomatic' acquired toxoplasmosis might in fact represent a serious and highly underestimated public health problem, as well as an economic problem.

 

An Internet search on Toxoplasmosis will return a great many research articles linking T. gondii to a variety of psychological issues, although causality is tough to prove.

 

We don’t know, for instance, whether T. gondii causes schizophrenia or whether schizophrenics are just more susceptible to T. gondii parasite.

 

On a more `macro scale’ the cultural personality of entire nations, it has been hypothesized, may hinge on the prevalence of  T. gondii infection among their population.

In 2006, USGS ecologist Kevin D. Lafferty published an article in the Proceedings of the Royal Society: Biological Sciences that looked at that very possibility.

 

Can the common brain parasite, Toxoplasma gondii, influence human culture?

1. Kevin D Lafferty 

 

It’s a complex question, and his article raises some intriguing possibilities. First, Lafferty noted a couple of things:

1. The rate of T. gondii infection varies widely around the world, from a low of just over 4% in South Korea, to over 45% in France.
2. Subtle psychological changes have been observed in people with T. gandii infection, including guilt-proneness in both men and women.
• Infected women tend to be more dutiful, rule conscious, and conforming. 
• Infected men were more rigid, frugal, reactive emotionally and easily upset.

If one assumes a nation’s culture is, at least to some degree, dependent upon the sum of the individual personality traits of its citizens, then toxoplasmosis might be a cultural driving force.

 

Lafferty looked for a correlation between reported levels of neuroticism – the tendency to experience negative emotional states (anxiety, anger, guilt & depression) – in various countries and the seroprevalence of T. gondii in its people.

And in many instances, he believes found that correlation.  He wrote:

 

The associations between prevalence and cultural dimensions are consistent with the prediction that T. gondii can influence human culture. Just as individuals infected with T. gondii score themselves higher in the neurotic factor guilt-proneness, nations with high T. gondii prevalence had a higher aggregate neuroticism score.

 

It is, admittedly, a bit disconcerting to think that our individual cultures, and perhaps – even the course of human history - may have been subtly influenced by this common parasite over the years.

 

On the other hand, as a long-time cat owner, if I’m ever involved in car accident I fully intend to cite these research articles as part of my defense.

 

For the 77% of Americans who are not infected – and would like try to stay that way – the CDC has a webpage on Toxoplasmosis Prevention & Control. As you might expect, the primary focus is on safe food handling and preparation.

 

And finally, for a truly fascinating (albeit sometimes technical) discussion of Toxoplasmosis, I can heartily recommend the 80 minute podcast:

 

This Week in Parasitism - TWiP #13 - Toxoplasmosis

Hosts: Vincent Racaniello and Dickson Despommier

An Increasingly Complex Flu Field

 

(Click to enlarge)

 

# 6534

 

 

Up until 1977  it was considered normal that only one strain of influenza A circulated at a time.

 

When a new pandemic strain appeared (as it did in 1918, 1957, and 1968), the existing seasonal strain – for reasons that weren’t well understood – would vanish, and in time the new pandemic virus would settle in as the seasonal flu.

 

But in 1977 something unprecedented happened.

 

The H1N1 flu virus – which had been replaced by the pandemic H2N2 virus in 1957 (only to be replaced by the H3N2 strain 11 years later) - suddenly reappeared after 20 years absence.

 

The theory is that it escaped from a Russian or Chinese lab’s freezer, as it was almost unchanged from a strain not seen since the early 1950s. 

 

It was dubbed the `Russian flu’, and for a while, slammed Emergency rooms and Flu wards in a big way.

 

Most adults had some immunity left over from their exposures before 1957, and so kids under 20 were the hardest hit.  But unlike in 1918, 1957, and 1968 – this new flu didn’t depose the old flu.

 

Instead we ended up with two major Influenza A strains bumping shoulders and jockeying for position.  Some years H3N2 would dominate, and other years it would be H1N1.

 

Further complicating matters we also have Influenza B viruses, which while generally regarded as less serious than influenza A, have divided into two distinct lineages (Yamagata & Victoria.

 

And they too compete each year for dominance.

 

Which leaves us with (currently) four major flu strains to contend with; 

• A/H1N109
• A/H3N2
• B/Victoria
• B/Yamagata

 

These viruses constantly change and evolve over time, and we often have several clades of each strain at any given time. The most recent ECDC: Influenza Virus Characterization found 5 genetically distinct H3N2 strains in circulation across Europe.

 

The recent emergence of a new – antigenically different – H3N2 strain, along with the recent dominance of the Yamagata influenza B virus, has prompted a major change in this year’s flu vaccine.

 

• The H1N1 component remains essentially unchanged, with the A/California/7/2009 (H1N1)pdm09-like  still recommended.
• But the old A/Perth/16/2009 (H3N2)-like virus now gives way to the A/Victoria/361/2011 (H3N2)-like virus.
• And the Victoria lineage B/Brisbane/60/2008-like virus will be replaced by a Yamagata strain; the B/Wisconsin/1/2010-like virus. 

 

Which makes getting the flu vaccine this fall doubly important, as it is likely that community immunity to both of these strains is low.

 

Beyond these four, keeping researchers up late at night is the fact that there are no fewer than six influenza viruses that – while not well adapted to humans  – keep trying to nudge their way into the human host pool.

 

Most people by now are aware of the concerns over the H5N1 `bird flu’, but less well known are the H7 avian strains, which have managed to jump to humans several times over the past decade.

 

• In 2003 an outbreak of H7N7 at a poultry farm in the Netherlands went on to infect at least 89 people. Most of the victims were only mildly affected, but one person died.
• In 2004 two people in British Columbia tested positive for H7N3 (see Health Canada Report) during an outbreak that resulted in the culling of 19 million birds.
• In 2006 and 2007 there were a small number of human infections in Great Britain caused by H7N3 (n=1)  and H7N2 (n=4), again producing mild symptoms.

 

H9N2 is another avian strain that has, on rare occasions, infected humans and is believed to have some pandemic potential. Over the past dozen years a small handful of cases have been identified – mostly in Hong Kong (see CIDRAP Avian Influenza (Bird Flu): Implications for Human Disease).

 

• In January of 2010, in H9N2: The Other Bird Flu Threat, I wrote about the World Health Organization  recommending the creation of a candidate vaccine virus for H9N2.

• And in November 2010, in Study: The Continuing Evolution Of Avian H9N2, we looked at computer modeling that suggested that the H9N2 virus moving towards becoming more `human-adapted’.

 

And since 2005 the CDC has been reporting a growing number of swine flu variants that have managed – on rare occasions – to jump to humans.

 

The three main flu strains circulating in pigs are:

• H1N1
• H1N2
• H3N2

When one of these swine viruses jumps to a human host, it is then called a `variant’ virus. 

 

Up until last year, it was the trH1N1 swine virus (now called H1N1v) that had been most commonly reported. The numbers were very low – rarely more than 2 or 3 infections each year.

 

Over the past year, the focus has shifted to the H3N2v virus, which emerged in the summer of 2011. After a quiet winter and spring, this summer it has infected several hundred people in the Midwest – most (but not all) appear to have contracted it directly from exposure to pigs.

 

And as an added surprise, on Friday of last week we learned of 1 confirmed and 2 suspected cases of a variant flu strain that had only been reported twice during the previous 7 years, in Minnesota Reports Swine H1N2v Flu.

 

Next week this chart will likely need updating.

 

There are other flu strains out there, of course.

 

Earlier this year, concerns were raised over an H3N8 flu virus that had killed seals off the coast of New England, and which conceivably could infect other mammals as well (see mBio: A Mammalian Adapted H3N8 In Seals).

 

And given the propensity for flu viruses to reassort (swap gene segments), the possibility of seeing an entirely new flu strain emerge can’t be ignored.

 

Nature’s laboratory is open 24/7, and unlike human researchers suffers neither from bureaucratic rules or budgetary constraints.

 

That said, history has shown that pandemic events only happen rarely; just three times during the last century (albeit with a couple of close-but-no-cigar events thrown in to keep us on our toes). 

 

Even with all of these potential threats on the viral horizon we could easily see average flu season.

 

So far, none of these novel viruses has demonstrated the ability to transmit among humans in a sustained and efficient manner while producing significant illness.

And if we get lucky, they never will. 

 

But as schools open, and cooler weather arrives, the conditions conducive for the spread of influenza improve. And that holds true whether we are talking seasonal flu, or one of these upstart strains.

 

Today is day three of National Preparedness Month, and while most people think of emergency preparedness as something you do for hurricanes and earthquakes, flu epidemics are also worth planning for as well.

 

Preparedness should include practicing good flu hygiene (hand washing-sanitizing, covering cough & sneezes, staying home if sick) all year round, and getting the flu shot early each year.

 

No one can predict with certainty the kind of flu year we will see, and I certainly have no special insight into the matter. The CDC states it pretty succinctly:

 

What sort of flu season is expected this year?

Flu seasons are unpredictable. The CDC and WHO closely monitor flu cases to identify new viruses or potential epidemics or pandemics.

 

The CDC and the WHO obviously take pandemics and epidemics very seriously, which is reason enough for us to take a more in-depth look at pandemic preparedness later this month as National Preparedness Month continues.

EID Journal: HFMD Cluster Due To CVA6

 

Vesicular eruptions in A) hand, B) foot, and C) mouth of a 6.5-year-old boy from Turku, Finland, with coxsackievirus (CV) A6 infection.  Credit - CDC EID Journal

# 6533

 

 

In 1969, Surgeon General of the United States William H. Stewart, famously (and incorrectly) declared,  "The war against diseases has been won."

 

Unfortunately, viruses, bacteria and fungi had other plans.

 

Which is why every few months we hear of a new emerging (or re-emerging) infectious disease somewhere in the world. 

 

One of those recent arrivals - first detected in Finland in 2008 - is Coxsackievirus A6, which I initially wrote about in February of this year (see HFMD: An Old Illness With A New Cause).

 

 

HFMD is a very common viral infection, usually seen in young children during during late summer or early fall (although adults may be vulnerable as well).

 

It is caused by several of the non-polio enteroviruses.  The two most common causes of HFMD have been the Coxsackie A16 virus, and the Enterovirus-71 (EV-71), and rarely, the Coxsackie A10 virus.

 

in the United States the disease is normally caused by  the Coxsackie A16 virus and is generally mild.

 

Over the past decade we've seen outbreaks, particularly in the Far East, caused by the more pathogenic EV-71 virus. This version of HFMD can occasionally be quite serious (see EV71: Cambodia’s Prime Suspect).

 

After popping up around the globe (in Finland, Japan, Singapore & Taiwan) the past four years, late in 2011 coxsackievirus A6 was finally reported in the United States (in Alabama, California, Connecticut & Nevada (see MMWR: Coxsackievirus A6 Notes From The Field).

 

Unlike Coxsackievirus A16, CVA6 produces a more robust infection, and and can occasionally lead to serious illness.  While no deaths were reported, the MMWR dispatch above indicated that nearly 20% of cases were hospitalized.

 

All of which serves as prelude to a letter recently published in the CDC’s EID Journal that describes a cluster of 8 patients who were treated last winter for CVA6 HFMD at Boston Children’s Hospital.

 

Volume 18, Number 10—October 2012

Letter

Hand, Foot, and Mouth Disease Caused by Coxsackievirus A6

Flett K, Youngster I, Huang J, McAdam A, Sandora TJ, Rennick M, et al.

(Excerpt)

In contrast to the typical manifestation, the patients in the Boston cluster exhibited symptoms in late winter (Table) and had perioral (Figure, panel A) and perirectal (Figure, panel B) papules and vesicles on the dorsal aspects of the hands and feet (Figure, panel C). Patients experienced a prodrome lasting 1–3 days, consisting of fever (8 patients), upper respiratory tract symptoms (4 patients), and irritability (7 patients).

This prodrome was followed by the development of a perioral papular rash (8 patients), which was often impetiginized with secondary crusting; a prominent papulovesicular rash on the dorsum of the hands and feet (6 patients); and a perirectal eruption (7 patients). Half of the patients had intraoral lesions. Fever abated in most of the patients within a day after onset of the exanthem.

The rash resolved over 7–14 days with no residual scarring. Samples from the oropharynx, rectum, and vesicles from these patients were sent to the Centers for Disease Control and Prevention (Atlanta, GA, USA) for analysis. Reverse transcription PCR and sequencing by using primers specific for a portion of the viral protein 1 coding region identified CVA6 (1) (Table).

(Continue . . . )

 

The authors caution:

 

Given the numerous CVA6 outbreaks in multiple countries in 2008 and a US population that may be relatively naïve to this serotype, CVA6 is likely to spread throughout North America.

 

Clinicians should be aware that, although standard precautions are routinely recommended for managing enteroviral infections in health care settings, contact precautions are indicated for children in diapers to control institutional outbreaks (10)

 

 

And indeed, just over two weeks ago we saw an alert out of the Washoe County Health Department (see Nevada: HFMD Coxsackievirus A6 Outbreak) over a fresh outbreak of CVA6 in their area.

 

 

While seemingly not as serious as the EV71 virus, CVA6 is a strong reminder of just how quickly emerging pathogens can appear, and that oceans are no longer effective barriers to their international spread.

 

For information, you may wish to visit the CDC’s extensive website on HFMD, where you’ll find audio podcasts by a CDC pediatrician on the illness, and links to other resources. 

 

For more on HFMD, including the more severe Enterovirus-71 (EV-71) version found mostly in southeast Asia, you may wish to revisit the following blogs:

 

Vietnam’s HFMD Outbreak

China: A Recombinant EV-71

HFMD Rising In China

China Sounds Alert Over EV-71 Virus

 

NPM12: Surviving Disaster – Texas Style

 

 

# 6532

 

September is National Preparedness Month, and along with thousands of others across the country, AFD blog is part of this year’s NPM coalition. All this month, in addition to my regular infectious disease blogging, I’ll be running preparedness articles as well. 

 

Some will be new, like today’s entry, and some will be reposts (often updated) of earlier preparedness essays.

 

Today, from Texasprepares.org (part of the Texas Department of State Health Services) we’ve a series of preparedness videos (available in both English and En Español) that highlight how Texans – who are hardly strangers to natural disasters – prepare for and cope with emergencies.

 

The 7 videos are:

 

Introduction from Dr. David Lakey, Commissioner – 1:20

Surviving Hurricanes: Grab it and Go – 9:50

A Community Rebuilds: Recovering from Wildfires – 9:46

Back to Business: Planning for Disasters – 7:35

Ready for Anything: Preparing for the Next Flood – 8:02

Winds of Destruction: A County's Lessons – 8:45

Facing Disasters: A Plan for Work and Home – 8:17

 

You can click the image below to watch the videos, or follow the link below it to the download page, where you can access, and download, all of their videos.

 

 

Surviving Disaster: How Texans Prepare - Download and Accessible Videos

 

Beyond the videos, you’ll find plenty of emergency preparedness resources on the Texasprepares.org page, including:

 

 

You needn’t be one of the 25 million residents of Texas to find these videos, and resources useful. But you can also find emergency preparedness resources at the FEMA and Ready.gov websites.

 

Regardless of where you go, today would be an excellent day to to take a hard look at your family’s emergency plans, and begin taking steps to improve them.

Making The Most Of The Day Before Tomorrow

Credit FEMA/READY.GOV 

 

# 6531

 

 

A week ago, soon-to-be Hurricane Isaac was threatening peninsular Florida as it emerged off the Cuban coast and ambled north towards an eventual landfall along the Mississippi/Louisiana coast. 

 

And like millions of others within the `forecast cone’, I was considering what I would do if the storm turned my way over the next 24-48 hours.

 

Luckily, I already had an emergency plan, a pre-arranged place to go, and an emergency kit (see Inside My New Bug Out Bag) packed and ready to go.

My Bug-out-bag, Canteen, & Toiletry kit

 

Earlier this summer, my home emergency preparedness and supplies proved useful when a large tree limb came crashing down across my roof (see At The End Of My Rope) in the middle of the night.

 

Over the years, my emergency medical training and my well stocked first-aid kit have been called upon more times than I can remember.

 

And the single most important thing that has kept me from being a bystander – or worse, a victim – during an emergency has been my ongoing efforts in being prepared.

 

Blame it on early scout training, my decade working as a EMT/Paramedic, or (more likely) my 12 years living aboard a sailboat – but emergency preparedness has been an integral part of my life for nearly a half century.

 

Before anyone asks . . .

 

No, I’m not preparing for `doomsday’ like the folks you see profiled on cable TV. I’m an Everyday Prepper, who believes in preparing for more likely disasters I might actually have a chance to survive.

 

You know . . . earthquakes, hurricanes, floods, pandemics, wildfires . . . things that actually happen with some regularity around the world.

 

Which is why every September I join in with FEMA and Ready.gov to promote National Preparedness Month  (NPM12), by running preparedness essays in this blog.

 

Kicking off NPM this year, Ready.gov has a very effective graphic showing a `day before disaster’ for all 50 states. 

 

The date when it was still not too late to prepare.

 

Click through to the interactive map, to see each state’s date with destiny.

 

 

If you click on Florida, for example, you’ll get:

While Missouri yields:

 

You get the idea. 

 

One day the sun is shining, the birds are chirping, and all seems well.  The next day, quite abruptly, the bottom falls out and life for some people changes forever.

 

The Federal government wants all of us to be prepared for emergencies, as they know that during a `normal’ disaster (of which dozens occur every year) citizens may be on their own for up to 72 hours. 

 

In an extreme disaster (like we saw with Katrina in 2005), some people may end up having to fend for themselves for a week or longer.

 

With the kickoff of NMP12, Ready.gov urges all of us to:

 

 

And to do it today . . .while the sun is still shining.