Surviving, or better still, preventing heart attacks: Part 1: After it happens

May 18th, 2012

Heart attacks frequently cause sudden cardiac arrest

The April 17, 2012 edition of The Wall Street Journal had an article titled “The Guide to Beating a Heart Attack.” It had both good news and bad: since the 1970s the annual number of American deaths from heart attacks (the “med-speak” term is myocardial infarction or MI) has diminished by three fourths; on the other hand nearly a million of us will have an MI this year and many of those will die.The National Vital Statistics Reports estimate for 2010 was 595,000 deaths from heart disease (of all kinds)  and the Seattle-King County 2012 estimate is 480,000 adults dying from an MI or its complications.

A quarter million die from sudden cardiac arrest (SCA) and the majority of those happen in a non-hospital location. Only 7.6% of people who  have an SCA outside a hospital survive to be discharged to home. This figure varies markedly according to where you live. If you happen to reside in Rochester, NY, your odds are much better. Bystander-witnessed cardiac arrest victims there who have the typical heart rhythm disorder that leads to sudden cardiac arrest (it’s usually due to a chaotic quivering called ventricular fibrillation{VF}), have a 50% chance of survival to discharge from the hospital.

My mother, as I’ve mentioned before, was one of the fortunate ones. She didn’t live in Rochester or in the Seattle area which also has a superb track record.  But she had a bystander-witnessed event, got prompt CPR and a rapid response from a trained Advanced Cardiac Life Support (ACLS) team, and lived another 16 years.

The Seattle-King County concept is termed “Community Responder CPR-AED.” They knew that most people who die from SCA have VF and the only “cure” was to use a defibrillator. Most non-medical people wouldn’t be able to operate the complex gadgets used in hospitals. The answer was the AED, an automated external defibrillator developed nearly twenty years ago.

The American Heart Association” Science Advisory commentary on AED use by non-medical people has a four-point program for out-of-hospital SCA: early recognition followed by a 911 call; early bystander-performed CPR; early AED use and then early ACLS.

look for this sign

They included several extra points I hadn’t thought about, having always performed CPR-defibrillation & ACLS in hospital settings. Early CPR increase the possibility that defibrillation will stop VF and the heart will then resume its normal rhythm; it does so while providing blood flow to the brain as well as the to heart. And all the AED does is stop the VF abnormal heart rhythm enabling the heart to restart normal beating, but the heart rate may be slow to begin with, so CPR may be necessary for several more minutes.

Early CPR also increases overall survival rates; if it’s not being provided, every minute between the patient’s collapse and defibrillation lowered that rate by 4-6%.

Given all that, one of the first things the state of Washington did was to pass a law granting immunity from civil liability for any person (or entity) who acquires a defibrillator. Then they started wide-spread CPR and AED training (learning to use an AED is easier than learning CPR) and markedly increased their paramedic numbers.

The life-saving results have been very impressive. My question now is whether to buy an AED for our home.

 

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The 1918 flu: Part 3: Gene sequencing and reconstructing the virus

May 15th, 2012

here's a starting point

So how do you re-create a virus? Or at least understand how it did what it did?

In the previous post I brought us up to 1995 when Jeffery K Taubenberger, who had received a combined MD/PhD degree at the Medical College of Virginia in 1986-87, and then went to the National Cancer Institute for pathology training, got interested in the 1918-1919 influenza virus.  He used the technique known as polymerase chain reaction (PCR ) which allows a researcher to make many copies of a short segment of DNA inexpensively (If you click on the link you can experience PCR yourself). It was invented by a scientist named Kary Mullis who won a Nobel Prize in 1993 for his novel approach to genetic information.

Taubenberger and his associates went to the National Tissue Repository (NTP) and found 70 of the 100 autopsy files from the pandemic had tissue samples; 13 of these seemed candidates for recovering RNA and two actually yielded suitable RNA fragments. Data from the first case showed the virus was an H1N1 subtype and the second NTP tissue plus that obtained by Hultin in Alaska enabled the next nine years of the project, sequencing the genome of the virus.

The process is described in the Human Genome Project Information (HGP) packet online, but in brief  the genetic material is broken into small chunks, each of which is used as a template, a model to be copied. Those models allow the research team to make duplicate fragments that have slight differences in which chemical bases (with abbreviations A, T, C, and G for DNA and U substituting for T in RNA) are present. Other steps, many of which are now automated, allow the re-creation of the sequence, the pattern, of the bases. In 2006 the HGP group finished enormous task of mapping the DNA sequence for all 24 human chromosomes.

In the meantime Taubenberger and his colleagues had moved into the field of reverse genetics technology, trying to find out what physical characteristics (the scientific term is phenotype) are due to a particular gene, by slightly altering the gene’s structure. Their 2007 paper, available in PubMed Central, a free digital database of full-text scientific literature in biomedical and life sciences, describes their efforts to sequence the entire genome (all of the biological information needed to build and maintain a living example of that organism) of the 1918-1919 influenza virus.

Then they could perform actual experiments with viruses that had at least one of the 1918 flu virus genes. They were very careful with this work; their research was performed two labs that had been through the laborious certification process as BioSafety Level 3 or higher. The new viruses that had all eight genes from the 1918 flu were considerably more damaging, in animals at least, than those that had less than the full complement of genes.

Their conclusions, at this point, were fascinating: the 1918 virus was likely brand new, at least to mankind and came from an avian source, but which bird was involved is unknown. They haven’t been able to determine yet exactly why the human infection was so deadly.

It could be a deadlier version of this one

They think we’re at a mid-point in understanding the worst flu pandemic and we clearly need to learn more about it.

Why? Because other influenza virus mutations will eventually be coming our way.

 

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The 1918 flu virus and its descendants: Part 2 Rediscovering the culprit

May 13th, 2012

many other major pandemics were associated with rodents, but not the 1918 flu

I re-read my last post a day after writing it and amended the first line, since I found it misleading. It was the worst flu pandemic ever, but I knew that smallpox, the Black Plague, AIDS, malaria and perhaps even typhus each have caused nearly as many or even more deaths over a period of years. I eventually found a rather strange, non-medical website with the “7 Worst Killer Plagues in history,” and confirmed my belief that no other bacteria or virus had wreaked as much havoc in brief span of time as the 1918-1919 H1N1 influenza virus.

I wanted to find out what happened to that highly pathogenic organism and, after searching the web, realized the PBS article on the “Spanish flu” was a good place to start. It mentions that the influenza virus was not identified until 1933 and that the actual genetic identity of the particular strain involved in that pandemic (as opposed to the basic type…H1N1) was not identified for many years. The influenza virus responsible for the 1918-1919 pandemic has had many descendants, none as deadly as their ancestor.

In 1950, Johan V Hultin, a graduate student starting his doctoral studies in microbiology, got a clue from a visiting professor who suggested hunting for the virus in bodies buried 32 years prior in the permafrost of the Arctic. Hultin and his faculty advisor traveled to Alaska where flu among the Inuits had been especially deadly with 50 to 100% death rates in five villages.

early days in the Far North

Gold miners, under contract with the Territorial government, had served as grave diggers in 1918-1919 and tissue samples were recovered from four bodies exhumed in 1951. Pathology slides fit with viral lung damage and, in some cases, secondary bacterial pneumonia. But tissue cultures from the samples did not cause disease in ferrets and no influenza virus was recovered.

It wasn’t until 1995 that science had advanced enough to for researchers to start the work necessary to identify the virus’s unique features. Jeffrey Taubenberger, a molecular pathologist then working at the Armed Forces Institute of Pathology (AFIP), began a ten-plus-year-long project starting with autopsy tissues from the time of the pandemic that had been preserved in the National Tissue Repository. His project was stimulated by a paper published in the journal Science in February, 1995, in which preserved tissue samples from the famous British scientist John Dalton (often called the father of modern atomic theory) were examined. Dalton was color-blind and had donated his eyes at his death in 1844 to determine the cause of the defect; his DNA was studied 150 years later and the resultant publication gave Taubenberger the impetus to do the same with the flu virus.

Hultin read the first paper from Taubenberger’s group, wrote to him and eventually went back to Alaska to exhume more flu victims. One was an obese woman whose lungs had the findings of acute viral infection. Samples of these permafrost-preserved tissue had RNA incredibly similar to those obtained from the AFIP National Tissue repository.

And so began an amazing chapter in the history of virology.

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The 1918 flu and its descendants: part 1

May 11th, 2012

In some years this sign should be in red

The worst flu pandemic of all time began near the end of World War I, in the fall of 1918. It killed, in the next year, somewhere between 20 and 50 million people across the globe.  The comparison to WW I deaths, eight and a half million from all countries involved, is striking.

There had been major influenza pandemics before and since, some severe and some relatively mild. The term itself conventionally refers to a worldwide outbreak of an infectious disease with some adults in every continent (except Antarctica) involved, but doesn’t imply how lethal the illness is.  For example the H1N1 “swine flu” pandemic in 2009-2010 involved 74 countries, but the death rate was relatively low.

Stanford University has a superb description of the so-called Spanish flu online. Usually flu kills the very young and the very old more than young adults; this time was different with far more deaths between the ages of 20 and 40 (some say 20-50 and others 15 to 34) than in the typical flu season. The influenza-related death rate, normally about 0.1%, has been estimated at 2.5 to 3% and may have been even higher. A fifth to a third of everyone alive at the time caught the virus, so half a billion victims may have been inflicted.

For Americans, including soldiers, the end of the war was near, but over 40,000 servicemen and nearly two-thirds of a million back home would die of this modern plague.

The precise origin of the disease is unclear; swine were affected in a nearly simultaneous fashion, but have not been blamed for the human ailment. The war itself and its resultant transportation of large numbers of troops, could have facilitated its spread globally. A first wave of the infection struck American army encampments in the United States, but was comparatively mild, at least when contrasted to the second and third outbreaks later in 1918 and then in 1919.

He was at risk as well

Public health measures were widely instituted, but the actual effectiveness of quarantine, gauze face masks, limited school closures and banning of public events is unknown.

In the midst of what for many was a typical flu infection, some developed a highly virulent form of the disease, with a strikingly abrupt onset, fever, exhaustion and rapid progression to pulmonary complications and death.

Many cases developed secondary bacterial infections and one species of bacteria was initially blamed for the disease. Then two French scientists reported a filter-passing virus in the British Medical Journal in November 1918. They used filtration to remove bacteria from the sputum coughed up by a flu patient and then injected the remaining fluid into the the eyes and noses of two monkeys. After their primate subjects were noted to have fevers, a human volunteer was given a subcutaneous injection of the same filtrate. He was the only person in their laboratory to develop the flu.

The extraordinary mortality rate of the 1918 influenza is shown on a graph plotting deaths in America from a variety of common infectious diseases over the years from 1900 to 1970. Another way to gauge the impact of the pandemic is to note that average life expectancy in the United States fell by ten years for that period.

And yet the incidence of influenza ebbed and since 1920 we’ve returned to the normal cycle of seasonal flu, intermittent epidemics and occasional pandemics, none as severe and deadly as the Great Flu of 1918-1919.

 

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Mutating the deadly H5N1 flu virus

May 5th, 2012

This ferret is healthy

There’s been a recent controversy as to whether potentially dangerous medical information should be made available to the public. Now it’s happened and I’m somewhat less concerned than I was a few weeks ago. The online version of Nature just published the work of the University of Wisconsin group on making the Highly Pathogenic Avian Influenza (HPAI) type A H5N1 virus transmissible from mammal to mammal, in this case ferrets.

This is potentially a terrible disease; it’s killed 355 of the 602 humans (~59%) known to have contracted the HPAI A(H5N1) virus to date. None of those cases involved human to human spread of the flu bug involved. But that’s roughly 600 times as lethal as an “ordinary” flu pandemic and more than 20 times as deadly as the 1918 flu.

So why am I less worried than I was?

When I read the article in Nature in detail (and it’s tough slogging even for a physician), I realized that the virus, in the process of making it capable of airborne transmission, had also been made less virulent. None of the ferrets used as research subjects died of the disease . The new virus was also found to be preventable by a vaccine and treatable with one of the existing anti-flu medications.

The other thing I quickly understood is this is not a process that the average man (or woman) on the street or even the vast majority of scientists and/or physicians could duplicate. It involved an enormously complex set of laboratory procedures, many of which would demand long-term expertise and experience in the field. Theoretically a virology lab could be influenced by links to a terrorist group or have their own “ultra-green” agenda; neither possibility sounds at all likely to me.

The other paper, detailing the work done on HPAI A(H5N1) in Rotterdam, is yet to be published. That one has me more concerned, but I’ve just read a paper “Dangerous for ferrets: lethal for humans?” that carefully explores the question involved.

The authors reminded us that a previous paper had discussed the recreation of the so-called Spanish flu virus that killed 50 million worldwide in 1918. I’ll write about that in detail some other time, but when that publication appeared, its authors were hailed as heroes, not as dolts.

The work of Ron Fouchier, a senior figure at the Erasmus Medical Center in Holland took the virology world by storm. He first announced his group’s alteration of H5N1 at an international meeting in Malta in September, 2011. Initially his variant of the flu virus was thought to be much more deadly to ferrets than the UW bug. A May 3, 2012 paper in Time Healthland discusses the infighting among scientists that followed, but notes that Fouchier’s paper should be out in the magazine Science in the near future.

Apparently Fouchier’s mutated virus also turned out to be less of a ferret-killer than was initially thought.

There's the normal flu season and the other kind

But that’s not the major issue here. Most of those working in the virology field feel a natural mutation of H5N1 or H1N1 or other flu strains is more to be feared than anything produced in a lab. Yet the relatively benign 1977 H1N1 flu pandemic, so-called Russian flu, may have escaped from deep freeze in a lab.

Every year has its flu season; some are much worse than others.

 

 

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Tick-borne Disease part four: the chronic Lyme Disease controversy

April 30th, 2012

Sometimes you need an expert panel to resolve a controversy

A March 27, 2012, Wall Street Journal article, “This Season’s Ticking Bomb,”predicted that the unusually warm weather most of the country has been experiencing meant we would also see many more cases of tick-borne diseases, If you click on the link, be sure to look at the section called “View Interactive” to get to a series of suggestions on reducing your family’s risk of tick bites.

The article itself talked mainly about Lyme disease. There is an International Lyme and Associated Diseases Society (ILADS), but much of their Lyme disease website information was from 2006.  They are on one side of a major medical controversy, how to care for patients who have had Lyme disease and continue to have problems, especially with short-term memory, fatigue, or musculoskeletal issues, well after they have been appropriately treated with short-term antibiotics.

Two articles were published on this subject in 2007-8: the first one, “Chronic Lyme Disease: an appraisal”  is available online; the other, “A Critical Appraisal of Chronic Lyme Disease,” appeared in the New England Journal of Medicine.

The real question is whether the bacteria involved, Borrelia burgdorferi, remains in the body of a patient after relatively short-term antibiotic therapy and if a considerably longer course of drug treatment is warranted. The ILADS says, “Yes” to both questions and refers back to a Harvard & Tufts study published in the Annals of Internal Medicine in 1994.

The most recent CDC online information states that 10 to 20% of those who receive standard therapy for Lyme disease will have some lingering symptoms. However they term this “Post-treatment Lyme disease Syndrome.” I found that European cases of Lyme and similar diseases are usually caused by our Borrelia borgdorferi’s cousins; data from that literature may not be relevant here.

In November 2006, the Attorney General of Connecticut (CAG) pushed the Infectious Disease Society of America (IDSA) into a detailed review of their Lyme Disease guidelines by starting an investigation to decide if they had violated existing antitrust laws. By April 2008, the IDSA and the CAG agreed to end the probe by convening a review panel, with members from Duke, the NIH, Dartmouth, the U.S. Navy, Baylor, Tulane and other centers, to decide if the original guidelines had been based on sound medical/scientific evidence and if they needed changes. An MD, PhD medical ethicist screened panel members for any conflict of interest. A public hearing was held to include other viewpoints. The Final Report of the Review Panel was published in April, 2010.

Some will think the decision ties their doc's hands.

It basically upheld the 2006 IDSA guidelines, but added 1). In some cases (non-pregnant adults or kids 8 or older who’ve had a tick of the Lyme-carrying species attached for 36+ hours in an area with high infectivity rate of ticks with B. burgdorferi), a single dose of doxycycline (if they have no allergy to this drug) may be given  if the tick was removed within 72 hours; 2). Antibiotics are appropriate for adults and children 8 or older with early, uncomplicated Lyme disease; 3).  ”Reports purporting to show the persistence of viable B. burgdorferi organisms after treatment with recommended regimens for Lyme disease have not been conclusive or corroborated by controlled studies.” and 4). “The risk/benefit ratio from prolonged antibiotic therapy strongly discourages prolonged antibiotic courses for Lyme disease.

And at the end of the report, they mentioned a disease I’d never heard of; I’ll do some more reading and write about it later.

 

 

 

 

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tick-borne disease part 3: Vanilla Lyme

April 29th, 2012

I’m finally ready to write about Lyme disease and will start with the basics; it results from the bite of a tiny tick and causes well over 20,000 cases per year in the US. It’s most common in the North-East and the Middle-West, most frequently affects kids under 16 (especially girls–ticks can hide in long hair) and can be prevented (DEET to keep ticks away; post-hike “tick checks”); prompt antibiotic treatment is indicated if signs or symptoms/history suggest this entity.

you have to look closely

I’ll save the controversy about post-treatment Lyme disease syndrome, AKA Chronic Lyme Disease, for another post as that issue deserves its own discussion.

We first heard about Lyme disease some years back when a relative was afflicted by a severe case of the illness. One of the best resources I’ve subsequently found on Lyme came from an emeritus at the place I got my formal medical training, the University of Wisconsin, now termed UW-Madison. Dr. Kenneth Todar, a PhD in the Department of Bacteriology, has a superb online textbook and his chapter on Lyme Disease is an extremely helpful reference.

The initial realization of the disease itself happened thirty-seven years ago. The website for NIAID, the National Institute of Allergy and Infectious Diseases has a great, though somewhat convoluted, detailed history of Dr. Willy Burgorfer’s isolation of the spirochete bacteria that would eventually be named for him.

In brief, there had been a 1975 outbreak that resulted in a considerable number of children living in or near the town of Lyme, Connecticut, being diagnosed with juvenile rheumatoid arthritis. The Yale physician looking for the cause of these Lyme disease cases realized most occurred in children who spent time in wooded areas and whose initial symptoms occurred in the midst of the tick season, summer. He thought the deer tick might be involved and, eventually, Dr. Burgdorfer  found the spirochetes in deer ticks sent to him from the affected area.

IDSA,  the Infectious Disease Society of America, has a one-pager titled “Ten Facts You Should Know About Lyme Disease” and the New York Health Department has a similar short discussion of Lyme Disease.

one example of a typical rash

To reiterate the concepts I think are crucial:  the groups involved, kids under 16 with more girls than boys, plus adult men;. the areas of the country: 93% of cases occur in ten states: Connecticut, Delaware, Maryland, Massachusetts, Minnesota, New Jersey, New York, Pennsylvania, Rhode Island and Wisconsin; the fact that early diagnosis is clinical (antibodies develop later); the tiny size (two mm) of the tick nymphs which usually are the agents for transmission of the bacteria; the difficulty in diagnosis unless the characteristic rash is present; and the need for prompt antibiotic treatment in prevention.

Symptoms begin to show anywhere from a few days to a month after the bite, but, in most cases, the tick itself has to remain attached for a day and a half to transmit the bacteria and there is no person to person spread of this disease. Early signs, in the absence of the characteristic rash, are very non-specific.

There is a sizable percentage of patents with Lyme who have long-term sequelae. I’ll write about them next time.

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Tick-borne disease part two: Tick paralysis & neurotoxins

April 23rd, 2012

I had almost finished my post on Colorado tick-borne diseases when I noticed an entity I was unfamiliar with, Tick paralysis.  The CDC’s comment on this says it’s a “loss of muscle function that results from a tick bite.” But as I read other websites, it’s also the only tick-borne disease that’s not caused by an infectious organism, e.g., a bacteria or a virus. Female, egg-laden ticks produce a neurotoxin, a substance poisonous to the normal function of the nervous system.

Typically children under 16, more girls than boys, are affected, and may develop an acceding paralysis, with leg weakness that can rise to the truck within a few hours and potentially cause death.

But if the tick, mostly found on the scalp, is removed, the symptoms usually resolve rapidly.

This particular chemical or mix of chemicals (it’s never been identified), is junior league compared to some of its cousins.

choose your sushi chef wisely

The other neurotoxins you may have heard about much more potent. Fugu poisoning  caused by eating a puffer fish/blow fish, was apparently found over 3,000 years ago in ancient Egypt and documented in the 1800s by Captain Cook’s journals of exploration. US cases are rare and the fish in question is found off Florida’s coast, the Gulf of Mexico and Baja California. But restaurants in Japan and Korea have served it as a delicacy for thousands of years. The chefs who do so go through rigorous training and have to pass both written and hands-on exams before they earn the license to prepare it in a restaurant.

The fish itself can only be offered in grocery store with a permit and, since the toxin, a thousand times as potent as cyanide, is mostly found in the skin, ovaries and liver of the fish, selling them whole is forbidden. There’s a great 2009 New York Times article on eating fugu here. I’m not about to try it myself.

It started as a way to catch dinner

And then there’s curare, the poison applied to darts in South America which caused paralysis of the muscles used in breathing. It was basically used in hunting as the preparation of this toxic brew (the name actually has been used for a number of substance, mostly made from a poisonous bark) was too laborious for it to be used in fighting other tribes. Eating the flesh of birds or mammals killed by this highly potent mixture has no toxic effect on humans. I’m unaware of any history of hunting using blowguns with curare-tipped darts in the US; instead  curare was used medically, initially in mitigating the seizures that resulted from shock therapy, later in keeping patents immobilized during some surgical procedures. Other drugs eventually were developed to replace it.

 

 

 

 

and curare

Tick paralysis affects cows and sheep, killing thousands, in other segments of the globe. Human cases in the US cases are uncommon and mostly occur in children under 16. Once the tick is removed the symptoms normally  go away rapidly, but rarely severe paralysis can develop before the tick is found and lead to death, Most commonly the tick is embedded in the scalp and two to seven days after it feeds, the child develops weakness in both legs. If nothg is done, the weakness can progress upward and eventually lead to respiratory failure.

Another initial sign of this disease is ataxia, defined on a Mayo Clinic website as a “Lack of muscle coordination during voluntary movements.” Tick bites can cause this syndrome without obvious muscle weakness, so be alert if your kids

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Tick-borne diseases: part one: Colorado ticks and related diseases

April 21st, 2012

a well-fed tick

The Wall Street Journal recently published an article titled “This Season’s Ticking Bomb,”  discussing the rise of tick-borne diseases, especially focusing on Lyme disease. It said two factors have been important contributors to this global trend: people have moved into turf harboring animal species which often carry ticks and, simultaneously, some kinds of those animals, e.g., squirrels, deer and mice, have increased their numbers.

I must confess I haven’t worried much about Lyme disease since our 1999 move to Fort Collins, Colorado, where our back porch is at an altitude of 5,206 feet. Then I found an online 2012 fact sheet from Colorado State University; its subject, “Colorado Ticks and Tick-borne Diseases” gave me pause until I read, “No human cases of Lyme disease have originated in Colorado.”

I was amazed to find that ticks here are especially common at higher altitudes; I would have guessed the opposite was true.

We have two species of Colorado ticks that are most relevant to humans: the American dog tick and the Rocky Mountain wood tick. They are three-host blood-feeding parasites, moving from rodents or other small mammals to dogs or deer typically and then, when available, on to human hosts. We’re more likely to encounter them in spring or early summer on paths through grassy areas or the brushy zones near the edges of field and woods.

I initially was concerned about the risk of Rocky Mountain spotted fever (RMSF), but it’s actually fairly rare here and most common in North Carolina, Oklahoma, Arkansas, Tennessee and Mississippi. From 2,000 to 2,500 cases occur a year in the US with those five states accounting for 60%. They see 19 to 77 cases a year per million while Colorado has 0.2 to 1.5 cases per million. The CDC webpage on RMSF notes the overall incidence of the disease has gone up considerably since 1920, but the fatality rate has plummeted. But in eastern Arizona, through 2009, over 90 cases were noted in a previously RMSF-free area. Ten percent of those who developed RMSF died and there was a marked association with communities with free-roaming dogs.

Colorado Tick fever is seen more frequently in my state than any other infection related to tick bites. It’s a viral disease with up to 15% of our campers being exposed, but is not as serious as many other tick-bite-caused illnesses. It usually goes away without causing complications, but 5-10% of those infected with the virus can develop encephalitis, meningitis or, rarely, hemorrhagic fever. Children are more prone to severe acute disease and more likely to have the nervous system complications, but most kids who contract this illness get well quickly. About 70% of adults over 30 may have prolonged symptoms.

make your body a no-tick zone

Half of those who develop Colorado tick fever have a so-called “saddle-back” temperature curve with initial fever then normal temperature followed by a single fever recurrence.

 I’m in the prime zone for this disease; it normally occurs in those living or traveling to altitudes of 4,000 to 10,000 feet. So it’s important for me and others living or visiting here to wear protective clothing, use DEET as a tick repellent, do a “tick check” after a day outdoors and, if any are found to remove them properly with blunt tweezers.

 

 

 

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Rabies and pet care

April 17th, 2012

make sure your dog's rabies vaccination is up to date

We got an older dog, a thirty-pound Tibetan terrier, eight months ago after not having a pet in the home for three years. He’s had all his immunizations, but he’s due for a repeat rabies shot in June. We plan to travel via car with him for the month of October and want to cross the Canadian border to see Vancouver. So we asked friends who have two much larger dogs and live in Washington State if they’ve been able to take their dogs into Canada.

“It’s no problem as long as you bring proof that his rabies vaccination is current,” my friend Bob said.

We joined the Rocky Mountain Tibetan Terrier Association and got their newsletter. One section was on preventing dog attacks, both outside the home and at home. The information came from the American Veterinary Association. More than 60% of dog bite victims are children; they need to learn not to play rough with family pets. One comment said, “Never put your face directly in front of a dog–even in play.”

‘Guilty as charged,’ I thought. Yoda and I play and he often licks my face. I don’t plan to change my behavior, but I will mention the ideas to the parents of his favorite kid, who is now one and a half years old. I do think the recommendation makes sense, for children in particular.

bats may carry the disease

So why is this important? I found an NIH National Library of Medicine article on rabies which said  that deadly viral infection is spread by infected animals. In the US the number of cases has fallen dramatically and most bites from rabid animals involve non-canines: bats, raccoons, foxes and skunks as well as cats are mentioned. We spend over $300 million a year on rabies prevention with the vast majority of that going to pet immunizations.

Worldwide rabies statistics are quite different:  over 90% of human exposure to rabies and over 99% of deaths are due to rabid dogs. Many developing countries, in spite of some having programs to vaccinate dogs and get rid of strays, can’t afford a complete program.

If your child or anyone else is bitten by a non-vaccinated animal, then immediate medical care is absolutely crucial. The CDC has an online helpful description of appropriate wound care and rabies post-exposure vaccinations. Let’s be clear: if your child or you are bitten, even by a beloved pet of yours that has had its shots, see your doctor right then or go to an ER. Animal bites can cause many complications outside of rabies.

Why is this so important? Well, I just read an article about a  survivor from clinical rabies, an eight-year-old girl from a non-urban area on the West Coast. That’s exceedingly rare!

Yes, that’s true; rabies is uniformly fatal…unless it’s prevented. In the US, there have been only three people who got rabies and survived. So urgent treatment with a series of shots of both human rabies immune globulin and rabies vaccine is critical.

Don’t delay; save a life.

 

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