Tuberculosis Part one: How long has it plagued us?

June 23rd, 2012

I was reading an article in The Wall Street Journal this morning about "Untreatable tuberculosis in India" and decided to explore the background data before writing about what we're facing now.

I have a personal acquaintance with TB; when I returned to Air Force Active Duty status in 1977, I got a TB skin test. Much to my surprise it was positive.

I'm glad my chest x-ray didn't look like this

My chest x-ray was normal; I had none of the symptoms of active TB: chronic cough with blood-tinged sputum, night sweats, fever and weight loss. So I didn't have active disease and could be treated with only one drug; the infectious disease specialist told me I would take a medicine called isoniazid (INH) for a year.

I found out that about a third of the entire world population has been infected with the human variant of TB, Mycobacterium tuberculosis. In the US, 5-10% of the population will have a positive skin test; in other parts of the world, especially in some Asian and African countries, up to 80% will test positive.

Around the world new TB infection are estimated to occur at the rate of one per second, nine million cases a year with 95% of those living in developing countries. The vast majority of those remain asymptomatic. Of those who have a normal immune system, roughly 5-10% will ever develop active disease. But if you have HIV you have at least a 30% chance of moving on to symptomatic disease & x-ray-positive TB; other studies place the risk even higher, at 10% per year.

Now that milk is pasteurized, most of us in the US don't have to worry about the bovine strain of TB. But that isn't true everywhere, so beware of drinking unpasteaurized milk when you travel abroad.

A detailed online history of TB from the New Jersey Medical School commented that 2-3 million people die of the infection every year; the vast majority of those lived in developing countries. The ancient Greeks called the disease phthisis. It's been with us for millennia; ~4,500-year-old spinal column bits and pieces from mummies in Egypt  were the earliest evidence of human infection that I had been familiar with, but I found an article that doubled that estimate. Bones from an ancient site off the coast of Israel, estimated to be 9,000 years old, not only had the characteristic signs of TB, but also had DNA and bacterial cell wall lipids that could be analyzed by modern techniques.

One of his ancestors had evidence of the earliest TB we're aware of

Researchers from England commented that the tuberculosis we see today came from a human strain of the bacteria, not from a bovine origin. They also said that the DNA was subtly different from that of TB organisms today and felt this meant there has been a very long linkage between this infection and people. But the very earliest animal to have clearcut evidence of TB was a long-horned 17,000-year-old bison with skeletal remains showing the disease.

TB outbreaks still occur in the US. The June 20, 2012 edition of JAMA has a CDC report of cases which occurred in a homeless shelter in Illinois. The majority of the 28 patents involved (82%) had a history of excess alcohol use  and many had longer stays in the men's section of the shelter and socialized in two bars in the area.

The risk factors seen in developing countries: lower socio-economic status and overcrowding, seem to me to have played a role in this US series of patients. Alcohol over-usage has been implicated as a risk factor for TB,  perhaps from repeated prolong close contacts in bars and perhaps from effects on the immune system.

I'll get back to the current issues with TB in my next post.

 

 

 

Tags: , , , ,
Posted in History of TB, infectious diseases, medical research, medically-oriented background info, TB risk factors, TB worldwide, tuberculosis | No Comments »

Thanks for the Memory: part 2: Dementias

June 19th, 2012

It's on the tip of my tongue

In 1990 I needed neurosurgery. The mass which was removed turned out to be benign, but I had a major post-op bleed and was left with a considerable scar on my right frontal cortex. Up to that point I'd had, as I often said, "the fourth best memory in the family."

Afterwards my brain worked well enough. But I had considerable problems moving information from short-term to long-term memory. So when I bought the Harvard Medical School booklet mentioned in my last post, I was intrigued by the research that has been done on the subject and how it applied to me and to others, especially as we age.

Most of us worry about dementia; the Aging, Demographics and Memory Study figures, published in 2007 looking at people 71 or older, estimated there were 3.9 million people with dementia in the US in 2002. Of that group, 2.4 million had Alzheimer's disease. The crucial factor, I thought, was the prevalence, the total number living with a disease, went up with age from 5% of people in the 71 to 79 year old group to 37.4% in those 90 and above. And there are lots more of us living to that age than before.

It's become clear that having a stroke, what used to be termed a "cerebrovascular accident" (CVA), is another major route for developing dementia. A 2010 study in the journal Stroke describes dementia associated with "first-ever stroke" in a French city of 150,000 inhabitants over a 24-year period. Out of nearly 4,000 patents suffering a CVA, 20.4% had dementia. Risk factors for the outcome included age, diabetes, prior heart attack, and atrial fibrillation (an irregular heart rhythm associated with a risk of emboli, blood clots that can be dislodged, travel to the brain and clog an artery).

These figures clearly included those with new-onset dementia, but, because of the study's design, didn't exclude those who may have had the problem prior to their stroke. Nonetheless a history of stroke nearly doubles the prevalence of dementia in people over 65.

Another group with an increased incidence of neurocognitive (thinking/memory) issues includes the roughly 40 million infected with HIV. At least 30% of that group have associated brain function impairment ranging from minor or mild symptoms to full-fledged dementia. With the newer anti-retroviral drug treatments, the incidence (new cases) of HIV-associated dementia (HAD) has markedly decreased, although with people living longer with the virus, overall there are more HAD patients.

There is a roadblock between the circulation and the brain itself, the blood-brain barrier (BBB), which serves, in usual circumstances, to prevent microbes from invading the central nervous system. The human immunodeficiency virus can penetrate the BBB in several ways: one of which is by hitching a ride inside one kind of immune cells called monocytes. This is termed a "Trojan Horse" method.

Another disease, affecting 1.3 million Americans, is termed Lewy Body Dementia (LBD). It's closely associated with the dementia seen in Parkinson's disease. Both have deposits of an abnormal protein that causes difficulties in brain function. In LBD these proteins are found in several areas of the brain; with Parkinson's they are more localized.

Let's get the right pill to help, not hinder

So why is it important to know what kind of dementia a person has?

Some types respond poorly to medications that may help other forms, at least to a limited extent. And LBD patients may be helped by meds that offer less benefit to Alzheimer patients.

It's not always easy, but an experienced neurologist can often sort out which person has which disease.

 

Tags: , , , , , , , , ,
Posted in Alzheimer's, atrial fibrillation, blood-brain barrier, embolus, HIV/AIDS, incidence versus prevalence, Lewy body dementia, memory loss, Parkinson's disease dementia, stroke, vascular dementia | No Comments »

Thanks for the Memory: Part one

June 14th, 2012

keep in touch with your older friends

My wife and I recently talked about the consequences of aging, physical and mental, and I decided to order a booklet from Harvard Medical School titled "Improving Memory: Understanding age-related memory loss." Then we set out on a Monday through Friday visit to old friends (literally, since most were more than 85 years old and at least five were over ninety). We flew from Denver to a city we once lived in and saw ten individuals/couples over the ensuing four days.

I remembered a family occasion fourteen years ago when my Dad and another elderly relative were talking about whether they'd rather be as they were, over ninety and suffering various aches and pains, but mentally sharp, or like another senior at the dinner was, a year or so older and healthy physically, but over the Alzheimer's cliff. They both voted for being creaky, but lucid.

The older friends we visited in three locales on the recent trip reminded me of Dad's discussion back in 1998. Most were a little frail and complained of a variety of back, leg and joint issues, but they were mentally right on target. On the other hand, I wondered if several had at least mild cognitive impairment.

Then we came home and I started reading the booklet. There are seven normal types of memory problems: a tendency to forget thing over time (transience), absentmindedness, blocking, misattribution, suggestibility, bias, and persistence. All of these can be worsened with age  without implying more severe brain issues: Alzheimer's, other dementias or even mild cognitive impairment.

The missing letters may not mean Alzheimers

I had the second of those seven problems yesterday, seeing a new member of my men's book group on the front steps of the house we were meeting in, introducing ourselves by first names and then sitting through a detailed discussion of a book, The Inventor's Dilemna, over the next two hours.

One of the seniors we visited on our trip had always been superb with names and even in her mid-80s is much better than most of us. I never had that talent and, of course, I have even less of it at age 71.

I had made no real attempt to store the other guy's name, didn't give him one of my usual memory-hook mental pictures, and totally forgot it by the time we left. One trick to overcome absentmindedness is using cues. I'm a "visual-verbal" person, and so I tend to superimpose an unusual tie or a mustache or something similar and then repeat  the cue to myself. When I do that, I remember names. In his case, I hadn't done so.

The book from Harvard has ten ways to promote memory health. One was very striking to me: "Get a good night's sleep." I sometimes read late into the night, 11:30 or 12 or even 12:30, and when I do I'm a tad groggy in the morning. That's not something I should do if I want to be at my best the next day.

So, having been in their company for a few minutes to several hours at most, I wouldn't even venture a guess as to whether the older friends we had eaten a meal with, or talked with for five or ten minutes, were mentally totally normal for their age and encountering one of the seven types of age-related memory problems we'll all have to cope with, or, possibly, had more severe issues.

But I will use the ideas in the book from Harvard Medical School.

 

Tags: , , , ,
Posted in age-related normal memory impairment, Azheimer's, Dementia, enough sleep, Harvard Medical School publications, memory loss, mild cognitive impairment, promoting memory health | No Comments »

Aspirin revisited

June 10th, 2012

They may be good for your heart, but.....

Some years ago I began to take a baby aspirin a day as a cardiovascular event preventive medication. In my case, it was primary prevention. I've not had a cardiovascular event and don't have major risk factors. Most of my relative lived until their 90s; the only exception was my older brother who smoked three packs of cigarettes a day, gained 50+ pounds after age 40, didn't always take his blood pressure meds and loved foods that I don't consider as "heart-healthy/" When he died of a heart attack at age 57, I couldn't find his car; Dad said, "Look in the parking lot of the closest Kentucky Fried Chicken," and that's where it was.

Now I plan to stop my daily 81 milligram aspirin having read an article in JAMA which studied the incidence of major bleeding episodes (mostly in the brain or in the bowel) of over 185 thousand people who were taking low-dose aspirin compared to carefully matched controls who weren't.

The authors started with a 4.1 million population base in Italy where aspirin taken to prevent cardiovascular events is paid for by a government prescription plan for all at high risk. A six-year period was selected (start of 2003 to the end of 2008) and those over the age of 30 who began taking low-dose aspirin during that time frame were the study subjects. There were nearly 600,000 people considered for the study, but after appropriate exclusions just under a quarter million current aspirin users were carefully matched with control subjects. From a random sample of nearly 850,00 non-aspirin users, matches were found for 186,425.

let's look at the statistics

I was impressed by the thoroughness of the statistical procedure using propensity scores  ( a way to get apples matched with apples, not with zebras or even melons) and a "greedy-matching algorithm" (this link is only for math fiends) as another way to reduce bias. The results convinced me to stop taking my baby aspirin a day. The number of study subjects who had their first major bleed was fairly low (6,907  or 1.85% of all those in the study were hospitalized for a hemorrhagic event) and the absolute difference between aspirin users and controls weren't huge  (5.58 per 1,000 person-years for those taking the drug versus 3.60 per 1,000 person-years in those who didn't take aspirin). But those numbers don't tell the whole story.

Men had considerably more bleeding episodes than women and older subjects had increased rates than younger ones. So as a 71-year-old man, I paid attention. I'm not diabetic, but noted that those who were had a higher risk of bleeding whether they took aspirin or not.

This wasn't a randomized controlled study, but its enormous size and careful methods were striking. The accompanying editorial by an MD, PhD from a university in Vienna looked at previous meta-analyses (lumped-together studies) and said that for a hypothetical large group of patents who took low-dose aspirin for secondary prevention, there was a 6 to 1 benefit-risk ratio. That supports giving the drug to people at high risk of a cardiovascular event.

But when you come to primary prevention, a similar large group of 10,000 could be expected to have 7 fewer cardiovascular events at the cost of 1 major bleed in the brain and 3 elsewhere. The odds are low enough that new guidelines in Europe don't recommend giving aspirin for primary prevention. This new study would certainly support that viewpoint.

I crossed off aspirin on my pill calendar.

Tags: , , ,
Posted in aspirin use, diabetes, greedy matching algorithm, low-dose aspirin, primary prevention, propensity scores, secondary prevention | 1 Comment »

Spinal cord injury: Amazing News

June 1st, 2012

I read an incredible article in The New York Times yesterday; scientists in a Swiss lab have been able to overcome an experimental spinal cord injury in rats, enabling them to walk again. Today I found the original scientific publication and decided it was a major breakthrough, well worth translating into human terms and language.

There may be rocks below

Let's start with the human statistics; there are about 12,000 non-fatal, but severe spinal cord injury (SCI) cases in the United States every year. Half of those SCI lead to chronic paralysis and a quarter of a million people with significant SCI were alive in the US in 2010. Most of those suffered their injury when they were relatively young and 80% of them are male.

Motor vehicle accidents account for roughly 40% of those cases; the next most common cause is termed "falls," but a typical story for a fall would be a young guy who dives into a pool or a water-filled abandoned quarry, not knowing its actual depth, and strikes the bottom or a rock.

I found a thoughtful blog post on diving. The author gave five suggestions of which one is clearly the most important: "Think First." The others included "Steer up," "Hands up and out" and "Control your dive." The last was also crucial, "Don't drink or take drugs and dive."

Let's go back to the rats. The article was published online in Science and is densely packed with medical terminology (I'd suggest you read the NYT article). The rodents had a partial severing of their spinal cords at two different levels, leaving normal tissue in between and connecting the parts of the spine involved. This corresponds to somewhere between 25% and 33% of human spinal injuries. A week after their SCI, the rats began training for 30 minutes a day.

They were fitted with little vests, held upright on their rear legs and given a goal, a piece of cheese to move toward. At the same time their spines were stimulated electrically above and below the spinal areas partially cut and they got a chemical infusion of several drugs that affect nerve cell activity.

The initial voluntary steps began after 2-3 weeks of daily training and, at that point, the time of exercise was gradually increased. Five to six weeks after the initial SCI all the rats could initiate full weight-bearing steps while the combined electrical and chemical stimulation was being applied. Eventually they could climb stairs and avoid obstacles. They also had anatomic evidence of new neuron (nerve cell) connections around the injury and, higher up, in the brain stem.

Control rodents placed on treadmills did not recover the ability for voluntary motion.

A neurologist from UCSF who was not involved in the research study was quoted as saying, "There's a huge potential to refine this model to mimic more humanlike conditions."

A Stanford medical school website captures the essence of what's going on; this is neural plasticity, the building of new wiring patterns in the nervous system.

Is it possible?

A simpler comment would be that this research, if extended and then repeated in human subjects, may possibly bring hope to some of those afflicted with spinal cord injuries and maybe even diseases. Perhaps some who otherwise would have been wheelchair bound will be able to walk again.

It's not at all clear to me that this will work in people who had a SCI some time ago and it doesn't appear to be applicable to those who have a complete transection (total severing) of the cord.

Time, as always, will tell.

 

 

Tags: , , , , ,
Posted in diving accidents, Motor vehicle accidents, neural plasticity, neuron regrowth after injury, paralyzing spinal injuries, SCI, spinal cord injury | No Comments »

Hantavirus syndromes part 2: the Four Corners and beyond

May 30th, 2012

I'm normally happy to see this sign, even in the Four Corners area

It's rare to have a "coup" in medicine, but one of mine happened just over 15 years ago. In mid-May of 1993 I was making rounds with my two staff Nephrologists and their Internal Medicine residents when I heard about a disease that had just been discovered in New Mexico. I was the "old man," the Commander of the Keesler Air Force Base medical center near Biloxi, not as current in my medical reading as my junior docs, so when I ventured a guess this would turn out to be a different Hantavirus syndrome and mentioned I have saved articles on the illness in my "War File," nobody paid much attention.

Several days later the CDC announced an unknown virus, presumed to be a Hantavirus, was causing a highly lethal pulmonary syndrome. There was an immediate scramble to borrow my War File.

El Nino had brought more rain than usual to the Four Corners area in the Fall of 1992 with a resultant growth of nuts, seeds and berries. Some of the local wild animals, including the deer mice, had markedly increased their population numbers.

The initial known victim was a young, physically fit Navajo man who had abrupt onset of breathing difficulties, was taken to a hospital and died soon afterwards.

Then it was found that his fiancé had also died, only a few days prior, with nearly identical symptoms. Another victim from the same locale and then a cluster of five others, reported independently, led to a massive effort to discover the cause. More cases turned up and 80% died.

this is how your chest x-ray should look; their's were diffusely white

Each had started with nondescript symptoms...fever, chills and muscle aches, but then they swiftly developed shortness of breath, low blood pressure and abnormal chest x-rays typical of Acute Respiratory Distress Syndrome (ARDS). That could be caused by any major injury to the lungs...trauma, severe infections, chemicals.

The short list of possible causes included Hantavirus and some of the blood samples from patients showed antibodies to several subspecies of those. No known member of the group could be be grown initially, and the causative agent was titled, Sin Nombre, "Nameless."  The new disease was named Hantavirus Pulmonary Syndrome, HPS. A laboratory test was developed to allow identification of the infecting virus from autopsy tissues and the deer mouse through its urine and droppings was thought to be the vector for the spread of the disease.

By the end of 2011, 587 cases have been reported in 34 states, with New Mexico, Colorado and Arizona leading the pack. Only 3 a year are seen in western Canada. Individuals with HPS and some outbreaks have been noted in a number of South American countries as well as Panama. Stored lung tissues from people who had died years back were examined and a Utah man who had ARDS in 1959 was found to test positive for the new virus which had eventually been grown by the Army's research lab.

Other viruses with other vector species have been reported to cause HPS. Some involve features overlapping with HFRS. An associate professor at Johns Hopkins has used satellite images to develop "risk maps" for outbreaks.

With current death rates at 35- 40%, presumably due to better handling of fluids given patients as well as discovery of milder cases, HPS is still a horrific disease.

But at least there has been no known instance of person-to-person spread.

Tags: , , , , ,
Posted in Acute respiratory Distress Syndrome, Centers for Disease Control and Prevention (CDC), deer mice, Hantavirus, Hantavirus pulmonary syndrome, rodent vectors, Sin Nombre virus | No Comments »

Hantavirus syndromes part 1: The rest of the world

May 26th, 2012

dialysis for acute kidney failure

It's been a long time since I've written about Hantavirus, but I recently saw mouse droppings in our basement storage area and that brought me back to the topic. My first knowledge of this organism came from an episode of "MASH" where Hawkeye encountered a patient with a low platelet count and acute kidney failure and had to send the man to a dialysis unit in Tokyo.  I got interested in the disease that soldier contracted and, since I was on Active Duty at the time, put it in my "War File." Years later I found articles showing exposure to the virus of longshoremen in a number of US ports and then in 1993, five young, previously healthy victims who lived in the Four Corners region, where Arizona, New Mexico, Utah and Colorado meet, died of a new manifestation of this virus.

There's a thorough paper on Hantavirus available online from the Center for Food Security & Public Health at Iowa State's College of Veterinary Medicine. The disease comes in two forms: the kind I first became aware of is hemorrhagic fever with renal syndrome (HFRS) and the newer variety is hantavirus pulmonary syndrome (HPS). There are huge differences between the two types.

Let's start with HFRS. The CDC's description of this "syndrome" (the term syndrome is normally used to describe a cluster of symptoms that together are characteristic of a disease) calls it a group of clinically similar illnesses. A number of different rodents and shrews (small, insect-eating, pointy-nosed mammals) carry the virus and four of the twenty hantavirsus subtypes identified are most frequently associated with HFRS in various countries/regions.

HFRS starts abruptly with fever, chills, headache, backache and exhaustion as the most common manifestations. After a few days to a week, severe cases develop hemorrhagic (bleeding) complications and kidney involvement with some going on to shock, kidney failure and death. Intensive nursing care, dialysis and an anti-viral medication called ribavirin are used to support the patients who have this dire form of HFRS.

The fatality rate varies considerably depending on which virus subtype is involved. For one particular hantavirus, found mostly in Europe, less than 1% of those affected may die; for the form I was first familiar with, caused by the Hantaan virus, 5 to 15% of patents will die.

Worldwide, up to 200,000 people are hospitalized with HFRS every year. Most of those cases occur in Asia (with much smaller numbers in Europe); up to 8% of the population there have antibodies indicating past infection with some form of the Hantavirus.

Other animals, including cats, dogs, pigs, horses and even moose may have antibodies to the virus, but don't appear to get sick from it.

Some mice are smarter than others.

Better than treating the disease, of course, is preventing it. Making your home or other buildings mouse-proof isn't easy, but storing food in secure containers and using traps and rodent poisons may go a long ways toward avoiding the disease. The CDC website has detailed instructions on safe ways to clean up rodent droppings and urine. CDC warns you should never start by sweeping or vacuuming!

Now I need to clean up the mouse debris in our furnace room.

Tags: , , ,
Posted in Hantavirus, Hantavirus pulmonary syndrome, Hemorrhagic fever with renal syndrome, HFRS, HPS, rodent-carried disease | No Comments »

Heart attacks Part 2: Prevention: risk factors & our kids

May 23rd, 2012

Here's a risk factor you can eliminate

This post pings off the April 17, 2012 article in The Wall Street Journal, "The Guide to Beating a Heart Attack." I initially wrote about surviving a heart attack (myocardial infarction {MI} is the medical term). Next I wanted to turn toward the prevention side.

I first found the Interheart study's article from 2004, "Nine modifiable risk factors predict 90% of acute MI." The study followed 29,000 people from 262 sites in 52 countries and concluded that the common belief that half of heart attacks can be predicted was clearly an underestimate.

The research group found the same impact of the nine variables everywhere in the world: abnormal blood lipids (fats, like cholesterol) and smoking were at the top of their list. Then came diabetes, high blood pressure, abdominal obesity, stress & depression, exercise, diet and alcohol intake.

I was used to measuring cholesterol and its HDL (so-called good cholesterol)  and LDL (bad cholesterol) components. This study actually used a more sophisticated lipid approach.

They measured the ratios of  the proteins that bind to and carry fats, apolipoproteins A and B. APOA is associated with HDL lipids while APOB is said to unlock the door to cells and in doing so acts as an unwelcome delivery van for cholesterol. When present in high levels, APOB can lead to plaque formation in blood vessels and an increased risk of coronary heart disease (CHD).

They also found some good news: as expected, eating fruits and vegetables daily, exercising and perhaps moderate alcohol intake were associated with lower risks of CHD. Again this was true everywhere in the world.

The WSJ article mentioned that hospital admissions for heart attacks had actually decreased among the elderly; these nine factors were better predictors in younger groups. What can be done to stop the looming specter of CHD among our younger population?

The CDC examined the parameters in a recent online article titled "A Growing Problem." One issue was "screen time." Our kids eight to eighteen average four an a half hours a day watching TV and three more on cell phones, movies, computers and video games. I even read an article about a two-year-old whose parents think learns a lot from their iPad. Maybe so, but how much exercise does that kid (and his older compatriots) get?

The CDC feels there is a dearth of quality physical activity in our schools; as of 2009 only a third of them provided daily PE for our kids. And after they leave school or when they're on vacation, many don't have safe access to biking, hiking, running, playing areas and trails.

Somerville chose healthier food in their schools

One Massachusetts community, Somerville, has gotten attention for their anti-obesity integrated program, "Shape Up Sommerville"  (You can watch the thirteen minute PBS special on their community-wide progress). The Robert Wood Johnson Foundation is attempting to help similar programs get started across the country, especially focusing on childhood obesity.

Recently I heard a NPR comment that caught my attention. If we don't do something to stop the epidemic of childhood obesity, we'll soon be seeing CHD rates soar in people in their 20s and 30s and maybe even younger.

A French researcher said, "Mankind is doing a good job of killing himself."

We need to try new approaches to help our kids. The Somerville plan sound like a good place to start.

 

 

 

Tags: , , , ,
Posted in anti-obesity programs, Cardiometabolic Risk factors, cholesterol, coronary heart disease, depression, diabetes type 2, Healthy eating, medical research, medically-oriented background info, mental health issues, Unhealthy eating, Vegetables | 1 Comment »

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.

 

Tags: , , ,
Posted in AED, coronary artery disease, coronary heart disease, heart attacks, Life extension, medically-oriented background info, ventricular fibrillation | No Comments »

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.

 

Tags: , ,
Posted in "bird" flu, 1918 flu pandemic, DNA, genome sequencing, PCR, reverse gentics | No Comments »

« Older Entries
Newer Entries »