Macular disease, cataracts and art

October 24th, 2013

My wife and I are supporters of two art museums, one locally and the other in Denver. I also have a personal interest in eye problems, especially cataracts and macular disease, as my father had lost an eye as an intern (a paper cut led to an infection and, in those days, before antibiotics, there was concern about the other eye developing problems, a medical issue called sympathetic ophthalmia). In his late 80s he had a cataract in his remaining eye and, when he was examined by an ophthalmologist at the Cleveland Clinic, was found to have macular degeneration, a chronic eye disease  usually seen in people over 50.

Someday my visions may deteriorate to this point.

Someday my visions may deteriorate to this point.

I became aware, as I read about Dad’s problem, that one day it might become mine as well; one of the risk factors for macular degeneration is a family history of the disease.

I’ve pasted in a list of symptoms from this condition (copied from a Mayo Clinic website).

  • The need for brighter light when reading or doing close work
  • Increasing difficulty adapting to low light levels, such as when entering a dimly lit restaurant
  • Increasing blurriness of printed words
  • A decrease in the intensity or brightness of colors
  • Difficulty recognizing faces
  • A gradual increase in the haziness of your central or overall vision
  • Crooked central vision
  • A blurred or blind spot in the center of your field of vision
  • Hallucinations of geometric shapes or people, in case of advanced macular degeneration

The National Eye Institute, a branch of the NIH, has a fact sheet on age-related macular degeneration (AMD) that’s worth looking at if you or someone in your family develops this problem. I’ll mention a few things from that website as AMD is a major cause of vision loss in older adults. To begin with the macula is the part of your eyes that gives you the sharpest, most detailed vision. It’s the extremely sensitive part of the retina, the layer of tissue  at the back of your eye that responds to light, converting images, focused by the eye’s lens on this equivalent of camera film, into electrical signals that travel via the optic nerve to the brain. If the macula is damaged, fine points of these images become less clear.

If this happens to a non-artist, someone who doesn’t make their living through images they put into a form that others can enjoy, it still leads to less sharp vision. You may have problems reading, driving or recognizing an image such as a face. Since your peripheral vision isn’t affected, you’ll probably be able to walk around without major difficulty.

But image that you’re an artist. You gradually realize your vision is becoming less clear. You used to be able to read an eye chart at the 20/20 level, meaning you can read the same row of small letters on the chart at 20 feet which those with normal vision can. Now your visual acuity, measured when you see your eye specialist, is slipping and you worry that it will affect your ability to paint as well as you once did.

Having 20/20 eyesight does not necessarily mean perfect vision. 20/20 vision only indicates the sharpness or clarity of vision at a distance. There are other important vision skills, including peripheral awareness or side vision, eye coordination, depth perception, focusing ability and color vision that contribute to your overall visual ability.

Some people can see well at a distance, but are unable to bring nearer objects into focus. This condition can be caused by hyperopia (farsightedness) or presbyopia (loss of focusing ability). Others can see items that are close, but cannot see those far away. This condition may be caused by myopia (nearsightedness).

I’ve written about these medical problems before, but was riveted by a pair of articles I found in two AMA publications yesterday. A Stanford eye surgeon, Dr. Michael F. Marmor, just published a supurb article on Edgar Degas’ progressive loss of vision in his later years. Degas was born in Paris in 1834 and died there in 1917. His painting altered from 1860 , when he had essentially normal vision, to 1870 and beyond  when first one eye, then the other progressively lost visual acuity. By 1897 he was seeing at a 20/200 level; that means he could would have to be twenty feet away from an eye chart to read the letters that someone with normal vision could read from 200 feet away.

The style and details of his paintings, especially his pastels, have been shown to change as Degas’ eye problems progressed, but Dr. Marmor’s article calls our attention to one oil painting, Scene from the Steeplechase: The Fallen Jockey. Here’s a link to the painting in the National Gallery of Art; it was originally painted in 1866 and reworked by the artist in 1880-81 and again in 1896 with considerable changes made which Dr. Marmor shows can be linked to Degas’ declining visual acuity.

A number of other significant artists have demonstrated visual loss in their work. An April, 2007 article in ScienceDaily focuses on Dr. Marmor’s work, mentioning he’s authored two books on art and eye sight: Degas Through His Own Eyes and The Artists’s Eye (I’ve ordered a copy of the latter book through Amazon).

The Blind with Camera School of Photography website mentions a number of other famous figures from the art world who struggled with visual issues. Among those were El Greco, Rembrandt, Van Gogh, Paul Cezanne, Claude Monet, Mary Cassatt, Camille Pissarro and Auguste Renoir. Georgia O’Keeffe, who lived to the age of 98, also suffered with significant eye disease in her later years; her almost complete loss of eyesight and ill health during the last fifteen years of her life significantly curtailed her artistic productivity. Her eye problems began in 1968, and by 1971 macular degeneration caused her to lose all her central vision.

How is this honeybee similar to Monet?

How is this honeybee similar to Monet?

Monet had cataracts which not only diminished his visual acuity, but also affected his perception of colors. He resisted having surgery, but eventually decided to have one cataract removed. After the operation, according to science writer Carl Zimmer’s review of the San Francisco Exploratorium’s free  publication, Color Uncovered, Monet, like honeybees, was able to see ultraviolet light (normally filtered out by the lens of your eye) and painted water lilies a pale blue. Bees are guided to pollen by light signals we are unable to perceive; Monet had lost a lens to surgery, but gained a spectrum of light perception the rest of us lack.

I have zero talent as a visual artist, but after bilateral cataract surgery my vision is correctable to 20/20…for now.

 

 

 

Nut allergies et al

October 8th, 2013
Warning, may contain some of these.

Warning, may contain some of these.

I recently heard from Kevin Thompson, a Colorado blogger who read one of my posts and wondered if I’d include a link to one of his on my website. I knew of tree nut allergies only in the most general terms, but found his post gripping and, for parents of a child with nut allergies, potentially life-saving.

But I wanted to do some reading on the subject myself and also needed to see what else Kevin had posted on his blog.

Before I move on to his recent ideas on nut allergies, I’d like to mention (and give you a link to) another of Kevin’s posts, “10 of the Most Common Food Allergies in Kids.” In that one he discusses, in non-technical terms, children’s alleges to eggs, milk, soy, wheat, peanuts, tree nuts, fish, shellfish, strawberries and (amazingly) kiwi fruit.

The American Academy of Pediatrics website has a July, 2013 update on diagnosing food allergies in children. That post mentions the most common pediatric food allergies are to dairy products, egg whites, poultry, seafood, wheat, nuts, soy and chocolate. Like any kind of allergy, those to food happen when your immune system, reacting to a substance foreign to your body, produces antibodies, chemicals that usually help to protect you from infections, or as the Mayo Clinic website on allergies says, “unwanted invaders that could make you sick.”

The reaction from your immune system leads to inflammation, but the area affected and the seriousness of the reaction varies. What Kevin was talking about is the high end of the spectrum, those forms of allergic responses that can be life-threatening.

Some years back a nurse at the allergy clinic my wife goes to (fifty miles north of us in Cheyenne, Wyoming), asked if someone in the home could give Lynnette her allergy shots. That would mean she didn’t have to drive a hundred miles every other week. I was drafted although I had never given shots in my years as a practicing physician. I learned quickly; after all I had performed kidney biopsies and, in my early days in nephrology, stuck large needles into arteries when a patient had acute kidney failure and needed dialysis.

But I needed some onsite drugs in case Lynnette had a medium or, heaven forbid, a major reaction to the allergy shots.

Here's what an EpiPen looks like.

Here’s what an EpiPen looks like.

I purchased some over-the-counter Benadryl and our family practice physician wrote us a prescription for epinephrine in the form of an EpiPen (there are other brands). This is an auto-injector, something you slam into the outer thigh of a person having a really serious allergic response to a foreign substance (i.e., an allergen) or to exercise or for unknown reasons. It’s available in an adult form with 0.3 milligrams of epinephrine or in a half dose (EpiPen Jr)  and I purchased a two-pack that came with a training device.

I hadn’t tried that before today, so I just got it out of its box and followed the instructions. I removed the Blue Safety Release, swung the device against my outer thigh and pushed it, hearing a click that, with the actual EpiPen would have meant a needle had extended and, while I held it against my thigh for ten seconds, would have injected me with the (hopefully) life-saving medicine. I would have been comfortable using the actual EpiPen, but thought I should simulate a non-medically-trained person practicing how they would use the real thing.

I hadn’t mentioned it yet, but you don’t take the time to lower the trousers of the person (whether that’s you or someone else) having serious allergic problems  to use the EpiPen; it goes right through the cloth in the event of a life-threatening emergency. It does have a needle and it does contain the epinephrine to counteract a major allergic reaction.

The Trainer  doesn’t contain any medication and has no needle; it’s also reusable, so somebody can practice with it until they are comfortable with the procedure.

Why in the world would you do this to yourself or someone else? The website of the American Academy of Allergy Asthma and Immunology describes this condition, medically termed anaphylaxis, as a serious, life-threatening allergic reaction, mostly commonly seen with foods, insect stings, medications and latex exposure. The signs and symptoms typically involve more than one part of the body . They require an immediate injection of epinephrine and a trip to the emergency room (call 911, don’t drive the person yourself).

Most commonly, anaphylaxis starts within a few minutes (five to thirty) after exposure to the allergen (the substance to which the person is allergic). It can lead to any combination of: hives, swelling in the throat or elsewhere, wheezing, difficulty swallowing, trouble breathing, a feeling of tightness in the chest, syncope (fainting), vomiting and/or diarrhea with cramps, a feeling of impending doom and/or paleness or redness of the body or face.

Occasionally it can have a delayed start, so I had my wife practice with the EpiPen Trainer also just in case I’ve left the house after I’d given her the shots, waited fifteen minutes to check the areas where they went in (one on each arm), and recorded the local reaction or lack thereof.

So let’s go back to Kevin Thompson’s blog post, “How to Keep a Child With Nut Allergies Safe at School.”It walks you, as a parent, step by step, through the means to safeguard your child’s health after they have been diagnosed with an allergy to nuts (tree nuts or peanuts). I think it’s well worth reading if you have a youngster with those kinds of potentially fatal allergic problems. From approaching the school’s personnel, to helping the child her- or himself be knowledgable, to ensuring the teachers and others at the school are prepared to deal with an anaphylactic reaction, to considering other options, the post is something I’d recommend you print multiple copies of and pursue with due diligence.

It’s best to be prepared and even over-prepared for a life-threatening situation.

 

 

Lyme Disease Redux

September 23rd, 2013

Yesterday’s edition of The New York Times had an article by an experienced academic physician that called for a new Lyme disease vaccine, Dr. Stanley A. Plotkin, a professor of pediatrics at the University of Pennsylvania said new CDC data had been released showing a ten-fold greater incidence of the disease than was previously thought. He explored the history of the vaccine put on the market in 1998 by a major US pharmaceutical company, then called SmithKlineBeecham (now it’s become GlaxoSmithKline).

I looked for that news release from the CDC and found their old numbers in an August, 2013 online site (30,000 cases a year reported by state and DC health departments) had been superseded by new preliminary figures coming from three different databases. So instead of the numbers we’ve thought represented human cases, 96% of which occur in thirteen states in the Northeast and upper Midwest, we have 300,000 cases a year, still heavily concentrated in those regions.

The white-footed mouse is the main reservoir for Lyme disease.

The white-footed mouse is the main reservoir for Lyme disease.

In 2011 Richard Ostfeld, a senior disease ecologist working at the Cary Institute in New York published an excellent book, Lyme Disease: The Ecology of a Complex System, aimed at a mixed readership of scientists and nonscientists. I’ve mentioned this before but should reiterate his finding that white-footed mice were a highly significant reservoir (host animal) for the bacteria that is then transmitted to humans by, in this country, one particular insect-like species, the black-legged tick.It’s actually an arachnid, cousin to spiders and scorpions. There are other host species and a variety of predators, weather/climate conditions and habitat factors also play a role.

His work predicted a surge in cases of Lyme disease in the spring of 2012, based on an acorn crop boom-and-bust cycle. The town of Whitman, MA, published an online summary of this prediction quoting the Cary Institute’s press release. In brief that mouse species’ population soars in a year with an abundant acorn crop and falls markedly when acorns are scarce. The organism that causes Lyme disease is a bacterial species called Borrelia burgdoferi, The white-footed mouse is a superb host for that bug; the mouse doesn’t get sick; the bacteria multiplies and there is an abundant supply of B. burgdorferi waiting to spread to other animals. Those mice are also frequently bitten by the tick in question, especially around their ears.

In the seasons of acorn abundance the mouse population soars and the ticks, which need a blood meal three times in their life span (once in the larval storage, once as a nymph and once as an adult), have plenty of mice to feed on.

But then comes a lean crop year for the acorns and the B. burgdorferi infected ticks have to find other blood sources for their next meal. Any mammal will do, but humans are certainly among those available. If we are camping or hiking through an area where the tiny tick nymphs or abound, we may never notice the bite. We may not even be wearing any  bug spray or perhaps have more skin exposed than is safest. The nymphs are cold-blooded, so the countryside has to warm up from Winter’s blasts before they are ready to feed. If it’s a milder cold season (and with global warming that may be the case), the nymphs may be out looking for a meal as early as April.

Forest ecologists from the Cary Institute noted 2010′s crop of acorns was very heavy;  mouse population numbers rose appropriately. Then, in the fall of 2011, their research site had a marked acorn scarcity. Mouse numbers plummeted leading to a prediction from the group of at least 20% more human cases of Lyme disease.

Let’s return to Dr. Plotkin’s article in the New York Times. Eight years ago he almost lost an adult son to a cardiac complication of a Lyme infection. Alec D. Plotkin was walking his dog on an August day in Pennsylvania when he abruptly lost consciousness and collapsed. In 2011 his father (Dr. Plotkin) published an article, “Correcting a Public health Fiasco: The Need for a New Vaccine against Lyme Disease,” in the Journal Clinical Infectious Diseases. At that time the yearly US case estimate was (reported cases only) roughly 20,000, but as Dr. Plotkin noted, “the extent of underreporting is unknown.” He mentioned that the state of Connecticut’s statistics would imply that 1% of its entire population could develop the ailment over a ten-year stretch and that nine of sixteen countries in Europe, where Lyme disease is caused by a different variant of B. burgdorferi, had data showing an increased case incidence over time.

But you may or may not have the pathognomonic rash.

But you may or may not have the pathognomonic rash.

On Septmeber 19, The New York Times published the obit of Dr. Stephen E. Malawista, who, as chief of rheumatology at Yale School of Medicine had, with his postdoctoral student, Allen C. Steere, defined Lyme disease. In the fall of 1975 two women from Lyme, CT and Old Lyme had developed joint swelling, peculiar rashes and neurological complaints undiagnosable by their local physicians. Each went to Yale seeking answers.

Researchers there noted that the clinical picture, which was originally felt to be juvenile rheumatoid arthritis, had occurred in clusters and at a rate 100 times that expected for JRA. It also was clustered in warm-weather months. Dr. Malawista suggested the name Lyme arthritis and he and his team made the eventual linkage with tick bites. In 1982 Dr. Willy Burgdorfer found the bacterium responsible and Yale scientists wnet to work to develop a vaccine.

It was finally licensed in 1998, but a series of events, detailed by Dr. Plotkin in his medical article, led to it being removed from the market four years later. In brief: the CDC’s Advisorty Committee on Immunization Practices (ACIP) gave greater emphasis to protective clothing, tick repellants and, in the event of an infection, consistent early diagnosis and antibiotic treatment, than to the vaccine, even for those at high risk. Then it was only tested in adults and more in the group who got the vaccine than in the control group experienced some transient joint soreness…but not actual arthritis (typically red,hot, swollen, painful joints. The marketing of the drug was inappropriately directed at a lay, not a medical audience. A class action suit was brought against Glaxo, the drug company which produced the vaccine and, in spite of later studies showing no increase in Lyme-related joint disease, was settled by Glaxo for $1 million in 2003. Only the lawyers involved got any money.

By then the vaccine was off the market.

It’s clearly time for it to come back, perhaps in a new version, perhaps developed by a different company, but, in any case a human Lyme disease vaccine is needed.

 

Ditch fad diets; use common sense instead

September 16th, 2013

When I returned home on September ninth from a twenty-eight-day trip, I found stacks of mail, magazines and newspapers plus about 650 emails to wade through. Most got short shrift and the old papers were pitched. But then I found four editions of JAMA and started reading selected articles. Over the years I’ve deplored the menagerie of fad diets that have been described, advertised and exploited for profit.

You don't have to weigh and measure each time you eat a pea

You don’t have to weigh and measure each time you eat a pea

So coming upon a Viewpoint piece in the Aug 21, 2013 edition, I read with intense interest  ”A Call for an end to the Diet Debates.” The pair of PhDs who authored the two-page discussion, Sherry L. Pagoto and Bradley M. Appelhans, are both academics, serving on the faculty of major medical schools. They commented on the host of studies and four recent meta-analyses that have reviewed the results of a variety of diets varying the amount of protein, carbohydrates and fats one is allowed.

Their conclusion is they don’t differ in their results in any significant way and that sticking to a diet and adding exercise is what counts.

There’s a second comment that was striking: in spite of markedly increased percentages of US adults being overweight or obese, the chances of their getting any counseling on the issue when they see their primary care physician have fallen. Researchers from the Penn State College of Medicine published an article in February of this year titled “A silent response to the obesity epidemic: decline in US physician weight counseling.” The National Center for Biotechnology, a National Library of Medicine section, published a short version of this study comparing outpatient visits in 1995-1996 to those in 2007-2008 (the most recent data available from an ongoing national ambulatory medical care survey).

What I think this means is that we still don’t pay physicians enough for preventive medicine interventions; we pay much more for procedures, what I think of as “Catch-up Medicine.”

Over the past forty-seven years, ever since I graduated from medical school in 1966, I’ve seen a host of fad diets come and go. The Rice Diet, invented at Duke where I served as an intern and resident, is still around, but was originally utilized as a very-low-protein approach for patents with severe kidney disease. Since then we’ve seen high protein, low protein, several that focus on carbohydrates, and, this year, in a blog from a Phoenix newspaper, an entertaining look at “5 Fad Diets to Avoid in 2013.”

Those include: a gluten-free diet (reasonable only for those who actually have been diagnosed, preferably by an experienced physician, as having gluten intolerance); the Dukan Diet (I’ll supply a link to the WebMD review of this French approach), essentially a high-protein and limited calorie approach that may work short-term, but doesn’t supply a balanced diet for the years to come; the alkaline diet (here’s another review from WebMD) which claims to alter your blood pH, which is nonsense, but basically is a fresh fruit and vegetable plus hydration approach which in itself isn’t unreasonable for those who don’t have kidney disease or severe diabetes. But the components of this diet can easily be purchased in your supermarket and therefore don’t need to be obtained through a website; the HCG diet, dangerously restrictive in calories and supplying a hormone that ought to be used only by a physician’s prescription, usually for fertility issues (here’s a Mayo Clinic review that says the diet dangerous); and finally, the beef tapeworm diet where some go over our southern border and actually pay to be infected with a parasitic disease. I don’t feel the need to even comment on the logic of that approach.

So what does make sense to me is, as always, eating less and doing more.

Of course that’s not as easy as it sounds. Some of my previous posts have alluded to the ways I’ve made this work for me, but you may or may not find them to fit your own lifestyle.

Use a good scale, but it doesn't have to be this fancy.

Use a good scale, but it doesn’t have to be this fancy.

So I’d suggest the following: 1). Don’t fall for the expensive fad diet ploy; eat in whatever pattern suits you (three meals a day is my habitual approach, but I sometimes eat two with a medium-sized brunch in anticipation of an evening event that includes food in abundance), but avoid snacking and late evening binges; 2) Eat balanced meals with more fruits and vegetables and less (or no) red meat than is typical for many Americans; 3). Find a form of exercise that you’re comfortable with and do it almost every day (We walk an hour a day and I spend another hour or often two in the gym six days a week; that may not work for you, especially if you have a full-time job.); 4). Don’t beat yourself up when you fall off your eating and exercise (figurative) bike, but get back on it ASAP. 5). Weigh yourself daily on a good scale, at the same time of day, wearing nothing (or as little as possible) and keep a record of your weight. 6). Don’t expect to lose twenty-five pounds in a few weeks. If you did that, my bet is you’d gain it all back in a year. Aim for a pound a week.

I took my eating plan, which I first decided on in 1996 or 1997, and really started using in early 2009, and wrote down all of the ideas and some recipes my wife added; I ended up with a 50,000 word book that I may eventually try to polish enough to publish. There are a number of specifics that I’ve added to the six basics concepts in the paragraph above, but I’ll mention those at another time.

I still occasionally struggle with one aspect of my eating plan; late-night reading can be a prelude to minor binging. And events with food are another potential minefield. But I’ve managed to get back to my diet whenever I’m above what I consider to be my acceptable range.

So I have four by six inch cards that tell me: “Don”t snack at events.”

I’ll bring one along tonight when I go to a writers’ meeting; there will be two speakers, but someone is bound to have lots of snacks for the group.

I don’t plan to eat them.

Cancer screening redux

August 12th, 2013

The JAMA article I’ve mentioned in my last two posts provided an interesting sequel. It mentioned lung and bronchus cancers in the group with breast cancer and prostate cancer, those whose incidence has gone up a fair amount, and death rates have gone down.

That confused me as the numbers showed only a smidge more being diagnosed (an 8% increase) and actually a death rate increase in the same ball park (eleven precent). The footnote said a National Lung Screening Trial looking at higher risk individuals concluded low-dose CT screening could reduce death rates by 20%. I had missed this article which was published in the New England Journal of Medicine in 2011 and had over 53,000 subjects who were randomly assigned to screening with either a single chest x-ray or low-dose CT. The point was CT scanning picked up early-stage cancers and their percentage was way up, while the proportion of later-stage cancers actually was less.

Lung cancer is the third most common in both genders in the United States and is the number one cause of cancer-related deaths. If you’re a heavy smoker, the chances of your dying from lung cancer go up immensely The CDC webpage on lung cancer risk factors calls cigarette smoking the major issue causing ~90% of all lung cancers in this country.

I’ve mentioned this before, but let me reiterate my Dad’s smoking cessation and mine. He had three rooms in his private practice office and one day realized he had put a lit cigarette in the ashtray of each room, He never smoked again and lived to ninety-four. I smoked as a youngster for four years, never heavily, and I quit as a senior in medical school when I saw one of my VA patients smoking through the trachesotomy he had had for cancer.

The August edition of the Annals of Internal Medicine, published one day after the piece in JAMA, has an article titled “Screening for Lung cancer with Low-Dose Computed Tomography” (AKA a CT scan). This one reviewed four trials of CT screening; only one was large and of good quality. It actually was the research reported in the NEJM article and the project was stopped at six and a half years when it was noted how much lung cancer mortality was reduced.

What’s interesting in this new review article is a series of comparisons: you need to screen 320 at-high-risk subjects by low-dose CT scanning to prevent one death from lung cancer and 219 to prevent one death from any cause. That wasn’t striking until I read you need to screen 1339 women aged 50 to 59 with mammography to prevent one breast cancer death and 817 people with flexible sigmoidoscopy (a shorter version of the colonoscope that can reach an estimated two of three colon polyps) to prevent one colon cancer death.

The third category of cancer screening focused on melanoma, the worst of the three common skin cancers (the others are squamous cell and basal cell cancers). In the time frame from 1975 to 2010 the incdence of melanoma went up 199% while the death rate from this tumor went up only 32%. I found a very recent online article on this cancer, reprinted from an April, 2011 publication, by US News and World Report. It focused on its warning signs and prevention as well as treatment.

We live at  an altitude of ~5,200 feet, so our exposure to damaging  UV rays from sunlight is considerable. My wife drives 55 miles to several times a year to see a dermatologist and the last few years I’ve gone with her on one of those visits and had a skin check,

Try to catch these very early

Try to catch these very early

Melanomas account for three quarters of all deaths from skin cancer and are felt to result from excessive exposure to UV light. We walk in the early morning and after dark, not during the middle of the day, don’t use tanning beds, my wife always wears sunscreen (I confess I don’t routinely do so, but I should), and neither of us has “fair or freckled skin’ or a family history of this disease.

The NCI says a change in the size or shape, color or texture of an existing mole, one of the black or brown patches that most of us, by adulthood have a number of (10-40 is common).I like the NCI’s ABCDE approach to look at moles: A stand for asymmetric, different parts of the skin lesion not looking the same; B means borders that are irregular, shaggy or ill formed (uneven or scalloped); C is for color that varies from part of the mole to another; D is for diameter (melanomas, while they may be smaller, usually are larger than a pencil eraser in size): and E is for evolving (changes in size, shape, color, elevation or even bleeding, crusting/scaling or itching).

Any of these signs should prompt a quick call to your doctor and perhaps a visit to a dermatologist.

Fortunately, the only skin cancer either of us has had thus far was a squamous cell and it was removed by the Mohs technique, in which a section of the lesion is surgically removed by a specially trained physician, and then immediately stained and examined under the microscope to make sure the borders are clear of any tumor. The process is repeated until safe borders are noted.

The last kind of cancer I want to mention is thyroid; during the thirty-five year period its incidence went up 185, but its death rate went down 7%.

Be sure your doc knows if you or your family member has had a thyroid problem

Be sure your doc knows if you or your family member has had a thyroid problem

In spite of having a first cousin who had this tumor, it was the one I knew the least about. So I went to the MD Anderson Cancer Hospital’s website on Thyroid Cancer Prevention and Screening. They mentioned on type that runs in families and is genetically linked, but for most of us, looking at our neck carefully twice a year, having our physician do a cancer-related exam yearly, making sure your salt has iodine, and knowing that most of these lesions occurs in women (3/4s), typically between age 20 and 55 is a good start. One other comment was exposure to radiation, especially in childhood is a significant risk factor.

There are other cancer screening procedures, but those are the common ones. Your physician may have a few more in mind.

 

 

 

 

Cancer screening Part 2: what works?

August 11th, 2013

A blog post in The New York Times online recently addressed this issue noting, “Definition of Cancer Should Be Tightened, Scientists Say.”

Here’s a typical scenario: We’ve had a screening test for some form of the illness many of us fear the most (actually, I fear Alzheimer Disease at least as much). Then we hear the words, the really scary ones. “You’ve got cancer.” We may not hear the modifiers that come before the C word, or anything else that follows. The National Cancer Institute’s (NCI) working group wants to clarify that some conditions are pre-malignant (they’re not cancer yet and, in certain cases, may never become carcinomas {another term for cancer}).

I want to return to the JAMA preprint article  I mentioned in my last post; it’s titled “Overdiagnosis and Overtreatment in Cancer? An Opportunity for Improvement

The group focused on cancer screening to include breast, lung, thyroid, colon, cervix, melanoma and prostate exams.  They tracked the incidence of a variety of cancers over the thirty-five-year period from 1975 to 2010 and found three different result patterns have been noted as more and more of us are screened for more and more conditions.

Some cancers have been diagnosed somewhat more frequently, but in many cases are less serious variants, less likely to kill us, so, overall, they are causing fewer deaths. Other malignancies are being found less frequently (due to improved and/or more frequent screening resulting in precancerous stages being treated) and the death rate from them has gone down considerably. And some cancers are being diagnosed much more often, but much of that increment is what the researchers termed “indolent disease,” less active or progressive disease and overall their death rate is nearly unchanged or increased much less than the percentage change of their being diagnosed would indicate.

Let’s take cancer of the prostate for an example of the first group. The incidence (rate of occurrence) in cases per 100,000 men has gone from 94 to 145.12, a fifty-four percent increase, while the death rate from the disease has gone down 30%.

So we’re doing better with treating this form of cancer, seeing a lower mortality rate, but we’re discovering considerably more cases that are not causing deaths. As I said in my last post, I’ve decided not to have any more PSA tests; at my age (72), other things are much more likely to kill me than prostate cancer. I clearly would have made the opposite choice (and did) at age 45 or 55.

Mammograms can save lives; they also can find pre-malignant lesions.

Mammograms can save lives; they also can find pre-malignant lesions.

The other tumor in the first group is breast cancer. Mammography has certainly become more of a routine procedure looking for breast lumps, but while the incidence of breast lesions has gone up 20% in the thirty-five year interval the NCI group looked at, the death rate has fallen by 30%. Much of that is due to what is termed adjuvant therapy, e.g., chemotherapy following surgery.

But another group of women with a positive mammogram have a less serious form of disease called ductal carcinoma in situ. The NCI webpage on this tumor says it is noninvasive, but some (uncertain) percentage of these can progress to an invasive form.

What is DCIS? It’s the most common type of non-invasive breast cancer, starts in the milk Ducts, has been termed a Carcinoma and is In Situ which means “in its original place.”

The NCI group who published the JAMA article terms it a premalignant condition and would prefer it not be called a carcinoma. Most of these lesions are small (~70% are less than 1 cm in size) and 80% are not found by breast examination, but show up on a mammogram.

Another NCI group, however, reviewed the medical literature on DCIS saying until recently the usual response to its discovery was a mastectomy. More recently there have been two randomized, controlled trials of breast-conserving surgery (lumpectomy) combined with radiation therapy and even more recently a double-blind prospective trial utilizing chemotherapy with the drug tamoxifen given daily for 5 years in addition to lumpectomy and radiation.

A control group had the surgery and radiation plus a placebo. The group that got tamoxifen did considerably better and other clinical trials are in progress.

The second group of tumors included colon cancer and cervical cancer. The statistics are fascinating. For colon cancer the incidence rate has gone down 31% and the death rate 45% and the trend is quite similar for cancer of the cervix (5 and 59% decrements)

We all have a colon, so let me focus on that cancer for a moment with a recent personal vignette.

My father had a large sessile polyp, a projecting growth without a stalk, in the very first part of his colon. It was initially benign, would have been difficult to remove and he was in his late 70s. so it was repeatedly observed and biopsied. Eventually it had a superficial layer that was cancerous. By then he was nearly ninety and the decision was to shave off layers until what was left was benign.

So that gives me a positive family history of colon cancer.

My previous colonoscopy (2006) was totally negative and without that family history my gastroenterologist would have said, “Come back in ten years.”

Some colon polyps are relatively easy to remove.

Some colon polyps are relatively easy to remove.

Because of Dad’s polyp, my GI doc wanted me back in seven years. And he was right; this time I had three small polyps, all of them benign and all on stalks (The technical term is pedunculated.), making them easy to snip off. I had decided to stay awake and watch and the procedure, while somewhat uncomfortable, was fascinating. I went home reasonably confident that my polyps were benign.

But there are three kinds of those colon polyps, according to the followup letter I received. Type one is of “minimal clinical significance.” Type two, which I had, is benign, but potentially precancerous. Early colon cancer screening for first-degree relatives is recommended. It was suggested I speak to parent (both dead), siblings (my only sib died at fifty-seven) and children (my daughter), so they can discuss colon cancer screening with their physician.

I copied the letter to bring to my daughter on a vacation trip we’re taking.

Type three is also benign, but there’s considerably more chance of it turning into a cancer.

So my next colonoscopy will be in five years this time.

If I had a totally normal colon at age 72, my GI doc had said he’d not suggest any more colonoscopies ever. My routine ten-year-interval next one would have been at age eighty-two and that, he felt, is too old to screen someone whose seventy-two-year-old colon was negative for any polyps.

But with their natural history of being potentially precancerous, the discovery of types two or three leads to a change in schedule and a family search is quite reasonable.

And, I take it, that’s why the incidence of colon cancer and the death rate from that malignancy have gone down over that thirty-five-year period. There’s presumably been better treatments developed for those who do end up with that form of cancer, but by dong colonoscopies and removing pre-cancerous lesions (i.e., polyps), we’re preventing many of them from altering into malignant tumors.

So those are examples of the group of tumors that are being discovered more often, but are causing fewer deaths and of one (colon cancer) that our screening is helping prevent.

I’ll write about cancer of the cervix and of thyroid cancer and melanomas next time.

 

 

 

Cancer Screening Part one: Incidentalomas & PSA

August 5th, 2013

I was reading the New York Times online today and noticed an important article in the Health section. A working group from the National Cancer Institute (NCI) had just published an article in the pre-print edition of JAMA that will likely change a highly significant face of medicine for many of us.

The issue is cancer diagnosis and, in many cases, over-diagnosis. Some pre-malignant conditions, in the viewpoint of this distinguished group, now come with the word cancer attached. That may lead to extensive testing, surgery or chemotherapy (or radiation therapy) and much mental anguish (and potential physical harm) for the patient involved.

Abnormalities, potentially malignant, can be discovered while scanning or even examining for something else. Dr. Peter Libby, chief of cardiovascular medicine at Brigham and Woman’s Hospital in Boston, a Harvard medical school teaching facility, wrote a June 8, 2010 piece in The New York Times titled “The ‘Incidentaloma’ Problem with Medical Scans.” A columnist for that paper had a CT scan for other reasons; a kidney mass was detected and a three-hour operation and eventually a six-inch scar ensued, yet the mass was benign. Dr. Libby’s review of the medical literature with his area of expertise in mind showed that greater than eight percent of cardiovascular imaging studies revealed incidental findings that led to further medical procedures.

His conclusion was we’re doing far too many CT scans.

Another physician wrote an April, 2011 piece in US News and World Report about a woman referred to him as a followup of an ER visit for abdominal pain that turned out to be viral gastritis. She too had a CT scan which showed her liver and intestines were normal, but one of her kidneys had a tiny mass, almost certainly a benign cyst. But the radiologist, while noting this lesion had all the features of something non-cancerous, covered his or her behind by saying, ”Cannot rule out malignancy. Clinical correlation required.” Translation: it was almost certainly nothing serious, but there was a very small chance that it might be cancer, and now it was the surgeon’s job to make sure it wasn’t.

But it’s not just those advanced radiologic procedures, or MRIs or other tests; It’s the mentality involved and that includes physical exams.

Let me give you a personal vignette. In 1969, as a second year clinical fellow in Nephrology, I went to see the Chief of Urology because of an abnormal lab test that involved my kidney function. A few questions later, he determined it was due to a diet I was on for a research project.

“But as long as you’re here, Peter,” he said, “I’ll check your prostate.”

It wasn’t quite normal, a tad bigger than it should have been. He said, “You’ll have a TURP (transurtheral resection of the prostate) by the time you’re sixty”

He recommended I monitor my symptoms (I had none at the time) and get repeat examinations at intervals.

Well, I’m seventy-two and haven’t had that surgical procedure. But what I did have, for many years, was a yearly digital prostate exam and, after 1994, a PSA (prostate specific antigen) blood test done periodically. At some point not only was the gland enlarged, but it the urologist involved thought it was also slightly asymmetric, so I had multiple biopsies, even though my PSA had consistently been less than 1.0, e.g., way below the level of concern.

All those biopsies showed benign (non-cancerous) tissue.

Now that I’m over seventy I don’t ask for a PSA test, wouldn’t agree with one if it were suggested and had my last digital exam of the gland several years ago.

But if I had that cancer at age 28 or 40, I would have been in real trouble. I would have been concerned about a malignancy that would likely kill me and would have welcomed any logical treatment for the disease. The NCI webpage on prostate cancer estimates nearly 240,000 new cases will be diagnosed in the United States this year and almost 30,000 men will die from that disease.

But the natural history of the tumor in most older men (>70 years old) is such that they will most likely die from something else (e.g., heart disease).

The NCI’s fact sheet on the PSA test is well worth reading. An initial statement is that the higher a man’s PSA level is, the more likely he has cancer of the prostate. Then the caveats begin: there are other reasons for the PSA to be elevated (I now have one of those, BPH or benign prostatic hypertrophy, an enlarged prostate). Half of all men over the age of fifty have BPH that is symptomatic with some hesitancy in starting their urine stream and/or a smaller stream.

If I had actually had cancer of the prostate at age sixty, my PSA may have been elevated. Then I would likely have had surgery to remove the tumor if it was localized to the gland and my physicians would then have periodically repeated my PSA testing to monitor if I had a recurrence of the neoplasm (a new and abnormal growth of tissue in some part of the body, especially as a characteristic of cancer).

A PSA level under 4.0 (nanograms/mililiter) was considered to be normal (my last PSA, done three years ago, was 0.7 ng/mL). In the past, if a man had a PSA level above 4.0 his physician  would have likely suggested biopsy to see if he had prostate cancer. But there are men who have that malignancy and yet have a PSA under 4.0 and, as I mentioned above, other, benign conditions can elevate the PSAwhile some medications used for BPH can lead to a lower PSA level. Only a quarter of those guys who have a prostate biopsy because of a PSA that’s elevated actually have cancer of the gland.

But now there’s considerable question whether PSA testing should be a routine, even though medicare and many private medical insurance plans cover a yearly screening using this test. The consensus seems to be that men should hear the pros and cons of the test before giving consent for it to be performed.

If 1,000 men in the 55 to 69 age range get screened with this test every one to four years, 100-200 will have false-positive results (no cancer, but an elevated PSA) and may have a biopsy recommended and, of course, worry about what’s going on with their prostate.

One hundred ten, according to the cancer.gov website, will be diagnosed as having prostate cancer and nearly half of those will have treatment complications (The National Cancer Institute website mentions sexual dysfunction, bowel or bladder control issues and infections.)

Four to five will actually die from prostate cancer, but five of every 1,000 who don’t have the screening will die from that cancer.

So the net is 1,000 have been screened to save 0-1 life.

And to further complicate things, the research done to determine what the normal upper limit of PSA is has largely been done in white men only.

So where do we go from here? There are studies being done to look at precursors of PSA, rate of change of PSA. free versus bound PSA etc.

We need  a better method to tell us if a man has a cancer or a benign prostate condition and to determine which prostate cancers are highly malignant fromt hose that are slow growing.

And all that’s just one cancer-screening tool.

 

Rabies Part one: background on a deadly disease

July 26th, 2013

Rabies is a viral disease affecting the brain and spinal cord, affecting warm-blooded mammals, passed to humans (the technical term is a zoonotic disease), with rare exceptions, via an animal bite , and, except for a very few recent cases, uniformly fatal in mankind.

It’s an ancient disease with written descriptions going back 4,000 years. A Codex (an early form of a book with individual handwritten pages on papyrus or vellum) in Mesopotamia described canine rabies ~3,400 years ago, but a timeline on the disease mentions dog owners in a Babylonian city being fined if their animal’s bites caused death, presumably from rabies,  nearly a thousand years before that.

In 1271 CE, rabid wolves in what is now Germany caused 30 deaths by attacking villagers. The disease was first reported in the Western Hemisphere in 1703 and caused canine rabies in Virginia in 1753.

In France, Louis Pasteur and a colleague, Emile Roux, started to work on a a vaccine for rabies in 1881. Roux made a candidate vaccine two years later using the spinal cord of an infected animal. In 1885 Pasteur, who was a chemist, not a physician, gave the vaccine to a nine-year-old child who had multiple deep bites by a rabid dog, saving his life. Over the next few years he inoculated over 700 people with only one failure (presumably a case where the virus had already reached the central nervous system). Donations helped start the institute named after him and rabies vaccination was launched widely.

You must vaccinate your dogs in order to license them

You must vaccinate your dogs in order to license them

Rabies in the United States has become a rare entity; we used to have more than a hundred case a year, but that fell to one to three each year by the 1990s. Previously one heard of rabid dogs; now, at a cost of over $300 million per year, an extensive vaccination program for companion animals has marked diminished their incidence, animal control programs are in place and rabies labs are maintained. Post exposure prophylaxis (PEP) used to involve a painful series of shots in the abdominal wall; newer protocols have been developed that are much less fearful.

We used to have to vaccinate our dogs every year and couldn’t get a city/county tag for them without proof of vaccination. Now a three-year canine vaccine is available. Since 1990 more cats than dogs have been found to be infected with rabies in the United States.

In the rest of the world rabies kills roughly 55,000 people every year with the vast majority of cases (95%) occurring in Africa and Asia. Almost all (97%) of those deaths start with a dog bite. India is “rabies central” with 20,000 cases a year. A 2001 law forbade the killing of dogs and Mumbai alone reported 80,000 people bitten by dogs in 2011. Strays survive on mounds of garbage, but Hindus oppose the killing of many kinds of animals. Scientists there are working on a canine contraceptive vaccine.

On the other hand Australia and Japan have eliminated rabies carried by terrestrial animals.

Here rabies is carried, not by dogs, but by bats (found in many parts of the country), raccoons in the eastern US, skunks in the north and south-central states (sometimes in the East), foxes in western Alaska and parts of Arizona and Texas as well as the East, and previously coyotes in the southern parts of Texas. Rabbits, rodents and hares rarely get the disease and haven’t been known to pass it to humans in the United States. Both raccoons and squirrels may carry a roundworm parasite that can be passed to humans and imitate rabies.

Opossums have a behavior to scare away predators (drooling, hissing and swaying), but are quite resistant to rabies.

In 2013 four Colorado livestock have been found to be infected with rabies, the most recent being a bull In Weld County a few miles to the east of where we live. The suspicion is a rabid skunk bit the bull. And in my county, where skunks exceed bats as the most common rabies carrier species, three adults and five children were recently bitten or scratched by a rapid kitten and got post-exposure prophylaxis.

I called a friend who has Shire (and other) horses, dogs and barn cats and she told me her son killed the seventh rabid skunk in the county several years back; since then all their animals have been vaccinated. She was aware that rabies vaccination is required at horse shows in some parts of the United States and at least four eastern states strongly recommend it for all horses. A 2008 Colorado State University online discussion of whether to vaccinate horses here mentions the sharp shift from bats to skunks as the common carrier species. Rabies here has also been found in raccoons, foxes and bison.

The World Health Organization, commonly known as WHO, has online recommendations for post-exposure prophylaxis (PEP). The administration of PEP should be prompt and local to the bite site, in an attempt to prevent the virus from migrating along nerves to the brain. In 2010 the PEP procedure was altered in the United States with one fewer dose of the vaccine being given.

Wound cleansing is crucial in rabies prevention. Animal studies have shown thorough attention to the wound markedly reduces the likelihood of rabies. For those who are not immunosuppressed and have not previously gotten PEP ( or been vaccinated because of high risk: e.g., veterinarians, spelunkers, international travelers to places where rabies is common), one dose of rabies immune globulin and four doses of rabies vaccine are given over a two-week period.

Survival from rabies wasn’t reported until recently.

Don't handle bats unless you're an expert

Don’t handle bats unless you’re an expert

In 2004 an adolescent American girl developed rabies (after handling a bat and being bitten by it), was placed into an induced coma and received a variety of medications to temporarily suspend brain function and fight the virus. She survived, graduated from college in 2011 and has a 2013 website describing her illness. The “Milwaukee protocol,” first tried in her and subsequently modified, has now been used on a total of forty-one other rabies patients worldwide with one source saying five survived.

The care involved is detailed and incredibly expensive; one report says $700,000 was spent in a futile attempt to save one patient.

I’d certainly get PEP after a bite if the animal involved had rabies. However, that’s not always obvious, even in bats; a recent study at the University of Calgary found roughly one percent of bats sampled had the virus. A comment from the report was that bats seldom come in contact with humans, so I think those that do in unusual settings should be suspect.

So vaccinate your animals and be wary of any with abnormal behavior.

 

West Nile: background and 2013 updates

July 22nd, 2013

We were a ways up in the mountains for a dinner yesterday and I cautioned the people who were hosting that mosquitoes could easily be found at their 7,600 foot level. I said the West Nile season was usually in August and September, but one of my gourmet group told me there had already been a first case in Colorado and West Nile positive mosquitoes in our county. What I discovered online was 94% of West Nile symptomatic cases occur between July and September.

Heed the warning!Today I found the West Nile advisory page for Larimer County where we live and the CDC’s West Nile statistics that mention 23 cases nationwide through July 16th with three deaths. Forty-three percent of the patients had West Nile Neuroinvasive Disease (WNND); the others had West Nile Fever (WNF). Twenty-nine states and the District of Columbia have reported human disease thus far.

And it’s still early in the Summer of 2013.

Then I went back to the last of the four articles in the July 17th edition of JAMA; this one covers information intended for physicians and goes into more depth than the others. Its title is West Nile Virus: Review of the Literature. I thought there would be a few nuggets of information that might be useful for an extended audience

To start with, West Nile is endemic in every state in our country except Alaska and Hawaii. That means it is found in each of those regions on an ongoing basis without the need to be imported each year. An example I found said chickenpox is endemic in the UK, but malaria is not. Canada has had no cases of either WNF or WNND thus far in 2013, but had 428 cases last year with five provinces reporting patents with the virus.

Here it is a much more frequent disease problem that has led to the three worst outbreaks of arbovirus neuroinvasive disease in US history, each leading to ~3,000 cases of encephalitis, meningitis or sudden onset of severe muscle weakness (AKA acute flaccid paralysis). Arboviruses are those carried by ticks, mosquitoes and similar species. Older adults don’t have a greater chance of developing WNF, but a markedly increased chance of WNND. One of fifty who catch West Nile and are over 65 get this dire form; that’s sixteen times the rate for those age 16 to 24. The death rate in patients with WNND is ~10%, lower in relatively young patents, higher in the 65+ age bracket: one series reported 0.8% mortality for those under 40 and 17% for patients over 70. It’s unknown how the virus crosses the blood-brain barrier, the super-tightly-packed cells that line the brain’s blood vessels, preventing passage of most substances.

2012 was a really bad year for human disease in this country. The CD’s final summary for that year included 5,674 cases, with 2,873 of those being WNND, and 286 deaths. The state of Texas had 37% of all reported cases and California, Louisiana, Mississippi, Michigan, Oklahoma and South Dakota were also hot spots for West Nile.

The virus has been found in over 325 bird species in the US and 65 different mosquito species, but only a few members of the Culex mosquito family have been shown to transmit West Nile to humans. Culex mosquitoes bite us from dusk to dawn, so, as I mentioned in my last post, I’ve changed what I wear when outside during those hours.

Passerine (perching) birds can infect mosquitoes; the robin isn’t as plentiful as some species, but has a high serum viremia (lots of the virus in its blood), so is an important reservoir. If we are bitten by an infected mosquito and go on to develop WNF we’d have a low serum viremia, so a second mosquito biting us won’t get the virus from us. Mosquito bites are responsible for almost all human cases; rarely one can occur after an organ transplant or a transfusion.

Higher-temperature areas both shorten the time a mosquito infected with the virus becomes infectious when it bites again and also improve the efficiency of it transmitting the virus to a bird. Of the 5 lineages of the virus only two have caused significant human outbreaks, but the 1999 New York City lineage has genetically altered subsequently to improve viral transmission. I don’t know if this is true worldwide, but there have been significant outbreaks in Russia, Israel, Greece and Romania since the early 1990s.

Most who get a West Nile infection, as I’ve mentioned before, remain subclinical (e.g., without enough symptoms to need medical attention). In a study of blood donors who had West Nile viremia, but no significant symptoms initially, 38% eventually saw a physician and 2% were hospitalized. Only 5% of those seeking a diagnosis got the correct one!

West Nile in pregnancy, in one study of 71 women who delivered 72 babies, did not result in any malformations or infected infants.

Fatigue may last a long time.

Fatigue may last a long time.

Full recovery is the norm for those who have either uncomplicated WNF or meningitis, but they may be fatigued for a considerable length of time. In a 2004 study of 98 patents, almost all had this symptom and its median duration was 38 days. The patient’s age didn’t predict the duration of symptoms.

There are four licensed equine vaccines, but none for us. Several candidate human vaccines have gone through early trials, but no large-scale clinical trials have been attempted. Given that, if amazes me that even during outbreaks few of us use insect repellents that have proven efficacy.

If this West Nile season is like last year’s, please heed the warnings, empty the water containers at intervals, avoid gardening at dusk or later and use an insect spray.

The brain and even the life you save may be your own.

 

 

 

West Nile: sex and the single mosquito

July 21st, 2013

Given that mosquitoes can carry a variety of diseases, West Nile among them, I wondered how best to deter them from biting us and transmitting viruses and other pathogens?

Now this would "bug" me

Now this would “bug” me

Let’s start with a brief overview of their life cycle. Most adult female mosquitoes must have a blood meal in order to lay eggs. Thus they are the only ones who bite us and other animals (Males feed on plant juices and unlike humans, apparently don’t extend their life span by doing so.) They live about a week, whereas their other-gender “mates” may live a month. They mate rapidly, finding each other by sound (males and females will match wing-beat sounds) and inseminated females will not mate again. That doesn’t hold true for the males, but some may lose their sexual apparatus in mating.

The females show a distinct preference as to where they lay their eggs; this varies by species, but must be on water. Of the 2,500 plus species worldwide and the 150 species of mosquitoes found in the United States, this water varies in quality, but can reside in almost any form of container you can imagine. The eggs are laid one at a time, but for the species we’re concerned with (West Nile vectors), they stick together to form egg rafts and hatch within 48 hours.

The next stage is called a larva. These larvae live in the water feeding on organic matter/microorganisms, but come to its surface to breathe. They shed their skin several times before becoming pupae, a non-feeding developmental stage which eventuates as an adult mosquito about two days later.

So we humans have some time in which we can interrupt their growth into the potentially disease-carrying adult females. These are not highly selective diners, but may feed on man, many domesticated animals, birds, some wild animals (e.g., deer and rabbits) and snakes, frogs, toads or lizards.

One of the easiest, very low-tech methods, is to keep track of water-containing vessels around your home and change the water every few days. I spotted the obvious ones (mentioned in my last post) and emptied the dog water dish into two potted plants and changed the water in our bird water container, spilling that onto the lawn a flight down.  But that may have been insufficient. I don’t know if any larvae in the pots would survive, though I doubt it, but I also put the hose into two larger containers that tomatoes are growing in. The fluid goes down a plastic pipe and spreads out into the dirt the plants are sprouting from. Could that be an area where mosquito progeny could live?

Since I’m discussing West Nile I’ll focus on Culex mosquito preferences Their eggs are laid on either fresh or stagnant water in ditches, creeks, puddles, tin cans, barrels and those are preferably sheltered from high winds (which we frequently have here) by weeds or grasses. The females lay the eggs at night, one at a time, to form rafts of two to three hundred edges which then hatch within 24 hours.

spray yourselves and your kids as well, but ask your pediatrician about little ones.

spray yourselves and your older kids as well, but ask your pediatrician about little ones.

Culex mosquitoes prefer to attack at dusk and after dark and are prone to enter buildings for blood meals. They only live a few weeks during the warm summer months. The Illinois Department of Public Health webpage on mosquitoes says they bite dogs and transmit heartworm disease to them, but the only canine case of West Nile I was able to find was from Africa in 1982. I’ll keep looking, but won’t worry about our Tibetan terrier as a reservoir for the virus. The Illinois website has lots of tips for reducing mosquito populations in your immediate area and thoughts on protecting yourself. I may change my short (I walked him 97 minutes starting at 6:35 a.m. today) late evening final-dog-walk of the day clothing from T-shirts to long sleeves and spray myself with DEET.

There are a variety of pesticides available; some of the commercial ones, for environmental use rather than personal spraying, are very toxic. That’s particularly a poignant question now when pesticide tainted school lunches in a village in India recently killed at twenty-three youngsters. That turned out to be a concentrated form of an organophosphate called malathion. It interfere with nerve signals in the bugs and kills them. Other chemicals include a triad compound marketed as Duet (Why isn’t it called Trio?). Current spraying is at night in ultra-low volume and the chemicals are broken down by light and soil, usually within hours of being applied according to a JAMA patient page from the July 17, 2013 edition. My take on the subject is there should be public announcements of such chemical application and I’d stay in that night.

We’re driving up to ~8,500 feet elevation for a meal with our gourmet club today so I wondered if that altitude made up safe from mosquito bites. I Googled the questioned and found a local source for an answer.

According to the Colorado State University Extension page on West Nile Virus: Culex tarsalis, one of the main West Nile virus vectors, commonly occurs up to altitudes of 8,500 feet and is found as high as 10,000 feet above sea level. Other potential vectors are more common above 8,500 feet and can be found well above this elevation. On the other hand, the transmission season becomes shorter as elevation increases, which probably reduces risk significantly. Given the lack of knowledge and experience with this disease in Colorado, it is prudent to use an effective repellent when mosquitoes are active, even at these higher elevations.

I remembered that while we were away I had seen a piece in The New York Times (that comes on my iPad) that would apply to preventing West Nile, “A Low-Tech Mosquito Deterrent.” According to this article mosquitoes fly at 1 to 1.5 miles an hour and a small rotating fan blows air at 10-15 MPH. It also disperses the chemical clue (our exhaled carbon dioxide) that female mosquitoes use to find their prey. So next time I plan an outdoor party in our yard, I’ll bring out the extension cord and put up a fan.

I mentioned this article to a friend at our health club and he said, “I already have a fan going in our bedroom at night; I’m going to buy another one for our son’s room.”