Archive for July, 2013

Rabies Part one: background on a deadly disease

Friday, 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

Monday, 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

Sunday, 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."

An enemy returns: East of the Sun and far West of the Nile

Friday, July 19th, 2013
epidemic warnings come late; prevention is better

epidemic warnings come late; prevention is better

We came home from a short trip to Texas and I realized my weekly copy of JAMA had four articles on West Nile disease, its complications and possible prevention. After several years of relative quiescence, West Nile was back with a vengeance in 2012. Between the original New York City outbreak in 1999 and 2010 the virus has been endemic in the United States with intermittent flares, overall infecting an estimated three million Americans, causing West Nile fever (WNF) in 780,000, the much more severe West Nile neuroinvasive disease (WNND: e.g., involving the brain and other portions of the nervous system)  in 16,196 and killing 1549 of those.

Until 1999, the West Nile virus lived, mostly in birds, in Africa, Europe and Asia, but was not known to be in the Western Hemisphere. Its hosts (reservoirs) were bitten by mosquitoes whose name comes from the Spanish or Portuguese for "little fly," but some think this insect is the most dangerous creature on earth as it also transmits malaria, yellow fever and a variety of encephalitis-causing illnesses (inflammation of the brain). The mosquito in turn can pass the virus on to another bird or to a human

A 2001 article in the New England Journal of Medicine reviewed the original Western Hemisphere outbreak, the 1999 epidemic in New York City. It began with two patients hospitalized for encephalitis in the New York City borough of Queens. A preliminary epidemiologic search of nearby hospital admissions revealed six more cases. All eight lived in a sixteen square mile area in northern Queens and all had participated in evening outdoor activities (e.g., working in their gardens).

A search of their environments showed breeding sites for the particular species of mosquitoes known to carry St. Louis encephalitis (its vector), so the mini-epidemic was presumed to be an arthropod-bourne disease (The term arthropod include insects, spiders and crustaceans such as lobsters and crabs.) Mosquito control measures were promptly begun.

Eventually fifty-nine New Yorkers were hospitalized in August and September of that year with this outbreak. Although their ages varied from 5 to 90, the median age of these severely ill patients was 71 (NB. The "mean" is the "average" you're used to, where you add up all the numbers and then divide by the number of numbers. The "median" is the "middle" value in the list of numbers, so in this case there were as many patents over 71 and under that age).

The overall attack rate of West Nile in this outbreak went sharply up with age. Nearly two-thirds of those affected had encephalitis with altered mental status along with fever and abnormalities in their cerebrospinal fluid (CSF, the fluid that cushions the brain and spinal cord, bring it nutrients and removes waste products). Some of those had moderate to severe muscle weakness and/or meningitis (inflammation of the membranes that cover the brain and spinal cord) with fever, abnormal CSF findings, headache and stiff neck symptoms.

Seven of the fifty-nine (12%) of those with the disease died and those over age 75 were especially prone to death in this epidemic. Diabetes was another risk factor for mortality.

At the same time, there was a seemingly unrelated fatal illness occurring in the area's birds, especially in crows. The connection initially was missed as St. Louis encephalitis doesn't usually kill off its avian reservoir hosts.

Eventually the West Nile virus was identified in tissue specimens taken from both crows and a Chilean flamingo that had died at a zoo in the vicinity.

Within five years the virus had spread to all forty-eight contiguous states and several provinces in Canada. There were major flares of WNF and WNND in 2002 and 2003 with almost 3,000 cases of WNND in those years.

Then things calmed down and, as is typical, the money available for mosquito control became less abundant. The disease spread to Argentina by 2005 and eventually to most of the Western Hemisphere countries. Strangely only the United States (and Canada) suffered major epidemics.

And then came 2012.

Dallas County had a population of nearly two and a half million humans; of those 255 developed WNF, another 173 got WNND and 19 of those died. The review article, published in the July 17, 2013 edition of JAMA, states there was "An usually rapid and early escalation of human cases (which) followed infection trends in mosquitoes."

As in the rest of the country, Dallas had experienced a considerably warmer than usual winter. Ever since 1966, when aerial spraying for mosquitoes was instituted for an epidemic of St. Louis encephalitis, researchers in the metropolitan area had a heightened awareness of arthropod-bourne disease. Blood studies of residents in a Dallas area prone to flooding had shown there had been recurring epidemics of related virus-caused illness.

As West Nile virus supplanted its predecessor, Dallas began to experience cases of WNND and to prepare for its flares. In May 2012 a mosquito trap yielded evidence of West Nile-infected insects and all area physicians were sent a recommendation to test patents with symptoms of potential WNND for the virus.

A "vector index" was developed and calculated weekly; the specific of the math doesn't matter, but it related to how many of the particular mosquito species which was the region's primary carrier of West Nile virus, Culex quinquefasciatus, were found and their infection rate. Human cases of WNND were noted to follow the vector index peaks by one to four weeks.

One means of prevention: avoid being bitten

One means of prevention: avoid being bitten

An 8-day aerial spraying of insecticide did not lead to an increase in emergency room visits for asthma or other respiratory problems, or, for that matter, to skin rashes.

As of today I'm unaware of any human vaccine for West Nile or any treatment for the disease other than supportive measures.

So what can we do to prevent WNF or WNDD?

At present our only method is to control the mosquito population and avoid being bitten. I decided to change the drinking water we put out for the birds we feed and any dog water that's outside every other day. And we don't garden in the evening.

I'll mention one other, low-tech preventive measure in my next post.










team-based home blood pressure control

Wednesday, July 10th, 2013

I was reading the July 3, 2013 edition of JAMA and came across an article and an editorial on better ways to manage elevated blood pressure (BP). The basic concept stems from data reviewed by the CDC in a 2012 online publication: high BP, AKA hypertension, is a major risk factor for both stroke and cardiovascular disease which jointly are the number one causes of preventable death in the United States.

Check your blood pressure and let your healthcare team know the reading

Check your blood pressure and let your healthcare team know the reading

Do you know what your BP is? Let's start from scratch with the kind of numbers you might hear about when you see your doctor or have your BP checked in other settings (e.g., the grocery store we usually shop at has a free automated system for BP measurement).

My BP usually runs about 116/ 68, but, similar to yours and everyone else's, my BP varies from those numbers from minute to minute. The top number, called my systolic pressure is always higher than the lower (diastolic pressure) It measures pressure in my arteries when my heart contracts (beats) while the bottom number measures it between heart beats when that muscular organ is resting and refilling with blood about to be pumped out to the rest of my body. The American Heart Association has a nice webpage explaining BP.

I'd like to see BPs under 120/80 and that seems to be a reasonable consensus figure in articles I read. Hypertension (HTN) is conventionally defined as a BP higher than 140/90 and the National Heart, Lung and Blood Institute's website calls any BP between 120/80 and 140/90 prehypertension. That's new to me, as the designation used to be applied to those with BPs between 130 and 139 for the upper number and 85 to 90 for the lower one. But I retired in 1998 and the BP goals changed in 2003.

My 2006 copy of Kaplan's Clinical Hypertension, the ninth edition of this amazing, mostly one-person work by a senior professor in Dallas (I just ordered a used copy of the 2010 tenth edition), mentions that 120-129/80-84 used to be considered normal  and 130-139/85-89 was thought to be borderline. But the 2003 report of the Seventh Joint National Committee  put BPs anywhere over 120/80 into the new category saying it wasn't a disease, but a designation to identify those at high risk of developing hypertension.

So what if one of your numbers is in this range, but not the other? The Harvard Medical School's Family Health Guide article on prehypertension notes that BPs vary from time to time and from arm to arm. If you have BP numbers over 120/80, the classification will depend on your average/usual readings, not the extremes. They suggest you always use the systolic or diastolic number that puts you in a higher category (normal, prehypertension, hypertension).  So, for example, if your average is 124/76 or 118/83, you're in the prehypertensive group

The CDC paper and others say the overall prevalence (i.e., the proportion of a population having a disease) of HTN in America is ~30%, but that increases with age with many estimates stating it's 70% in those of us 65 and older. That group is more prone to systolic HTN with only the upper number being elevated. That's still high BP and dangerous.

Treatment of HTN with diet, weight control and meds is associated with considerable decreases in the dire consequences of uncontrolled HTN: strokes, heart attacks and congestive heart failure (a condition where your heart can't pump out enough blood to keep up with the needs of your body).

All of us should be screened for HTN, even if our BP is less than 120/80. Screening intervals should be at least every two years for those with normal BP and every year for people with prehypertension. Your physician will also consider your other risk factors (weight, age, gender, your blood lipid levels {e.g., total cholesterol, HDL and LDL levels} presence or absence of diabetes, heart disease or chronic kidney disease, exercise patterns) and may, in some case recommend drug therapy even if your BP is <140/80. That's especially likely for those with any of the three chronic diseases I just mentioned.

So do we all need to be on medications if our BP is >140/80 (no, your physician may start with non-pharmacologic modalities such as cutting our salt intake) and if we do start on BP meds how often do we need to see our doc? After all, they're really busy these days and we may not be able to get an appointment for several months.

Let me start with my own experience (in the "Dark Ages") and then come up to the present.

When I was in my first Air Force assignment at Langley AFB, VA from 1970 to 1972, I set up a HTN clinic run by a public health nurse, an RN with extras training who didn't want to be a ward nurse. My immediate boss was a cardiologist and, after I set up protocols (e.g., which meds to start with, appropriate followup intervals for various levels of BP, when to call for help), our nurse felt quite comfortable running the BP clinic.

She didn't see other kinds of patients, got very savvy about HTN, read a lot of the current medical literature on the subject, was entirely at ease with calling either of her two consultants whenever she had a question and our HTN patient population could easily get appointments in her clinic.

Fast forward ~forty years.

In 2011 a Veterans Administration group from Durham (coincidentally a place I worked when I was a resident and nephrology fellow at Duke) published an article in the Archives of Internal Medicine (now called JAMA Internal Medicine). Its title was "Home Blood Pressure Management and Improved Blood Pressure Control: Results From A Randomized Controlled Trial."

In brief they followed nearly 600 HTN patients who were randomized into one of four groups. The first had usual care, i.e., being seen in a primary care clinic at intervals. The other three groups involved nurses who administered behavioral management concepts, worked with docs on medication management or did both. The patients had their BPs monitored at home with data transmitted to the researchers. Incidentally 48% of the patients involved were African American.

Overall the research group felt the intervention effects were moderate, but those patients who started with the worst BP control had much better resultant effects.

there are a number of options for HTN meds

there are a number of options for HTN meds

Now there's the new JAMA article, "Effect of Home Blood pressure Telemonitoring and Pharmacist Management on Blood pressure Control: A Cluster Randomized Clinical Trial." Researchers associated with an integrated health system in Minnesota using electronic medical records, noting that typically only half of HTN patients have adequately controlled BPs, followed 450 patients, roughly half of whom got usual care. The other half got home BP telemonitoring and had PhD pharmacologists following their data and making changes in their BP meds by a protocol worked out with physicians.

BP control was better in the latter group at 6 and 12 months and was even better 6 months after the year-long study ended.

Lesson one: other healthcare professionals can manage HTN. Lesson: doing this via home BP measurements may be the path of the future.

Typo and autocompletion error

Sunday, July 7th, 2013

I just looked at my last post and found one typo (agreement on subject and verb) of minor consequence and one instance where my MacBook Pro's autocompletion feature changed the meaning of a sentence.

I get frustrated when the latter happens. In this case it was referring to the Harvard Health Publications editor's review of several articles. I clearly did not mean for the word "artless to be substituted for articles.




Marijuana and Schizophrenia: What's the association?

Saturday, July 6th, 2013

My wife called my attention to an editorial page piece in the July 2, 2013 edition of The Wall Street Journal linking marijuana use to schizophrenia. I at first wondered who the paper had chosen as a distinguished medical figure to write on his or her research study of the association between use of this drug and the most severe mental illness, but read the commentary and realized it was written, not by a professor, but by a Yale psychiatry resident in training.

Having been a Duke resident more than 45 years ago, I was aware that young physicians at major teaching centers might, as I did, see a particular spectrum of the general patient population, in many cases the most ill portion of it.  Therefore I was less than certain of the strength of the basis for his viewpoint, but felt it was a highly significant topic and it was well worth perusing the literature pro and con.

Does this cause mental illness?

Does this cause mental illness?

In 2010 Time magazine published a well-balanced article titled "The Link between Marijuana and Schizophrenia." That led me to several medical research reports, but the lay press article itself was interesting.

It commented that studies showed those who were diagnosed with schizophrenia were approximately twice as likely to be marijuana smokers than groups who didn't have this dire diagnosis. Some studies, viewing things prospectively, suggested (note the word, please) that pot smokers were at double the risk of developing schizophrenia as those who never smoked the drug.

But, as the Time article noted  the portion of our US population diagnosed with this debilitating illness has remained constant at roughly 1%, and the current National Institute of Mental Health (NIMH) web-based discussion of schizophrenia agrees with this figure. It mentions that some drug abusers exhibit symptoms like those of patents with schizophrenia, but NIMH states that most researchers do not think that drug abuse is the cause of this mental illness.

A short piece from the CDC on childhood mental disorders in JAMA  for July 3, 2013, confirmed that schizophrenia is way down the list of mental disorders in US children. On the other hand, ADHD, behavioral/conduct disorders, anxiety, depression, use of illicit drugs or alcohol or cigarette, autism spectrum disorders and even Tourette syndrome (a neurologic disorder characterized by tics {repetitive involuntary movements and vocalizations} are listed as affecting multitudes of our youth.

In any given year, according to the CDC article, up to one fifth of our kids and adolescents have a mental disorder, while inpatient admissions have sharply increased for both mental health and substance abuse problems, especially for "mood disorders," e.g., anxiety and depression.

But there may be a subset of marijuana-using/abusing youngsters that merits special attention.

A 2011 Harvard Health Publications (HHP) blog piece by the then editor of the series, a woman whose bachelors degree was not in a medical field, but had a brother who developed schizophrenia, is titled "Teens who smoke pot at risk for later schizophrenia, psychosis."

I was concerned that she might have a biased slant on the disease, but impressed, as I read her blog piece by the articles she cited.

But then I went back to the articles themselves, as I routinely do. The first was in the British Medical Journal in 20111 and was a population based cohort study, a comparison of two different groups. The outcome was the "incidence and persistence of sub-threshold psychotic symptoms after adolescence." The verbiage used was that the use (and especially the continued use) of cannabis was a risk factor for developing severe mental illness.

I'd read the study as showing kids who end up psychotic often have smoked (or otherwise used) marijuana.

The second article cited was from the Archives of General Psychiatry, again a 2011 publication and was a meta-analysis (a study of a number of articles). The authors reviewed a large number of published research studies, picked 83 of them which met their standards for inclusion and pooled the results for statistical purposes.

That's a common way to look at data in order to have enough of it to reach a significant conclusion, which in this case was that the age of onset of psychosis was 2.7 years younger in the group who used cannabis.

Once again, that's only an association, but not a proof of causation.

The third article came from Lancet (in 1987) and was the result of  long-term followup of 45,550 Swedish military conscripts. Those who had smoked pot more than fifty times had a much higher rate of developing serious mental illness.

I want to go back to the blog in Harvard Health Publication, because here's where I have to differ with the author. Her statement that, "So far, this research shows only an association between smoking pot and developing psychosis or schizophrenia later on" makes sense; she admits the data don't prove marijuana causes psychosis.

But in the very next paragraph, she compares this research to that on cigarette smoking first being noted to be associated with lung cancer and later found to be a major cause of that disease.

Do troubled youngsters choice to smoke pot or does smoking it cause later troubles?

Do troubled youngsters choice to smoke pot or does smoking it cause later troubles?

Don't get me wrong; today's marijuana is reputed to be much stronger than that which was around when I was a young research fellow and volunteered time at the Long Beach Free Clinic. And some of the studies I've read in the last week would certainly make me want to caution a teenager with a family history of schizophrenia that pot smoking is really risky for them.

Maybe we're going to see an epidemic of the disease in those of our younger generation who smoke marijuana and don't any family history of schizophrenia or other major mental illness.

But I sure haven't see any data yet that convinces me that's going to happen.

Lyme disease: the battle continues

Wednesday, July 3rd, 2013
Stay away from ticks

Stay away from ticks

In April of 2012 I wrote a series of posts on tick-borne diseases. This is my 315th post so when the subject of chronic Lyme disease (called post-treatment Lyme Disease syndrome {PTLDS} by the CDC) came up in a well-balanced article in The New Yorker I needed to revisit what I had written 14+ months ago before I could determine if there was anything new on the subject.

It delineates the ongoing controversy which basically comes down to whether chronic Lyme disease actually occurs. Most academic physicians and organizations deny that this exists, but a large group of patents with a multitude of long-term symptoms have interacted with physicians who are willing to treat such an entity. They've formed an International Lyme and Associated Diseases Society who "argue that the traditional approach to diagnosis and treatment, put forth by most American physicians, all but guarantees failure."

A pamphlet from a group formed to fund-raise and increase awareness, the Lyme Action Network, is titled "It Might Be Lyme." The multitude of symptoms under this rubric is astounding as is the conclusion that years of (often intravenous and horrendously expensive) antibiotic therapy is needed to ensure a cure of the ailment.

The author of the New Yorker article was recently interviewed by Terry Gross on NPR. He comments that our current state of knowledge of the illness is incomplete, but notes that the symptoms of many of those who are said to have "chronic Lyme" are vague, commonplace and difficult to attribute to this disease when there are no positive tests and/or they don't live in region of the country known to have Lyme disease.

Let's start with a comment. I found only one medical article that shifted my point of view even a tad bit.

A research group headed by a Johns Hopkins-associated physician with infectious disease training published a study of patients with PTLDS symptoms in a journal I've never heard of before: Quality of Life Research.

His group enrolled 63 patients with the skin manifestation of Lyme disease and systemic symptoms (therefore people with pretty clear-cut diagnoses to fit the ailment) in a prospective cohort study. They followed this group and the control subjects for six months and saw each of them five times. After conventional treatment with a three week course of the antibiotic doxycycline all signs of Lyme disease went away, but after six months slightly over a third of the patents had new-onset fatigue, one fifth had widespread pain and 45% had neurocognitive problems (thinking issues that relate to a particular part of the brain).

This is the first article I've seen that prospectively followed patients with Lyme disease, but my caveats are: it was a small group (63 patients) with obvious Lyme disease and the followup period is relatively short.

I'd like to see a considerably longer prospective study of a much larger group.

Don't wait until the tick has finished its meal

Don't wait until the tick has finished its meal

The introduction to the article mentions that Lyme disease is caused by a spirochete bacteria (therefore a long, coiled member of the same family as the syphilis, but there hasn't been human to human spread that I'm aware of and of course, Lyme is not  a venereal disease). It is  the most common vector-borne (transmitted by a blood-sucking insect or arachnid (mites or ticks) infectious disease in North America. In 2009 nearly 40,000 cases were reported in this country, but most feel that there are likely at least 100,000 cases a year.

There are four other, less prevalent, illnesses that the deer tick vector can transmit, but funding for control of ticks is regarded as low especially when compared to that in Massachusetts for mosquito control in an effort to prevent other ailments, especially West Nile virus and eastern equine encephalitis.

Many academic physicians with infectious disease training feel strongly that Lyme disease should be treated with antibiotics for a month or less in most cases with an exception made for those who develop Lyme arthritis (who may require up to three months of treatment).

After realizing I hadn't done my due diligence, it was time to read lots of background material, including the article in The New Yorker. I downloaded the Kindle edition of Lyme Disease: The Ecology of a Complex System, a 2010 book written by Richard Ostfield, a Ph.D. field biologist.

This is a fascinating opus written from a different point of view, one of a scientist working at the Cary Institute of Ecosystem Studies, a private, not-for-profit in New York state with research focusing on the interactions among organisms that influence the risk of human exposure to vector-borne diseases.

Dr. Ostfeld outlines the natural history and ecology of LD and shows it is a much more convoluted ailment than I had realized. I had thought that the bacterium, the vector and the host were those I had read about, namely Borrelia burgdorferi, the black-legged tick and the white-footed mouse. But just focusing on the potential host species, chipmunks and shrews may carry the microorganism and the tick bites or tries to bite other animals, some of which are "less-efficient/competent reservoirs." So white-tailed deer and robins, depending on their abundance or lack thereof, may play a role in the likelihood of your catching LD, as may the terrain (e.g., densely forested versus subdivided into patches).

We had dinner recently with friends and one of the number was a physician who works for the CDC and has lectured extensively on Lyme disease. He feels quite strongly that the viewpoint of many of those who espouse long-term antibiotic therapy for LD is influenced by financial reward and that data is lacking to prove that this entity exists.

Allen Steele, the doctor who first discovered Lyme disease, now a rheumatologist at Massachusetts General Hospital, is the country's foremost Lyme disease researcher. These days he finds himself distrusted and sometimes harassed by those who feel Lyme disease often has chronic manifestations. A June 2, 2013 article in the Boston Globe highlighted the issue with its title "Drawing the lines in the Lyme disease battle."

I certainly don't agree with a fringe view  I found claiming that the LD bacterium was weaponized for bio-warfare.

At the end of my reading I side with the more traditional, academic view of Lyme disease. I think the other group has yet to prove its case.




A valid comment on aspirin withdrawal

Wednesday, July 3rd, 2013

I get tons of comments that come from for=profit websites or email addresses  that bounce.

But last month I received one that made sense, asked for links to medical sites and got those in a subsequent email.

Thanks, Rosey.



Hi Peter,
so far these are the papers I've found on the subject of withdrawing from aspirin:

and I've cut&pasted a quote below from

"There appears to be a rebound from reversing the “blood thinning” effects of aspirin when it is stopped suddenly. Over three times the expected risk of stroke occurs in patients with a previous history of heart disease when they suddenly stop taking aspirin.13 A similar increase in risk of heart attack has been reported when aspirin was stopped.

No one has determined a safe regime for discontinuing this therapy. I suggest that people needing to stop long-term use of aspirin should do so slowly. Since as little as 30 mg (1/3 of a baby aspirin) will deactivate all of the body’s platelets, slow withdrawal should begin at about this level. Cut a baby aspirin into quarters (now 20 mg). Take 20 mg then wait for 4 days to take the next 20 mg dose. Increase the interval between 20 mg doses by one day until a 10-day interval between doses is reached, and then stop taking the aspirin. This is not an easy task since the tablets are so small. Reduction or discontinuation should be done after obtaining a doctor’s advice on the risks and benefits for each individual patient. Even before reducing the aspirin, patients should change to the McDougall Diet in order to most effectively reduce their risk of strokes and heart attacks."

"13) Maulaz AB, Bezerra DC, Michel P, Bogousslavsky J.† Effect of discontinuing aspirin therapy on the risk of brain ischemic stroke.† Arch Neurol. 2005 Aug;62(8):1217-20."

(This reference is the first link above)
I haven't been able to find any other advice from doctors and scientists on how to safely get off aspirin without these risks.
Thanks for your interest,
Rosemary Faire