Archive for September, 2009

On Vitamin E and anecdotes

Monday, September 28th, 2009

   A better man than I am said:

   "I think the educational and psychological studies I mentioned are examples
of what I would like to call cargo cult science. In the South Seas there is a
cargo cult of people. During the war they saw airplanes land with lots of good
materials, and they want the same thing to happen now. So they’ve arranged to
make things like runways, to put fires along the sides of the runways, to make
a wooden hut for a man to sit in, with two wooden pieces on his head like
headphones and bars of bamboo sticking out like antennas – he’s the controller
– and they wait for the airplanes to land, exactly the way it looked before.
But it doesn’t work. No airplanes land. So I call these things cargo cult
science, because they follow all the apparent precepts and forms of scientific
investigation, but they’re missing something essential, because the planes
don’t land.
   "Now it behooves me, of course, to tell you what they’re missing. But it
would be just about as difficult to explain to the South Sea Islanders how they
have to arrange things so that they get some wealth in their system. It is not
something simple like telling them how to improve the shapes of the earphones.
But there is *one* feature I notice that is generally missing in cargo cult
science. That is the idea that we all hope you have learned in studying science
in school – we never explicitly say what this is, but just hope that you catch
on by all the examples of scientific investigation. It is interesting,
therefore, to bring it out now and speak of it explicitly. It’s a kind of
scientific integrity, a principle of scientific thought that corresponds to a
kind of utter honesty – a kind of leaning over backwards. For example, if
you’re doing an experiment, you should report everything that you think might
make it invalid – not only what you think is right about it: other causes that
could possibly explain your results, and things you thought of that you’ve
eliminated by some other experiment, and how they worked – to make sure the
other fellow can tell they have been eliminated.
   …
   "The easiest way to explain this idea is to contrast it, for example, with
advertising. Last night I heard that Wesson oil doesn’t soak through food.
Well, that’s true. It’s not dishonest, but the thing I’m talking about is not
just a matter of not being dishonest, it’s a matter of scientific integrity,
which is another level. The fact that should be added to that advertising
statement is that *no* oils soak through food, if operated at a certain
temperature. If operated at another temperature, they *all* will – including
Wesson oil. So it’s the implication which has been conveyed, not the fact,
which is true, and the difference is what we have to deal with."
   …
   "The first principle is that you must not fool yourself – and you are the
easiest person to fool. So you have to be very careful about that. After you’ve
not fooled yourself, it’s easy not to fool other scientists. You just have to
be honest in a conventional way after that." – from "Surely You’re Joking, Mr.
Feynman!", Bantam Books, 1985.

   I’ve been the target of a rising tide of attacks for my snide ridicule of
someone who contended that application of Vitamin E to an abrasion would cause
it to heal more quickly. My snideness was not justified (and for that I
apologize) but my attack was. I ended my article with a short paragraph in
which I said that anecdotal evidence is useless and that only double blind
experiments were important.

   Oddly enough, no-one defended the concept of using Vitamin E on abrasions,
they only attacked this comment about anecdotal evidence. I’d like to make a
more serious attempt to justify this position (and also alter it slightly).

   A double blind experiment is one which is designed to eliminate two very
important sources of error:
        1. Observer bias
        2. Multiple degrees of freedom.

   It has been demonstrated repeatedly that two observers, watching exactly the
same set of occurrences but told to expect different things, will report what
they expected to find, even though they contradicted each other. Each will
swear that they have reported honestly, and each will be wrong. (An unbiased
observer can demonstrate that both have misreported.) (One version of this
experiment had people observing rolls of 2 dice, being told that the dice were
dishonest and would show more 6’s or more 1’s. Each did report finding such a
bias, even though the dice were actually honest, and the experiment was filmed
for later analysis which *showed* they were honest.)

   Multiple degrees of freedom are a problem when you compare two occasions,
but there are multiple differences between them. [If I pour water from one
container to another, it remains clear. If I add salt, sugar, pepper and blue
food coloring to the water, it turns blue. Thus from this I conclude that salt
makes water blue.] The problem is amplified when you don’t even know what all
the degrees of freedom are. [My lab assistant added the blue food coloring when
my back was turned. For a more serious example of this, read any article about
"Piltdown Man".]

   The specific case in point is an anecdote about improved healing of a cut by
application of Vitamin E. He reports that healing was speeded, but how was this
measured? (It turns out it was a subjective feeling of "Boy, this sure is
healing fast!") How do we know what other factors may have changed between this
specific case and other times he cut himself? (Maybe his nutrition is better,
and he healed faster because of it. Maybe there are other factors involved as
well. We just don’t know.) More important yet, how do we know it really healed
any faster? It could just be that this was a less serious cut, or that it took
exactly the same length of time as some other cut, but was observed wrongly.

   A serious study of this case would require making 10 or 20 deliberate cuts,
to a controlled depth, two to a person. You then treat one with Vitamin E, and
the other with corn oil. (But beware, it may be that it is the OILINESS of the
Vitamin E which helps, and corn oil may have the same effect. You have to
choose something which you KNOW doesn’t help.) Neither the patient nor the
doctor know which cut got which treatment. You can then observe whether Vitamin
E helped more than corn oil (or whatever you use for a placebo).

   I stated that anecdotal evidence is useless – this was a bit too strong. It
is very premature to use anecdotal evidence as if it were an established fact,
but it does repesent a source of potential investigation for the future.

   However, not all anecdotes are created equal. Suppose someone says "You know
how slowly I heal when I cut myself? Well, a couple of weeks ago I cut myself,
and it was a full moon, so I went out into the woods near my house and took my
clothes off and danced and sang under the moon, and you know? Darned if I
didn’t heal faster than I usually do!"

   Immediately this spurs a series of questions: Does it matter whether he sang
in English, or would Latin work better? What were the details of the dance?
Does it matter whether it was the full moon? If he danced fully clothed, would
that make a difference? But before asking ANY of those
questions, we apply a test of reasonableness, and come to the conclusion that
it is exceedingly unlikely that dancing naked under the moon had anything to do
with of his cut. It is much more likely that dancing under the moon made him
FEEL better, and thus made it SEEM to him as if his cut healed faster even
though it didn’t.

   Whenever one hears an anecdote, one applies a test of reasonableness to it,
rejecting it based on prior knowledge. There is no rule on how to decide
whether it is reasonable (application of bread-mold to a cut makes it heal
faster) or unreasonable (dancing naked under the moon makes a cut heal faster)
– and as such we can sometimes waste a lot of time investigating something
which turns out to be unimportant – and equally we can sometimes pass by
something which is very important. ("Stones from the sky" is surely a classic
example of this.)

   That’s the breaks. No human endeavor is without error, but the scientific
method is intended to be conservative: Better than 10 truths be missed than
that we believe one falsehood. If we’re going to make errors, let’s make
erroneous exclusions rather than erroneous inclusions. Thus it can seem to
those outside that science moves slowly and seems dogmatic and thick headed.

   The body of scientific knowledge is not complete, but what is
within it is as trustworthy as we can make it. Very occasionally, we must
replace a section wholesale, but as time goes on such changes alter
proportionally smaller parts of the whole body, and there are some parts of it
that haven’t changed in millenia. (Euclidean geometry, for one.)

   In this particular case (Vitamin E and cuts) my intuition was as follows:
"The list of vitamins represent 50 or so chemicals distinguished only by the
fact that our bodies need them but cannot produce them internally. They are not
particularly distinguished in any other way from the millions of chemical
compounds running around internally in our bodies. As such, they should be no
more likely to have special biochemical properties than any randomly chosen
list of organic chemicals, and thus reports of special properties are more
likely to be the result of improper observation or improper reporting. Given
hundreds of millions of potential organic compounds available, there is no
reason to give this list of 50 or so any special attention."

   I will try to summarize what I believe to be his position, without being
snide: "There are a large number of conditions for which no reasonable
treatment is available, or for which the treatment can only be dispensed by a
doctor at great expense. I want to control my own body and my own health, and
when something goes wrong I want to be involved in the

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Re: Some more data on drug legalization

Monday, September 28th, 2009

> The following was in today’s (Sunday, Oct.8) N.Y. Times. I didn’t kow
> this, but heroin is essentially decriminalized in Italy. It is legal
> to possess and use for personal use. In the last three years, the
> number of deaths by overdose has tripled, to almost a thousand last
> year. Furthermore, almost half of the country’s 300,000 addicts are
> infected with HIV.

I was in Italy (Rome) when pres. Bush declared ‘The war on drugs’. I
didn’t hear anything about heroin being *legal*, nor did I read anything
about it in the papers. On the contrary, Italians seemed to be quite
concerned about drug dealing, in view of the problems they have with
organized crime over there.

Here in The Netherlands many drugs have been *decriminalized*.
Possession of a small quantity (for personal use) will usually not land
you in jail. But selling heroin or cocain is still very much illegal.
Selling marihuana or hashish is technically illegal, but in practice
it’s tolerated. Buying these ’soft drugs’ is easy. You walk into shops,
that are clearly marked and easily recognizable. A sign on the wall or a
menu on the tables has the prices for the different kinds of drugs. No
problems, no interference by the police. It’s become so easy to get
these drugs, it’s almost boring. The use of soft drugs has been
declining steadily over the past few years.

Although dealing, selling or smugling cocain or heroin is illegal,
merely using it is not considered a crime. The idea behind this is, that
a drug user is not considered a ‘criminal’, but someone who is ‘ill’ and
needs treatment. Because drug users are not forced to hide, they are
easier to reach, by for example, anti-drug treatment programs, or AIDS-
prevention programs. There are methadone programs in the major Dutch
cities and needle exchange programs, where used needles can be exchanged
for clean new ones.

The result of this open policy is, that there now is a slight decline in
the use of heroin and cocain. OD’s have definitely dropped. Crack cocain
never caught on in Holland. The ‘domino theory’ (use of marihuana or
hashish will eventually lead to the use of more dangerous drugs) does
not seem to be valid at all over here. HIV-infections are still rising,
but there is no ‘explosion’ of AIDS. There is much concern about AIDS
reaching the heterosexual/ non drug-user population, through ‘heroin-
whores’, but that does not seem to have happened yet (prostitution has
always been legal in The Netherlands).

OD’s still happen, a lot are tourists (West-Germans) who don’t know the
strength of Dutch heroin.

Amsterdam city council and the Rotterdam health department have argued
in favor of legalizing heroin (with supervision on the use of the drug),
but because of international treaties this was not possible. I therefore
think it’s unlikely that legalization would really be possible elsewhere
in Europe.

King Han Gan – Erasmus University of Rotterdam – School of Medicine and
Health Sciences (almost MSc, two years to go for my MD)

Re: Voting with Feet (free market medicine)

Monday, September 28th, 2009

We don’t have anything like a free market in medical care
in the USA. The AMA has kept things as close to monopoly
as they could. Plus there are lots of socialist gadgets
attached that tend to drive up prices (doctors and patients
more or less conspire together to maximize the bills when the
government or insurance is paying).

You can get very good, inexpensive health care from what
free market medicine is available, but you have to be
an intelligent consumer. If consumers are stupid, don’t expect
free markets to give good products and services at low prices.
Consumers have the responsibility to exercise their right of
choice, choosing the best the market makes available, if they
hope to drive poor quality and high prices out of the marketplace.

Socialism means "protect the stupid, so they can safely become
even more stupid", in effect. It has to break down eventually,
so why wait until catastrophe strikes to reform? Eventually the
ignorant masses will become unmanageable by sheer weight of numbers,
if you keep feeding them at the expense of the productive. Then
comes chaos and revolution.

************************************************************
"A general must prove himself to be an arch-plotter, a cheat,
a thief, and a robber, so that he may overreach his opponent
at every turn …" — Xenophon

medical education

Monday, September 28th, 2009

Shortening the pre-med portion of the education process by one year would allow
those who are non-traditional students a break in that the system is one year
shorter.  You could still encourage students to go for a BS.  Adding two
classes to the SPARSE pre-med curriculum guidelines will not break anyone, and
in fact may produce better education in basic micro and biochem, as these two
seem particularly vulnerable to the curriculum knife in med school.

Making med school three years would also entail shortening the first section of
basic science from two academic years to one and one half,
allowing more pre-clinical instruction and time for rotations.  As for the
frustration level, I can only speak for myself.  I was SOO poor, that I
couldn’t do anything during the break beetween years one and two, and the short
break between two and three was taken up studying for boards.  I had a whole
week off between year three and four, which was spent traveling home from my FP
clerkship.  In my experience, you are in med school formally or informally all
four years, so why not make it three and cut the studs some slack.

Tuition can be lowered slightly and can be capped at current usurious
levels.  That should be the AMA’s TOP priority re: new students.

The NY laws are an example of a good intention with bad results.  The
houseofficers need overnight call for both medical and psychological education.
Call nights make you an independent physician because they are your opportunity
to practice independently.  What we don’t need is to work 24hrs then be
expected to give grand rounds and admit four more patients and lecture to the
students during the next 12hrs.
The NY laws are too vague and don’t deal with the problem of the last 12 of the
36 hour shift.

I agree that we should clean our own house, but we will need some legal
support.  If the American Board of Whatever inspects a rat-hole residency, and
orders it closed, it should be closed–Even if its Harvard.  We should attend
to the problem of residency slave programs
at once, that should be the AMA’s top priority re: MD’s in training.
A residency program is not a system of finding cheap phlebotomists who have no
protection under the wage and hour laws, it is a training program which exists
to teach and train medical school graduates to be practitioners of a given
specilaty of medicine.

–  
Uucp: …{gatech,ames,rutgers}!ncar!noao!asuvax!stjhmc!3601!14.0!Jim.Harper
Internet: Jim.Har…@p0.f14.n3601.z1.fidonet.org

bone marrow donation

Monday, September 28th, 2009

Did you know that bone marrow can be banked like blood?  Did you know that we
can now do bone marrow transplants from people that are unrelated to the donor?

Its possible.  With the help of the National Bone marrow Donor Registry in
Minneapolis, we can match patients needing a transplant with potential donors.  

This is an incredible advance for those patients who need a transplant.  
Patients with certain kinds of leukemia, and certain life-threatening anemias
need transplants to be cured.  Before, the problem was that only about 30% of
the patients had a compatible sibling donor.  70% died.  With the registry,
another 30-40% can find a match.  The registry works great for white people
because there are a lot of them on the registry.  Black and Hispanic patients
are not nearly as fortunate.  For them, finding a match is quite rare.
If you would like to be a bone marrow donor, especially if you are black or
hispanic, please contact you local blood bank, or the National Registry, or
leave me a message on the echo.  By the way, there are similar registries in
Europe, and Canada, so if you would like to register in Europe, please contact
them at you locale.

Jim Harper, MD
Ped. Heme/Onc
Gainesville, Fla

ATH: 3601/14 151/1003 265/7 103/501

–  
Uucp: …{gatech,ames,rutgers}!ncar!noao!asuvax!stjhmc!3601!14.0!Jim.Harper
Internet: Jim.Har…@p0.f14.n3601.z1.fidonet.org

Haemochromatosis ..?

Monday, September 28th, 2009

Haemochromatosis.

I’ve discovered that I am no expert on this… what are
the neurological or (if any)
psychiatric complications? – brain rusting..or whatever.?

5 255/64

–  
Uucp: …{gatech,ames,rutgers}!ncar!noao!asuvax!stjhmc!2!255!64!Carl.Littlejohns
Internet: Carl.Littlejo…@f64.n255.z2.fidonet.org

What drugs shall I get in Canada while visiting from the USA.

Monday, September 28th, 2009

Steve Dyer writes:
> I’ve heard of the research on its use in impotence, but whether
> it would be generally available now for such use would require that
> an injectable form be already available (thereby allowing doctors
> to use the drug for any condition they care to).  Otherwise,
> an NDA for the injectable preparation would have to be filed,
> safety and efficacy studies reported, etc.  Given that papaverine
> is a common, totally unpatentable drug, I’d be surprised if a company
> went to all the trouble.
> I still wince every time I read of its method of administration.

I wince too but the patients don’t. Believe me these intrapenile injections
work. The patient is taught to inject himself. It is effective for all types of
impotence EXCEPT that do to circulation
(the drug requires the circulation to be intact). Primary application
is neurogenic impotence. In fact, the injection can be used as a test for the
patency of the penile circulation. Major (occasional) complication is priapism
– antidote: epinephrine. One injection and patient is rock hard for 30 minutes,
depending on dose.

The drug is available by prescription in Canada. I will find out who makes it.
I have never personally prescribed it – that’s usually done by the urologist.
I’ll forward more info later.

…Michael

–  
Uucp: …{gatech,ames,rutgers}!ncar!noao!asuvax!stjhmc!167!1.0!Outremed*.Mr
Internet: Outremed*…@p0.f1.n167.z1.fidonet.org

Declining Medical Applica

Monday, September 28th, 2009

I certainly agree with all that you said about why medicine is taxing
and long road to travel carrer, however, I must disagree with your
proposals to change the system.

>    1>  Make Premed 3 years long, and teach Biochem and Micro

This seems to forget that college is probably the last chance many
people get to try new things and learn a few things about the arts,
culture, other related fields, sonthing to diversify ones interests,
give them something to do other than just medicine, basically makes us
all a little more interesting to talk with (and maby a little easier to
talk to)

> in premed. 2>Make Medschool 3 years long by going all year long.

So many students in medical school are already pressed for time and
frsutration having to make early descisions about internships and
residencies, I just don’t see where this will help the learning process.
 First and second years are so much lecture time and so much information
that a restructuring of the system may be in order.  Seems a more topic
or organ system oriented approach would be a better move than decreasing
the time. Most undergraduates are not ready to take a medical course in
Micro/ID (that is what it really  is) or medical biochem.  Unless what
you are saying is to turn medical school into a 6 year frolic.

> Having eliminated
>   Biochem and Micro, you could then spend more time on pre-clinical
>   instruction and pathology.
> 3>Cap tuition in state schools and demand honest accounting of "the
>   cost of medical educaton."

I would love to see something done about the high cost of tuition, but
that seems it has reached the point where only a restructuring of the
entire medical system could help there i.e cheaper socialized system
that pays tution (in part), medical costs, salaries etc.    

> 4>Approach residency certification with a knife.  If a program is

What do you think about the new laws instituted in NY?  They certainly
address the problem.  I personally wish that we could better manage our
own house rather than state and federal legislatures.

141/205 132/127 119 101 265/7 103/501

–  
Uucp: …{gatech,ames,rutgers}!ncar!noao!asuvax!stjhmc!141!205!Aaron.Waxman
Internet: Aaron.Wax…@f205.n141.z1.fidonet.org

Re: Ethics And Oragn Transplantation

Monday, September 28th, 2009

 > The uniform donor card might solve some of the problems
 > involving the family,  but the suspicion could always be
 > raised that the transplant surgeons were too  quick to
 > pronounce irreversible brain death. There is really no way
 > to  separate the emotional aspects from the need for
 > organs.

Yes, you are very right in regards to the family of not being able to separate  
emotions from organ transplantation.  They have the choice to use  
transplantation as a means of dealing with their grief, and are given the  
option to or not to.  No guilt is supposed to be given if they choose not to.  
However, transplant surgeons *do not* pronounce brain death.  It is the  
neurosurgeons who do that, usually two different ones to make sure that brain  
death occurs. There are several things that are involved in brain death that  
must occur first.  Some hospitals also have a neurosurgeon and an internist do  
the test separately and if both come up with the same results, (brain death has  
occurred), and if the person is a good possible organ donor, then the family is  
approached, and they are given the option of donating organs or not.   The  
donor card is a good tool, but the final decision must be made by the family.

 280/9 290/627 132/101 265/7 103/501

–  
Uucp: …{gatech,ames,rutgers}!ncar!noao!asuvax!stjhmc!280!9!Melanie.Thornton
Internet: Melanie.Thorn…@f9.n280.z1.fidonet.org

HICN237 News Part 2/4

Monday, September 28th, 2009

— begin part 2 of 4 cut here —
100-fold: 6.1 in the Mid-Atlantic region, 3.7 in New England, 0.7 in the North
Central  states,  0.6  in  the  Pacific  states  (1987  data only),  0.2 in 16
Southeast and Southwest states, and less than 0.1 in the Mountain region (2).

Reported  by:  State  and  local  health  departments.   Div  of  Vector-Borne
Infectious Diseases, Center for Infectious Diseases, CDC.

Editorial Note:

    National  surveillance  for  LD relies on states for reports.  Since 1982,
when national surveillance began,  state  surveillance  systems  for  LD  have
changed  considerably.  LD has been made a reportable disease in 31 states and
the District of Columbia, and surveillance for LD has intensified,  especially
in areas where the disease is endemic.

    Since 1982, 13,825 cases of LD have been reported. From 1982 through 1987,
the  number  of  cases  increased  nearly fivefold from 492 to 2368;  in 1988,
reported cases doubled (4572 cases)  (Figure  2).  LD  is  the  most  commonly
reported vectorborne disease in the United States (Figure 3).

>From  1983  through  1987,  LD accounted for 50% of the vectorborne infections

reported to CDC.  Tickborne diseases (e.g.,  LD,  Rocky Mountain spotted fever
(RMSF)) accounted for 95% of these infections; fleaborne typhus and plague and
mosquitoborne arboviral infections accounted for the remaining 5%.

    The  increased  incidence  of  reported  LD  probably  is  due to improved

Health InfoCom Network News                                             Page 11
 Volume  2, Number 37                                        October  9, 1989

awareness and recognition of the disease,  as well as to an actual increase in
incidence  and  geographic  spread.  Other  factors may also contribute to the
increase. For example, because the clinical and laboratory diagnosis of LD may
be imprecise (3),  other conditions possibly may be misdiagnosed and  reported
as  LD.  In  addition  to  differences  in clinical interpretation of erythema
migrans (EM), misdiagnosis may also result from the lack of standardization of
serologic testing and from cross-reactivity  with  Treponema  and  with  other
Borrelia (3). In areas with endemic LD, persons with illnesses other than LD–
but who previously have been infected with B. burgdorferi (the causative agent
for  LD)–also  may  be misdiagnosed (4).  Conversely,  several factors may be
responsible for failure of a case of LD to be diagnosed  and/or  to  meet  the
case  definition.  These  include  early  treatment  of  symptoms resulting in
abrogation of the specific antibody  response  (3),  the  low  sensitivity  of
serologic  tests  in early LD (3),  and the failure of approximately 25% of LD
patients to manifest EM (4,5). The extent of underreporting of LD is unknown.

    Until more sensitive  and  specific  laboratory  diagnostic  tests  become
available,   diagnosis  of  LD  relies  predominantly  on  clinical  features.
Serologic testing may be of greatest diagnostic utility in patients  who  have
symptoms compatible with late-stage LD. The validity of serologic test results
depends  largely  on  the  experience  of  the  diagnostic  laboratory and its
quality-control procedures.  No published data exist on the diagnostic utility
of  antigen-detection assays in the laboratory diagnosis of LD.  A comparative
study of licensed LD diagnostic kits is planned by the  Association  of  State
and Public Health Laboratory Directors.

    State-  and  community-based  epidemiologic  studies  have  documented  an
increase in human cases and an expansion of affected areas (5-8).

Entomologic surveys have detected  local  increases  of  Ixodes  dammini,  the
principal  tick  vector in northeastern and central states,  and its spread to
new areas (7-10).  However, because the risk for acquiring LD varies widely by
locality,  the  disease  appears  to  be  of public health consequence only in
certain regions–specifically,  coastal counties  on  both  seaboards  and  in
certain counties in the upper Midwest.  In the southeastern, southwestern, and
Mountain states,  RMSF remains the  leading  vectorborne  disease:  from  1983
through 1987,  3160 RMSF and 658 LD cases were reported from the Southeast and
Southwest,  and 37 RMSF and seven LD cases were  reported  from  the  Mountain
states.

    Data  concerning  risk  factors for acquiring LD are limited.  In suburban
areas where LD is  endemic,  infection  may  be  acquired  principally  around
patients’  residences  (11,12),  and risk of exposure may be continuous during
the  transmission  season.   Under  these  circumstances,   certain   personal
protection  measures  (e.g.,  the  daily application of repellents) may not be
practical.  Further efforts  are  needed  to  evaluate  the  effectiveness  of
environmental  modifications  and  focal  application of acaricides (chemicals
effective  against  ticks)  for  the  control  of  vector   ticks   in   these
circumstances.  Where  LD  is  transmitted  sporadically through occasional or
brief exposures during recreation or work,  personal protection  measures  are
most appropriate for prevention.

    Measures  recommended  to  reduce exposure to ticks include avoiding areas
endemic for LD; using repellents;  wearing long-sleeved shirts and long pants,
and tucking pants into the top of socks;  wearing light-colored clothing;  and

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inspecting clothing and skin frequently for ticks. Animal studies suggest that
I.  dammini may not efficiently transmit infection until  after  48  hours  of
attachment  and  that  prompt removal of attached ticks may limit transmission
(13). However, it is unknown how long a tick must attach to human hosts before
infection occurs.

    N,N-diethyl-m-toluamide (DEET) is effective in repelling  I.  dammini  and
other vector ticks. In view of the possible risk for toxicity (14), the use of
DEET-containing  repellents solely to prevent LD may be inappropriate in areas
without endemic LD.  Permethrin (0.5%) sprayed onto clothing also is effective
in  reducing  the numbers of adherent ticks,  including I.  dammini and others
(15,16).  However,  permethrin aerosols are available only in  certain  states
that   have  obtained  Environmental  Protection  Agency  approval  for  their
distribution.

References

 1.  Schmid GP, Horsley R, Steere AC,  et al.  Surveillance of Lyme disease in
the United States, 1982. J Infect Dis 1985;151:1144-9.

 2. Tsai TF, Bailey RE, Moore PS. National surveillance of Lyme disease, 1987-
1988. Conn Med 1989;53:324-6.

 3.  Barbour AG. The diagnosis of Lyme disease: rewards and perils. Ann Intern
Med 1989;110:501-2.

 4. Steere AC. Lyme disease. N Engl J Med 1989;321:586-96.

 5.  Cartter ML,  Mshar P,  Hadler JL.  The epidemiology of  Lyme  disease  in
Connecticut. Conn Med 1989;53:320-3.

 6.  Steere  AC,  Taylor E,  Wilson ML,  Levine JF,  Spielman A.  Longitudinal
assessment of the clinical and epidemiological features of Lyme disease  in  a
defined population. J Infect Dis 1986;154:295-300.

 7.  Lastavica CC,  Wilson ML,  Berardi VP,  Spielman A,  Deblinger RD.  Rapid
emergence of a focal epidemic of Lyme  disease  in  coastal  Massachusetts.  N
Engl J Med 1989;320:133-7.

 8.  Hanrahan  JP,  Benach  JL,  Coleman JL,  et al.  Incidence and cumulative
frequency of endemic Lyme disease in a community.  J Infect Dis  1984;150:489-
96.

 9.  Spielman A,  Wilson ML, Levine JF, Piesman J.  Ecology of Ixodes dammini-
borne human babesiosis and Lyme disease. Annu Rev Entomol 1985;30:439-60.

10.  Davis JP,  Schell WL,  Amundson TE,  et al.  Lyme disease  in  Wisconsin;
epidemiologic,  clinical, serologic and entomologic findings.  Yale J Biol Med
1984;57:685-96.

11.  Falco RC,  Fish D.  A survey of tick bites  acquired  in  a  Lyme-disease
endemic area in southern New York State. Ann N Y Acad Sci 1988;539:456-7.

12.  Falco  RC,  Fish  D.  Prevalence of Ixodes dammini near the homes of Lyme
disease patients in Westchester County, New York. Am J Epidemiol 1988;127:826-

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 Volume  2, Number 37                                        October  9, 1989

30.

13.  Piesman J, Mather TN, Sinsky RJ, Spielman A.  Duration of tick attachment
and Borrelia burgdorferi transmission. J Clin Microbiol 1987;25:557-8.

14. CDC. Seizures temporally associated with use of DEET insect repellent–New
York and Connecticut. MMWR 1989;38:678-80.

15.  Schreck CE,  Snoddy EL,  Spielman A.  Pressurized sprays of permethrin or
DEET on military clothing  for  personal  protection  against  Ixodes  dammini
(Acari: Ixodidae). J Med Entomol 1986;23:396-9.

16. Mount GA, Snoddy EL. Pressurized sprays of permethrin and DEET on clothing
for  personal  protection against the Lone Star tick and the American dog tick
(Acari: Ixodidae). J Econ Entomol 1983;76:529-31.

*The surveillance case definition for  LD  varies  among  states  and  between
states and CDC. Some states use the CDC case definition adopted in 1988, i.e.,
physician-diagnosed  erythema  migrans (EM) in a person who acquired infection
in a county with endemic LD or, for persons who acquired infection in a county
without endemic LD,  laboratory evidence  of  infection  in  addition  to  the
presence of EM.  Other states (e.g.,  New York,  Wisconsin, Connecticut) use a
previous,  more inclusive,  CDC case definition for LD,  which counts as cases
persons  with  appropriate  systemic manifestations and laboratory evidence of
infection (1).

Differences in the case definitions used by states  must  be  considered  when
state and regional incidences are compared.

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 Volume  2, Number 37                                        October  9, 1989

                              International Notes
                            Lyme Disease — Canada

    From  1977  through  May  1989,   30  cases  of  Lyme  disease  (LD  (Lyme
borreliosis)) were reported to Canada’s Laboratory Centre for Disease  Control
(LCDC).  Ontario  is  the only province in which LD is a reportable condition;
however,   active  laboratory  surveillance  for  LD  is  conducted  in  other
provinces. In Ontario, the diagnosis of LD is based on recognition of erythema
migrans  (EM),  with  involvement  of  at least two of the three organ systems
usually affected by LD (joints, nervous system, and cardiovascular system), or
EM and an indirect immunofluorescence antibody titer greater than or equal  to
1:128  or an enzyme-linked immunosorbent assay optical density greater than or
equal to 0.40,  or EM and  isolation  of  Borrelia  burgdorferi.  Without  EM,
diagnosis  is  based  on involvement of at least one organ system and positive
serology  or  isolation  (C.  LeBer,  Ontario  Ministry  of  Health,  personal
communication, 1989).

    For 25 (83%) of the 30 cases,  exposure probably occurred in Canada.  Four
patients  had  a  documented  history  of  tick  bite  during  travel  to  the
southeastern United States before onset of symptoms;  one case was acquired in
Germany.  Seventeen (68%) of the 25 indigenous cases were reported in Ontario,
and five (20%),  in Manitoba (Figure 1).  The areas in Canada with the highest
number of cases border on  the  American  states  with  the  highest  reported
incidence of LD.

    Sixteen (53%) of the 30 cases occurred in 1988.  Of the 25 cases for which
month of onset was reported,  cases occurred most commonly in July  (28%)  and
June (16%).  The mean age of LD patients was 40 years (range:  18 months to 70
years). Males accounted for 53% of all cases.

    A tick bite was documented for 47% of  the  patients;  the  remainder  had
either  no  history  of  a  bite  or  no available information.  For 48% of LD
patients, EM was documented. The most frequently documented presenting symptom
was rash (38%),  followed by  arthralgia/arthritis  (28%)  and  influenza-like
illness  (13%).  Most  had  multiple  symptoms;  five  patients had neurologic
involvement. Five (17%) of the 30 LD patients were hospitalized.

Comment:  In several provinces,  studies are being planned  to  determine  the
prevalence  of  infected  vectors  in  Canada.  The  Department of Entomology,
University  of  Manitoba,  identified,  and  the  Smithsonian  Institution  in
Washington,  D.C.,  confirmed,  two  female  Ixodes dammini ticks collected in
Gunton and Winnipeg,  Manitoba,  in May and June 1989.  These  are  the  first
reports  of  this vector species in Manitoba.  The only other Canadian reports
are from Long Point,  Ontario.  Intensive sampling efforts for I.  dammini  in
other  regions of Manitoba in 1989 found only Dermacentor variabilis (American
dog tick).

    To acquire more complete incidence data for Canada,  LCDC is interested in
receiving  reports  of  any  additional  cases  through provincial/territorial
epidemiologists.

Adapted from:  Canada Diseases Weekly Report 1989;15:135-7 and 1989;15:185, as
reported by:  MJ Todd,  MHSc,  AO Carter,  MD, Disease Surveillance, Bureau of
Communicable Disease Epidemiology,  Laboratory  Centre  for  Disease  Control,

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 Volume  2, Number 37                                        October  9, 1989

Ottawa,  Ontario;  TD  Galloway,  PhD,  Dept of Entomology,  Univ of Manitoba,
Winnipeg.

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 Volume  2, Number 37                                        October  9, 1989

                        Epidemiologic Notes and Reports
    Seizures Temporally Associated with Use of DEET Insect Repellent — New
                             York and Connecticut

    In August 1989,  epidemiologists from the New  York  State  Department  of
Health  (NYSDH)  investigated  five reports of generalized seizures temporally
associated with topical use of N,N-diethyl-m-toluamide (DEET).  Three  of  the
case-patients,  one from New York and two from Connecticut, were reported by a
pediatric neurologist who practices in both  states.  One  case  was  reported
initially to an entomologist in New York, and one was reported directly to the
NYSDH. The cases occurred in June through August 1989.

    The  patients,  four boys aged 3-7 years and one 29-year-old man,  had few
prodromal symptoms and recovered quickly.  All five had  unremarkable  medical
histories,  and  none had had a previous seizure or neurologic event.  All had
normal nonfocal neurologic examinations after their  seizures,  and  four  had
normal  complete  laboratory  examinations  and normal computerized tomography
and/or magnetic resonance imaging examinations. Each had had topical cutaneous
exposure to varying concentrations of DEET;  four had  had  fewer  than  three
applications.  The  interval  between  last  use of DEET and onset of seizures
ranged from 8 to 48 hours. One patient developed urticaria before his seizure;
he was one of two patients who developed an urticarial reaction  to  phenytoin
administered to control seizures.

    While  reinforcing  the  importance of DEET in preventing Lyme disease (LD
(Lyme borreliosis)), health officials in New York, Connecticut, and New Jersey
issued a health alert on August 22  advising  caution  in  the  use  of  DEET-
containing repellents.  The NYSDH is planning to conduct epidemiologic studies
to evaluate the association between DEET and neurologic events.

Reported by:  S Oransky,  MD,  Hudson Valley Poison Control Center,  Nyack;  B
Roseman,  MD,  Pediatric  Neurologic Associates,  White Plains;  D Fish,  PhD,
Medical Entomology Laboratory, New York Medical College, Valhalla;  T Gentile,
MS,  Center  for  Environmental  Health,  J  Melius,  MD,  State Environmental
Epidemiologist, New York State Dept of Health.  ML Cartter, MD, JL Hadler, MD,
State  Epidemiologist,   Connecticut  State  Dept  of  Health  Svcs.   Div  of
Environmental Hazards and Health Effects,  Center for Environmental Health and
Injury Control; Div of Vector-Borne Infectious Diseases, Center for Infectious
Diseases; Div of Field Svcs, Epidemiology Program Office, CDC.

Editorial Note:  For health officials in New York and Connecticut,  two of the
states where LD is of growing concern,  inquiries about the potential  adverse
effects  of  insect  repellents  have  increased.  Recent anecdotal reports of
seizures temporally associated with the use of  DEET  have  heightened  public
awareness of DEET’s potential adverse effects.
    DEET  has  been marketed in the United States since 1956 and is used by an
estimated 50-100 million persons each year.  Since 1961, at least six cases of
toxic  systemic  reactions  from repeated cutaneous exposure to DEET have been
reported (1-6). Six girls, ranging in age from 17 months to 8 years, developed
behavioral  changes,  ataxia,  encephalopathy,  seizures,  and/or  coma  after
repeated  cutaneous exposure to DEET;  three died.  Another six systemic toxic
reactions have been reported following ingestion of  DEET  (7).  Additionally,
episodes  of  confusion,  irritability,  and  insomnia  have  been reported by
Everglades National Park employees following repeated  and  prolonged  use  of

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 Volume  2, Number 37                                        October  9, 1989

DEET (8).

    DEET  is  partially absorbed through the skin and has been used to enhance
dermal delivery  of  other  drugs  (9).  Adverse  reactions  include  allergic
responses,  direct  neurotoxicity,  and dermatitis.  One of the girls who died
after  dermal  exposure  was  partially  deficient  in  the  enzyme  ornithine
carbamoyltransferase  (3);  DEET  may  interfere with the urea cycle metabolic
pathway (10).

    Anecdotal reports of seizures are difficult  to  interpret.  None  of  the
recent cases in New York and Connecticut have been clearly established as DEET
toxicity.  In  contrast to cases described in the medical literature,  the New
York and Connecticut patients were all male,  DEET exposure was less  intense,
few  prodromal  symptoms  or  encephalopathy were seen,  and recovery was more
rapid and complete.  With the dramatic increase in the prevalence of DEET  use
in areas with endemic LD, the reported cases of seizures temporally related to
DEET use may be coincidental.  However, these cases may represent a different,
previously unreported spectrum of toxic  reactions.  Careful  toxicologic  and
epidemiologic  studies must be conducted,  including adequate documentation of
DEET levels in affected and unaffected persons.

    Clinicians evaluating patients with unexplained seizures  should  consider
the  possibility of exposure to DEET.  However,  since the exact circumstances
under which DEET-related neurotoxicity may occur are unclear,  DEET should not
be  accepted  as  the  cause  of  a  seizure  until appropriate evaluation has
reliably excluded other possible etiologies.

    The optimal concentration of DEET for prevention of tick bites is unknown.
However,   repellents  containing  20%-30%  DEET  applied  to   clothing   are
approximately  90%  effective in preventing tick attachment (11).  To minimize
the possibility of adverse reactions to DEET,  the following  precautions  are
suggested:

–  Apply  repellent  sparingly  only  to  exposed  skin  or clothing.
—  Avoid  applying  high-concentration products to the skin,  particularly of
    children.
—  Do not inhale or ingest repellents or get them into the eyes.
—  Wear long sleeves and long pants, when possible, and apply repellent
    to clothing to reduce exposure to DEET.
—  Avoid applying repellents to portions of children’s hands that are
    likely to have contact with eyes or mouth.
—  Never use repellents on wounds or irritated skin.
—  Use repellent sparingly; one application will last 4-8 hours.
    Saturation does not increase efficacy.
—  Wash repellent-treated skin after coming indoors.
—  If a suspected reaction to insect repellents occurs, wash treated
    skin, and call a physician. Take the repellent can to the
    physician.Specific medical information about the active ingredients
    in insect repellents is available from the National Pesticide
    Telecommunications Network, telephone (800) 858-7378.

References

 1. Edwards DL, Johnson CE. Insect-repellent-induced toxic encephalopathy in a
child. Clin Pharm 1987;6:496-8.

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 Volume  2, Number 37                                        October  9, 1989

 2.  Gryboski J,  Weinstein D,  Ordway  NK.  Toxic  encephalopathy  apparently
related to the use of an insect repellent. N Engl J Med 1961;264:289-91.

 3.  Heick HMC, Shipman RT, Norman MG, James W.  Reye-like syndrome associated
with use  of  insect  repellent  in  a  presumed  heterozygote  for  ornithine
carbamoyl transferase deficiency. J Pediatr 1980;97:471-3.

 4.  de  Garbino  JP,  Laborde  A.  Toxicity  of  an  insect  repellent:  N-N-
diethyltoluamide. Vet Hum Toxicol 1983;25:422-3.

 5.  Roland EH, Jan JE,  Rigg JM.  Toxic encephalopathy in a child after brief
exposure to insect repellents. Can Med Assoc J 1985;132:155-6.

 6. Zadikoff CM. Toxic encephalopathy associated with use of insect repellant.
J Pediatr 1979;95:140-2.

 7.  Tenenbein M.  Severe toxic reactions and death following the ingestion of
diethyltoluamide-containing insect repellents. JAMA 1987;258:1509-11.

 8. McConnell R, Fidler AT, Chrislip D, NIOSH. Everglades National Park health
hazard evaluation report.  Cincinnati, Ohio: US Department of Health and Human
Services,  Public Health Service, 1986;  NIOSH health hazard evaluation report
no. HETA-83-085-1757.

 9. Windheuser JJ, Haslam JL, Caldwell L, Shaffer RD.  The use of N,N-diethyl-
m-toluamide  to enhance dermal and transdermal delivery of drugs.  J Pharm Sci
1982;71:1211-3.

10. Heick HMC, Peterson RG, Dalpe-Scott M, Qureshi IA.  Insect repellent, N,N-
diethyl-m-toluamide, effect on ammonia metabolism. Pediatrics 1988;82:373-6.

11.  Schreck CE,  Snoddy EL,  Spielman A.  Pressurized sprays of permethrin or
DEET on military clothing  for  personal  protection  against  Ixodes  dammini
(Acari: Ixodidae). J Med Entomol 1986;23:396-9.

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 Volume  2, Number 37                                        October  9, 1989

              Deaths Associated with Hurricane Hugo — Puerto Rico

    At 9 a.m.  eastern daylight time on Monday, September 18, 1989, the eye of
Hugo, the North Caribbean’s strongest hurricane (a category four on a scale of
five) in a decade,  struck the northeast corner of Puerto  Rico.  Hugo’s  path
extended  from  the Lesser Antilles and the Virgin Islands (where it struck on
September 17) to South Carolina and areas of North  Carolina  (where  it  came
ashore  during  the  late evening and early morning of September 21-22).  Wind
velocities in San Juan were measured at up to 100 mph;  wind  gusts  elsewhere
measured  as  high  as  140  mph.  These  winds damaged nearly 25% of homes on
Puerto Rico,  left approximately 75% of the island without power,  and created
30-foot  swells  off  the  east coast.  Heavy rains accompanying the hurricane
caused some flash flooding.

    From September 18 to September 29,  the medical examiner  in  Puerto  Rico
investigated nine deaths considered to be related to the hurricane.  One death
(case  1)  occurred  before the storm (preimpact phase);  two (cases 2 and 3),
during the storm  (impact  phase);  and  six  (cases  4-9),  after  the  storm
(postimpact).  The  medical  examiner  categorized the manner of death for all
cases as "accident."*

    Case 1.  A 57-year-old man was electrocuted  while  trying  to  remove  an
outside television antenna before the storm.

    Case  2.  A  94-year-old  woman drowned while waiting out the storm in her
home.

    Case 3. A 60-year-old man drowned on his boat during the storm.

    Cases 4-8.  Five electric company workmen, ages 28,  30,  35,  37,  and 42
years, were electrocuted in five separate incidents while attempting to repair
downed power lines after the storm.

    Case  9.  A 35-year-old man was electrocuted when he contacted an electric
cable lying on the ground where he was chopping a tree.

Reported by:  P Rechani,  PhD,  Director,  Instituto de Sciencias Forenses  de
Puerto  Rico,   San  Juan;   JV  Rullan,  MD,  State  Epidemiologist,  Div  of
Epidemiology, Puerto Rico Dept of Health. Div of Field Svcs,

Epidemiology Program Office;  Div of Environmental Hazards and Health Effects,
Center  for  Environmental Health and Injury Control;  Div of Safety Research,
National Institute for Occupational Safety and Health, CDC.

Editorial  Note:   In  the  past,  hurricane-related  mortality  has  occurred
primarily  as  a  result  of drownings during the impact phase.  Most of these
drownings have been associated with storm surges rather than heavy rains  (1).
For  most  parts  of the world,  however,  this pattern may be changing.  This
decrease  in  impact-phase  drownings  may  be  a  consequence   of   improved
forecasting  and  early  warnings  about  approaching  hurricanes,  as well as
increased compliance of persons potentially at risk with effective  evacuation
programs.

    The  principal  public health response to Hurricane Hugo was early warning
and a coordinated evacuation plan.  By the evening of  Sunday,  September  17,

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 Volume  2, Number 37                                        October  9, 1989

Puerto  Rican  officials  had  evacuated  greater than 18,000 persons who were
residing in low-lying, flood-prone areas.  Cases 2 and 3 were the only impact-
phase   deaths  in  Puerto  Rico.   Despite  repeated  pleas  from  government
authorities,  these persons refused  to  leave  their  property  and  move  to
temporary shelters.

    The  contribution to mortality of causes other than impact-phase drownings
was highlighted by Tropical Storm Isabelle,  which struck Puerto Rico in 1985.
Of the 95 deaths investigated by the medical examiner,  21 (22%) resulted from
drowning;   the  rest  resulted  from  other  traumatic  injuries,   primarily
associated  with  a  landslide  and collapsed bridges (CDC,  unpublished data,
1987).

    Public health officials and health-care providers must recognize that  the
mortality  and  morbidity  risks  associated with hurricanes extend beyond the
impact phase.  Efforts to minimize injury and  other  health  risks  for  both
disaster-relief  workers  and the general population are crucial.  These risks
include electric hazards,  floodwaters,  lacerations  from  storm  debris  and
unfamiliar equipment (e.g.,  chain saws), operation of motorized vehicles, use
of sump pumps and generators in confined spaces,  and exacerbation of existing
or unknown medical conditions as a result of fatigue,  stress,  or unavailable
medical support.

    CDC and other Public Health Service agencies are providing  assistance  to
the Virgin Islands,  Puerto Rico,  South Carolina, and other areas affected by
Hurricane Hugo.  At least five of the seven electrocutions reported here  were
work-related.  A Fatal Accident Circumstance and Epidemiology (FACE) team from
the National Institute for Occupational Safety and Health, CDC, has arrived in
Puerto Rico to assist local health  officials  in  the  investigation  of  the
occupational fatalities that occurred during the postimpact phase.

Reference

1.  French J.  Hurricanes.  In:  Gregg MB,  ed.  Public health consequences of
disasters.  Atlanta: US Department of Health and Human Services, Public Health
Service (in press).

*"Manner  of  death"  and  "accident"  are  medicolegal  terms  used  on death
certificates that refer to the  circumstances  under  which  a  death  occurs;
"cause  of  death"  refers to the injury or illness responsible for the death.
When a death occurs  under  "accidental"  circumstances,  the  preferred  term
within  the  public  health community for the cause of death is "unintentional
injury."

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 Volume  2, Number 37                                        October  9, 1989

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              News from the National Institute of Dental Research

                            DENTAL PROJ NOW ONLINE

DENTALPROJ is now online.  The  file  contains  summaries  of  ongoing  dental
research  projects  funded  in  the  current  fiscal year.  NIDR developed the
database and collaborated with the National Library of Medicine in  adding  it
to  MEDLINE.  The  file  consists of active dental projects supported by DHHS,
and some projects (as many as could be collected) sponsored  by  the  Veterans
Administration  and  the  Department  of  Defense.  The  new  database  can be
accessed through MEDLINE by entering the command: FILE DENTALPROJ.

The purpose of DENTALPROJ is to expedite the  transfer  of  information  about
ongoing  dental research projects.  DENTALPROJ allows the scientific community
to access information  while  research  is  in  progress–before  results  are
published, indexed, and otherwise available.

DENTALPROJ  has  approximately  1300  research  projects  listed.  It  will be
updated bi-annually and  replaced  annually.  Included  in  its  listing  are:
grants  and contracts administered by NIDR,  career awards and the Institute’s
intramural (on-campus  research).  The  file  does  not  contain  training  or
fellowship awards.

               UPDATE ON LONG RANGE RESEARCH PLAN FOR THE 1990S

As  part  of the planning process to develop the NIDR Long-Range Research Plan
for the 1990s,  NIDR recently sponsored two special meetings involving private
industry  and  representatives  of minority groups.  On May 16,  NIDR hosted a
session   on   "Dental   Research–Industry    Collaboration."    Twenty-three
representatives  from industry,  joined by six dental scientists from academia
and  26  NIDR  staff  members,   discussed  the  potential  for  collaborative
arrangements   between  academic  dental  research  institutions  and  private
industry.  On May 22,  NIDR convened a session to discuss Dental Research  and
Minority  Group  Issues.  The  meeting  considered  the  oral  health needs of
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