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Volume: 1
Issue: 19
Date: 12-Aug-93


Table of Contents:

              Notes From The Sixth Annual Rheumatology
                     Symposium on Lyme Disease
                           Yale University


Newsletter:

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                     Volume 1 - Number 19 - 8/12/93


                        ***** SPECIAL ISSUE *****
           ***** NOTES FROM THE SIXTH ANNUAL RHEUMATOLOGY *****
                  ***** SYMPOSIUM ON LYME DISEASE *****


I.    Introduction
II.   Special Section
III.  How to Subscribe, Contribute and Get Back Issues



I. ***** INTRODUCTION *****

In this issue, Frank Demarest offers us his notes from the 6th Annual
Rheumatology Symposium on Lyme Disease, sponsored by the Yale University
School of Medicine.  As with Dr. Lloyd Miller's notes from the conference
in Atlantic City, the notes are *not* abstracts written by the presenters.
They represent notes taken by the attendees at the respective conferences.  
Special thanks to Frank for sharing his notes with us.


Warning: Some of the opinions presented in this issue are highly
controversial and are by no means the final word on Lyme disease.  Some
individuals will be outraged at the declarations of certainty made my
some physicians when unambiguous data is not present.  If you are one
of these individuals, please resist the urge to publicly shred this issue
of the newsletter.


For example, one opinion leader declared that:
You will never see a negative ELISA with a positive blot.


I had a negative ELISA and a "positive" Western Blot at Dr. Dattwyler's lab
at SUNY Stony Brook.


Never say never.

-Marc.


II. ***** SPECIAL SECTION *****

Sender: Frank Demarest <76116.2065@compuserve.com>

Notes and other information from:
The Sixth Annual Rheumatology Symposium on Lyme Disease.
Wednesday, June 16, 1993.
Yale University School of Medicine, New Haven, CT.


Each item has the title of the presentation and the speaker's name.  All the
speakers are associated with Yale except as noted.  The bracketed numbers
refer to related articles in the proceedings, listed at the end.  Text
bracketed with {{ and }} are my own comments.


Disclaimer: These notes may contain errors, although I tried to accurately
represent what was said. Extra care was taken with the statements shown as
quotes. The opinions presented are those of the speakers.


Frank C. Demarest, July 1993.
------------------------------------------------------------


Opening remarks.
Robert T. Schoen, MD.


About 160 people in attendance.  Each presentation 15-20 minutes long.
------------------------------------------------------------


Lyme Disease Epidemiology. [1]
Patricia Mshar (Connecticut State Dept of Health Services)


The incidence of LD in 1992 was 55 per 100,000, the highest rate for any
state.  The surveillance case definition is to establish uniform criteria for
reporting, NOT as sole criteria for: clinical diagnosis, standard of care,
guidelines for quality insurance, or reimbursement, or sole criteria for
initiating a public health action.


Lyme surveillance started in CT in 1977. In 1992 they did active surveillance
in the 12 towns around Lyme, and in Litchfield County (same areas studied in
1977).  Passive surveillance is done through labs and health care providers.
People less than 10 years old are at greatest risk.  Most cases are infected
during June, July, August.  In 1991, 43% had EM, 57% no EM.  Of those without
EM: 22% met CDC case definition for late Lyme; 16% no clinical information
given; 15% late Lyme, unknown serology; 5% late Lyme, negative serology; 39%
no late manifestations, positive serology.  Arthritis was the most frequent
symptom of late Lyme with unknown or negative serology.  The surveillance case
definition and system has limitations.  It is not sensitive enough to describe
the clinical manifestations of the disease.  The goal is to describe
epidemiology by person, place, and time.


A case control study examined risk factors for LD, "persons with EM were more
likely to live in a rural area and to have found ticks on their pets.  No
other variables, including those found to be risk factors in other studies,
were significant.  Protective measures that did not contribute significantly
to the model included: wearing long pants, use of repellent sprays, and
checking for ticks."


A study in 1991-1992 (also published in MMWR) found that only 7% of
physicians from four specialties (general/family practice, internal medicine,
pediatrics, and dermatology) reported LD.  This suggests that either most
physicians don't diagnose LD or that underreporting is common.
------------------------------------------------------------


Ecological Risk Factors in Lyme Disease. [2,3]
Sam Telford, MD. (Harvard)


Studies were done in the Nantucket, Martha's Vineyard, Elizabeth Islands,
Cape Cod area of Massachusetts.  Number of deer in the area is related to
risk of LD.  Babesiosis is an emerging disease in RI and southeastern CT,
also carried by the same ticks (about 40% of LD).


The population of the larval stage of the tick peaks in July-Sept., and the
nymph stage peaks in May-July, showing that the larva survives nearly a full
year on a single feeding.  The larva normally detaches in 2-3 days in the
late afternoon, in the mouse nest.  The adult usually feeds in the late fall
and lays eggs in about June which hatch in July.  Total life cycle may be 3
or 4 years.  The nymph population peak is at the same time that people come
to the island for the summer.  Based on the life cycle and time of infection,
the nymph (size of a sesame seed, usually not noticed) is most often the
carrier to humans, although the adult (size of an apple seed, usually
noticed) has twice the rate of infection.


Reducing the number of deer reduces the number of ticks.  Each adult tick
lays 1500-2000 eggs, each deer may have 100-1000 ticks.  Ticks are sensitive
to drying out, require humidity > 90%.  Mice in areas with woody stems had
more ticks than mice in areas with grass.  Piles of brush and woods between
yards increase deer, mouse, and tick populations.


Doing tick drags over 10-meter sections, it was found that areas of
infestation occur in clumps, half the drags gave nothing, some had as many as
ten ticks.  Not all clumps are infective.  Half the clumps are not infected,
others clumps range from 20% to 100% infection.  In one example an average of
16% of the ticks were infected, but almost 50% of the clumps had some
infected ticks, half the ticks in each infected clump was infected.  Not all
animals can act as reservoir hosts, lizards cannot infect ticks, incompetent
hosts can reduce the number of infected clumps.


The concept of enzootic overflow was presented, where there are more ticks
than the host population can support. This increases the chances of people
being infected.


{{ He referred to Ixodes dammini as a distinct species of tick that they
first discovered on Nantucket. This has recently been found to be the same
as Ixodes scapularis.}}
------------------------------------------------------------


Tick bites; Prevention and Prophylaxis. [4]
Eugene D. Shapiro, MD.


The risk of a tick bite is related to the proportion of infected ticks and
the duration of attachment.  The risk is substantial if a nymph has been
attached 36-48 hours, or an adult has been attached 48-72 hours.  A clinical
trial was done treating tick bites with either amoxicillin (250mg TID) or a
placebo for 10 days.  In the area of the study, 4% of larva, 12% of nymphs,
and 28% of adult ticks were infected.  Active surveillance was done for 1
year.  The risk of infection was determined to be 1.2% for a placebo, or 0%
for amoxicillin.  Conclusion is that risk "is so low that prophylactic
antimicrobial treatment is not routinely indicated."


    {{ A question was asked if tick removal technique affects risk, the
reply was no, unless you have an opening in the skin, but did not address
risk if the tick is squeezed while still attached.  Dr. Telford recommends
treatment if the tick has been attached more than 48 hours. (The LDF
recommends treatment in all cases.) }}
------------------------------------------------------------


Differential Diagnosis of Erythema Migrans. [5]
Irwin Braverman, MD.


A presentation of slides showing many variations of ECM.  ECM is slowly
expanding, usually leaving a clear center.  The edge is usually elevated due
to edema, does not have a solid feel.  There may be concentric rings, may be
necrosis in center, may look like cellulitis.


Other rashes that may look like ECM are: erythema annularis centripitum
(looks similar but may persist for many months), ringworm, granulum
annularis, subacute cutaneous lupus erythematosus (large lesions), erythema
pershing, or erythema marginatum.
------------------------------------------------------------


Lyme Carditis. [6]
Janine Evans, MD.


    Lyme carditis is relatively uncommon, reported in about 8% of those
untreated.  It is less common now due to early treatment.  LD can cause heart
block (1st degree to complete, may fluctuate), myocarditis, pericarditis,
dilated cardiomyopathy (in Europe), and ventricular tachycardia.  Typically
are self-limiting and resolve in several weeks, even without antibiotics.
Seven cases were summarized, 2 recalled a tick bite, 3 had an EM rash.  Many
had other symptoms first, fatigue, palpitations, shortness of breath,
headache, fever, arthralgias.  One patient was seronegative, then
seroconverted.  All improved within 48 hours on treatment.  Conclusion that
Lyme Carditis is a significant problem, with a dramatic presentation,
expect complete resolution with rarely long term sequelae.
------------------------------------------------------------


Evaluation of Neurologic Manifestations of Lyme Disease. [7]
Thomas N. Byrne, MD.


Lyme disease is a clinical diagnosis, with supporting laboratory data.
Often anxiety contributes to depression, mood disturbances, and memory
problems.  Early disease, within a month or so after EM, may have pain,
headache, symptoms of meningitis.  Bell's palsy (7th nerve) is most common,
meningitis sometimes seen, also radiculoneuritis.  Pleocytosis common,
glucose usually normal, protein usually elevated, all 12 bands frequently
present.  Spinal fluid is not important in diagnosis of peripheral
neuropathy.  Neuropsychological testing is difficult to interpret.


    {{Much of this material was from L. Reik's book "Lyme Disease and the
Nervous System" (1991).  He also referred to a paper in JAMA in spring 1992
(Luft), 1990 NEJM paper on chronic neurological manifestations (Logigian),
and Jan. 1993 paper in Neurology. }}
------------------------------------------------------------


Lyme Arthritis. [8]
Robert T. Schoen, MD.


Diagnosis uses recognition of clinical features.  Knee involvement common,
both here and in Europe.  Reviewed old studies of cases before antibiotics
were used.  Most have EM, exposure in geographic area, onset of symptoms in
characteristic time of year.  Most patients (> 95%) are ELISA positive by the
time they have arthritis.  Difference between mild and severe cases may
involve both the infection and host immunogenetic response.  Organism
disseminates widely, and to certain preferential sites.  Severity of onset
of disease correlates with later arthritis.  Host antibody response increases
with time.  HLA-DR4 and HLA-DR2 seen in patients with chronic arthritis.
Failures of antibiotic therapy in late Lyme disease may underlie an
immunogenetic susceptibility on the part of the host.  "When you evaluate
treatment protocols and success rates in treatment of Lyme Disease,
particularly late Lyme disease, you need to consider ... whether you're
getting a sampling that is biased by refractory cases."  Reported on study

of 50 patients, 80% arthritis and 20% neurological problems, who had 2 or 4
weeks of ceftriaxone, success at completion of treatment about 50%, 6 month
follow-up showed 85% success rate.  Success of 2 and 4 week therapy about
the same.  Suggests 2-4 week treatment, then watching for several months.
Oral treatment for mild arthritis and children, parenteral therapy for
severe arthritis.  There is no "head-to-head" comparison of oral versus
intravenous therapy.  A few refractory cases were discussed.


    {{ He seems more concerned with absolute certainty in diagnosing and
treating the average case than with the seronegative or difficult cases. }}
------------------------------------------------------------


Laboratory Testing in Lyme Disease.
Mark Mamula, Ph.D.


Connecticut has 10% of the US total cases of LD.  Testing relies either on
detecting the Borrelia burgdorferi organism (culture - not easy; or PCR), or
detecting the immune response (serum antibody response - IIF, ELISA; WB; or
T-cells - for late disease or serologically negative).  Antibody response
has early IgM and later IgG response.  Factors that influence test accuracy
are timing (too early), quality assurance of test, syphilis, relapsing fever,
and rheumatoid factor.  They have developed a more sensitive and specific
test using the P39 with ELISA.  One study found 6% of ELISA negatives were
positive for P39.  This test also has promise for earlier detection of Lyme
disease.


LD diagnosis is both a clinical an laboratory one.  Single positive ELISA may
be good enough with clear clinical criteria.  With ambiguous clinical
criteria, use both ELISA and Western blot.  If the Western blot has only a
positive 41kD band (not specific), then use the P39 ELISA.


Three years ago they did a comparison among Yale, Tufts, and U of Minnesota,
and found 96% (IgM) to 100% (IgG) correlation of negative results, and
73% (IgM) to 78% (IgG) correlation of positive results.


    {{ 78% correlation is no comfort if you are among those going
undiagnosed. They seem more concerned with false positives than false
negatives.}}
------------------------------------------------------------


Differential Diagnosis of Late Lyme Disease. [9,10]
Leonard Sigal, MD. (Robert Wood Johnson University Hospital, New Brunswick,
                   NJ)


Early disseminated neurologic disease occurs weeks to months into the
infection.  Children more often develop meningitis, and adults more often
develop radiculoneuritis.  "Tertiary neuroborreliosis can be differentiated
from the early disseminated neurologic disease by the fact that it is
later, very frequently in association with inflammatory joint disease, but
quite frequently it will be on its own, and sometimes it will be the very
first manifestation of Lyme disease."  The IgG and IgM responses may be
delayed.  The IgG and IgM responses may be suppressed, the potential for
seronegative Lyme exists but is "a very, very, uncommon phenomenon".


Immunoglobulin level may stay elevated despite adequate therapy.  Chronic
inflammatory disease can cause false positives in ELISA but not Western
Blot.  Use a lab doing clinical research in Lyme disease for best results.  
A major problem is overdiagnosis.  Lyme is often an incorrect diagnosis in
pediatric and adolescent fibromyalgia (Paper in Pediatrics, Oct. 1992).


Treat fibromyalgia with tricyclic antidepressants at bedtime, and exercise.
There is a paper to be published in the Annals of Internal Medicine.
Another study of 77 patients with fibromyalgia, mostly female, found 43 had
prior Lyme, 25 not Lyme, and 9 Lyme.  Using estimates for overdiagnosis of
Lyme disease, and extrapolating, the cost to find and cure one case of Lyme
disease in Montana, where Lyme is uncommon, will be approximately twenty
million dollars.


    {{Dr. Sigal often mixes his opinions with his data. He made several
interesting comments during this presentation:}}


"People in practice in New Jersey, certainly not Connecticut but in New
Jersey anyway will wind up drawing test after test after test to see whether
or not the person is cured. The patient is asymptomatic but is still
seropositive and so obviously we treat patients and not blood tests."


In "a university laboratory much more care is taken and certainly if you have
a question about the results the likelihood is that you are going to get
somebody who probably knows something about Lyme disease as opposed to a
technician who barely knows how to spell the thing."


"Kids who have been treated and treated and treated and treated a mean of 1.8
times per patient have been tested and tested and tested and tested I believe
the mean is 2.4 tests per patient. ... 40% of these kids describe a major
disruption in their lives due to their chronic illness.  No one's going to
school, home tutoring, which is by the way destroying the budgets of the
boards of education of a variety of counties of central and southern New
Jersey.  Some of these kids have been out of school for as long as two years
now.  Psychological stresses were found in 30% of these children, divorces,
child abuse, sexual abuse, major arguments with parents, that sort of thing.
Prior tick bite was relatively uncommon."
------------------------------------------------------------


Case Presentation.
Robert T. Schoen, MD.


The case presented was a 43 year old male in Stamford, CT.  This case was
picked as an example of a real diagnosis that had "shades of gray".


4/90  Multiple deer tick bites, physician documented EM, treated with
     amoxicillin, improved.


5/90  Recurrence of EM, treated with doxycycline for 28 days.

6/90  While on doxycycline, developed stiff right shoulder.

6/90-7/90  ceftriaxone, 6 weeks, 2g BID.  Developed more significant
     arthritis of hands, shoulders, neck, and knees.  Symptoms fairly
     symmetric.  Patient believed increased symptoms related to treatment.


7/90-6/91  Full symmetrical polyarthritis with morning stiffness.  RF
     negative, ANA negative, HLA-B27 negative, Lyme titer 1:1280, 5 bands
     on western blot.  Received 2 more courses of IV antibiotics, both
     approx. 4 weeks ceftriaxone.


6/91-1/92  Because of lack of response to treatment, and pattern of
     symmetric polyarthritis, decided that it was seronegative rheumatoid
     arthritis.  Started on therapy for arthritis.


4/92  Arthritis flared, IV corticosteroids for arthritis - little improvement.

4/92-3/93  Continued joint problems.  Headaches, impaired concentration,
     fatigue, depression.


3/93  Lumbar puncture, protein 9.5, 6 mononuclear cells, 41 red cells, 8
     bands on western blot.


Patient has been out of work most of this time.  Discussion followed. Dr.
Schoen asked for a show of hands:


Not Lyme in CNS? - A few people.
Definitely Lyme in CNS? - A few people.
Might be Lyme in CNS? - Most people.
Treat it? - Most people.


    Then we heard a short report from the patient's doctor. They chose to
start IV penicillin.  After 6 weeks, patient was marginally improved, Lyme
serologies have fallen, and Western blot is now negative.


    {{ This is a good example of how serious Lyme disease can be, even with
prompt treatment.  I would consider a case like this a red flag, rather than
a "gray area".  The "experts" should be researching better treatment of
cases like this, rather than complaining about overdiagnosis. }}
------------------------------------------------------------


A short mention was made, and a slide was shown, of an advertisement in a
local newspaper to call 1-800-TICK-BITE if you think you may have Lyme
disease.  The ad was from an infusion company.  It was viewed simply as the
infusion company's attempt to increase business.
------------------------------------------------------------


Panel Discussion (Answers from various doctors.)

Comments: You will never see a negative ELISA with a positive blot.

Q: Is 28 days of treatment enough?
A: It is 90-95% effective for early Lyme.  If there are secondary lesions,
  then it is a later stage.


Q: What do you do if you keep treating and have several consecutive
  treatment failures?


A: Then it is either not Lyme disease, or the symptoms may be slow to go,
  sometimes months are required.  Neuropsychological testing for some cases
  to reduce subjective complaints.


Q: (inaudible)
A: For early disseminated disease, 10 days is too short, 21 is needed, and
  continue for at least a week after patient is feeling okay.  Probenecid
  is not used any more, not very helpful and increases possibility of
  allergy to antibiotics.
------------------------------------------------------------


Polymerase Chain Reaction.
Stephen E. Malawista, MD.


    The urine antigen test was never validated and is not useful.  The PCR
test can detect the DNA of the spirochete.  It was first used to test ticks
from museums.  There was a brief description of the amplification process,
which can amplify a single piece of genetic material several million or
trillion times, in 30 to 45 doublings.  Contamination is a problem, because
the large amount of multiplied DNA in the lab can produce all positive or
false positive results.  They use isopsoralen which is activated by UV light
after the processing and binds with the amplified DNA so it cannot be
multiplied anymore.  They prefer working with spinal fluid or synovial
fluid, urine is more difficult to get right.  They would be happy to receive
samples for testing.
------------------------------------------------------------


Lyme Disease Vaccine. [11]
Erol Fikrig, MD.


    The reasons for a Lyme vaccine are that there are some refractory
cases, the EM rash is not always present, and the tick bite is sometimes
missed.  OSPA antibodies can protect against 10,000 spirochetes, OSPB
antibodies can only protect against 100.  OSPC antibodies can offer some
protection.  Bb can survive in the presence of neutralizing antibodies, both
in vitro and in vivo.  There are different strains of Bb, protection against
one may not protect against others.  They have developed both OSPA and OSPB
vaccines which appear to work, even with wild ticks.  The vaccine also
appears to kill the spirochetes in infected ticks that feed on vaccinated
mice.
------------------------------------------------------------


Lyme Disease Animal Model. [12]
Stephen W. Barthold, DVM, Ph.D.


They did experiments with a type of mouse (C3H) that develops visible
leg swelling after infection.  After infection with either a syringe or a
tick, the mouse develops symptoms of disseminated disease in 5 days.  In 15
to 30 days, the disease is at its peak, with polysynovitis, carditis, and
vasculitis.  At 90 days, the disease goes into regression.  At 180 to 360
days, there is exacerbation, then persistent infection.  Many spirochetes in
early acute stage of disease.  Smaller number of organisms in late disease.
The antibodies rise after 180 days.  The antibodies in the serum of a
chronically infected mouse will protect another mouse, but are apparently
not sufficient to clear the disease.  Serum antibodies given another mouse
24 hours after infection offer no protection.
------------------------------------------------------------


Pathogenesis of Lyme Disease. [13]
Leonard Sigal, MD. (Robert Wood Johnson University Hospital, New Brunswick,
                   NJ)


This discussed possible autoimmune reactions that cause symptoms not
directly caused by the Borrelia burgdorferi.


Bb is alive at the site of inflammation, induces septic process, cytokine
production.


Persisting antigen, organism may be dead.  Antigen induced arthritis.
Immune complex formation.  Vasculitis.


Molecular mimicry, organism may be absent.  Component of microorganism
resembles human tissue.  Immune response causes human tissue damage.  May
also occur in Lyme neurologic disease.
------------------------------------------------------------


Panel Discussion:

Borrelia does not destroy tissue with septic process, it is a very good
antigen.  That is why Lyme treatment with corticosteroids worked before
antibiotics were used. Much of disease is not because of lots of organisms,
but because they are very good antigens.
------------------------------------------------------------


{{ It is  interesting to note that little or no useful information was
presented on seronegative Lyme disease, ophthalmologic problems, persistent
infection, or Lyme during pregnancy. }}
------------------------------------------------------------


1.  "Lyme disease in Connecticut"; Matthew Cartter, MD; State of
   Connecticut Department of Health Services.


2.  "Clustering of host-seeking nymphal deer ticks (Ixodes dammini)
   infected by Lyme disease spirochetes (Borrelia burgdorferi"; SR
   Telford III, SS Urioste, & A Spielman; Am J Trop Med Hyg, 47(1),
   1992, pp 55-60.


3.  "Deer reduction & control of Ixodes dammini populations"; SR
   Telford; Ecology & Environmental Management of Lyme Disease ed. H.
   Ginsberg. Rutgers U. Press, 1993 In press.


4.  "A controlled trial of antimicrobial prophylaxis for Lyme disease
   after deer-tick bites"; ED Shapiro MD, MA Gerber MD, NB Holabird
   LPN BS, AT Berg PhD, HM Feder Jr MD, GL Bell BLT, PN Rys MS, DH
   Persing MD PhD; N Engl J Med 1992; 327:1769-73.


5.  "Diagnosis of Lyme disease based on dermatologic manifestations";
   MS Malane MD, JM Grant-Kels MD, HM Feder Jr MD, SW Luger MD; Annals
   of Internal Medicine 1991:114:490-498.


6.  "Lyme Carditis"; J Evans, L Rosenfeld, RT Schoen.

7.  "Neurological involvement in Lyme disease"; TN Byrne MD.

8.  "Epidemiology, clinical features, and diagnosis of Lyme disease";
   JD Cooper MD, RT Schoen MD; Current Opinion in Rheumatology 1992,
   4:520-528.


9.  "Lyme disease: Recommendations for diagnosis and treatment"; DW
   Rahn MD, SE Malawista MD.; Annals of Internal Medicine 1991;
   114:472-481.


10. "Lyme disease: testing and treatment"; LH Sigal MD; Rheumatic
   disease clinics of North America; V19 N1 Feb 1993 pp 79-93.


11. "A recombinant vaccine for Lyme disease"; E Fikrig, SW Barthold, JE
   Sears, SR Telford III, A Spielman, FS Kantor, RA Flavell; Lyme
   Disease: Molecular and Immunologic Approaches; Cold Spring Harbor
   Laboratory Press.


12. "Lyme Borreliosis in the laboratory mouse"; SW Barthold, M de
   Souza, E Fikrig, DH Persing; Lyme Disease: Molecular and
   Immunologic Approaches; Cold Spring Harbor Laboratory Press.


13. "Possible autoimmune mechanisms in Lyme disease"; LH Sigal;  Lyme
   Disease: Molecular and Immunologic Approaches; Cold Spring Harbor
   Laboratory Press.



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