Web-Page: http://www.ariplex.com/lyme/lymbur12.htm

Das englische Original dieser Web-Seite ist im Usenet veröffentlicht worden. Dr. Burrascano hat sein Manuskript einem Patienten gegeben, der es gescannt hat. Ich verstehe nicht, warum man so ein Manuskript nicht direkt auf Diskette weitergeben kann. Das würde Übertragungsfehler vermeiden.
14.11.98, Aribert Deckers

Dr. Burrascano überarbeitet seine "Guidelines" und gibt neue Versionen in unregelmäßigen Abständen weiter. So sind sie unter anderem auch im Usenet zu finden. Der hier vorliegende Text ist die Version 12 von 1998.

Die zur Zeit aktuelle Version ist Version 14!:

Wer sich tiefer mit der Materie beschäftigen möchte, benötigt hierzu auch die älteren Versionen. Aus diesem Grund archiviere ich die alten Versionen. Zur Zeit gibt es:
Version 14 http://www.ariplex.com/lyme/lymbur14.htm
Version 13 http://www.ariplex.com/lyme/lymbur13.htm
Version 12 http://www.ariplex.com/lyme/lymbur12.htm
Version 11 http://www.ariplex.com/lyme/lymburg1.htm

13.12.2002, Aribert Deckers

From: "Rita Stanley" <ritastan@worldnet.att.net>
Newsgroups: sci.med.diseases.lyme
Subject: Dr. Burrascano's "New Lyme Disease" '98 
Date: 28 Oct 1998 00:23:01 GMT
Message-ID: <715o55$e19@bgtnsc03.worldnet.att.net> Part 1
Message-ID: <715olu$gq1@bgtnsc03.worldnet.att.net> Part 2




Twelfth Edition
Copyright October, 1998


        PIROPLASMOSIS (Babesiosis)      5
        EHRLICHIOSIS        5
          ERYTHEMA MIGRANS       5
          DIAGNOSTIC CRITERIA       7
          SYMPTOM CHECKLIST       8
   PIROPLASMOSIS (Babesiosis)       10
        ANTIBIOTICS         13
        ANTIBIOTIC CHOICES       15
        PROPHYLAXIS        17
        FOR KNOWN TICK BITES       17
             1.early         17
             2.late          17
             1. pulse therapy        18
             2. combination therapy       18
             1. responsive to antibiotic therapy      18
             2. non-responsive to antibiotic therapy     19
   SAFETY          19
   Rationale for treating tick bites       27
   Rationale for treatment recommendations     28


THE NEW LYME DISEASEI humbly propose we redefine what we have been calling
Lyme. A huge body of research and clinical experience has demonstrated the
nearly universal phenomenon in Lyme patients of co-infection with multiple
tick-borne pathogens. As many have heard me say, coinfection is not
surprising, for ticks are arachnids that literally live in dirt and drink
the blood of wild animals. To think that a significant tick bite transmits
only one infection is narrow minded indeed. Studies have shown that
concurrent Borrelial and Ehrlichial and/or Babesial infections result in a
change in their individual clinical presentations, with different symptoms,
atypical signs, decreased reliability of standard diagnostic tests, and most
importantly, the creation of chronic, persistent forms of each of these
infections. As time goes by, I am convinced that more pathogens will be

 Therefore, Lyme, as we had come to know it, probably represents a mixed
infection. I will leave to the reader the implications of how this may
explain the discrepancy between laboratory study of pure Borrelia
infections, and what front line physicians have been seeing for years in
real patients.

It is still early in our efforts to sort out the individual contributions of
each of these pathogens in the coinfected patient, so the suggestions that
follow are quite preliminary. However, I believe this information is so
important, I did not want to delay any further this edition of my

I will refer to the general symptom complex as "Lyme", but will refer to the
separate entities as Lyme Borreliosis (LB) or Borrelia burgdorferi (Bb),
Babesia microti (Bm), and the Ehrlichia species as a group.
In past editions, I mentioned how the diagnosis and treatment of Lyme
Disease had entered a new era, as simplistic approaches were being replaced
by more modern ones based on better knowledge, more experience, and the
application of common sense. Seronegativity, the existence of chronic
persistent infection, relapses and treatment failures had all been
confirmed, as well as the need for many months of therapy in those ill for a
long time.  Unfortunately, many health care workers and health reporters
have not kept up with these facts. It is only through knowledge that we will
be able to conquer this misinformation.  Please continue your efforts to
educate the unaware.

The concept of a "therapeutic alliance" between the caregiver and patient
must again be emphasized.  This means that the patient has to work with and
become part of the medical team, and must take responsibility for complying
with the recommendations given, maintaining the best possible health status,
reporting promptly any problems or new symptoms, and especially in realizing
that despite all our best efforts, success in diagnosis and treatment is
never assured. The medical team must make great efforts to listen carefully
to the patient and not be too quick to dismiss seemingly bizarre or
illogical complaints.

I extend my best wishes to the many patients and caregivers who deal with
Lyme, and a sincere thank you to my colleagues whose endless contributions
have helped me shape my approach to tick borne illnesses. I hope that my new
approach proves to be useful. Happy reading!


The evaluation of a Lyme patient must begin with testing for all currently
known tick borne pathogens. Serological studies for Borrelia, Babesia and
Erlichia should be combined where appropriate with direct  antigen assays.
Antigen detection tests (antigen Capture and PCR) are especially helpful in
evaluating the seronegative patient and those still ill or relapsing after
therapy.  Unfortunately, over a dozen protozoans other than Babesia microti
can be found in ticks, yet commercial tests for only B. microti are
available at this time, so as in Borrelia, clinical assessment is the
primary diagnostic tool. In Erlichiosis, test for both the monocyte and
granulocytic forms. Many presently uncharacterized Ehrlichia-like organisms
can be found in ticks and may not be picked up by currently available
assays, so in this illness, too, serologies are only an adjunct in making
the diagnosis.

Babesia are parasites, and I suggest that if a coinfection is found
involving this organism, treat this first, so that subsequent therapy for
Borrelia and Ehrlichia will be more effective.

Experience has shown that collateral conditions exist in those who have been
ill a long time. Test B12 levels, and be prepared to aggressively treat with
parenteral formulations of the B-vitamins: 100mg each of Bl and B6 and 1000
mcg of B12 IM at least weekly in the more ill patient. Magnesium deficiency
is very often present and quite severe. Magnesium is predominantly an
intracellular ion, so blood level testing is of little value.  Oral
preparations are acceptable for maintenance, but most need parenteral
dosing: 1 gram IV or IM at least weekly until neuromuscular irritability has
cleared. Because the Lyme syndrome has been associated with faulty
activation of T4, measure free T3 levels by RIA and basal A.M. body
temperatures.  If hypothyroidism is found, treat with T3 preparations.

SPECT scanning of the brain, if done by knowledgeable radiologists using
high-resolution equipment, will show characteristic abnormalities in Lyme
encephalopathy.  This not only helps with the differential diagnosis, but if
done before and after acetazolamide, it will guide in the use of
vasodilators, which may clear up some cognitive symptoms.  Therapy can also
include serotonin agonists, pentoxiphylline and even Gingko biloba.
Therapeutic trials may be needed.

Tilt table testing is another powerful tool which, just as in CFIDS, may
demonstrate neurally mediated hypotension(NMH).  If found, therapy is based
on blood volume expansion (increased sodium and fluid intake and possibly
Florinef plus potassium). If not sufficient, beta blockade may be added
based on response to Isuprel challenge during testing. If NMH is present,
treatment can dramatically lessen fatigue and palpitations, and increase


Lyme is diagnosed clinically, as no currently available tests, no matter the
source or type, are definitive in ruling in or ruling out infection with
these pathogens, or whether these infections are responsible for the
patient's symptoms. The entire clinical picture must be taken into account,
including a search for concurrent conditions and alternate  diagnoses, and
other reasons for some of the presenting complaints.  Often, much of the
diagnostic process in late, disseminated Lyme involves ruling out other
illnesses and defining the extent of damage that might require separate
evaluation and treatment.

       Consideration should be given to tick exposure, rashes (even atypical
ones), evolution of typical symptoms in a previously asymptomatic
individual, and results of tests for tick borne pathogens. Another very
important factor is response to treatment-presence or absence of Jarisch
Herxheimer-like reactions, and improvement with therapy.


Classic teachings state that acute infections are usually only seen in those
with some form of  immune compromise. Flu-like symptoms rapidly evolve to
include shaking chills, high fevers, hemolysis and pancytopenia. Fatalities
have been reported. Visualizing Babesial forms on peripheral smears can make
the diagnosis in this situation.  In those with intact immune systems, a
mild flu-like illness appears one to two weeks after exposure and clears
without treatment over six to eight weeks. In either case, it is imperative
to test for Borrelia and Ehrlichia.

However, when coinfection exists, this acute presentation is much less
common, and it is rare to see parasite forms on smear. Signs of coinfection
include severe headaches, dizziness and encephalopathy out of proportion to
the other Borrelial symptoms. Testing is not at all definitive, yet should
include CBC, Babesia smear (very low yield), serologies (IgG and IgM) and if
necessary, PCR of peripheral blood.  Newer direct assays are currently being
researched, as this is an active area of investigation.  Always consider
coinfection in your current Lyme patients who are not responding fully.


While it is true that this illness can have a fulminant presentation, I am
convinced that milder forms do exist, especially when other tick-borne
organisms were transmitted. When present in a Lyme patient, persistent
leucopenia is an important clue. Thrombocytopenia is much less common, but
likewise should not be ignored. Headaches, myalgias, and ongoing fatigue
seem to relate to this illness, but are extremely difficult to separate from
symptoms caused by Bb. At this time, we only have serologies for laboratory
diagnosis, as no direct assay currently exists. There is no way at this time
to judge the accuracy of these tests, especially since there may be a
variety of pathogenic Ehrlichia-like organisms that will not be picked up by
current testing technology. Direct visualization of this organism in
leukocytes has been reported, but is rare.  Again, consider this diagnosis
in a LB patient not responding well to therapy.



     Erythema migrans (EM) is diagnostic of Bb infection, but is present in
fewer than half. Even if present, it may go unnoticed by the patient. It is
an erythematous, centrifugally expanding lesion that is raised and warm.
Sometimes there is mild stinging or pruritus. The EM rash will begin four
days to several weeks after the bite, and may be associated with
constitutional symptoms. Multiple lesions are present less than 10% of the
time, and represent disseminated disease. Some lesions have an atypical
appearance and skin biopsy specimens may be helpful.  When an ulcerated or
vesicular center is seen, this may represent a mixed infection, involving
other organisms besides B. burgdorferi.

 After a tick bite, serologic tests (ELISA, IFA, western blots, etc.) are
not expected to become positive until several weeks have passed. Therefore,
if EM is present, treatment must begin immediately, and one should not wait
for results of Borrelia tests. You should not miss the chance to treat early
disease, for this is when the success rate is the highest. Indeed, many
knowledgeable clinicians will not even order a Borrelia test in this


 When reactive, serologies indicate exposure only and do not directly
indicate whether the spirochete is now currently present. Because Bb
serologies often give inconsistent results, test at more than one laboratory
using if possible different methods. I recommend ordering both ELISAs and
western blots.
Be aware that in late disease there may be repeatedly peaking IgM's and
therefore a reactive IgM may not differentiate early from late disease, but
it does suggest an active infection. When late cases of LB are seronegative,
36% will transiently become seropositive at the completion of successful

         Western blots are reported by showing which bands are reactive.
41KD bands appear the earliest but cross react with T. pallidum and several
other spirochetes. The 18KD, 23-25KD (Osp C), 31KD (Osp A), 34KD (Osp B),
39KD, 83KD and the 93KD bands are the most specific but appear later or may
not appear at all. You need to see at least the 41KD and one of the specific
bands. 55KD, 60KD, 66KD, and 73KD are nonspecific and nondiagnostic.

         Antigen detection tests including PCR are now available, and
although they are very specific, sensitivity remains poor, possibly less
than 30%.  This is because Bb causes a deep tissue infection and is only
transiently found in body humors. Therefore, multiple specimens must be
collected to increase yield, and a negative result does not rule out
infection, yet a positive one is significant. The patient must be antibiotic
free for at least six weeks before testing. Antigen capture can be done on
urine, CSF, and synovial fluid. PCR can be done on blood (buffy coat is
best), urine, CSF, any other body fluid including breast milk, and on tissue
biopsy specimens.

Spinal taps are not routinely recommended, as a negative tap does not rule
out Lyme. Antibodies to Bb can be detected in the CSF in just 20% of
patients with late disease. Therefore, spinal taps are only performed on
patients with pronounced neurological manifestations, if they are
seronegative, or are still significantly symptomatic after completion of
treatment. When done, the goal is to rule out other conditions, and to
determine if Bb antigens are present. It is especially important to look for
elevated protein and mononuclear cells, which would dictate the need for
more aggressive therapy, as well as the opening pressure, which can be
elevated and add to headaches, especially in children.

To aid the clinician, a workable set of diagnostic criteria were developed
with the input of dozens of front line physicians. The resultant document
has proven to be extremely useful not only to the clinician, but it also can
help clarify the diagnosis for third party payers and utilization review
committees. It is important to note that the CDC's published reporting
criteria are for surveillance only, not for diagnosis.


Tick exposure in an endemic region        1
Historical facts and evolution of symptoms
consistent with Lyme          2
Systemic signs & symptoms consistent with Bb infection
(other potential diagnoses excluded):
Single system. e.g. monoarthritis       1
 Two or more systems. e.g. monoarthritis
and facial palsy          2
Erythema migrans, physician confirmed       7
Acrodermatitis Chronica Atrophicans, biopsy confirmed     7
Seropositivity           3
Seroconversion on paired sera        4
Tissue microscopy, silver stain        3
Tissue microscopy, monoclonal immunofluorescence     4
Culture positivity          4
B. burgdorferi antigen recovery        4
B. burgdorferi DNA/RNA recovery         4
Lyme Borreliosis Highly Likely        7 or above
Lyme Borreliosis Possible         5-6
Lyme Borreliosis Unlikely         4 or below
I suggest that when using these criteria, you state Lyme Borreliosis is
"unlikely', "possible", or "highly likely" based upon the following
criteria - then list the criteria.


This is not meant to be used as a diagnostic scheme, but is provided to
streamline the office interview.  Note the format - complaints referable to
specific organ systems are clustered to better display multisystem

NAME _______________   DATE _______________


Tick infested area__ Frequent outdoor activities__ Hiking__ Fishing ___
Camping ___ Gardening ___ Hunting ___ Ticks noted on pets ___
Do you remember being bitten by a tick? No__ Yes__ When? _________
Do you remember having the "bull's eye rash"?  No__ Yes__ Any other rash?
No__ Yes__
Have you had any of the following? (CIRCLE ALL YES ANSWERS)
1. Unexplained fevers, sweats, chills, or flushing
2. Unexplained weight change--loss or gain
3. Fatigue, tiredness, poor stamina
4. Unexplained hair loss
5. Swollen glands: list areas_____________________________________________
6. Sore throat
7. Testicular pain/pelvic pain
8. Unexplained menstrual irregularity
9. Unexplained milk production: breast pain
10.Irritable bladder or bladder dysfunction
11.Sexual dysfunction or loss of libido
12.Upset stomach
13.Change in bowel function-constipation, diarrhea
14.Chest pain or rib soreness
15.Shortness of breath, cough
16.Heart palpitations, pulse skips, heart block
17.Any history of a heart murmur or valve prolapse?
18.Joint pain or swelling: list
19.Stiffness of the joints, neck, or back
20.Muscle pain or cramps
21.Twitching of the face or other muscles
23.Neck creeks and cracks, neck stiffness, neck pain
24.Tingling, numbness, burning or stabbing sensations, shooting pains
25.Facial paralysis (Bell's Palsy)
26.Eyes/Vision: double, blurry, increased floaters, light sensitivity
27.Ears/Hearing: buzzing, ringing, ear pain, sound sensitivity
28.lncreased motion sickness, vertigo, poor balance
29.Lightheadedness, wooziness
31.Confusion, difficulty in thinking
32.Diffculty with concentration, reading
33.Forgetfuiness, poor short term memory
34.Disorientation: getting lost, going to wrong places
35.Difficulty with speech or writing
36.Mood swings, irritability, depression
37.Disturbed sleep-too much, too little, early awakening
38.Exaggerated symptoms or worse hangover from alcohol



         Piroplasms are not bacteria, they are protozoans. Therefore, they
will not be eradicated by any of the currently used Lyme treatment regimens.
Therein lies the significance of coinfections- If a Lyme patient has been
extensively treated yet is still ill, suspect a piroplasm.

         Just as in Lyme Borreliosis, the longer one has been infected, the
longer the course of therapy must be. Similarly, clinical assessment is the
only guide to treatment endpoint.

         Treatment choices are limited. Pentamidine is a treatment given as
daily IM shots- very painful, they cause sterile abscesses and permanent
fibrous scars on the buttocks. More importantly, response is poor, and the
patient risks development of glucose intolerance. Clearly, not a first

   Clindemycin, 600 mg qid plus Quinine, has been the published standard but
the suggested two week course is nearly impossible to tolerate (hearing
loss, rash, fever, headache) and treatment failures have been reported.

         Gentamicin in combination with either penicillin or a first
generation cephalosporin is used in treating livestock infected with
piroplasms. There are only anecdotal reports of efficacy in Humans and the
dose and duration of therapy (14 days) has not been well worked out. The
main side effect is hearing loss from the gentamicin, and the need for IM or
IV doses.

         Mepron (atavoquone), 750 mg bid, has demonstrated efficacy, but
should be given concurrently with azithromtcin, 250 to 600 mg daily, or
resistance may develop. Efficacy is by far the best with this combination,
but surprisingly, Herxheimer-like reactions are almost always seen at the
fourth day, and at the fourth week of therapy. Does this represent a newly
described phenomenon in treating Piroplasms, or does this combination have
heretofore unrecognized efficacy in killing Bb? Although I do not have the
answer, I suspect the latter simply based on the familiar (in Bb) four-week
cycle. In late, longstanding cases, one month of treatment is the minimum,
and four or more months are often needed. Problems during therapy include
diarrhea, mild nausea, the expense of Mepron ($600.00 per bottle- enough for
one month of treatment), and rarely, a temporary yellowish discoloration of
the vision. Regular blood counts and liver panels are recommended during any
prolonged course of therapy.


         Treatment recommendations at this time are very preliminary, mainly
due to the lack of direct detection methods needed to guide us in developing
a solid clinical feel. The mainstay of treatment is doxycycline, either
orally or IV, given for at least two weeks for an early infection, or at
least four weeks in a longstanding one. Interestingly, the unexpected
efficacy of IV doxycycline in treating Lyme cases which had previously
responded poorly to cell wall agents, may in fact reflect concurrent therapy
of coinfection with Bb and Ehrlichial species. The new concern for Ehrlichia
is the main reason that Doxycycline is now the first choice in treating tlck
bites and early Lyme, before serologies can become positive.


After a tick bite, Bb undergoes rapid hematogenous dissemination, and for
example, can be found within the central nervous system as soon as twelve
hours after entering the bloodstream. This is why even early infections
require full dose antibiotic therapy with an agent able to penetrate all
tissues in adequate concentrations to be bactericidal to the organism.

         It has been shown that the longer a patient had been ill with Bb
prior to first definitive therapy, the longer the duration or treatment must
be, and the need for more aggressive treatment increases.
         Bb contains beta lactamases, which, with some strains, may confer
resistance to cephalosporins and penicillins. This is apparently a slowly
acting enzyme system, and may be overcome by higher or more continuous drug
levels especially when maintained by continuous infusions (cefotaxime) and
by depot preparations (benzathine penicillin). Nevertheless, some penicillin
and cephalosporin treatment failures do occur and have responded to
sulbactam/ampicillin, imipenim, and vancomycin, which act on different cell
wall sites than penicillin and the cephalosporins.

         There is now evidence that B. burgdorferi can remain viable within
cells, such as macrophages, lymphocytes, endothelial cells, neurons, and
fibroblasts, and evade the effects of antibiotics in vitro by sequestering
in these intracellular niches. In addition, Bb secretes a glycoprotein that
can encapsulate the organism (an "S-layer"). This may impair immune
recognition and block antibiotic penetration. Because this glycoprotein
binds host IgM, it is possible that Borrelial antigens are hidden by host
protein, and in theory at least, this will interfere with immune
recognition, and cause seronegativity.

        There are multiple strains of Borrelia burgdorferi and they vary in
their antigen profile and antibiotic susceptabilities. In addition, L-forms
exist which do not contain cell walls, and thus cell wall antibiotics will
not affect them. Apparently, Bb can shift between the two forms during the
course of the infection and cause the varying serologic responses seen over
time, including seronegativity. Because of this, it may be necessary to
change antibiotics or even prescribe a combination of agents.

        Vegetative endocarditis has been associated with Borrelia
burgdorferi, but the vegetations may be too small to detect with
echocardiography. Keep this in mind when evaluating patients with murmurs,
as this may explain why some patients seem to continually relapse after even
long courses of antibiotics.
        As the spirochete has a very long generation time (12 to 24 hours in
vitro and possibly much longer in living systems) and may have periods of
dormancy, during which time antibiotics will not kill the organism,
treatment has to be continued for a long period of time to eradicate all the
active symptoms and prevent a relapse, especially in late infections. If
treatment is discontinued before all symptoms of active infection have
cleared, the patient will remain ill and possibly relapse further. In
general, early disseminated LB is treated for four to six weeks, and late LB
usually requires a minimum of four to six months of continuous treatment.
All patients respond differently and therapy must be individualized. It is
not uncommon for a patient who has been ill for many years to require open
ended treatment regimens: indeed, some patients will require ongoing
maintenance therapy to remain well.

        It has been observed that symptoms will flare in cycles every four
weeks. It is thought that this represents the organism's cell cycle, with
the growth phase occurring once per month. As antibiotics will only kill
bacteria during their growth phase, therapy is designed to bracket at least
one whole generation cycle. This is why the minimum treatment duration
should be at least four weeks. If the antibiotics are working, over time
these flares will lessen in severity and duration. The very occurrence of
ongoing monthly cycles indicates that living organisms are still present and
that antibiotics should be continued.

        With treatment, these monthly symptom flares are exaggerated and
presumably represent recurrent Herxheimer-like reactions as Bb enters its
vulnerable growth phase. For unknown reasons, the worst occurs at the fourth
week of treatment. Observation is that the more severe this reaction, the
higher the germ load, and the more ill the patient. In those with
long-standing highly symptomatic disease who are on I.V. therapy, the
week-four flare can be very severe, similar to a serum sickness reaction,
and be associated with transient leucopenia and/or elevations in liver
enzymes. If this happens, decrease the dose temporarily, or interrupt
treatment for several days, then resume with a lower dose. If you are able
to continue or resume therapy, then patients dramatically improve. Those
whose treatment is stopped and not restarted at this point usually will need
retreatment in the future due to ongoing or recurrent symptoms.  Patients on
I.V. therapy who have a strong reaction at the fourth week will need to
continue parenteral antibiotics for several months, for when this monthly
reaction finally lessens in severity, then oral or IM medications can be
substituted, indeed, it is just this observation that guides the clinician
in determining the endpoint of I.V. treatment. In general, I.V. therapy is
given until there is a clear positive  response, then treatment is changed
to IM or po until free of signs of active infection for 4 to 8 weeks. Some
patients, however, will not respond to IM or po treatment and I.V. therapy
will have to be used throughout. As mentioned earlier, leucopenia may be a
sign of persistent Ehrlichiosis, so be sure to look into this.
        Repeated treatment failures should alert the clinician to the
possibility of an otherwise inapparent immune deficiency, and a workup for
this may be advised.

        There are three things that will predict treatment failure
regardless of which regimen is chosen: Non-compliance, alcohol use on a
regular basis, and failure of the patient to obtain proper rest.  Advise
them to take a break when (or ideally before) the inevitable mid afternoon
fatigue sets in.
        All patients must keep a carefully detailed daily diary of their
symptoms to help us judge the effects of treatment, the presence of the
classic four week cycle, and treatment endpoint. One must follow such
diaries, temperature readings in late afternoon, physical findings, notes
from physical therapists, and cognitive testing to best judge when to change
or end antibiotics.

         Remember-there currently is no test for cure, so this clinical
follow-up assumes a major role in Lyme Disease care.

        There is no universally effective antibiotic for treating LB. The
choice of medication used and the dosage prescribed will vary for different
people based on multiple factors. These include age, weight,
gastrointestinal function, blood levels achieved, and patient tolerance.
Doses found to be effective clinically are often higher than those
recommended in older texts.  This is due to deep issue penetration by Bb,
its presence in the CNS including the eye, within tendons, and because very
few of the many strains of this organism now known to exist have been
studied for antibiotic susceptibility. In addition, all animal studies to
date have only addressed early disease in models that behave differently
than human hosts. Therefore, begin with a regimen appropriate to the setting
and modify it over time based upon responses and refer to the suggested
reading list and the appendix at the end of this document.

        There are four types of antibiotics in general use for Bb treatment.
The tetracyclines, including doxycycline and minocycline, are bacteriostatic
unless given in high doses. If high blood levels are not attained, treatment
failures in early and late disease are common. However, these high doses can
be difficult to tolerate. For example, doxycycline can be very effective but
only if adequate blood levels are achieved ether by high oral doses (300 to
800 mg daily) or by parenteral administration.

        Penicillins are bactericidal. As would be expected in managing an
infection with a gram negative organism such as Bb, amoxicillin has been
shown to be more effective than oral penicillin V. Because of its short
half-life and need for high levels, amoxicillin is usually administered
along with probenecid. Since blood levels are extremely variable they should
be measured.

        Cephalosporins must be of advanced generation: first generation
drugs are not effective, and second generation drugs are comparable to
amoxicillin and doxycycline both in-vitro and in-vivo. Third generation
agents are currently the most effective of the cephalosporins because of
their very low MBC's (0.06 for ceftriaxone) and have been shown to be
effective in penicillin and tetracycline failures. Cefuroxime axetil
(Ceftin), a second generation agent, is also effective against staph and
thus is useful in treating atypical erythema migrans that may represent a
mixed infection, containing some of the more common skin pathogens in
addition to Bb. Because of this agents GI side effects and high cost, it is
not used as first line drug.

        When choosing a third generation cephalosporin, there are several
points to remember: Ceftriaxone is administered once daily (an advantage for
home therapy), but has 95% biliary excretion and can crystallize in the
biliary tree with resultant colic and possible cholecystitis. GI excretion
results in a large impact on gut flora. Biliary and superinfection problems
with ceftriaxone can be lessened if this drug is given in interrupted
courses, such as five days in a row each week. Cefotaxime, which must be
given at least every twelve, and preferably every eight hours, is less
convenient, but as it has only 5% biliary excretion, it never causes biliary
concretions, and may have less impact on gut flora. It is the experience of
some clinicians that cefotaxime can be even more efficacious if given as a
continuous infusion, rather than in   interrupted doses.

        Erythromycin has been shown to be almost  ineffective as
monotherapy. The advanced macrolides and azalides such as azithromycin and
clarithromycin can be difficult to tolerate orally due to their  tendency to
promote yeast overgrowth and poor GI tolerance at the high doses needed. As
they have impressively low MBCs and do concentrate in tissues and penetrate
cells, they theoretically should be ideal agents.  However, initial clinical
results were disappointing, it has been suggested that when Bb Is within a
cell, it is held within a vacuole and bathed in fluid of low pH, and this
acidity may inactivate this class of antibiotics.  Therefore, they are
administered concurrently with hydroxychloroquine or amantadine, which raise
vacuolar pH, rendering these agents much more effective. It is not known
whether this same technique will make erythromycin a more effective
antibiotic in LB. Another alternative is to administer azithromycin
parenterally.  Results are excellent, but expect to see abrupt
Jarisch-Herxheimer reactions.

        Other agents with demonstrated in-vitro efficacy have been used
successfully in treating patients with Bb and are listed further below.
         Drug levels are measured until the most acceptable dose is found,
and then at any time major changes in the treatment regimen occur. With
parenteral therapy, CBC and chem/liver panels are done at least twice each
month during symptom flares, with urinalysis and prothrombin time monitored


ORAL THERAPY: Always check blood levels when using agents marked with an *,
and adjust dose to achieve a peak level in the mid-teens and a trough
greater than five. Because of this, the doses listed below may have to be
raised.  Consider Doxycycline first due to concern for Ehrlichlia.
Adults: 1g q8h plus probenecid 500mg q8h; doses up to 6 grams daily are
often needed
Pregnancy: 1g q6h and adjust.
Children: 50 mg/kg/day divided into q8h doses.
Adults: 100 mg tid with food; doses of up to 600 mg daily are often needed,
doxycycline is only effective at high blood levels. Not for children or in
If levels are too low at tolerated doses, give parenterally
*Cefuroxime axetil
Oral alternative that may be effective in amoxicillin and doxycycline
failures. Useful in EM rashes co-infected with common skin pathogens.
Adults and pregnancy: 1g ql2h and adjust.
Children: 125 to 500 mg ql2h based on weight.
Tetracycline- Adults only and not in pregnancy. 500 mg tid to qid
Erythromycin-Poor response and not recommended.
Azithromycin- Adults: 500 to 1200 mg/d. Adolescents; 250 to 500 mg/d
        add hydroxychloroquine, 200-400 mg/d or amantadine 100-200 mg/d
        Cannot be used in pregnancy or in younger children.
Clarithromycin- Adults: 250 to 500 mg q6h plus hydroxychloroquine 200-400
        or amantadine 100-200 mg/d. Cannot be used in pregnancy or in
younger children.
Augmentin- Cannot exceed three tablets daily due to the clavulanate, thus is
given with amoxicillin.
Chloramphenicol- Not recommended as not proven and potentially toxic.


Ceftriaxone- Risk of biliary sludging can be minimized with intermittent
breaks in therapy
(ie: infuse five days in a row per week).
Adults and pregnancy: 2g q24h. For large body habitus or more severe
illness: up to 4g daily
         Children: 75 mg/kg/day up to 2g/day
Cefotaxime- Comparable efficacy to ceftriaxone: no biliary complications.
Adults and pregnancy: 2g q8h; may dose as high as 12g daily. Consider
continuous infusion.
         Children: 90 to 180 mg/kg/day dosed q6h (preferred) or q8h, not to
exceed 12 g daily.
*Doxycycline- Requires central line as is caustic.
Surprisingly effective, probably because blood levels are higher when given
         Always measure blood levels.
         Adults: 400 mg q24h and adjust based on levels
         Cannot be used in pregnancy or in younger children.
Azithromycin- Requires central line as is caustic.
Dose: 500 to 1000 mg daily in adolescents and adults.
Penicillin G- IV penicillin G is minimally effective and not recommended.
Benzathine penicillin- Surprisingly effective IM alternative to oral
therapy.  May need to begin at lower doses as strong, prolonged (6 or more
week) Herxheimer-like reactions have been observed.
Adults: 1.2 million U once to twice weekly
         Adolescents: 300,000 to 1.2 million U weekly.
Should not be used in pregnancy.

Poorly studied but anecdotally effective

Vancomycin- observed to be one of the best drugs in treating Lyme, but
potential toxicity limits its use. It is a perfect candidate for pulse
therapy to minimize these concerns. Use standard doses and confirm levels.
Imipenim and Unisyn-similar in efficacy to cefotaxime, but often works when
cephalosporins have failed.
        Must be given q6 to q8 hours.

Cefuroxime- useful but not demonstrably better than ceftriaxone or
Ampicillin IV- more effective than penicillin G. Must be given q6 hours.

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PROPHYLAXIS of high risk groups- education and preventive measures.
Antibiotics are not given.

TICK BITES - Embedded Deer Tick With No Signs or Symptoms of Lyme (see

Decide to treat based on the type of tick, whether it came from an endemic
area and percent infected, how it was removed, and length of attachment
(nymphs; at least one day: adults; anecdotally, as little as four hours).
The risk of transmission is greater if the tick is engorged, or if it was
removed improperly allowing the tick's contents to spill into the bite
wound. High risk bites are treated as follows (remember the possibility of

1)Adults: Oral therapy for 21 days.
         2) Pregnancy: Amoxicillin 1000 mg q6h for 6 weeks. Test for Babesia
and Ehrlichia.
             Alternative: Cefuroxime axetil 1000 mg q12h for 6 weeks.

3) Young Children: Oral therapy for 21 days.

EARLY LOCALIZED-Single erythema migrans with no constitutional symptoms:
         1) Adults: oral therapy for 6 weeks.
         2) Pregnancy: 1st and 2nd trimesters; I.V. X 21 days then oral X 6
            3rd trimester: Oral therapy x 6 weeks.
              Any trimester- test for Babesia and Ehrlichia
3) Children: oral therapy for 6 weeks.

DISSEMINATED DISEASE-Multiple lesions, constitutional symptoms,
lymphadenopathy. or any other manifestations of dissemination.

EARLY DISSEMINATED: Milder symptoms present for less than one year and not
complicated by immune deficiency or prior steroid treatment:

1) Adults: oral therapy until no active disease for 4 weeks (4-6 months
         2) Pregnancy: As in localized disease, but duration as above. Some
experienced clinicians
treat throughout pregnancy
         3) Children: Oral therapy with duration based upon clinical

PARENTERAL ALTERNATIVES for more ill patients and those unresponsive to or
intolerant of oral medications:

1) Adults and children: I.V. therapy for 6 weeks or until clearly improved.
Follow with oral therapy or IM benzathine penicillin until no active disease
for 8 weeks. I.V. may have to be resumed if oral or IM therapy fails.
         ) Pregnancy: IV then oral therapy as above.

LATE DISSEMINATED: present greater than one year, more severely ill
patients, and those with prior significant steroid therapy or any other
cause of impaired immunity:

         1) Adults and pregnancy; extended IV therapy (6 to 10 or more
weeks), then
             oral or IM, if effective, to same endpoint.
         2) Children; IV therapy for 6 or more weeks, then oral or IM follow
up as above.



        Pulse therapy consists of administering antibiotics (usually
parenteral ones) two to three days in a row per week. This allows for
several advantages:
        *Dosages are doubled (ie: cefotaxime, 12 g daily), increasing
        *More toxic medications can be used with increased safety (le;
        *May be effective when conventional, daily regimens have failed.
        *IV access may be easier or more tolerable
        *More agreeable lifestyle for the patient
        *Often less costly than daily regimens

Note that this type of treatment is expected to continue for a minimum of
ten weeks, and often must continue beyond twenty weeks. The efficacy of this
regimen is based on the fact that it takes 48 to 72 hours of continuous
bactericidal antibiotic levels to kill the spirochete, yet it will take
longer than the four to five days between pulses for the spirochetes to
recover. As with all Lyme treatments, specific dosing and scheduling must be
tailored to the individual patients clinical picture based upon the
treating physician's best clinical judgment.


        This consists of using two or more dissimilar antibiotics
simultaneously for antibiotic synergism and to better compensate for
differing killing profiles and sites of action of the individual
medications. A typical combination is the use of a cell wall agent plus a
protein inhibitor (ie: amoxicillin plus clarithromycin). Note that GI
intolerance and yeast superinfections are the biggest drawbacks to this type
of treatment.  However, these complications can often be prevented or easily
treated, and the clinically observed benefits of this type of regimen
clearly have outweighed these problems in selected patients.



        Patients in this group improve on antibiotics yet relapse repeatedly
when medications are
Discontinued.  Some patients in this category have been proven, in peer
reviewed medical literature, to have persistent infection. The treating
physician may decide on chronic therapy in order to avoid clinical
deterioration.  Recommend you confirm blood levels, and study immune
competence. This includes T- and B- cell function and counts, Natural Killer
cell functional assays, complement levels, neutrophil function, and vaccine

Options for treatment:
- Longer duration. including open ended maintenance therapy
- Increased dose
- Different drug
- Change method of administration (oral to IV)
- Combination or pulse therapy
- Synovetomy
- Search for and treat concurrent illnesses
- Supportive therapy as needed


- Reconsider the diagnosis, and perform specific Bb antigen tests after
antibiotic free for 6 to 12 weeks.
- Search for and treat concurrent illnesses and coinfections
- Supportive therapy based on symptoms
- NSAIDS and hydroxychloroquine
- Antidepressants, analgesics, muscle relaxants, and amantadine
- Synovectomy
- Psychiatric/psychometric evaluation and treatment if indicated
- Long-term follow-up
- Consider retreatment if condition changes



- daily yogurt and acidophilus preparations
- multivitamins and B complex 50 mg daily
- Physical therapy, rehabilitation, and a graded exercise program

PRESCRIBE AS NEEDED, especially in more severe cases:

- vitamin and nutritional supplements as listed below
- Psychosocial evaluation and possibly refer for counseling
- NSAIDS and remittive agents
- antidepressants, analgesics, muscle relaxants, and amantadine
   - immune globulins and other immunotherapy if indicated
   - Sinequan (DAW) in low doses (5 to 50 mg daily) reportedly improves
T-cell function


- alcohol use
- excessive caffeine intake
- any avoidable stresses
- sleep deprivation


        Over a decade of experience in treating thousands of patients with
Lyme has proven that therapy as described above, although intense, is
generally well tolerated.  The most common adverse reaction seen is allergv
to probenecid.   In addition, yeast superinfections are seen, but
these are generally easily recognized and managed. The induction of
Clostridium difficile toxin production is seen most commonly with
ceftriaxone, but can occur with any of the antibiotic regimens mentioned in
this document. However, regular use of the lactobacillus preparations seems
to be helpful in controlling yeast and antibiotic related colitis, as the
number of cases of C. difficile in Lyme patients is low when these
guidelines are followed.

        When using PICC lines (peripherally inserted central catheters), if
ANY line problems arise, it is recommended that the line be pulled for
patient safety.  Salvage attempts (urokinase,  repairing holes) are often
ineffective and may not be safe

        Please advise all patients who take the tetracyclines of skin and
eye sensitivity to sunlight and the proper precautions. When doxycycline is
given parenterally, do not freeze the solution prior to use!

        Years of experience with chronic antibiotic therapy  in other
conditions, including rheumatic fever, acne, recurrent otitis, recurrent
cystitis, COPD, bronchiectasis, and others have not revealed any consistent
dire consequences as a result of such medication use. Indeed, the very real
consequences of untreated chronic persistent infection by B. burgdorferi can
be far worse than the potential consequences of this treatment.


        Studies on patients with chronic Lyme Disease and in those with the
Chronic Fatigue Syndrome have demonstrated that some of the late symptoms
are related to cellular damage and deficiencies in certain essential
nutrients. Double blinded, placebo controlled studies, and in one case
direct assay of biopsy specimens have proven the value of the supplements


        Studies show that when EFAs are taken regularly, statistically
significant improvements in fatigue, aches, weakness, vertigo, dizziness,
memory, concentration and depression are likely. There are two broad
classes: GLA and EPA, derived respectively from plant and fish oils. The
plant sources are many, so choose one from the list below.

         Plant Oils:  evening primrose oil
                     black currant seed oil
                     borage oil (probably the best choice)
         Fish oil:   'MAX EPA" (or any similar preparation containing 1,000
mg of EPA)

RECOMMENDATION: four plant oil capsules and two to four EPA capsules dairy,
taken with the largest meal of the day.  Benefit begins within several days,
but further improvement continues to occur over time.  Continue for three to
four months.

CO-Q 10 (ubiquinone):

        This is a vitamin B- like compound essential to every living cell.
Deficiencies have been related to poor function of the heart, limitations of
stamina, and poor resistance to infections. Tissue biopsy studies have
resulted in the recommendation that a patient with chronic Lyme should take
between 200 and 300 mg daily, in two or three equal doses.   Improvements in
stamina and general well being do not begin for several weeks. The body will
manufacture its own Co-Q 10 when the original infection is controlled, but
only if stimulated by aggressive exercise.  Therefore use this supplement
until the patient is feeling well and is exercising  regularly, usually
three to four months.


         Studies in the 1950s demonstrated the need for supplemental
vitamin B in infections with other Borrellia. This enhances clearing of
neurological symptoms. I recommend one 50 mg B-complex capsule daily long


         Magnesium supplementation very helpful for the tremors, twitches,
cramps, muscle soreness, arrhythmias and weakness. It may also help in
energy level and cognition. Unexplained hyperreflexia is an indicator of Mg
deficiency. The best source is magnesium chloride ('Bio-Mag', one or two
qid) or magnesium oxide (Mag-Ox, 400 mg one or two daily). DO NOT rely on
"cal-mag", calcium plus magnesium combination tablets, as they are not well
absorbed.  In many cases, I.M. or I.V. magnesium is necessary.  Continue
long term.


         I recommend the Life Pack family of supplements - choose LifePak
for males under 40, LifePak Women for hormonally active women, and Lifepak
Prime for post menopausal women and men over 40.  These are unique
supplements-Pharmaceutical grade and USP certified, and the only products
clinically proven to raise antioxidant levels in the blood and lipids. They
are available by mail order- call 1-800-487-1500, reference # US 9256681.
Continue long term.

All of these products are available without a prescription.


Those with long-standing tick borne illnesses end up in poor physical
condition. Even with successful treatment of the infections, they will not
return to normal unless they take an active role in personal rehabilitation.

        In late stage disease, many negative effects to the body are
occurring: muscles atrophy, and to some degree, the heart muscle also
suffers, as do the joints, tendons, nerves, etc. The percent fat content of
the body as a whole rises, the cholesterol rises, and the balance between
HDL and LDL becomes less favorable.  In at least 50% of the patients,
significant weight gain occurs.

Because of the extreme fatigue and body pain, many Lyme sufferers end up
spending inordinate amounts of time in bed, and get far less exercise than
they did before they became ill. This begins a debilitating downward spiral
that can be very difficult to reverse.

         As a result, Lyme patients are stiff, weak, tired, have poor
stamina, and are at increased risk for cardiovascular disease and diabetes.
Antibiotic treatment alone cannot correct these effects. Therefore, it is
necessary to prescribe physical therapy, the extent of which depends on an
individual patients' condition, followed by a graded exercise program.

         The earliest phase involves multiple modalities (massage, heat,
TENS, MENS, ultrasound. etc.) and aggressive range of motion exercises
supervised by a physical therapist.  The goal is to relieve discomfort and
to promote better sleep and flexibility. This then evolves into stretching
and mild muscular toning which can lessen joint pain and increase mobility
and stamina. Finally, the program must expand to include muscular
conditioning and strengthening, ideally under the supervision of a
credentialed exercise physiologist. 'Body sculpture'  classes are ideal.
Aerobics are not recommended until the patient has fully recovered.

This is the time for the very best of health habits. I recommend light, low
fat food, with high quality nutritional value, minimal amounts of starch and
other simple carbohydrates, absolute abstention from alcohol, elimination of
caffeine, and, if applicable, a serious commitment to weight loss. Consider
recommending books that outline "Arthritis diets", as they can help some

         Cessation of smoking is extremely important and must be addressed
         As written orders for physical therapy are required to initiate the
program, an example of the format of a typical prescription for Lyme
rehabilitation follows.


NAME  ________________________________________________________

D.O.B. __________________________ DATE ________________________

Please enroll this patient in a program of therapy to rehabilitate him/her
from the effects of Lyme
Disease.  If necessary, begin with classic physical therapy, then progress
when appropriate to a whole body conditioning program.  Such therapy must be
graded, carefully individualized, and be performed on a one-on-one basis, at
least initially, to ensure the maximal amount of  supervision and guidance.

THERAPEUTlC GOALS (to be achieved in order as the patient's ability allows):


1.  Relieve pain and muscle spasms utilizing multiple modalities as
available and as indicated: massage, heat, ultrasound, TENS, "micro amp",
2. Increase mobility while protecting damaged and weakened joints, tendons,
and ligaments, to increase range of motion and relieve stiffness.

EXERCISE: Begin with a private trainer for careful direction and education.

PATIENT EDUCATION AND MANAGEMENT (to be done during the initial one-on-one
sessions and reinforced at all visits thereafter):

1.  Instruct patients on correct exercise technique, including proper
warm-up, breathing, joint protection, proper body positioning during the
exercise, and how to cool-down and stretch afterwards.

2.  Please work one muscle group at a time and perform extensive and
extended stretches to each muscle group immediately after each one is
exercised, before moving on to the next muscle group.

3.  A careful interview should be performed at the start of each session to
make apparent the effects, both good and bad, from the prior visits therapy,
and adjust therapy accordingly.

1.  Improve strength and reverse the poor conditioning that results from
Lyme, through a whole-body exercise program ("stretch and tone", or "body
sculpture" classes). This consists of light calisthenics and weight lifting,
using small weights and many repetitions.

2.  Exercise no more often than every other day

3. Each session should last one hour. If the patient is unable to continue
for the whole hour,
the program to decrease the intensity to allow him/her to do so.

4. This is what is required to achieve wellness and is the main focus of
rehab. Simply placing the patient on a treadmill or an exercise bike is not
acceptable, nor is a simple walking program.

5.  Aerobic exercises are not allowed, not even low impact variety, until
the patient has fully recovered.

Please feel free to contact my office if you would like to discuss this
client's situation in more detail.
PHYSICIAN'S SIGNATURE______________________________________


Many patients with Lyme Disease develop an overgrowth of yeast. Therefore,
it is recommended that on a daily basis the patient eat a full container or
yogurt that contains active cultures, and take acidophilus, two after each
meal.  Here are some suggestions on how to control yeast:

MOUTH: A tongue with a beige coating, bad breath, and dysgeusia are signs of
thrush. The patient must brush the tongue whenever they brush their teeth,
and use antiseptic mouthwashes then. Because the effectiveness of a
mouthwash is related to how long it is in contact with the germs, it should
be kept in the mouth while brushing.

Since yeast germs feed on sugars, have patients avoid simple carbohydrates,
starches, fruits, and juices for at least two weeks, or until the problem is

Prescription medications may be necessary. Mycelex troches and Nystatin
liquid are not
recommended for they contain large amounts of simple sugars. Nystatin powder
is used, mixed with water, to be swished end swallowed qid (pc and hs).
Systemic antifungals (Diflucan, Nizoral) may be necessary.
The most effective (and drastic) treatment, employed as a last resort,
consists of using "Dakin's Solution" as a mouth rinse.  This is a mixture of
household liquid bleach (Clorox), one teaspoon in four ounces of water. A
small amount is held in the mouth while brushing, then spit out, and
repeated until the mouth has cleared. This is usually a one-time treatment,
but may have to be repeated every few weeks.
After using an antiseptic to clean the mouth, it is necessary to immediately
eat yogurt or
liquid acidophilus, or chew an acidophilus capsule to replenish the
beneficial flora in the mouth.
Because the germ count after such a cleaning will be artificially reduced,
and because yeast germs are opportunists, they would be the first to come
back.  By having the yogurt or acidophilus then, a more normal oral flora
will result and thrush will be better controlled.

INTESTINAL TRACT: An overgrowth of yeast here will ferment dietary sugars
and starches, forming acids, gas, and alcohols. Symptoms include gas,
heartburn and/or pain in the stomach area, and because of the alcohol, there
can be headaches, dizziness. lightheadedness, and wooziness. To clear
intestinal yeast, first the tongue and mouth must be cleared so yeast does
not reenter the system with every swallow. Avoid sweets, starches, fruits
and juices for two weeks or longer to starve the germs. Systemic antifungals
(Diflucan, Nizoral) usually are needed.

VAGINAL: An occasional vaginal yeast infection can be controlled with
products such as Monistat cream or suppositories.  If it is a recurrent or
ongoing problem, then it often reflects a simultaneous intestinal infection,
reinfecting the genital area with every bowel movement. Therefore treat the
patient as above for intestinal overgrowth, and prescribe topical
preparations such as Monistat concurrently for two weeks.



PROPERTY  Remove wood piles, rock walls, and bird feeders as these attract
tick-carrying small animals and can increase the risk of acquiring Lyme.

INSECTICIDES: Property should be treated with a product called "Damminix".
This consists of cardboard tubes containing cotton balls that have been
dipped in insecticide.  These tubes are placed around the property in the
wooded areas and below shrubs. Mice, which are a key link in the propagation
of Lyme disease, find the cotton and bring it back to their burrows to be
used as nesting material, with the result being a big decrease in the number
of ticks in the area.  Unfortunately, after two years tick populations may
rise again as other small animals that do not gather cotton become hosts to
the ticks, Therefore, Damminix alone is not sufficient.  Use this product in
conjunction with liquid or granular insecticides.

LIQUID & GRANULAR PESTICIDES: Products meant for widespread application
include Dursban, Tempo, permethrin, and sevin. They are available as a
liquid concentrate and as granules. If liquid insecticides are used,
application should be by fogging, not by coarse sprays. Apply these products
in a strip a few feet wide at the perimeter of the lawn at any areas
adjacent to woods and underbrush. Also treat any ornamental shrubs near the
house that may serve as a habitat for small animals. The best time to apply
these products is in late Spring and early Fall.

CLOTHING  When wearing long pants, tuck the cuffs into the socks so any
ticks that get on shoes or socks will crawl on the outside of the pants and
be less likely to bite. Also, light colored clothing should be worn so the
ticks will be easier to spot.  Smooth materials such as windbreakers are
harder for ticks to grab onto and are preferable to knits, etc.

Tick repellents that contain "permethrin" (Permanone, Permakill) are meant
to be sprayed onto clothing. Spray the clothes before they're put on, and
let them dry first. Do not apply this chemical directly to the skin.
Ticks are very intolerant of being dried out. After being outdoors in an
infested area, place clothes in the dryer for a few minutes to kill any
ticks that may still be present.

SKIN  Insect repellents that contain "DEET" are somewhat effective when
applied to the arms, legs, and around the neck.  Do not use any repellent
over wide areas of the body as they can be absorbed causing toxicity. Also,
it is inadvisable to use a product that contains more than 50% DEET, and 25%
concentrations are preferred. Use repellents cautiously on small children,
as they are more susceptible to their toxic effects. Be aware that this
repellent evaporates quickly and must be reapplied frequently.
Check carefully for ticks not only when home but frequently while still


         Using a tweezer (not fingers!), grasp the tick as close to the skin
as possible and pull straight out.  Then apply an antiseptic. Do not try to
irritate them with heat or chemicals, or grasp them by the body, as this may
cause the tick to inject more germs into your skin. Tape the tick to a card
and record the date and location of the bite. Remember, the sooner the tick
is removed, the less likely an infection will result.



The Medical Advisory Committee of the Lyme Disease Foundation now recommends
antibiotic prophylactic treatment upon a known tick bite for:

1. People at higher health risk bitten by an unknown type of tick or tick
capable of transmitting Borrellia burgdorferi, e.g. pregnant women, babies
and young children, people with serious health problems, and those who are

2. Persons bitten in an area endemic for Lyme Borreliosis by an unidentified
tick or tick capable of transmitting B. burgdorferi,

3. Persons bitten by a tick capable of transmitting B. burgdorferi, where
the tick is engorged, or the attachment duration of the tick is greater than
four hours, and/or the tick was improperly removed. This means when the tick
is squeezed between the fingers, irritated with toxic chemicals in an effort
to get it to back out, or disrupted in such a way that its contents were
allowed to contact the bite wound.  Such practices increase the risk of
disease transmission.

4. A patient, when bitten by a known tick, clearly requests oral prophylaxis
and understands the risks.  This is a case-by-case decision.

The physician cannot rely on a laboratory test or clinical finding at the
time of the bite to definitely rule in or rule out Lyme Disease infection,
so must use clinical judgment as to whether to use antibiotic prophylaxis.
Testing the tick itself for the presence of the spirochete, even with PCR
technology, is not reliable enough to guide your decision to treat, as false
positives and false negatives occur.

          An established infection by B. burgdorferi can have serious,
long-standing or permanent, and painful medical consequences, and be
expensive to treat. Since the likelihood of harm arising from
prophylactically applied spirochetal antibiotics is low, and since treatment
is inexpensive and painless, it follows that the risk benefit ratio favors
tick bite prophylaxis.

It is the Medical Advisory Committee's recommendation that antibiotic
prophylactic treatment for tick bite in many circumstances is not only
justified but warranted. The ultimate decision for treatment on tick bite
should be determined jointly between the physician and patient.


When I began treating Lyme Borreliosis (LB) in the mid 1980s, I recognized
that in disseminated disease, the then recommended ten to fourteen day
courses of antibiotics would either result in only a lessening of the
illness, or an initial good outcome followed by a relapse of symptoms. These
patients would then respond again to a repeat course of antibiotics.

          Published studies by Steere and others (1) had, at that time,
defined success as the elimination of the "major" symptoms of Lyme
(arthritis, carditis, and Bell's Palsy) even though they usually resolve
over time without treatment.  These same studies go on to report the
persistence of "minor symptoms" of Lyme even after antibiotic therapy, and
the authors call it the "post Lyme syndrome".

          In 1987 I participated in a study in which twenty six patients
with active disseminated LB who were culture positive for Borrelia
burgdorferi (Bb), were treated with ceftriaxone I.V. for fourteen days,
using either two or four grams a day.  Although culture negative at the
immediate end of therapy, all patients became culture positive again within
several weeks, which corresponded to the time when their symptoms recurred.
I concluded then that the persistence of symptoms after this type of therapy
in fact represented ongoing infection.  The results of this study were
presented in 1989 at the national meeting of the Lyme Borreliosis
          Upon the advice of colleagues who for years have been involved in
seminal LB research (2), I then studied the effects of lengthened duration
of treatment.  I found a direct correlation between treatment duration and
the ultimate outcome of patients' symptoms.  Using amoxicillin 3g/day plus
probenecid 1 .5g/day in divided doses, the per cent success was tabulated
for therapies lasting for from one through six months.  Success here is
defined as the elimination of all LB symptoms, both major and minor, without
a relapse by three months after completion of treatment.

The data clearly demonstrated a direct relationship between duration and
success, starting at 17% for one month of therapy, and reaching a plateau at
67% at five months duration. These data were also presented at the 1989
meeting mentioned above.

Next, using ceftriaxone, results of therapy were tabulated based on
duration.  Even with 45 days of continuous antibiotic, none of the patients
returned to or maintained their well, pre-Lyme state. However, if oral
medications were continued after ceftriaxone, to the endpoint of being free
of signs and symptoms of active disease, then relapses did not occur. Again,
the average duration of antibiotic treatment necessary to achieve this was
at least four months.

Further culture studies involving 74 patients confirmed that the patients
had to be free of signs and symptoms of active Borreliosis before
antibiotics were discontinued in order to be both culture negative, and not
experience a relapse during three months of follow up.

          There are now a growing number of published reports utilizing
various forms of Bb antigen detection that demonstrate the persistence of
infection in antibiotically treated patients (3,4,5,6,7,8), confirming my
earlier work. Even Steere has proposed this as a mechanism for chronic
arthritis in Lyme (9).

          Although syphilis perhaps is not a synonymous spirochetosis to
Lyme, similar findings of organism persistence despite presumed adequate
(short course) therapy has been reported in those who later became immune
deficient (10). Indeed, Wassermann in 1936 recommended a minimum of twenty
six weeks of treatment for established infection, based upon generation-time

I had participated in an NIH study utilizing the antigen detection method of
Dorward et at (11) in testing over 130 patients with Chronic Persistent LB,
in whom symptoms of active disease continued despite even prolonged
treatment (indeed, some would describe as excessive the treatment given to
several participants), Bb could be recovered from blood, CSF, urine, and
tears.  Indeed, many of these patients had received months to years of
aggressive, often parenteral therapy for LB.  For example, one had received
continual antibiotics for three years, while another was treated for 18
months with repeated courses of parenteral therapy. As a matter of record,
neither one was a patient of mine.

These examples clearly indicate what researchers have recognized as the
ability of Bb to evade host defenses (1,12,13,14,15) even in the presence of
antibiotics (5,6,7,8).

          I do not now recommend treatment forever, but I point out the
above results to be able to make several points:

1.  There has never been a study in the history of this illness that even in
the simplest way proves that currently recognized short-course (two to four
week) therapy results in a bacteriologic cure.

2.  There has never been a consensus in patients still symptomatic after
short treatment courses as to what constitutes the post Lyme syndrome, how
Bb induces it, and what perpetuates it if bacteriologic cure is indeed

3. Patients must be kept on therapy until free of active symptoms or they
either will never recover fully, or suffer a relapse.

4. Extended durations of antibiotic therapy clearly have helped literally
thousands of patients who were not helped by short courses of treatment.

5.  Finally, we have to recognize that in some patients, LB may not be
curable in a strict
bacteriologic sense.

Until sensitive and specific antigen detection tests become widely
available, treatment of LB will remain difficult, controversial, and the
subject of much discussion.

                                        J.J. Burrascano, Jr., M.D


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lesions of patients with erythema chronicum migrans Afzelius and
acrodermatitis Chronica atrophicans. Acta Pathol Microb Immunol Scand 1985;
Sect B, 93: 161-163
2. Berger, B.W., Johnson, R. C., Schwann, T.G. Clinical and microbiologic
findings in six patients with erythema migrans of Lyme Disease, Am J Acad
Dermatol 1989: 21:1186-91
3. Cimmino, M.A., Azzolini, A., Tobia, F., Pesce, C.M. Spirochetes in the
spleen of a patient with chronic Lyme Disease. Am J Clin Pathol 1989;
4. Dorward, D.W., Schwan, T.G., Garon, C.F.  Immune capture and detection of
Borrelia burgdorferi antigens in urine, blood, or tissues from infected
ticks, mice, dogs, and humans. J J Clin Microbiol 1991:29(6):1162-70
5. Harris, N.S., Stephens, B. Detection of Borrellia burgdorferi antigen in
urine from patients with Lyme borreliosis, 1995; 2(2):37-41
6. Hassler, D., Riedel, K., Zorn, J., Preac-Mursic, V.  Pulsed high dose
cefotaxime therapy in refractory Lyme Borreliosis, Lancet 1991:338:13
7. Kirsch, M. etal.  Fatal adult respiratory distress syndrome in a patient
with Lyme Disease. JAMA 1989; 259:2737-39
8. Lavoie, P.E.  Lyme Disease. IN Conn's Current Therapy 1991 pp 101-105
9. Lawrence, C., Lipton, R.B., Lowy, F. D., Coyle, P.K.  Seronegative
chronic relapsing neuroborreliosis, Eur Neurol 1995 35(2):113-117
10. Liegner, K.B.  Lyme Disease: the Sensible Pursuit of Answers. J Clin
Microbiol 1993; 31(8): 1961-63
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manifestations of Lyme Disease. N Engl J Med 1990; 323:1438-44
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13. MacDonald, A.B., Berger. B.W., Schwann, T.G.   Clinical implications of
delayed growth of the Lyme Borreliosis spirochete, Borrelia burgdorferi.
Acta Tropica 1991; 48:89-94
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Neurology  1990; 40:1535-40
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neuroborreliosis: Presence of Borrelia burgdorferi in the CSF without
concurrent inflammatory signs.  Neurology 1989: 39:1118-20
17. Preac-Mursic, V., Marget, W., Busch, U., Pleterski-Rigler, D., Hagl, S.
Kill kinetics of Borrelia burgdorferi and bacterial findings in the relation
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Formation and cultivation of Borrelia burgdorferi spheroplast L-form
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Treatment of late Lyme Borreliosis    Journal of Infection 1994: 29:255-261

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