Web-Page: http://www.ariplex.com/lyme/lymbur14.htm

Das englische Original dieser Web-Seite ist im Usenet veröffentlicht worden.

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 aktuelle Version 14 von 2002.

Die zur Zeit aktuelle Version ist Version 14!:
http://www.ariplex.com/lyme/lymbur14.htm

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" 
Newsgroups: sci.med.diseases.lyme
Subject: 2002 Burrascano's Diagnostic & Treatment Guidelines (LONG)
Message-ID: <TyPG9.209041$WL3.71734@rwcrnsc54>
Date: Mon, 02 Dec 2002 20:40:20 GMT


As reported on Robynn's Lyme List:
http://groups.yahoo.com/group/Robynns_Lyme_List/

Dr. Burrascano sent me his latest Guidelines with encouragement to send them
along to you.  The original format is a Word document, so please forgive any
formatting irregularities.  To view the original Word document please see
the Files section at http://groups.yahoo.com/group/Robynns_Lyme_List/
-Robynn


ADVANCED TOPICS IN LYME DISEASE

DIAGNOSTIC HINTS AND TREATMENT GUIDELINES FOR LYME AND OTHER TICK BORNE
ILLNESSES


INTERNATIONAL LYME AND ASSOCIATED DISEASES SOCIETY



JOSEPH J. BURRASCANO JR., M.D.

Fourteenth Edition
November, 2002


Copyright, November, 2002
TABLE OF CONTENTS

INTRODUCTION  3
BACKGROUND INFORMATION..4
DIAGNOSTIC HINTS
PIROPLASMOSIS (Babesiosis)..5
EHRLICHIOSIS........5
LYME BORRELIOSIS
     ERYTHEMA MIGRANS 5
     DIAGNOSING LATE DISEASE 6
     DIAGNOSTIC CRITERIA 7
     SYMPTOM CHECKLIST 8

LYME DISEASE TREATMENT GUIDELINES
PIROPLASMOSIS  (Babesiosis). 9
EHRLICHIOSIS.  9
LYME BORRELIOSIS  9
GENERAL INFORMATION 9
COURSE DURING THERAPY 10
TREATMENT INFORMATION 11
ANTIBIOTICS 11
MONITORING OF THERAPY 12
ANTIBIOTIC CHOICES 12

TREATMENT CATEGORIES
PROPHYLAXIS 13
FOR KNOWN TICK BITES 13
EARLY LOCALIZED DISEASE 13
DISSEMINATED DISEASE 13
1. early   13
2. late   14
ALTERNATE SCHEDULING OF ANTIBIOTIC TREATMENTS 14
ADVANCED TOPICS 14
1. Cystic form 14
2. Borrelia Neurotoxin 15
REFRACTORY DISEASE 15
1. responsive to antibiotic therapy 15
2. non-responsive to antibiotic therapy 16
ADJUNCTIVE THERAPY 16
SAFETY   16
NUTRITIONAL SUPPLEMENTS IN CHRONIC LYME DISEASE 17
LYME DISEASE REHABILITATION 18
REHAB THERAPY PRESCRIPTION 19
MANAGING YEAST INFECTIONS.20
PATIENT INSTRUCTIONS ON TICK BITE PREVENTION AND TICK REMOVAL 21
APPENDIX
Rationale for treating tick bites 22
Rationale for treatment recommendations 23
SUGGESTED READING 25

INTRODUCTION

Welcome to the fourteenth edition of the "Guidelines". With the passage of
time, our understanding of tick-borne illness has grown, so new information
is presented to help us further refine our management techniques.

"Lyme Disease" is not simply an infection with Borrelia burgdorferi, but a
complex illness potentially complicated by multiple tick-borne
co-infections. In later stages, it also includes a very significant degree
of immune suppression. This not only serves to perpetuate the infections,
but it is probably responsible for the reactivation of latent infections,
such as herpes-type viruses. Many collateral conditions result in those who
have been chronically ill so it is not surprising that damage to virtually
all bodily systems can result. To fully recover, all of these issues must be
addressed in a thorough and systematic manner. No single treatment or
medication will result in full recovery of the more ill patient. Only by
addressing all these smaller issues and engineering treatments and solutions
for all of them will we be able to restore full health to our patients.

Once again, the full spectrum of Lyme Borreliosis will be addressed, from
the new bite, through early and late disseminated infections, and certainly
to chronic Lyme Disease.

A very important issue is the definition of "Chronic Lyme Disease". Based on
my clinical data and the latest published information, I offer the following
definition. To be said to have chronic Lyme, these three criteria must be
present:
1. Illness present for at least one year
2. Have persistent major neurologic involvement (such as
encephalitis/encephalopathy, meningitis, etc.) or active arthritic
manifestations (active synovitis).
3. Still have active infection with B. burgdorferi, regardless of prior
antibiotic therapy (if any).

It is clear that in the great majority of patients, chronic Lyme is a
disease affecting predominantly the nervous system. Thus, careful evaluation
often includes neuropsychiatric testing, SPECT and MRI brain scans, CSF
analysis when appropriate, regular input from Lyme-aware neurologists and
psychiatrists, pain clinics, and occasionally specialists in
psychopharmacology.

As an extension of the effect of chronic Lyme Disease on the central nervous
system, new information has demonstrated a deleterious effect on the
hypothalamic-pituitary axis. Varying degrees of pituitary insufficiency are
being seen in these patients, the correction of which has resulted in
restoration of energy, stamina and libido, and resolution of persistent
hypotension. Unfortunately, not all specialists recognize pituitary
insufficiency, partly because of the difficulty in making the laboratory
diagnosis. However, the potential benefits of diagnosing and treating this
justify the effort needed for full evaluation.

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 once again 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 edition proves to be useful.  Happy reading!

BACKGROUND INFORMATION

SPIROCHETE LOAD AND IMMUNE SUPPRESSION IN LYME DISEASE

The spirochete load has a direct bearing on the severity of Lyme
presentation. Low spirochete loads result in mild or even inapparent
infections that can be missed and remain present for years. As spirochete
load increases, especially from subsequent tick bites, the morbidity of Lyme
increases. Symptoms become apparent and more debilitating the larger the
load, and testing for Lyme can become more accurate. Studies have shown that
higher loads also begin to clinically impact the immune system, with
invasion and killing of B- and T-lymphocytes, including Natural Killer
Cells, and inhibition of lymphocyte transformation and mitogenesis. A
corollary to the issue of spirochete load is the delicate balance between
defense efficacy vs. pathogen strength. In other words, more severe illness
also results from weakened defenses, such as from severe stress,
immunosuppressant medications, and severe intercurrent illnesses.

The longer one is ill with Lyme, the more likely the illness will be more
severe and treatment resistant. The same studies that demonstrated
lymphocyte inhibition and lysis from high spirochete loads also demonstrated
increased negative effects on the immune system the longer the spirochetes
were present. We have seen this clinically, with the ultimate result being
full blown Chronic Lyme Disease.

CO-INFECTION

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. Significant numbers of Lyme patients have been shown
to also carry Babesia species, Ehrlichias, Anaplasmas, Mycoplasmas,
Bartonellas and viruses. Rarely, yeast forms have been seen in peripheral
blood. Studies have shown that co-infection results in a more severe
clinical presentation, with more organ damage, and the pathogens become more
difficult to eradicate. It is known that Babesia infections, like Lyme
Borreliosis, is immunosuppressive. There are changes in the clinical
presentation compared to when each infection is present individually, with
different symptoms, and atypical signs. There may be decreased reliability
of standard diagnostic tests, and most importantly, the recognition that
chronic, persistent forms of each of these infections do indeed exist.  As
time goes by, I am convinced that even more pathogens will be found.

Therefore, real, clinical Lyme as we have come to know it, especially the
later and more severe presentations, 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.

The evaluation of a Lyme patient must begin with testing for all currently
known tick borne pathogens.  Serological studies for Borrelia, Babesia and
Ehrlichia 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 and WA-1 are
available at this time, so as in Borrelia, clinical assessment is the
primary diagnostic tool.  In Ehrlichiosis, test for both the monocytic 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.

COLLATERAL CONDITIONS

Experience has shown that collateral conditions exist in those who have been
ill a long time. The evaluation should include testing both for differential
diagnosis and for uncovering other subtle abnormalities that may coexist.

Test B12 levels, and be prepared to aggressively treat with parenteral
formulations.

Pituitary and other endocrine abnormalities are far more common than
generally realized. When testing the thyroid, measure free T3 and free T4
levels and TSH. Nuclear scanning and testing for autoantibodies may be
necessary.

Activation of the inflammatory cascade has been implicated in blockade of
cellular hormone receptors. One example of this is insulin resistance, which
may partly account for the dyslipidemia and weight gain that is noted in 80%
of chronic Lyme patients. Clinical hypothyroidism can result from receptor
blockade and thus hypothyroidism can exist despite normal serum hormone
levels.  In addition to measuring free T3 and T4 levels, check basal A.M.
body temperatures.  If hypothyroidism is found, you may need to treat with
both T3 and T4 preparations until blood levels of both are normalized.

Tilt table testing is another powerful tool which, just as in CFIDS, may
demonstrate neurally mediated hypotension (NMH). NMH can result from
autonomic neuropathy and endocrine dyscrasias. If NMH is present, treatment
can dramatically lessen fatigue, palpitations and wooziness, and increase
stamina. This test should be done by a cardiologist and include Isuprel
challenge. This will demonstrate not only if NMH is present, but also the
relative contributions of hypovolemia and sympathetic dysfunction. 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 the Isuprel challenge.

Magnesium deficiency is very often present and quite severe.  Hyperreflexia,
muscle twitches, myocardial irritability, poor stamina and recurrent tight
muscle spasms are clues to this deficiency. Magnesium is predominantly an
intracellular ion, so blood level testing is of little value. Oral
preparations are acceptable for maintenance, but most need additional,
parenteral dosing: 1 gram IV or IM at least once a week until neuromuscular
irritability has cleared.

SPECT scanning of the brain, if done by knowledgeable radiologists using
high-resolution equipment, will show characteristic abnormalities in Lyme
encephalopathy.  What these scans demonstrate is cerebral vasculitis, which
is the underlying mechanism for much of the symptoms of Lyme. 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
some cognitive symptoms. Therapy can include acetazolamide, serotonin
agonists and even Ginkgo biloba.  Therapeutic trials of these may be needed.

Two different researchers have provided evidence that B. burgdorferi, like
many other pathogenic bacteria, can produce neurotoxins. Early clinical
trials aimed at removing these toxins have proven quite promising! I will
discuss this in more detail in a later section.




LYME BORRELIOSIS

DIAGNOSTIC HINTS

Lyme is diagnosed clinically, as no currently available test, no matter the
source or type, is 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, the classic four-week cycle of waxing and waning of symptoms, and
improvement with therapy.


ERYTHEMA MIGRANS

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, but do 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
circumstance.

DIAGNOSING LATER DISEASE

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. The suggestion that two-tiered
testing, utilizing an ELISA as a screening tool, followed, if positive, by a
confirmatory western blot, is illogical in this illness. The ELISA is not
sensitive enough to serve as an adequate screen, and there are many patients
with Lyme who test negative by ELISA yet have fully diagnostic western
blots. I therefore recommend against using the ELISA. Order IgM and IgG
western blots- but 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 therapy.

Western blots are reported by showing which bands are reactive.  41KD bands
appear the earliest but can cross react with other spirochetes.  The 18KD,
23-25KD (Osp C), 31KD (Osp A), 34KD (Osp B), 37KD, 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.

PCR tests 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, just as in routine blood culturing, multiple specimens must be
collected to increase yield; a negative result does not rule out infection,
but a positive one is significant. You can test whole blood, buffy coat,
serum, urine, spinal and other body fluids, and tissue biopsies. Several
blood PCRs can be done, or you can run PCRs on whole blood, serum and urine
simultaneously at a time of active symptoms.  The patient should be
antibiotic free for at least six weeks before testing to obtain the highest
yield.

Antigen capture is becoming more widely available, and can be done on urine,
CSF, and synovial fluid. Sensitivity is still low, but specificity is high.

Spinal taps are not routinely recommended, as a negative tap does not rule
out Lyme.  Antibodies to Bb most commonly are found in Lyme meningitis, but
are rarely seen in non-meningitic CNS infection, including even advanced
encephalopathy. Even in meningitis, antibodies are detected in the CSF in
less than 20% of patients with late disease. Therefore, spinal taps are only
performed on patients with pronounced neurological manifestations in whom
the diagnosis is uncertain, 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 or nucleic
acids 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.

I strongly urge you to biopsy all unexplained skin lesions/rashes and
perform PCR and careful histology. You will need to alert the pathologist to
look for spirochetes.


DIAGNOSTIC CHECKLIST

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


LYME BORRELIOSIS DIAGNOSTIC CRITERIA      RELATIVE VALUE

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

DIAGNOSIS

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.

SYMPTOM CHECK LIST
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
involvement.
NAME_______________________________________DATE__________________

RISK PROFILE (PLEASE CHECK)
Tick infested area__   Frequent outdoor activities__   Hiking__   Fishing__
Camping__
Gardening__   Hunting__   Ticks noted on pets__   Other household members
with Lyme__

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- circle one)
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 or abdominal pain
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
joints_________________________________________________
19.Stiffness of the joints or back
20.Muscle pain or cramps
21.Twitching of the face or other muscles
22.Headache
23.Neck creaks and cracks, neck stiffness, neck pain
24.Tingling, numbness, burning or stabbing sensations, shooting pains, skin
hypersensitivity
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.Increased motion sickness, vertigo, poor balance
29.Lightheadedness, wooziness, unavoidable need to sit or lie down
30.Tremor
31.Confusion, difficulty in thinking
32.Difficulty with concentration, reading
33.Forgetfulness, poor short term memory, poor attention, problem absorbing
new information
34.Disorientation: getting lost, going to wrong places
35.Difficulty with speech or writing; word or name block
36.Mood swings, irritability, depression
37.Disturbed sleep- too much, too little, fractionated, early awakening
38.Exaggerated symptoms or worse hangover from alcohol

LYME DISEASE TREATMENT GUIDELINES


LYME BORRELIOSIS:

GENERAL INFORMATION

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 concentrations known 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 of 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 through different
cell wall mechanisms than penicillin and the cephalosporins.

TREATMENT RESISTANCE

There is evidence that B. burgdorferi can remain viable within cells, such
as macrophages, lymphocytes, endothelial cells, neurons, and fibroblasts. Bb
has been shown to evade the effects of beta lactam antibiotics in vitro by
sequestering in these intracellular niches. In addition, Bb can coat itself
with host cell membranes, and it secretes a glycoprotein that can
encapsulate the organism (an "S-layer"). Because this glycoprotein binds
host IgM, it is possible that host protein as well as cell membrane hide
Borrelial antigens. In theory at least, these coatings interfere with immune
recognition, thus affecting the clearing of Bb, and also cause
seronegativity.

There are multiple strains of Borrelia burgdorferi and they vary in their
antigen profile and antibiotic susceptibilities. It has also been recognized
that B. burgdorferi can exist in at least three different morphologic forms:
spirochetal, spheroplast (or l-form), and the recently discovered cystic
form.
L-forms and cystic forms do not contain cell walls, and thus beta lactam
antibiotics will not affect them. Spheroplasts seem to be susceptible to
tetracyclines and some erythromycins, yet the cyst has so far only been
proven to be susceptible to metronidazole. Apparently, Bb can shift among
the three 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 antibiotic or even prescribe a
combination of agents.

More evidence has accumulated indicating the severe detrimental effects of
immunosuppressants including steroids in the patient with active B.
burgdorferi infection.  Never give steroids or any other immunosuppressant
to any patient who may even remotely be suffering from Lyme, or serious,
permanent damage may result, especially if given for anything greater than a
short course. If immunosuppressive therapy is absolutely necessary, then
potent antibiotic treatment should begin at least 48 hours prior to the
immunosuppressants.

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.

COURSE DURING THERAPY

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.

Several days after the onset of appropriate antibiotic therapy, symptoms
often flare due to lysis of the spirochetes with release of increased amount
of antigenic material and possibly bacterial toxins. This is referred to as
a Jarish Herxheimer-like reaction. Because it takes 48 to 72 hours of
therapy to initiate bacterial killing, the Herxheimer reaction is therefore
delayed. This is unlike syphilis, in which these reactions can occur within
hours

It has been observed that symptoms will flare in cycles every four weeks. It
is thought that this reflects the organism's cell cycle, with the growth
phase occurring once per month (intermittent growth is common in Borrelia
species).  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 then are lysed. For unknown reasons, the worst occurs at the
fourth week of treatment.  Observation suggest 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 continue to 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 because the
infection was not eradicated.  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. Obviously, evaluation for co-infection should be performed, and a
search for other or concurrent diagnoses need to be entertained.

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.

BORRELIA NEUROTOXIN (With thanks to Dr. Shoemaker)

Two groups have reported evidence that Borrelia, like several other
bacteria, produce neurotoxins. These compounds reportedly can cause many of
the symptoms of encephalopathy, cause an ongoing inflammatory reaction
manifested as some of the virus-like symptoms common in late Lyme, and also
potentially interfering with hormone action by blocking hormone receptors.
At this time, there is no assay available to detect whether this compound is
present, nor can the amount of toxin be quantified.  Indirect measures are
currently employed, such as measures of inflammation and neuropsychiatric
tests. A visual contrast sensitivity test (VCS test) reportedly is quite
useful in documenting CNS effects of the neurotoxin, and following effects
of treatment. This test is available at some centers and on the internet.

It has been said that the longer one is ill with Lyme, the more neurotoxin
is present in the body.  It probably is stored in fatty tissues, and once
present, persists for a very long time.  This may be because of
enterohepatic circulation, where the toxin is excreted via the bile into the
intestinal tract, but then is reabsorbed from the intestinal tract back into
the blood stream.  This forms the basis for treatment.

Synthetic fiber agents, available by prescription for the treatment of high
cholesterol, have the ability to bind some bacterial toxins.  When take
orally in generous amounts, the neurotoxin, present in the intestinal tract,
binds to the resin, is trapped, and then excreted.  Thus, over several
weeks, the level of neurotoxin is depleted and clinical improvement can be
seen.  Current experience is that improvement is first seen in three weeks,
and treatment continues for two to four months.  Retreatment is always
possible.

Two prescription medications that can bind these toxins include
cholestyramine resin (Questran), and Welchol pills. These medications may
bind not only toxins but also many drugs and vitamin supplements. Therefore
no other oral medications or supplements should be taken from one hour
before, to three hours after a dose of one of these fiber agents.

Cholestyramine must be taken four times daily, and Welchol is prescribed at
three pills twice daily. While the latter is obviously much simpler to use,
it is less effective than cholestyramine. The main side effects are bloating
and constipation, best handled with increased fluid intake and gentle
laxatives.


LYME DISEASE TREATMENT INFORMATION

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 duration and severity of illness,
presence of co-infections, immune deficiencies, prior significant
immunosuppressant use while infected, 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 tissue penetration by Bb, it's 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 of susceptibility 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
if necessary, modify it over time based upon response.

ANTIBIOTICS

There are several 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 either by high oral
doses (300 to 600 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
rarely 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 they 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.

When choosing a third generation cephalosporin, there are several points to
remember: Ceftriaxone 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 three to five days in a row each week. More recently,
chenodeoxycholic acid, used to dissolve gallstones, is being prescribed
along with ceftriaxone as prophylaxis. Cefotaxime is less convenient to
administer because of the need for either multiple daily doses or continuous
infusions, 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, especially with oral azithromycin.  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
antibiotics 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.

Metronidazole (Flagyl) is commonly used in select patients with treatment
resistant, chronic Lyme. When present in a hostile environment, such as
growth medium lacking some nutrients, or spinal fluid, or serum with certain
antibiotics added, Bb will change into a cystic form. This cyst seems to be
able to remain dormant, but when placed into an environment more favorable
to its growth, the cyst can open, and an intact spirochete emerges. The
conventional antibiotics used for Lyme, such as the penicillins,
cephalosporins, etc do not kill the cystic form of Bb. Furthermore, the cyst
lacks the usual surface antigens found on the spirochete (these are the
markers detected by ELISAs and western blots). This may be another reason
for the chronically sick Lyme patient remaining seronegative.

There is evidence that metronidazole will kill the cystic form. This fits
with the now well known clinical observations that metronidazole can be
remarkably effective for many chronic Lyme patients. However, this
medication apparently has no effect on intact spirochetes. Therefore, the
trend now is to treat the chronically infected patient who has resistant
disease by combining metronidazole with one or two other antibiotics to
target all forms of Bb. Because there is laboratory evidence that
tetracyclines may inhibit the effect of metronidazole, this class of
medication may not be as useful as others in these two- and three-drug
regimens. There have been some recent reports that Bb does not contain genes
that would confer susceptibility to metronidazole. However, this clearly
does not fit with in vitro and a large body of clinical data, which have
demonstrated the usefulness of this agent in the Lyme patient. Perhaps we do
not have all the genetic information needed to dismiss the use of this
agent. Once again, real world experience is one step ahead of bench
research.

Important precautions:
1. Pregnancy while on metronidazole is not advised, as there is a risk of
birth defects.
2. No alcohol consumption! A severe, "antabuse" reaction will occur,
consisting of severe nausea, flushing, headache, and other unpleasant
symptoms.
3.  Metronidazole is potentially neurotoxic. Peripheral neuropathy may
result. Therefore, breaks in treatment are commonly prescribes, such as
using this agent every other week.
4. Yeast overgrowth is especially common. A strict anti-yeast regimen must
be followed.
5. VERY severe Herxheimer-like reactions are seen in the more ill patient
during the first week of therapy, and again four weeks later.

COMBINATION THERAPY

This consists of using two or more dissimilar antibiotics simultaneously.
There are several reasons for this. Combinations should utilize dissimilar
antibiotics for antibiotic synergism, to better compensate for differing
killing profiles and sites of action of the individual medications, and to
cover the three known morphologic forms of Bb. The idea is to work in body
fluids and in deep tissues, outside and within cells, and effect killing by
different mechanisms for synergism. An example is a combination of
amoxicillin and clarithromycin. Note how complimentary these two are for
treating infection with Bb. 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.

PULSE THERAPY

This 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 efficacy
· More toxic medications can be used with increased safety (ie: vancomycin)
· 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 patient's clinical picture based upon the
treating physician's best clinical judgment.

MONITORING THERAPY

Drug levels are measured, where possible, to confirm adequate dosing. The
regimen may have to be modified to optimize the dose, and again 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, especially during
symptom flares, with urinalysis and pro- time monitored monthly.

INDICATORS FOR PARENTERAL THERAPY

The following are guidelines only and are not meant to be absolute. It is
based on retrospective study of over 600 patients with late Lyme disease.

· Illness for greater than one year
· Prior immunosuppressive therapy
· Major neurological involvement
· Active synovitis with high sedimentation rate
· Elevated protein or cells in the CSF


ANTIBIOTIC CHOICES

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 Ehrlichia.

*Amoxicillin- 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.
*Doxycycline-  Adults:  100 mg qid with food; doses of up to 600 mg daily
are often needed, as
doxycycline is only effective at high blood levels. Not for children or in
pregnancy.
   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 q12h and adjust.  Children:  125 to 500 mg q12h
based on weight.
Tetracycline-  Adults only, and not in pregnancy.  500 mg tid to qid
Erythromycin-  Poor response and not recommended.
Clarithromycin- Adults: 500 to 1000 mg q12h. Add hydroxychloroquine, 200-400
mg/d
or amantadine 100-200 mg/d. Cannot be used in pregnancy or in younger
children
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. Oral azithromycin is not as effective as
clarithromycin.
Augmentin-  Cannot exceed three tablets daily due to the clavulanate, thus
is given with amoxicillin. This
combination can be effective when Bb beta lactamase is felt to be present.
Chloramphenicol- Not recommended as not proven and potentially toxic.
Metronidazole (see text): 500 to 1500 mg daily in divided doses. Adults
only.

PARENTERAL THERAPY
Ceftriaxone- Risk of biliary sludging can be minimized with intermittent
breaks in therapy (ie: infuse five
  or less days in a row per week).
Adults and pregnancy: 2g q12h, four days in a row each week.
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.  Suggest a
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 higher overall, and spiked blood
levels when given
parenterally.
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 three times per week (higher doses with large body
habitus)
Adolescents:  300,000 to 2.4 million U weekly.
May 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
cefotaxime.
Ampicillin IV- more effective than penicillin G.  Must be given q6 hours.


TREATMENT CATEGORIES

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
appendix):

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 of 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
coinfection!):
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 weeks
3rd trimester:  Oral therapy  X 6 weeks.
Any trimester- test for Babesia, Bartonella, 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 immunosuppressive treatment:
1) Adults:  oral therapy until no active disease for 4 weeks (4-6 months
typical)
2) Pregnancy:  As in localized disease, but duration as above. Treat
throughout
pregnancy, and do not breast feed.
3) Children: Oral therapy with duration based upon clinical response.

PARENTERAL ALTERNATIVES for more ill patients and those unresponsive to or
intolerant of oral medications:
1) Adults and children:  I.V. therapy for at least 6 weeks (until clearly
improved).  Follow with oral
  therapy or IM benzathine penicillin until no active disease for 6-8 weeks.
I.V. may have
  to be resumed if oral or IM therapy fails.
2) 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 I.V. therapy (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.


CHRONIC LYME DISEASE

By definition, this category consists of patients with active infection, of
a more prolonged duration, and most likely have higher spirochete loads,
weaker defense mechanisms, possibly more virulent or resistant strains, and
probably are significantly co-infected. Neurotoxins may also be significant
in these patients. Search for and treat concurrent illnesses including
viruses, chlamydias, and  mycoplasmas. These patients require a full
evaluation for all of these problems, and each abnormality must be
addressed.

This group will most likely need parenteral therapy, especially high dose,
pulsed therapy, and antibiotic combinations, including metronidazole.
Antibiotic therapy will need to continue for many months, and the
antibiotics may have to be changed periodically to break plateaus in
recovery. Be vigilant for treatment-related problems such as
antibiotic-associated colitis, yeast overgrowth, intravenous catheter
complications, and abnormalities in blood counts and chemistries.

If treatment can be continued long term, then a remarkable degree of
recovery is possible. However, attention must be paid to all treatment
modalities for such a recovery- not only antibiotics, but rehab programs,
nutritional supplements, enforced rest, low carbohydrate, high fiber diets,
attention to food sensitivities, avoidance of stress, abstinence form
caffeine and alcohol, and absolutely no immunosuppressants, even local doses
of steroids (intra articular injections, for example).

Unfortunately, not all patients with chronic Lyme disease will fully recover
and treatment may not eradicate the active Borrelia infection. Such
individuals may have to be maintained on open-ended, ongoing antibiotic
therapy, for they repeatedly relapse after antibiotics are stopped.
Maintenance antibiotic therapy is thus mandatory.

SAFETY

Nearly two decades 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 allergy 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, pulsed dose therapy and 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 central intravenous lines including 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, and advise birth control
if appropriate. When doxycycline is given parenterally, do not refreeze the
solution prior to use!

Remember, years of experience with chronic antibiotic therapy in other
conditions, including rheumatic fever, acne, gingivitis, 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.


CO-INFECTIONS IN LYME

PIROPLASMOSIS (Babesiosis)

GENERAL INFORMATION
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 co-infections- if a Lyme patient has been
extensively treated yet is still ill, suspect a co-infection.

Babesia infection is becoming more commonly recognized, especially in
patients who already have Lyme Disease. It has been published that as many
as 66% of Lyme patients show evidence of co-infection with Babesia.  It has
also been reported that Babesial infections can range in severity from mild,
subclinical infection, to fulminant, potentially life-threatening illness.
The more severe presentations are more likely to be seen in
immunocompromised and elderly patients.  Milder infections are often missed
because the symptoms are incorrectly ascribed to Lyme. Babesial infections,
even mild ones, may recrudesce and cause severe illness. This phenomenon has
been reported to occur at any time, even up to several years after the
initial infection. Furthermore, asymptomatic carriers pose a risk to the
blood supply as this infection has been reported to be passed on by blood
transfusion, and Babesia may be passed to the unborn child from an infected
mother. Some quotes from the literature:

Krause, PJ. Spielman, A, Telford, SR et.al.. Persistent parasitemia after
acute Babesiosis N Engl J Med 1998. 339:160


"The clinical spectrum of human Babesiosis ranges from an apparently silent
infection to a fulminant malaria-like disease."
"When left untreated, silent Babesial infection may persist for months to
years."
"Silent infections, which occur in about a third of infected people, may
recrudesce."
"Babesial infection may recrudesce after many months of asymptomatic
parasitemia."
"Although parasites were initially detected microscopically in the blood of
two of the untreated subjects, and all of the treated subjects, none could
be found a week after the onset of illness."
"Persistent symptoms of Babesiosis accompanied persistent blood-borne
Babesial DNA"
"The persistence of seroreactivity increasingly correlated with the
persistence of Babesial DNA."
"In those with only subtle symptoms, Babesiosis often remains undiagnosed."
"Furthermore, physicians tend not to recognize Babesial infection in those
who are co-infected with the agent of Lyme Disease, because Babesial
symptoms tend to be ascribed to Lyme Disease."
"Physicians caring for patients with moderate to severe Lyme disease should
consider obtaining diagnostic
    tests for Babesiosis and possibly other tick-borne pathogens. especially
in patients experiencing
    "atypical Lyme disease" or patients in whom the response to antibiotic
treatment is delayed or absent."

Krause, PJ, Telford, SR, Spielman, A, et.al. Concurrent Lyme disease and
Babesiosis. JAMA 1996. 275(21):1657

"Subjects with evidence of both infections reported a greater array of
symptoms than those infected by the spirochete or piroplasm alone."
"Co-infection generally results in more intense acute illness and a more
prolonged convalescence than accompany either infection alone."
"Spirochete DNA was evident more often and remained in the circulation
longer in co-infected subjects than in those experiencing either infection
alone."
"Co-infection might also synergize spirochete-induced lesions in human
joints, heart and nerves."
"Babesial infections may impair human host defense mechanisms."
"The possibility of concomitant Babesial infection should be considered when
moderate to severe Lyme Disease has been diagnosed."

SYMPTOMS
In milder forms, symptoms may include a vague sense of imbalance without
true vertigo, headache, mild encephalopathy, fatigue, sweats, air hunger and
occasionally cough. When present as a co-infection with Lyme, initial
symptoms of the illness are often more acute and severe. Suggestions of
co-infection include the above symptoms, but the headaches are more severe,
and encephalopathy is out of proportion to the other Borrelia symptoms. The
fulminant presentations include high fevers, shaking chills and hemolysis,
and can be fatal.

DIAGNOSTIC TESTS
Diagnostic tests are insensitive and problematic. There are at least
thirteen Babesial forms found in ticks, yet we can currently only test for
B. microti and WA-1 with our serologic and nuclear tests. Standard blood
smears reportedly are reliable for only the first two weeks of infection,
thus are not useful for diagnosing later infections and milder ones
including carrier states where the germ load is too low to be detected.

Krause, PJ, Telford, SR, Spielman, A, et.al. Concurrent Lyme disease and
Babesiosis. JAMA 1996. 275(21):1660
"As is common in the case of Babesial infections, parasites frequently
cannot be seen in blood films."

Therefore, multiple diagnostic test methods are available and each have
their own benefits and limitations. Always consider co-infection in your
current Lyme patients who are not responding fully to Lyme treatment, and be
prepared to treat based on clinical presentation, even with negative tests.

SEROLOGY
Unlike Lyme, Babesia titers can reflect infection status. Thus, persistently
positive titers or western blots suggest persistent infection.

PCR
This is more sensitive than smears for B. microti, but will not detect other
species.

ENHANCED SMEAR
This utilizes buffy coat, prolonged scanning (up to three hours per sample!)
and digital photography through custom-made microscopes. Although more
sensitive than standard smears, infections can still be missed. The big
advantage is that it will display multiple species, not just B. microti.

FLUORESCENT IN-SITU HYBRIDIZATION ASSAY (FISH)
This technique is also a form of blood smear. It is said to be 100-fold more
sensitive than standard smears for B. microti, because instead of utilizing
standard, ink-based stains, it uses a fluorescent-linked RNA probe and
ultraviolet light. The Babesial organisms are then much easier to spot when
the slides are scanned. The disadvantage is that currently only B. microti
is detected.


TREATMENT
Treating Babesia infections had always been difficult, because the therapy
that had been recommended until 1998 consisted of a combination of
clindamycin plus quinine. Published reports and clinical experience have
shown this regimen to be unacceptable, as nearly half of patients so treated
have had to abandon treatment due to serious side effects, many of which
were disabling. Furthermore, even in patients who could tolerate these
drugs, there was a failure rate approaching 50%.

Krause, PJ. Spielman, A, Telford, SR et.al.. Persistent parasitemia after
acute Babesiosis N Engl J Med 1998. 339:162

"Of the treated subjects, almost half had symptoms that were consistent with
reactions to quinine, including hearing loss, tinnitus, hypotension, and
such gastrointestinal symptoms as anorexia, vomiting, and diarrhea"
"Although treatment with clindamycin and quinine reduces the duration of
parasitemia, infection may persist and recrudesce and side effects are
common."


Because of these dismal statistics, the current regimen of choice for
Babesiosis is the combination of atovaquone plus azithromycin. Combination
was initially studied in animals, and then applied to Humans with good
success, because when atovaquone was used alone, resistance developed in 20%
of cases, but reportedly did not occur when azithromycin was added.  Fewer
than 5% of patients have to halt treatment due to side effects, and the
success rate is clearly better than that of clindamycin plus quinine.

The duration of treatment with atovaquone plus azithromycin for Babesiosis
varies depending on the degree of infection, duration of illness before
diagnosis, the health and immune status of the patient, and whether the
patient is co-infected with Borrelia burgdorferi. Typically, a three-week
course is prescribed for acute cases, while chronic, longstanding infections
with significant morbidity and co-infection will require several months of
therapy. Relapsed have occurred, and retreatment is occasionally needed.

Problems during therapy include diarrhea, mild nausea, the expense of
atovaquone (over $600.00 per bottle- enough for three weeks of treatment),
and rarely, a temporary yellowish discoloration of the vision.  Regular
blood counts, liver panels and amylase levels are recommended during any
prolonged course of therapy.  Patients who are not cured with this regimen
can be retreated but with higher doses, as this has proven effective in many
of my patients. Artemesia (a non-prescription herb) may be added, but is not
effective when used alone. Metronidazole can also be added to increase
efficacy, but there is minimal clinical data on how much more effective this
regimen is.

EHRLICHIOSIS

GENERAL INFORMATION
While it is true that this illness can have a fulminant presentation, and
may even become fatal if not treated, milder forms do exist, as does chronic
low-grade infection, especially when other tick-borne organisms are present.
The potential transmission of Ehrlichia during tick bites is the main reason
why doxycycline is now the first choice in treating tick bites and early
Lyme, before serologies can become positive. When present alone or
co-infecting with B. burgdorferi, persistent leukopenia is an important
clue.  Thrombocytopenia and elevated liver enzymes are 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.

DIAGNOSTIC TESTING
Testing is problematic with Ehrlichia, similar to the situation with
Babesiosis. More species are known to be present in ticks than can be tested
for with clinically available serologies and PCRs. In addition, serologies
and PCRs are of unknown sensitivity and specificity. Standard blood smears
for direct visualization of organisms in leukocytes is of low yield.
Enhanced smears using buffy coats significantly raises sensitivity and will
indicate a wider variety of species. Despite this, infection can be missed,
so clinical diagnosis remains the primary diagnostic tool.  Again, consider
this diagnosis in a Lyme Borreliosis (LB) patient not responding well to
therapy.

TREATMENT
Standard treatment consists of Doxycycline, 200 mg daily for two to four
weeks. Higher doses, parenteral therapy, and longer treatment durations may
be needed based on the duration and severity of illness, and whether immune
defects or extreme age is present. However, there are reports of treatment
failure even when higher doses and long duration treatment with doxycycline
is given. In such cases, consideration may be given for adding rifampin, 600
mg daily, to the regimen.

BARTONELLA

Bartonella henselae, the agent of cat scratch disease, has been found in
Ixodid ticks and as a co-infection in patients with Lyme Disease. With
co-infection, symptoms of Bartonella are almost impossible to distinguish
from Lyme, but may include lymphadenopathy, splenomegaly, hepatomegaly,
headache, encephalopathy, somnolence, flu-like malaise, weight loss, sore
throat, and a papular or angiomatous rash. In acute cases, there can be
hemolysis with anemia, high fever, weakened immune response, jaundice,
abnormal liver enzymes, and myalgias. Endocarditis and myocarditis have been
reported. More severe infections are associated with immune deficiency and
possibly occurrence of opportunistic infections. As in Lyme Disease and
Babesiosis, Bartonella may be transmitted to the fetus in the infected
pregnant patient.

Diagnostic tests include serology, blood and CSF PCR, and biopsy of skin
lesions and lymph nodes.

In the co-infected Lyme patient, eradication may be difficult. Many
antibiotic agents have been reported to be effective, including
cephalosporins, fluoroquinolones, erythromycins, gentamicin, rifampin and
streptomycin. In practice, these patients seem to do best with a combination
regimen that utilizes agents that can penetrate cells. Typical combinations
include an erythromycin, plus a fluoroquinolone or rifampin. Treatment
progress is most commonly assessed by PCR post treatment and serial titers.


NUTRITIONAL SUPPLEMENTS IN DISSEMINATED LYME DISEASE

Studies on patients with chronic illnesses such as Lyme and Chronic Fatigue
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 some of the supplements listed.  Some are required,
while others are optional -see below. They are listed in order of
importance.

The quality of supplements used is often more important than the dose.  In
fact, "mega doses" are not recommended.  Instead, seek out, if possible,
pharmaceutical grade products, especially if USP certified. Pharmanex brand
products are recommended because they fit these criteria. In the list below,
it is indicated whether the product should be gotten from Pharmanex, or
whether a generic substitute is OK. To order Pharmanex brand products, call
1-800-487-1000 and give the following U. S. reference #: 9256681.

BASIC DAILY REGIMEN

ACIDOPHILUS (required when on antibiotics)
Essential daily supplement to maintain the normal balance of bowel flora,
especially if on antibiotics, or if gastrointestinal disturbances are
present.  Always try to get enteric coated, milk-free acidophilus.  The best
kinds are frozen or refrigerated to ensure potency.  Take two with each meal

MULTI-VITAMIN (required)
I recommend the Life Pack family of multivitamins. These are unique
supplements-Pharmaceutical grade and USP certified, they are the only
products clinically proven in double blinded, placebo controlled crossover
studies to quench free radicals and raise antioxidant levels in the blood
and lipids.  Choose LifePak for males under 40, LifePak Women for hormonally
active women, and LifePak Prime for postmenopausal women and for men over
40.  They are available through Pharmanex.  Continue long term.

CO-Q10 (ubiquinone)- required if not taking the prescription drug atovaquone
(Mepron)
Deficiencies have been related to poor function of the heart, limitations of
stamina, gum disease, and poor resistance to infections.  Heart biopsy
studies in Lyme patients indicated that they should take between 200 and
300mg daily of standard CoQ 10, or 90 mg of the well absorbed, highly
purified, crystalline CoQ 10 product sold by Pharmanex, (surprisingly, the
Pharmanex brand is far less expensive than the generic).  The body will
manufacture its own C0Q 10 when the original illness is controlled, but only
if stimulated by aggressive exercise.  Therefore, use this supplement until
you are feeling well and exercising regularly.

VITAMIN B (required).
Clinical studies demonstrated the need for supplement vitamin B in
infections with Borrelia, to help clear neurological symptoms. Take one 50
mg B-complex capsule daily. If neuropathy is severe, an additional 50 to 100
mg of B6 daily may be helpful. Generics are OK.

MAGNESIUM (required)
Magnesium supplementation is very helpful for the tremors, twitches, cramps,
muscle soreness, heart skips and weakness.  It may also help in energy level
and cognition. The best source is magnesium L-lactate dehydrate ("Mag-tab
SR", sold by Niche Pharmaceuticals: 1-800-677-0355, and available at
Wal-Mart).  DO NOT rely on "cal-mag", calcium plus magnesium combination
tablets, as they are not well absorbed.  Take at least one to two tablet
twice daily.  Higher doses may cause diarrhea, and you should check with
your physician before using more than this.  In some cases, injections or
intravenous doses may be necessary. Continue long term.

ESSENTIAL FATTY ACIDS: (required)
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
(omega-6 oils) and EPA (omega-3 oils), derived respectively from plant and
fish oils.  This is what to take:
Plant Oils: borage oil, evening primrose oil, or black currant seed oil
(choose one). Do NOT use Flax seed oil!
Fish Oil: Omega-3 (Fish Oil) capsules, 1000 mg per capsule. Use "Optimum
Omega" by Pharmanex, if a higher quality product is desired, or to minimize
the "fishy" aftertaste.
RECOMMENDATION: four plant oil capsules and four fish oil capsules daily,
taken with meals.  Continue for three to four months then try to taper down
the dose.

OPTIONAL SUPPLEMENTS FOR SPECIAL CIRCUMSTANCES

CORDYMAX (optional)
Cordyceps is a well-known herb from Tibet and has been shown in clinical
studies to improve stamina, fatigue, and enhance lung and antioxidant
function.  It also raises superoxide dismutase levels.  The positive effects
can be so dramatic, I strongly urge all people with fatigue to try this.
Available only from Pharmanex as "CordyMax".

METHYLCOBALAMIN (Methyl B12)  (optional)
This is a prescription drug made from vitamin B12 that has several
documented benefits: it helps to heal damage to the nervous system, enhances
diminished T-cell function, can restore the normal diurnal cycle, and can
help with memory and cognition. Methyl B12 must injected into the muscle as
it will not be absorbed if swallowed. Dose ranges from 25 to 50 mg daily,
based on weight.

REISHI MAX (optional)
This enhanced extract from cracked spores of the reishi mushroom has been
shown in clinical studies to augment function of the Natural Killer Cells
and macrophages. Take two a day for maintenance, and four a day in disease
states. Available only from Pharmanex.

ECHINACEA (optional)
May be helpful in fighting acute and chronic viral illnesses.  Choose a
pharmaceutical grade brand ("Immune Formula" by Pharmanex), and do not use
the liquid form as this contains alcohol. Do not take daily on a long-term
basis, as the benefit may wear off. For a chronic illness, double the usual
daily dose but take in cycles- use daily three weeks on, one week off each
month.

BIO-GINKGO (optional)
The most effective ginkgo brand in my experience- pharmaceutical grade, and
very high potency to assure full bioavailability. Available only from
Pharmanex.  Ginkgo has been shown to increase blood flow to many organs,
including the brain.  Patients report clearer thinking and better memory.
Be aware that this brand is strong- start with a low dose, then increase
every few days or a pressure-type, vascular headache may result from all the
increased circulation.

GLUCOSAMINE (optional)
Can be of long term benefit to the joints. Do not be mislead into buying a
product that also contains chondroitin, as this chemical does not add
anything, but it can make the product more expensive. Look for a product
that contains the herb Boswellia serrata- this is a non-irritative
anti-inflammatory. Although many generics exist, the Pharmanex product,
"Cartilage Formula" has the right ingredients and is of proven efficacy.
Expect improvement only over time (several weeks), but plan to use this
indefinitely to maintain joint health.

CREATINE (optional)
Creatine has been shown to be of benefit in neuromuscular degenerative
diseases such as Lou Gherig's Disease (ALS) and can be very helpful in
supporting low blood pressure, as in NMH.  Important: To use this safely,
you must have an adequate fluid intake. The creatine product should contain
taurine, an amino acid needed to enhance creatine absorption, plus some
carbohydrate to aid creatine entry into muscle.  You will need a 20 gram
loading dose for the first five days, then 4 to 10 grams daily maintenance.
Try "Cell Tech" from the Vitamin Shop, and follow label directions.

MILK THISTLE   (optional)
Useful to support liver function. Take 175 mg three times daily- use an 80%
Silymarin extract.

MUSCLE FIX (optional)
This blend of nutrients from Pharmanex really helps sore, tight muscles.
Must be taken on an empty stomach- either two, twice daily between meals, or
four at bedtime. Can be used intermittently as needed, or daily.

LYME DISEASE REHABILITATION

Those with long-standing tick borne illnesses end up in poor physical
condition.  Even with successful treatment of the infections, chronic Lyme
patients will not return to normal unless they pursue a formal program of
therapeutic exercise, as outlined below.

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 per cent 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 80% 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, to relieve discomfort and to promote better sleep and
flexibility. The goal of physical therapy is to prepare the patient for the
required, gym-based exercise program. This starts with stretching and mild
muscular toning.  Then, 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
testing for food hypersensitivities and recommending books that outline
"arthritis diets", as they can help some patients.

Cessation of smoking is extremely important and must be addressed
immediately.

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.

LYME REHAB-PHYSICAL THERAPY PRESCRIPTION

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.

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

PHYSICAL THERAPY (if needed):
1.  Relieve pain and muscle spasms utilizing multiple modalities as
available and as indicated:  massage, heat, ultrasound, TENS, "micro amp",
etc.
2.  Increase mobility while protecting damaged and weakened joints, tendons,
and ligaments, to increase range of motion and relieve stiffness.
3.  The role of physical therapy here is to prepare the patient for the
required, preferably gym-based, exercise program outlined below.

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 stretching 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 visit's
therapy, and adjust therapy accordingly.

PROGRAM:
1.  Aerobic exercises are NOT allowed, not even low impact variety, until
your stamina improves.
2.  Conditioning: work to improve strength and reverse the poor conditioning
that results from Lyme, through a whole-body exercise program, consisting of
light calisthenics and weight lifting, using small weights and many
repetitions. This can be accomplished in exercise classes called "stretch
and tone", or "body sculpture", or can be achieved with or exercise
machines, or carefully with free weights.
3.  Each session should last one hour.  If the patient is unable to continue
for the whole hour, then modify the program to decrease the intensity to
allow him/her to do so.
4.  Exercise no more often than every other day. You may need to start by
exercise every 4th or 5th day initially, and as your abilities improve, work
out more often, but NEVER two days in a row. The days you do not exercise
should be spent resting.
5.  This whole-body conditioning program is what is required to achieve
wellness. Simply placing the patient on a treadmill or an exercise bike is
not acceptable (except briefly, as part of a warm-up), nor is a simple
walking program.


PHYSICIAN'S SIGNATURE____________________________________________


MANAGING YEAST OVERGROWTH

Many patients with chronic illnesses including Lyme Disease develop an
overgrowth of yeast.  A basic strategy to combat this is to eat a full
container of sugar-free, non-fruit flavored yogurt that contains active
cultures daily, and take acidophilus, two after each meal.  Here are some
other suggestions:

MOUTH:  Yeast problems usually begin in the mouth, for when thrush is
present, organisms may repeatedly pass down into the GI tract where they
cause the most problems. A tongue with a beige coating, bad breath, and a
bad taste in the mouth are signs of oral yeast. Patients should use a
toothpaste that contains surfactants (detergent-like cleaning agents), and
antiseptic mouthwashes (Scope, Listerine, etc.), and brush the teeth,
tongue, gums, cheeks and the roof of the mouth while holding the mouthwash
in the mouth.

The most effective 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
thrush 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 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 yeasts 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.

Since yeast germs feed on sugars and starches, avoid simple carbohydrates
including sugars, starches, and some fruits. Refer to the diet outlined
below.

Prescription medications may be necessary.  Mycelex troches and Nystatin
liquid are not the best choice, for they contain large amounts of simple
sugars.  Instead, Nystatin oral powder is preferred, as it does not contain
sugar. It is mixed with water, and swished and swallowed four times daily.
Systemic antifungals tablets (Diflucan, Lamisil, Nizoral) may be necessary.

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, wooziness and post-meal
fatigue.  To clear intestinal yeast, first the oral cavity must be cleared
so yeast does not reenter the system with every swallow.  Avoid sweets,
starches, fruits and juices to starve the germs. Use PLAIN yogurt daily, and
acidophilus, 2 capsules three times daily after meals. Systemic antifungal
medications may be 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,
re-infecting the genital area with every bowel movement.  Therefore follow
the above protocol for intestinal overgrowth, and use topical preparations
such as Monistat concurrently for up to two weeks.



YEAST CONTROL DIET (Restricted carbohydrate regimen)

FOODS ALLOWED
Meat, fish, fowl, cheese, eggs, dairy, tofu

FRUITS
q Only high fiber fruits are allowed
q Fruits are only allowed at the end of a meal, and never on an empty
stomach

ALLOWED
Grapefruit, tomatoes, avocado, lemons, limes

SMALL AMOUNTS ONLY!
(The high fiber content in these makes up for the carbohydrates)
Pears, apples, strawberries, etc.

NOT ALLOWED
Oranges, watermelons, bananas, grapes, etc. (too much sugar and not enough
fiber)

VEGETABLES
Green vegetables and salads are O.K.  Avoid starchy vegetables (potato,
rice, beans, etc.)

STARCHES
If it is made from flour, it is not allowed! (No breads, cereals, cake,
etc.)

SWEETENERS
NOT ALLOWED
No sugars at all; no fructose or corn syrup, and no honey

ALLOWED (if tolerated)
Aspartame, Nutrasweet, Equal; saccharin products allowed but not recommended

DRINKS
ALLOWED
Vegetable juices, water, seltzer, diet sodas, coffee and tea without sugar
or caffeine

NOT ALLOWED
Fruit juices, regular sodas, any drinks sweetened with sugars, syrups or
honey




PATIENT INSTRUCTIONS ON BITE PREVENTION AND TICK REMOVAL

HOW TO PROTECT YOURSELF FROM TICK BITES

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
such as permethrin and its derivatives are preferred. 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
outside!

HOW TO REMOVE AN ATTACHED TICK
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.


APPENDIX

RATIONALE FOR TREATING TICK BITES

Prophylactic antibiotic treatment upon a known tick bite is recommended for
those who fit the following categories:

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

2. Persons bitten in an area highly 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
body of the tick is squeezed upon removal, 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.

SUGGESTED READING


1.  Liegner, K.B. Lyme Disease: the sensible pursuit of answers. J Clin
Microbiol 1993; 31(8): 1961-63

2.  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 Clin Microbiol 1991; 29(6):1162-70

3.  Harris, N.S., Stephens, B. Detection of Borrelia burgdorferi antigen in
urine from patients woth Lyme
borreliosis. 1995; 2(2):37-41

4  Preac-Mursic, V., Marget, W., Busch, U., Pleterski-Rigler, D., Hagl, S.
Kill kinetics of Borrelia
burgdorferi and bacterial findings in the relation to the treatment of Lyme
borreliosis. Infection 1996; 24(1):11-18

5  Preac-Mursic, V., Wanner, G., Reinhardt, S., Wilske, B., Marget, W.
Formation and cultivation of
Borrelia burgdorferi spheroplast L-form variants. Infection 1996;
24(3):218-225

6  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

7  Pfister, H.W., Preac-Mursic, V., Wilske, B. Latent Lyme neuroborreliosis:
Presence of Borrelia burgdorferi in the CSF without concurrent inflammatory
signs. Neurology 1989; 39:1118-20

8  Preac-Mursic, V., Weber, K., Pfister, H.W., Wilske, B. Survival of
Borrelia burgdorferi in antibiotically treated patients with Lyme
Borreliosis. Infection 1989; 17(6):355-359

9  Phillips, S.E., Mattman, L.H., Hulinska, D., Moayad, H.  A proposal for
the reliable culture of Borrelia burgdorferi from patients with chronic Lyme
Disease, even from those aggressively treated.  Infection. 1998; 26(6):
364-367

10. Lawrence, C., Lipton, R.B., Lowy, F.D., Coyle, P.K.  Seronegative
chronic relapsing neuroborreliosis.
Eur Neurol 1995; 35(2):113-117

11. Borson, O., Brorson, S. An in vitro study of the susceptibility of
mobilke and cystic forms of Borrelia burgdorferi to metronidazole. APMIS;
1999; 107 (6): 566-576

12.  Hassler, D., Riedel, K., Zorn, J., Preac-Mursic, V. Pulsed high dose
cefotaxime therapy in refractory Lyme Borreliosis.  Lancet 1991; 338:13

13. Cimmino, M.A., Accardo, S. Long term treatment of chronic Lyme arthritis
with Benzathine penicillin.  Ann rheum Dis 1992; 51: 1007-1008

14.  Logigian, E.L., Kapan, R.F., Steere, A.C. Chronic neurologic
manifestations of Lyme Disease. N Engl J Med 1990; 323:1438-44

15. Fallon, B.A., Nields, J.A., Burrascano, J.J., Liegner, K., DelBene, D.,
Liebowitz, M.R. The neuropsychiatric manifestations of Lyme Borreliosis.
Psychiatric Quarterly; 1992; 63 (1): 95-117

16.  Musher, D.M. Syphilis, Neurosyphilis, Penicillin, and AIDS. J Infect
Dis 1991; 163:1201-1206

17. Miklossy, J. Alzheimer's Disease- a spirochetosis? NeuroReport 1993; 4:
841-848

18.  MacDonald, A.B. Gestational Lyme Borreliosis. Implications for the
fetus. IN Rheumatic Disease Clinics of North America 1989; 15(4):657-677

19.  Asbrink, E., Hovmark, A. Successful cultivation of spirochetes from
skin lesions of patients with erythema chronicum migrans Afzelius and
acrodermatitis Chronica atrophicans. Acta Pathol Microb Immunol Scand 1985;
Sect B, 93:161-163

20.  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;
91:95-97

21.  Kirsch, M. etal. Fatal adult respiratory distress syndrome in a patient
with Lyme Disease.  JAMA 1989; 259:2737-39

22.  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; 21:1188-91

23. Bou-Holaigah, I., Rowe, P.C., Kan, J., Calkins, H. The relationship
between neurally mediated hypotension and the chronic fatigue syndrome. JAMA
1995; 274(12): 961-967

24. Wahlberg, P., Granlund, H., Nyman, D., Panelius, J., Sppala, I.
Treatment of late Lyme Borreliosis
Journal of Infection 1994; 29:255-261

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