Back to main report








W.T. Harvey, MD, MPH







Table of Contents


I.          Introduction                                                      Page 3

II.         Background/Illness Model                                Page 3

III.       Potentially Infected Groups                               Page 8

IV.       Diagnosis                                                          Page 9

V.        Treatment                                                         Page 19

VI.       Valuable Medical Contacts                               Page 23

VII.      Information Sources                                          Page 23

VET     Appendix                                                         Page 23

IX.       References                                                       Page 35









This manual is intended for medical professionals. Its contents have been derived from an extensive review of peer-reviewed medical articles, select books, and the author's clinical experience.

As of now, this guideline is outside presently accepted concepts, and "Standard Medical Care". Nevertheless, its conceptual framework has evolved into unexpectedly successful treatment outcomes in many chronic illnesses, heretofore treated with only minimal or no success. Simply considering this viewpoint in patients with complex, poorly understood illnesses may provide insights where none presently exists.






Numerous "Syndromes" presently exist with a similar, multi-systemic presentation but without clear etiology. For the most part, these are associated with singular, but dissimilar viewpoints. They have been derived within differing assumed frameworks, and may or may not have a single proposed etiology. We believe that most of these Syndromes, all with different names, are variants or distinct but separate parts, of a single illness.

We came to this perspective as we systematically evaluated representative patients from most of these syndromes over a four-year period. As the numbers examined increased, it became clear that all had fundamentally similar physical findings, similar but intermittent laboratory abnormalities, and eventually, common etiologic agent(s). Treatment derived from this "unifying" concept became more successful as it evolved, until presently most patients improve significantly if not fully, and treatment time and complexity has diminished.

We began with the assumption that a controversial illness, labeled "Chronic Lyme Disease" was the possible common thread among all these syndromes. As testing for the known etiologic agent for "Lyme disease" (a limited, tightly-defined zoonosis), Borrelia burgdorferi sensu stricto, proceeded, results were at first disappointing. Dissection of the test criteria (NTH Dearborn Criteria, 1994) provided insights that led to increased numbers of test positives, until present percentages are now between 80 and 90%. As the numbers of positives rose and treatments directed at Borrelia became more successful, our certainty of a Borrelia etiology for all syndromes we evaluated became the foundation of our diagnosis and treatment.     





Interwoven into the progression of our understanding were the findings of credible explanations of symptoms, signs, laboratory abnormalities, and treatments. As these findings became more numerous, we began constructing a "working model" of the larger disease that connected these Syndromes. To our surprise, it later began to explain illnesses far outside the Syndromes, providing improvement or recovery in patients that earlier had no effective treatments available.

A synopsis of the evolutionary steps in our conceptual model of these illnesses follows:

1.   Barrel'ia bvrgdorferi was first considered the singular etiology.

2.   Treatment evolved from oral antibiotics that took one to several years for

effective outcomes, to IM Ceftriaxone (8 months), to higher-dose IV Ceftriaxone that in many cases resolved symptoms in 12 weeks.

3.  As the faster, more effective treatments were used, a follow-on illness "flare" or recrudescence emerged that had strong CNS characteristics.

4.   Babesia microti began to be found in increasing numbers in these patients for reasons similar to the difficulty of finding Borrelia initially. Repeated testing revealed even higher percentages of Babesia co-infection.

5.   Use of the anti-Babesial combination Atovaquone and Azithromycin produced dramatic resolution of about 75% of the many symptoms (CNS related) in both the Babesia positive and the Babesia negative groups with Borreliosis.

6.   Our model now shifted to the assumption that these illnesses had a common etiology consisting of TWO interdependent agents, Borrelia and Babesia. Treatment became yet more effective and shorter.

7.  Comprehensive literature search of NLM strongly suggested Toxoplasmosis as a candidate etiological agent, as did treatment outcomes (Both Toxoplasmosis and Babesia are treated effectively with Atovaquone and Azithromycin). Standard testing (IgG/TgM and PCR) for Toxoplasmosis gondii rarely revealed this agent, however. Test methods and sensitivity remain questionable, as specialty labs have not yet developed sensitive procedures for finding this agent.

8.   We thus find ourselves at the paradoxical position of having two possible

fundamental co-agents, one moderately supported by laboratory identification and the other strongly supported by credible theory but no test "proof. Fortunately, treatment for both is the same.

9.   Insight into this/these illnesses continues to evolve...

In summary, virtually all our patients fall outside the rigid definition of Lyme disease. Many, however, fall within one or more overlapping "Syndromes". Unexpectedly, many others within the current mainstream medical model fit our model with varied additional symptoms or signs. All appear to encompass a broad range of illnesses that have in common chronicity, persistent inflammation, and unknown primary cause.




How symptoms are caused: a hypothetical conceptualization in progress Borrelia bwgdorferi enters the body either by trans-ovarial passage before birth or from sexual contact. Globally (outside all highly endemic areas such as Texas), its' entry is thus unlikely from tick bite, particularly when the organism is present as a part of the body during its initial development in the womb (Vertical transfer). This may allow some tolerance, or the opportunity for more effective cloaking. Horizontal transfer is assumed to be sexually via mucous membranes or as a blood-borne pathogen. In any case, effects may appear immediately (fetal damage or miscarriage), slowly (frequent infections, fatigue) or rapidly (sudden onset of multi-symptom disability). Reasons for the differences are unknown.

The spirochete's mechanisms of pathology are simple but essential: (1) to create immune deficiency, and (2) to cause chronic, low grade inflammation. Until recently, we conceptualized these Syndromes as involving only Borrelia burgdorferi. Lately, the realization that most patients are infected with an enormous range of unexpected, activated agents has led us to believe that some or many illness symptoms come from a pan-immune deficiency state. Particularly, a co-infection that may have initially entered humanity via arthropods is being found in large numbers in these patients (Babesia). Additionally, activation of common, usually dormant human pathogens such as the Herpes group and Toxoplasmosis are also symptom-generation candidates. Recent highly successful experience treating with the drugAtovaquone leads us to speculate that either Babesia or Toxoplasmosis may be the primary generator of pathology. If so, these syndromes may be unique in nature as dual agent diseases.

Complicating the Syndromes is a characteristic of most bacteria: pleomorphisra (multiple forms). Borrelia, for example, is thought of only as a moving, coiled bacterium. However, use of time-lapse microscopy shows it or one of the co-agents appears to exist within red cells in a form without walls, and within serum as buds and strings (L-forms). More developed forms can be seen multiplying within human phagocytes.

Borrelia also changes into a "cyst" form when in the presence of either an activated immune system or antibiotics... then back again when no threat exists. These multiple forms and phagocyte neutralization can credibly explain many of the syndromes' disbelieved characteristics: persistence with and without symptoms, detection impediment, and treatment difficulties. The existence of Borrelia cyst forms gives plausibility to an often-seen scenario: (1) acquiring the disease at birth, (2) having minimal symptoms for years or decades, then (3) erupting when significant physiologic stress (such as participating in the Gulf War) drops immune competence, permitting the pathogens to emerge or activate.









The hypothetical etiologic agents

Agent one; Borrelia: We postulate that Borrelia is one of two essential pathogens responsible for most unexplained chronic human illness. It operates in these two ways:

    Chronic inflammation of the body via an initial pan-vasculitis

    Immune damage, encompassing the anti-viral, anti-bacterial, anti-parasitic and anti-fungal systems

Inflammation: Borrelia appears to stimulate parts of the immune system considerably. Certain T-cells, mainly macrophages and monocytes, contact the spirochete and after identifying it as foreign, send out cytokines to shorten the expected short infection. The process is not appropriate for continuous, unremitting infection. The primary cytokines responsible for many inflammation symptoms are IL-lb, IL-6, and TNF-alpha (Tumor Necrosis Factor-alpha), although others may also contribute. TNF-alpha predominates. Other cytokines counter the inflammatory effect but in chronic illness are actually down-regulated. SimplisticaHy, pathogenic agent attracts T-cell; T-cell releases high levels of TNF-alpha; TNF-alpha circulates throughout the entire circulatory system inciting inflammation in any susceptible tissues. Unless the spirochete is gone or dormant, the tendency to inflame is ceaseless.

What becomes inflamed seems to depend on several factors, some obvious, some unexplainable as yet. Clearly, tissues under mechanical stress from overuse, continuous use, or overloading are susceptible. Other tissues that become slightly inflamed from various causes such as the friction of bile passage can cascade into full inflammation. Yet others may simply be random events. Some tissues or organs may swell simply in the presence of these cytokines.

The one process in patients caused mainly by excess TNF-alpha that is not attributable to inflammation is insulin resistance. TNF-alpha blocks insulin receptors, denying entry of blood glucose into most or all cells. Insulin receptor blockade then causes blood glucose to rise (hyperglycemia), insulin production and response to increase (Hyperinsulinemia), and lowered functional capacity of all affected cells. This effect likely contributes to fatigue as well as diminished function of most organ systems.

Immune damage: These Syndromes appear to have in common diminished immune competence. The effect spans immunity against bacteria, protozoa, viruses, fungi, and small symbiotic biological entities seldom seen on humans from animals and plants. Rarely do most resulting infections become severe. More likely, they are numerous and disconcerting. Activation of the agents causing central nervous system effects (such as Babesia or Toxoplasmosis) seems to be the most serious consequence of Borrelia's effect on immunity. We now believe most symptoms and signs of these Syndromes are caused by one or both of these agents.









Agent two (Candidate 1): Babesia Our most recent observation concerns awareness of the high prevalence of Babesia microti in our 56-infected patients. It seems to be associated only with central nervous system symptoms and signs where pain, motor function, and behavioral effects predominate. We repeatedly verify this association by seeing the disappearance or diminution of global CNS complaints when treating with the anti-Babesial drugs atovaquone and azithromycin. Patients where chronic, severe pain predominates are virtually all in this category.

Agent two (Candidate 2); Toxoplasmosis This agent remains a serious candidate for CNS activation in these patients for many indirect reasons. First 30-50% of humans are infected with the latent cyst form. Second, copious data exist on the CNS effects of activation from the HTV literature. Except for degree, most effects are the same. Third, identifying activated Toxoplasmosis remains extremely difficult for pathologists, blinding our attempts to see if this agent is present in all these syndromes. Supporting its' presence is the remarkable response to the medications also effective against it: atovaquone and azithromycin.

Central Nervous System effects: The full extent of CNS effects continues to be evealed. The control center for the entire body is the brain, composed mainly of neurons and neurochemicals. Documented effects include changing set points (breathing rate), disrupting control loops (such as most if not all hormones), and altering behavior, emotion, equilibrium, sensory mapping, memory, sleep architecture, etc. How these neuronal effects occur is not yet understood.

This introduction does not (nor can it presently) address every symptom found associated with persistent Borreliosis. It is intended to provide a plausible way to understand the disease and its symptoms. We call this toll an Illness Model. It remains theoretical and is built from patient diagnosis and treatment experience, credible published data, and rationally based imagination. Continued observation of new patient information and treatment outcomes is iterated into the model to continue its evolution toward accurate explanation. Eventually, extensive research must validate all aspects of the model. Only then does "proof exist.






























The follow ing focus specifically on these Syndromes. It is not intended as part of a "differential diagnosis". That said, vigilance for many other illnesses with some symptoms in common is imperative, as serious states such as cancer and coronary heart disease must not be overlooked. Following a singular mindset or viewpoint is, in fact, the cause of most error in medical diagnosis.

Below are the specific data points we find most useful and most common among patients with these Syndromes. They lend themselves, in fact, to use as a checklist to simplify initial and repeat evaluations.


           Birth state/country

           Residence locations and length

           Travel destinations and activities relative to animal, vector and human endemicity
            for Borreliosis (incompletely determined globally, however)



           Mate gender preference

Family History

Characterize illnesses in the following family members. Focus on symptoms and signs of these Syndromes listed further down. Include onset dates. If possible have patient construct a family tree with known diagnoses, age, age at death, and cause of death.






Medical History-inclusive

Patients found to be infected with Borrelia burgdorferi typically give several patterns of illness presentation:

1.   In true "Lyme disease", illness symptoms begin (days to weeks) shortly after inoculation by a tick or other vector arthropod or insect.

2.   In congenital transfer cases, symptoms appear sporadically throughout early life until (or if) full activation occurs (at any age, but most commonly, it appears beyond age 40). Most common are








recurrent headaches, seldom-recognized activity limits, and frequent viral-like illnesses. Most children (There are many pediatric cases) have some degree of ADD or ADHD. Many babies are born with some physical defect, often palate or digit aberrancies. "Full" Activation" later is common.

3.   Fully Active Borreliosis cases are usually quite ill, many are not able to hold jobs, most are home-bound if not bed-ridden, and the breadth among body systems of symptoms often astonishing. By the time most find effective medical care, they have experienced the following repeatedly: Outright rapid rejection by physicians as being ill (with minimal or no exam or tests), diagnosed as a psychiatric case (usually depressed), or have had numerous surgeries related to various chronic pains. Most slowly deteriorate, and review of their family histories suggests shortened lifespan of parents and siblings from cardiovascular causes or cancer (death in mid-50s is typical).

4.  Asymptomatic Borreliosis is common. An average of several epidemiological surveys of large populations finds that about 50% who test positive for the organism show "no symptoms". More of these are male than female, and are often spouses of infected mates. Examination of Borrelia-infected patients since CY 2000 reveals, however, that even in the most "symptom" free and active Bb-positive person, some signs and lab abnormalities typical of the disease can be found.

History of present illness

The following points, embellished as time permits, are present in most, if not all Borrelia-infected patients. The degree may vary extensively, however.

    When did the illness begin?

   Were ANY "typical" symptoms (see below) present before significant symptoms began?

   What was the FIRST symptom noticed?

   What were the subsequent symptoms/signs, how fast did they progress, and what was the course of their intensity?

Review of Systems

Review by organ system or anatomic region.

1.   HEENT:

a.   Sores?

b.   Hair/Eyebrow loss? c.   Flushing episodes? d.   Recurrent acne?








e.         Chronic/recurring "sinus" or "allergy" problems?

f.          Sensitivity to light or sound? Intermittent blurring of vision?

g.         Recurrent eye pain or vision loss?

h.         Constant bilateral tinnitus?

i.          Tender lymph nodes or salivary glands?

j.          Recurrent mouth sores?

k.         Recurrent ear infections?

1.         Throat frequently sore or excessive mucus?

m.        Recurrent laryngitis?

n.         History of Bell's Palsy?

o.         Neck sore, chronically hurts to move?

p.         Recurrent nose or gingival bleeding?

2-   NECK:

a.   Thyroid problems?

b.   Neck discomfort?

c.   Recurrent node tenderness?

3.   BACK:

a.   Chronic pain in any part of back or shoulders?

b.   Any prior disc problems diagnosed or surgery performed?


a.         Asthma?

b.         Any frequent wheezing?

c.         Ever have pneumonia?

d.         Smoker?

e.         Episodic dyspnea when inactive (frequent sighing, yawning)?

f.          Current dyspnea with exertion?

g.         Able to jog or walk long distances?

h.         Chronic dry or productive cough?


5.   SKIN: Note and describe all unusual skin abnormalities, particularly:

a.         Pigmentation patterns

b.         Raised but discrete growths?

c.         Excessive epidermal sloughing?

d.         Erythema-either confluent or blotchy?

e.         Sores?

f.          Thick skin on feet (esp. heels)?

g.         Any eczema-like patches?

h.         Thickened and dark areas on ankles or lower arms?

i.          Roughness (like sand) on outer arms between shoulders and elbows?

j.          Hair loss on toes, lower legs, scalp, eyebrows, eye lids?

k.         Toe fungus?






a.         Recurrent pain?

b.         Recurrent arrythmias?

c.         Dyspnea with effort? When resting (Sighing, "breath-catching")?

d          History of murmurs or other Cardiological diagnoses?

e.         On medicine for hypertension?

f.          Has Mitral Valve Prolapse been diagnosed?

g.         Chronic high resting heart rate (>75 bpm)?


a.         GERD?

b.         IBS (Recurrent, alternating diarrhea and constipation)?

c.         HX gallstones, cholecystitis? cholecystectomy?

d.         Hx pancreatitis?

e.         Appendicitis?

f.          Hx intestinal parasites?

g.         Hx swollen liver or spleen?

h.         Hx hepatitis?

i.          Liver cysts?

j.          Intestinal polyps?

k.         Swallowing problems?

1.         Esophageal procedures?

m.        Hiatal hernia?


a.         Chronic/recurrent bladder pain?

b.         Kidney stones?

c.         Kidney cysts?

d.         Neurogenic bladder?

e.         Frequent urination, day or night?

f.          Difficulty starting stream?

g.         Incontinence?

h.         Hx enuresis in childhood?


a.         (Females) Irregular periods?

b.         PMS?

c.         Dyspareunia?

d.         Polycystic ovaries?

e.         Uterine fibroids?

f.          Endometriosis?

g.         Miscarriages?

h.         Abnormal newborns?

i.          Low libido?

j.          Chronic pelvic pain?







k.         (Males) Chronic/recurrent prostatitis?

1.         Recurrent epididymitis?

m.        Early low libido?


a.         Sleep quality?

b.         Sleep apnea DX?

c.         Unstable weight?

d.         Significant, progressive weight gain?

e.         Habitual smoker?

f.          Alcohol intake excessive?

g.         Chronic tiredness?

h.         Exercise level, type and frequency?


a.         Bipolar?

b.         ADD?

c.         OCD?

d          Chronically anxious?

e.         Rage attacks?

f.          Panic attacks?

g.         Dysnomia?

h.         Delusional/psychotic episodes?

i.          Night terrors?

j.          Memory considered worsening?

k.         Recurrent depression?

1.         Agoraphobia (does not want to leave the house; asocial)?

m.        Unreasonably fearful?









Physical Examination

Examine by organ system or anatomic region.

1.   HEENT:

           Sores in scalp?

           Hair loss? Eyebrow loss?

           Red, flushed face or ears?

           Excessive acne for age?

           Lymphocytomas on edge of pinna (small, firm white growths on edge of

           Sluggish or contrary pupillary response to penlight?

           Anisocoria (pupil diameter difference)?

           Enlarged or tender lymph nodes (any location) or salivary glands?

           Check tongue for white matting, sores along edge.

           Lips: Dry? Cold sores? 7th nerve outlet: tender (just below ear lobes)?

           Check ear canals for cheesy/inflamed external otitis.

           Pharyngeal lymphoid patches inflamed?

           Voice strong?

           Facial asymmetry (even small droop to one side)?

           Check all 18 Fibromyalgia tender points (Atch.).

2.   NECK:

   Thyroid: check for size, shape, and tenderness.

   Check neck for full movement in all axes.

3.   BACK:

           Continue Fibromyalgia tender point check around scapulae.

           Check shoulder joints for full ROM in all axes without pain.

           Check shoulder bursae for tenderness.

           Have patient point out any other areas of back that are tender or painful.

           Any CVA tenderness?

           SI joints tender?

           Lungs clear to auscultation from back, w/o wheezing?

           Check skin for microangioma (many vs. few vs. none).

4.   CHEST:

           Heart: Listen for murmurs.

           Determine rhythm and rate over 15-30 seconds.

           Check skin for microangioma.

           Check abdomen for RUQ, LUQ tenderness or swelling.

           Palpate abdomen for masses.

           Palpate pelvis for tenderness.

           Can patient sit up without assistance? Does it hurt to do so?







5.   SKIN:

           Describe any lesion in terms of size, location, texture, color, and any

           Livido reticularis on forearms, upper legs, palms?

           Capillary refill time on palm (Grade as 0, Yz, 1,2, or 3 seconds)

           Microangioma number and relative size (1 mm = small; 3-5 mm large)

           Hyperpigmentation of outer ankles?

           Multiple superficial bruises?

           Thick, dark (elephant) skin areas?

           Toenail fungus?

           Tinea cruris?

           Small or large (> 1 cm) skin ulcers?

           Multiple healed "bluish" ulcer scars?



           Recurrent itching (visible excoriation) of "normal" skin?

           Erythema of face, forearms, palms, upper chest?

           Purple feet if hung from examining table over one minute,

           Toe, foot, or lower leg hair loss? Describe extent.


   Decreased shoulder, neck ROM

    Tender wrists, fingers, L-T spine, sacroiliac joints.

    Swelling, erythema, heat in any joint MUSCLES/TENDONS:

      Any tenderness or atrophy?

      Look for snuff-box and forearm dip of both arms.

      Check grip strength, standing from a squat, and ability to raise arms.

      Can patient fully extend all fingers and toes?

      Are shins tender?






Are all limb movements purposeful and coordinated?

Check all Cranial nerves.

Look at tongue for fasciculations.

Are fasciculations obvious anywhere?

Is voice strong ? Speech slurred?

Facial asymmetry pronounced?

Look for abnormal pupillary response to light.

Check Babinski (usually normal)

Romberg (always abnormal)

Check reflexes (Kneejerk usually abnormally increased) and for reflex


Test toes and fingertips for vibratory sensory loss with a 120 Hz tuning fork

(virtually always present).










Laboratory relevant testing

1.  Initial testing includes the following that are to exclude similar illnesses and where abnormalities are usually found (Common results from these patients follow in parentheses):

   CBC (LOW: WBC, RBC, Hct: HIGH: RBC size and color, Eos, Monocytes; EITHER: RBC indices)

   CMP (LOW: K+, CO2; HIGH: Ca++, SGOT, SGPT, Glu, BUN)

   RPR (Normal)

    HIV (Normal)

    Sedimentation rate (Sometimes slightly high, rarely very high)

   ANA (usually slightly elevated)

    TSH (Normal)

   IgG subclasses (Often S-C 1 and 3 are low. Occasionally Total IgG is low)

   EBV panel (IgGs always elevated)

   C-reactive protein (Often high or high-normal)

    Test for possible infectious etiological agents. (See below.)

2.  Follow up testing, done at all routine subsequent office visits:



Testing for Borrelia-associated agents

WHERE these tests are done is crucial. Borrelia and its associated agents can be difficult to find even with the most recent, carefully crafted tests. Rationale is brief here but stems from the initial test criteria being set 10 years ago, where inclusion criteria of specimens were for recently-infected individuals with high antibody levels, where test positivity depended strictly on antibodies (then state-of-the-art), and where two of five crucial Outer Surface proteins (P31, P34) were removed for vaccine research. Detection methods now available are for antigenic material, and are more sensitive and specific, such as PCR and DFA.

The following specialized laboratories are recommended because they have given us the highest correlation with successful treatment, and greatly minimized the number of tests presently needed to find these agents at "standard" commercial clinical laboratories. See relevant attachments.

    Igenex Laboratories

   Bowen Research Foundation (We use only the testing arm of that organization)




The agents we seek to find are these:

   Borrelia burgdorferi (We presently believe this single agent is ultimately responsible for all patient illness, but may carry out its symptom creation via other organisms allowed guest status because of the immune deficiency it creates.)

    Babesia microti

    Taxoplasmosis Gondii

    We acknowledge the occurrence of possibly high levels of other co-infections in endemic regions (11 states) such as Bartonella and Erlichia. We seldom find these in our patients from any region, and when we treat these organisms see little effect on the overall illness. Our patients differ, of course, from the typical "Lyme disease" patient by time. Ours have been symptomatic for years to decades, almost guaranteeing that the acute effects of co-infections (sometimes serious) have passed.

Igenex tests using several methods and is CLIA approved. Their amplified and expanded Western Blot for Borrelia is very sensitive now. Use Western Blotting when Insurance is causing problems. Igenex has the most sensitive Babesia test panel we find available, but does not yet test for Toxoplasmosis. Igenex tests are recoverable from insurance but must include a check on submission. Their tests are at no cost to Medicare recipients.

Bowen Research is not a clinical lab but a research lab. Their IFA test for Borrelia appears to be the most sensitive available. Their test also crudely scales the bacterial load (0-8) that can be quite helpful in assessing recovery status. Their Babesia testing is visual only, but is a part of the standard Borrelia test (Qribb). Pictures follow that are interesting. The cost of the full Bowen Qribb is $250, and is not recoverable from medical insurance but IS partially recoverable as a research foundation tax deduction.






Given the plethora of symptoms, signs, illness levels, disease expressions, and unexpected response to medical agents of any kind, all treatment is necessarily empirical, thus highly individualized. Presently, treatment is directed at TWO distinct organisms with distinctly different symptoms and signs. These are Borrelia, and Babesia/ Toxoplasmosis. This new paradigm and its ease and enhanced treatment effectiveness now drives us to a single FIRST approach in most patients:

Treat with oral Azithromycin and Atovaquone (see B or C below)

1.     Atovaquone, 750 mg/ 5ml, 210 ml bottle or packs. Take one teaspoon (5 ml) twice daily with food. Refill X 2.

2.     Azithromycin, 250 mg, #60. Take one tablet twice daily with food. Refill X 5.

3.     Diflucan, 100 mg, #10. Take one tablet weekly and as needed for yeast overgrowth. Refill X 5.

4.     Metronidazole ER, 750 mg, # 5. Take one weekly. Refill X 5.

In variants of the illness with serious neurological or psychiatric presentation, we presently begin by substituting the 12-week Ceftriaxone protocol for the Azithromycin, but combine with the Atovaquone.




A. Antibiotics effective against BORRELIA:

1.   Orals Best choices in our experience to date are

(considering efficacy, low flare effects, and compliance. If cost is a consideration, the level is shown below as H, M or L):

                                      Azithromycin, 600 mg QD (H)

    Clarithromycin XL, 500 mg QD (H)

                                        Cefuroxime, 500 mg BID (M)

    Minocycline, 100 mg BID (L/M)

                                         Cephalexin, 500 mg BID (L)

                                      Amoxicillin, 1,000 mg TDD (L)

    Metronidazole ER, 750 mg QD (M), or 250 mg TK>
      "Cyst form" only (H)

2.   Intramuscular (IM) [Most of our parenteral experience is with this single drug. It is several times more effective than any oral, and has minimal flare effect.]

    Ceftriaxone, one gram IM daily.

3.   Intravenous (IV) (As above, one drug, high efficacy, low flare effect.)

   Ceftriaxone, 2 grams BID for 12 weeks. Repeat cycle only once if required.

B. Antibiotics effective the protozoans BABESIA and TOXOPLASMOSIS:

1.   The only recommended safe and effective treatment of these two organisms are the following two drugs:

   Azithromycin, 250 mg twice a day with meals (breakfast and dinner)

   Atovaquone (Mepron), 5 ml (one teaspoonful) also twice a day with the same meals.

C. Antibiotics effective against both Borrelia and a presumed protozoan: The same as B.



D. Sources:

1.  All oral antibiotics are PDA approved, and purchased through local or US Mail-Order pharmacies, typically through medical insurance co-pay. Long-term high-cost antibiotics such as azithromycin are sometimes not approved, or at least often require "Prior Approval" paperwork. Biaxin may be substituted. Diagnostic codes should include Babesia (088.82) if it is found or part of treatment rationale.

2.   IM ceftriaxone (Presently only sold as Rocephin until December 2004, when it becomes available as a generic.) One-gram vials seem to be readily gotten through local or Mail-Order pharmacies via prescription. Concurrent prescriptions are required for the following required equipment:

   Lidocaine. 1%, 100 cc/month (two 50 cc bottles preferred). Mix 2. Ice with each one-gram vial of ceftriaxone until clear yellow.

    Syringes, disposable, 30cc, 30 per month. Use one daily.

   Needles, 25 gauge, 1 Vz inches, 30 per month. Use only for the actual injection.

   Needles, 18-20 gauge, 1 inch, 30 per month. Use only for fluid transfer between bottles (that can cause tip bending).

3.   IV Ceftriaxone should be given by professionals trained to do so, such as Home Health agencies. Insurance often will not cover this method because of exorbitant cost. Orders (describing details) for the only effective protocol we now consider useful are attached.

4.   Patients whose insurance will not cover IV ceftriaxone, but who have extremely debilitating or progressive courses can find alternative, less expensive drug sources. Safety, however, is paramount, and there must be assurance of quality line placement and care, and medication mixing and infusion. See attached information.





1.   Azithromycin: Continue from the first day without a break until symptoms have disappeared or plateaued for more than 3 months.

2.   Atovaquone: Give one course (bottle or box... typically for 21 days). Stop a week, then give the second course. Most patients will not require more than three courses, although CNS recovery will continue for another 3-4 months to resolution.


The technique is straightforward, and involves only in cutting the dose back... or even stopping the antibiotic briefly... until bacterial load drops sufficiently that severe flare effects are no longer a big problem. Patient and physician have to "feel" their way through treatment startup in some patients. Most can begin and continue at full dosing, however.



1.   Yeast control: Give one 100 mg Diflucan or one 200 mg Ketoconazole weekly as prophylaxis. Supplement for breakthroughs.

2.   Borrelia cyst removal: Give one Metronidazole ER, 750 mg, once each week during antibiotic therapy.

3.   Bile sludging: Give Ursodiol, 300 mg twice a day when on Ceftriaxone only. This is the only effective prophylaxis against gallbladder failure on this drug.


1.   Sleep/Pain: Give Gabatril, 2 mg qhs. Move up in two week increments to a max of 12 mg.

2.   Attention, alertness, memory/Sleep: Give Provigil, 100-200 mg twice a day (On awakening and 6-8 hours later).

3.   Avoid; Antidepressants, narcotics, and benzodiazepines.






   PEDIATRICS-Charles Ray Jones, M.D. New Haven, CN 203-772-1123

   PSYCHIATRY-Robert Bransfield, M.D. Red Bank, NJ 732-741-3263

    OB-GYN-Bvron Holt, M.D. Houston, TX


    Pub Med: http://www.ncbi.nlm.nih. gov/entrez/query. fcgi

    Lots of Links on Lyme Disease:

http://www. geocities. com/HotSprings/Oasis/6455/lyme-links.html


   References below





   Igenex test instructions form

   IM Ceftriaxone (patient-administered) instructions

   IV Ceftriaxone (patient-administered) instructions

   Ceftriaxone foreign source information

   Liability release form for self-administered parenteral medication

   Home Health Orders for IV Rocephin (Cichon protocol)

   Patient Informational Manual template

   Physical Therapy Orders for Borreliosis patient rehab

    Bowen Research Labs Test information for patients

    Fibromyalgia tender-point map