Amsterdam Rotation Protocols Dr H Training

Rotation of Antibiotics and
Integrative/Herbal Protocols
in the Difficult-to-Treat Lyme

Patient

Amsterdam

June 19th 2019

Dr. Richard Horowitz,
Medical Director HVHAC, Hyde Park, N.Y.

Board Certified Internal Medicine
Member, HHS Tick-Borne Disease Working Group 2017-2019
Co-chair, HHS Other Tick-borne Diseases and Co-infections, 2017-2019

Healing: Compassionate Empathetic

Attuned Presence: Matt Liotta PhD

Decety, J. Why empathy has a beneficial impact on others in medicine:
unifying theories. Front Behav Neurosci, 2014;8:457

7 Point Action Plan for Lyme-MSIDS:

How Can I Get Better? St Martin’s Press 2017
◼ Rule One: Symptoms Drive Diagnosis and

Treatment
◼ Rule Two: Lower Inflammation
◼ Rule Three: Detoxify, Detoxify, Detoxify
◼ Rule Four: Repair the Damage
◼ Rule Five: Provide Internal Balance:

Cytokines, Hormones, Microbiome
◼ Rule Six: Master the Big Three:

Sleep, Food, and Exercise
◼ Rule Seven: Heal Your Emotional Wounds

16 Point MSIDS Map: Evaluate all of
the Sources of Inflammation

◼ Primary Sources: ◼ Downstream effects:

◼ 1) Chronic infections ◼ 7) Endocrine disorders:
low T, low adrenal (f)
◼ 2) G.I.: Dysbiosis of
intestinal bacteria ◼ 8, 9) Neurological,
Psychological dysfunction
◼ 3) G.I. : Leaky gut w/ Food
allergies and sensitivities ◼ 10) POTS/dysautonomia

◼ 4) Sleep disorders:↑ IL-6 ◼ 11) Mitochondrial Dys(f)

◼ 5) Environmental toxins ◼ 11) Pain Syndromes
(heavy metals, mold…) ◼ 12) Liver Dysfunction

◼ 6) Nutritional Deficiencies ◼ 13) Autoimmune phen.

Initial History & Physical

◼ Initial visit: fill out the Horowitz MSIDS
questionnaire (HMQ) to determine the probability
of Lyme and associated tick-borne disease

◼ Do a complete History and Physical with the chief
complaints, past medical history, & current
symptoms, defining severity and frequency

◼ Social history, Family history

◼ Environmental history (? Mold ? Chem exposure)

◼ Review of Systems & Physical examination

◼ Differential Diagnosis and Testing

Empirical Validation of the Horowitz MSIDS

Questionnaire for Suspected Lyme Disease

Citera M, Freeman PR, Horowitz RI. International Journal of General Medicine 2017:10 249–273.
http://www.ncbi.nlm.nih.gov/pubmed/28919803

Step 1: Prioritize Likely Abnormalities on the

16 point MSIDS Map Based on an H and P

◼ History: HMQ score > 63? (c/w Lyme), Migratory pain?

(Lyme, other Borrelia spp.), questions 1/22 + (sweats) ?
(Babesia). Perform differential diagnostic work-up based on
history. Focus on key questions: ? Multiple tick-bites (↑
risk co-inf’s) ? Pain bottom feet (? Bart), ? New onset
seizure d/o (Bart, POWV), ? Dizziness standing (POTS)

◼ Physical: ? Rashes (EM), striae (Bartonella), granulomas

(Bartonella), other rashes (BMD, STARI, RMSF..), large LN’s
(? Bart), Bells palsy (? Lyme), evidence of PNP (? Lyme,
Bartonella, heavy metals, DM, hypothyroidism, CTS…), √
sitting/standing BP/pulse (POTS), dermatographism(MCAD)

Step 1: Prioritize the Most Important
Abnormalities on the 16 point MSIDS Map

◼ Other Important History: Timing of the illness:

◼ ? After being in woods, or highly endemic area (TBD)

◼ ? After being in a mold exposed building (Mold S)

◼ ? Recent renovations or chemical exposure (VOC’s,
formaldehyde…). ? Feel better out of the house (MCS,
Mold)

◼ ? Recent travel inside US, or outside the country (↑ risk
malaria, dengue, chikungunya, parasites..)

◼ ? Recent trauma, i.e., physical, emotional (PTSD
component, with concomitant adrenal stress)

◼ Do full H+ P, ROS to evaluate all major organ systems

Step 1: Prioritize the Most Important
Abnormalities on the 16 point MSIDS Map

◼ Other Important History: Past Medical & Social

History:

◼ Other inflammatory or AI disease? (RA, SLE, UC/IBD,
MS…). On immunosuppressive medications?

◼ History of gluten sensitivity/celiac: ? Compliant w/ diet

◼ History of CVID, CIDP? (20% + Lyme patients have immune
deficiencies, interfering with treatment)

◼ ? Smoking/ETOH history (? Risk ASHD, cirrhosis, liver abN)

◼ ? Psych history: new sudden onset psychiatric illness
without a clear trigger (schizophrenia post tick-bite), or
not responding to classical therapies, wrong age for illness

Step 1: Prioritize the Most Important
Abnormalities on the 16 point MSIDS Map

◼ Other Important History: Past Medical & Social

History:

◼ Recent long term antibiotic use for TBD’s (? Candida
issue, ? Mitochondrial dysfunction). Sx worse w/carbs?

◼ History of itching, wheezing, sneezing, anaphylactic
reactions (? Food allergies/? leaky gut/? mast cell
activation/? alpha gal allergy…apart from prior allergic
rhinitis/asthma history..)

◼ Are you sensitive to all meds/herbs/diet? (MCS, trauma)

◼ Change in symptoms? Do you crash after exercise?
(mitochondrial dys(f), adrenal fatigue, deconditioning..)

Step 1: Prioritize the Most Important
Abnormalities on the 16 point MSIDS Map

◼ Other Important History: Change in symptoms, what

makes it better or worse?

◼ ? Feel better or worse with antibiotics or herbs (Lyme, co-
inf’s, Herxheimer reactions)

◼ ? Feel better or worse with detoxification, i.e., GSH, CSM,
charcoal/clay (Detoxification issues)

◼ ? Feel better or worse with methylation (Detox issues)

◼ ? Change in symptoms based on hormonal cycles (women
with Lyme disease tend to flare around the menses)

◼ ? Change in diet w/ ↑ carbs, w/ mid am +/or aft fatigue
that is sudden, profound (hypoglycemia, Candida)

Step 2: Evaluate Potential
Medication Side Effects

◼ Psychiatric medication: can cause drowsiness/fatigue

◼ Sleep medication: ? Hangover effect with sleep
walking/eating/driving, ↓ memory/conc… (Benadryl and
other anti-H1’s like Atarax, Ambien, Lunesta, Sonata..)

◼ Stimulants: caffeine, chocolate, Vyvanse: ? Interfering
with sleep, and increasing anxiety due to long ½ life

◼ Hormonal imbalance: ? Too much thyroid medication
causing jitteriness, anxiety; too little thyroid medication
(? Needs to be in upper 1/3 of normal range), ? not
enough adrenal support..

◼ Check PDR for SE’s/interactions of all medications!

Step 3: Create A Differential Diagnosis
For Every Symptom

◼ Every symptom should have several differential diagnoses

◼ See pages 50-64 “How Can I Get Better?” for a list of
extensive differentials to be considered. Often more than
1 etiology is ↑ symptoms in the Lyme-MSIDS patient

◼ Ex: Neuropathy symptoms: seen in up to 94% of all Lyme
patients. Differential includes: Borreliosis, Bartonella,
Autoimmune disorders (MS), carpal and cubital tunnel
syndrome, or any nerve entrapment (thoracic outlet), DM,
hypothyroidism, heavy metals (Hg, Pb, As), other
environmental toxins (TCE, mold), vitamin deficiencies (B
vit’s, B12, folate, MMA, HC), immune deficiency (CVID),
mitochondrial dys(f), hx CVA, pregnancy, hyperventilation..

Differential Diagnosis Pain

◼ Pain syndromes associated with Lyme Disease and
associated co-infections (ie., Bart, Mycoplasma):

- Chronic fatigue syndrome/ Fibromyalgia w/ widespread pain

- Autoimmune diseases (RA/SLE/MS) with inflammation

- Neurologic: headaches/migraines, neuropathy, radiculopathy,

encephalopathy, cranial nerve palsies, carpal tunnel/ulnar nerve

- GI/GU: IBS/IBD, interstitial cystitis (Lyme, Bart)

- GYN: pain syndromes: dysparaneuria, neuralgia (Lyme, Bart)

- Cardiac: chest pain (costochondritis, pericarditis..), palpitations..

- Psych: depression, psychosis, OCD, anxiety→↑pain (Lyme, Bart)

- Ophthalmology: painful eye syndromes (conjunctivitis, uveitis,

retinitis, optic neuritis..). If unresponsive to NSAIDS, narcotics,
neuroleptic medication, ? Underlying source(s) of infection..

Establish a Differential Diagnosis: Table 2.1:

Symptoms and Associated Medical Conditions on the

MSIDS Map

Symptoms Possible Medical Laboratory Testing

Conditions to Consider

Unexplained fevers, • Lyme disease (chronic and • CBC with a white cell count
sweats, chills, or
flushing other bacterial, viral, parasitic, • CMP with liver functions
and • Giemsa stain and malarial
fungal infections) smears

• Babesiosis • Babesia IFA

• Malaria • Babesia WA- 1/duncani
titers
•Brucellosis • Babesia FISH and PCR

• Hyperthyroidism • Thyroid function tests (TFT’s)
• Hormonal failure (early • Sex hormone levels
menopause) • Chest X-ray/PPD
• Tuberculosis* • ANA, RF
• Non- Hodgkin’s lymphoma* • Erythrocyte sedimentation rate
• Panic disorders (ESR),C-reactive protein (CRP)
• Autoimmune disorders • Cytokine panel
• Inflammation

Step 4: Address Inflammation To Heal

◼ 1. Block NFKappa-B and Activate Nrf2 with
antioxidants (curcurmin, green tea, resveratrol) and

phytochemicals (sulforaphane..)

◼ 2. Block Activation of Glial cells in the brain: LDN:

Blocks NFKappa-B and TLR4 signaling (decreasing glial cell
activation) and shifts immune responses from TH2 to TH1

◼ 3. Do an Anti-inflammatory diet: ↑ omega 3, ↓

omega 6 FA (Medit diet)→ ↓ arachidonic acid, avoid
allergic/sensitive foods, reduce simple sugars, red meat,
eggs, dairy, gluten, ? histamine

◼ 4. Replace minerals (zinc, copper, magnesium)

◼ 5. Get proper sleep and exercise (insomnia:↑ IL-6)

Address Inflammation To Heal

◼ 6. Treat the Infections causing inflammation, immune

dysfunction (The 3 I’s): antibiotics and natural therapies

◼ 7. Detoxification: Remove chemicals and inflammatory

cytokines causing inflammation

◼ 8. Balance the hormones, cytokines, & the microbiome

◼ 9. Heal the Damage to the Body: Repair the

mitochondrial damage from free radicals and oxidative
stress (may improve energy; neuro/card)

◼ 10. Heal the Damage to the Mind/Emotions: role of

meditation, love and compassion
◼ Annie Hopper, Dynamic Limbic Neural Retraining (DNRS)

Commonly Seen Obstacles to Healing

◼ The most difficult to treat, sensitive patients
usually have certain things in common:

◼ 1. Often they suffer from MCS and detoxification
problems

◼ 2. They often have GI issues: with disruption of
the microbiome, +/- SIBO, gluten sensitivity, leaky
gut, parasites, +/- enzyme deficiencies…

◼ 3. MCAD is often present, triggered by infections
like Lyme (PIMCAD) and/or environmental toxins
like mold

Commonly Seen Obstacles to Healing

◼ 4. Multiple chronic infections are often present:

◼ Bacteria we have seen persist: Borrelia spp and

Bartonella spp. are on the top of the list, with Mycoplasma
spp., tularemia, & brucella right behind. We have only seen
a rare case of a chronic rickettsial infection (Q-fever)

◼ Parasites we have seen persist: Babesia spp. persist

despite most rotations of anti-malarial medications/herbs

◼ Viruses we have seen persist: HHV6 reactivation was

seen in our practice, w/ 4x ↑ titers and + PCR’s. EBV PCR+
was occ. found. Also, chronic candidiasis possible…

◼ Horowitz, R.I.; Freeman, P.R. Precision Medicine: retrospective chart review and data analysis of 200
patients on dapsone combination therapy for chronic Lyme disease/post-treatment Lyme disease
syndrome: part 1. International Journal of General Medicine 2019:12 101–119

Commonly Seen Obstacles to Healing

◼ 5. There is immune deficiency: over 20% of our

practice had immunoglobulin deficiencies & subclass
deficiencies

◼ 6. There is immune overactivation: autoimmune

markers and inflammatory markers were elevated in up to
70% of our sickest patients

◼ 7. There are disrupted sleep patterns: including

DSPS, circadian rhythm disorders and insomnia/hypersomn

◼ 8. There is a history of emotional trauma, with PTSD
& unresolved issues of abuse

◼ Horowitz, R.I.; Freeman, P.R. Precision Medicine: The Role of the MSIDS Model in Defining, Diagnosing,
and Treating Chronic Lyme Disease/Post Treatment Lyme Disease Syndrome and Other Chronic Illness:
Part 2. Healthcare 2018, 6, 129.

Commonly Seen Obstacles to Healing

◼ 9. There is resistant POTS/dysautonomia with
severe autonomic dysfunction

◼ 10. There is mitochondrial dysfunction w/the cell
danger response (CDR). Difficult to find a safe
environment without continuous exposure to toxins

◼ 11. Whatever underlying medical problems are
present (including endotoxemia from dental/GI
sources), they are not well controlled, & contribute
to the burden of illness, w/ genetic predispositions

◼ Horowitz, R.I.; Freeman, P.R. Precision Medicine: The Role of the MSIDS Model in Defining, Diagnosing,
and Treating Chronic Lyme Disease/Post Treatment Lyme Disease Syndrome and Other Chronic Illness:
Part 2. Healthcare 2018, 6, 129.

Use Of Compounded Medications In
This Patient Populations is Essential

◼ Compounded Medications Provide Some Solutions
for this sensitive patient population:

◼ Compounded medications provide flexible dosing
(LDN, DMSA, hormones), liposomal formulations
(GSH, oregano oil), dye/excipient free compounds
(MCS), medications otherwise unavailable
(methylene blue for Dapsone, Bartonella)

◼ Compounders: Ex’s: Infuserve America (Fla),
Hopkinton Drug (Mass), Fallon Pharmacy..

Liposomes and Drug Delivery

◼ Liposomes localize preferentially to sites of inflammation
and infection → ideal for targeting biofilms (liposomal
oregano oil). Compounders can make liposomal formulas

◼ Liposomes are able to concentrate antimicrobial agents
at biofilm interfaces.

◼ Liposomes can carry both hydrophobic/hydrophilic and
lipophilic drugs over long periods of time and changes
the pharmacokinetics of antimicrobial agents, increasing
the circulation time and reducing the toxic side effects

Compounded Liposomal Herbal
Preparations/Medications

◼ Compounded pain creams (neuropathy:
ketoprofen (NSAID), local anesthetic, gabapentin,
amitriptyline)

◼ Compounded hormones: thyroid, sex hormones

◼ Liposomal formulations (Artemesia, Curcurmin,
oregano oil) for Babesia, inflammation, biofilms

◼ Compounded antibiotics (dye, excipient free) for
those with Environmental Illness/Chem Sensitivity

◼ Yadav, et al. Immunomodulatory effects of curcurmin. Immunopharmacol Immunotox. 2005;27
(3):485-97

◼ Feng J, et al. Front. Med, 11 October 2017

I. Multiple Chemical Sensitivity (MCS)

◼ Avoidance of chemicals: #1, + Measure body burden of
mold, metals, VOC’s, pesticides..(DD, PacTox..)

◼ Air and water purifiers, + fresh, clean food…? EMF free

◼ Evaluate detoxification pathways (Genova, Great Plains..)

◼ Support detoxification: Skin (FIR saunas), GI (fiber, flax,
binders [clay/charcoal], pre/probiotics, saccharomyces..),
liver (phase I and II support: NAC, ALA, DIM, sulforaphane
glucosinolate [Oncoplex ES] , GSH, methylation, MedCaps
DPO…), kidney (> 2 L fluid/day) + remove mold, metals..

◼ Mental detox: Annie Hopper’s Dynamic Limbic Retraining

◼ ? Low dose Keppra (250 mg +) HS

◼ Kakisaka, Y. et al. Levetiracetam improves symptoms of multiple chemical sensitivity: Case report. J
Med Invest. 2017;64(3.4):296-298.

Mycotoxin testing: Positive in Many
Patients With Mold Exposure

II. Gastrointestinal Issues

◼ Testing: upper GI: H. pylori (titer, breath test), ?

Achlorhydria (Heidelberg gastric analysis test), + test
pancreatic enzymes (amylase, lipase), Liver (NH3, LFT’s)

◼ Lower GI: CDSA: Genova, DD, Diagnos-Tech: (microbiome
eval [Prevotella spp., Clostridium spp, O+P..], ? Candida
overgrowth, ? adequate enzyme levels, ? Fat in stool
[malabsorption], pH, inflammatory markers [Eosinophil
protein X, calprotectin, lactoferrin, SCFA’s/butyrate levels]

◼ Breath testing (SIBO, leaky gut, fructose intolerance)

◼ Zonulin levels, IgE & IgG food profile, sIga (? Leaky gut)

◼ Antigliadin/TTG levels for gluten/celiac ? Cyrex lab

◼ Check for Mast Cell Activation Syndrome! If resistant sx

III. MCAS: Affects Different Disease

Processes

Slide thanks to Bob Miller, ISEAI, 2019

MCAS: ↑ Inflammatory Mediators (ASD)

Slide thanks to Bob Miller, ISEAI, 2019

III. Mast Cell Activation Syndrome

◼ May involve 1/5-10 people: check tryptase, histamine,
chromogranin A, PGD2 (blood,urine), mold in sinuses, urine

◼ Also: urinary N-methyl histamine, leukotriene E4, biopsy
with CD 117 staining. Triggers: mold, inf’s, trauma (MIT)

◼ Rapid reaction to anything PO (food, liquid)→ think MCAS

◼ ↑ Sensitivities: if sensitivity is increased to chemicals
(MCS), food, touch, smell, light, EMF → think MCAS

◼ Symptoms: pruritis, wheezing, sneezing, sinus congestion,
laryngitis, n. drip.. G.I.: after eating: sweating, flushing,
palpitations, N+, V+, diarrhea, bloating, gas, pain, headache
migraines, potentially anaphylaxis, + dermatographism

◼ Skin: rashes of every type (itching, flushing, hives), paresth.

◼ CV: POTS, palpit’s, arrythmias, lightheadedness, vertigo

III. Mast Cell Activation Syndrome

◼ Gen Symptoms: malaise, fatigue, temp dysreg, wt loss/gain

◼ Pelvic: bladder pain, cystitis. Neuro Psych: tics, seizures,
brain fog, ANS dysregulation!! + mood/sleep d/o’s (labile)

◼ Triggers: Mold and mycotoxins, infections(PIMCAS), trauma

◼ Mast cells coordinate the immune response to infectious
agents and toxins. Treat mold, inf’s, trauma (DNRS)…(MIT)

◼ Treatments: Mold: PC 3 g PO BID, GSH 1 g BID, NAC 600
BID, ALA 600 BID, N-butyrate 500 mg BID, binders
(charcoal/bentonite clay, CSM), dose is based on tolerance.
Intranasal Therapy : Amphot B, itraconazole, Nystatin +
biofilm agents (colloidal Ag, EDTA); Bactroban synergistic

◼ Mekori, Y. et al. Integrating innate and adaptive immune cells: Mast cells as crossroads between
regulatory and effector B and T cells. C Eur J Pharmacol (2015)

III. Mast Cell Activation Syndrome

◼ Systemic Antifungals: itraconazole (not well absorbed with
Zantac or PPI’s), voriconazole, posaconazole, isavuconazole

◼ Consider limbic retraining program if reactivity is
prominent & limiting symptom w/ MCAD/mold sensitivity

◼ Treat inf’s (Lyme, co-inf’s) and use Mast cell stabilizers:

◼ MCAD: H1 and H2 blockers (Zyrtec 10 mg + Zantac 150 mg
QD-BID, or Claritin 10 mg + Pepcid [famotidine] 10-20 mg,
vs fexofenadine [Allegra] 180 mg/day w/ H2 blocker)

◼ Mast cell stabilizers: Cromolyn Na (Gastrocrom…) +
Ketotifen: compounded: 0.5mg cap’s HS, then AC

◼ Diet: Low histamine diet

◼ Molderings, G. et al. Mast cell activation disease: a concise practical guide for diagnostic workup and
therapeutic options. Hematol Oncol 2011; 4: 10

IV. Multiple Chronic Infections

◼ Bacteria: goal is to treat multiple IC pathogens at once,

and address different forms of borrelia during the
treatment course, following the clinical response to each
drug/botanical as its added, personalizing treatment

◼ Cell wall forms: penicillins, cephalosporins (Ceftin 500 BID)

◼ Round body/cystic forms: Plaquenil 200 BID, GSE 2 PO BID
(Pure Encap’s), occ Flagyl/Tindamax (body wt), Alinia

◼ Intracellular location: tetracyclines, macrolides, quinolones,
rifampin, rifampicin, sulfa (dapsone), PZA. Extracell: Gent

◼ Biofilm/persister forms: dapsone, PZA, + add on treatment
for Bartonella (? methylene blue, clotrimazole, berberine) +
add on treatment for Babesia (malarone, herbs, rotations)



New Bartonella “Persister” Drugs

◼ Bartonella has been shown to have stationary persister
forms, like borrelia. Methylene blue, Gent, daptomycin &
clotrimazole were among the most active agents.? Berberine

◼ 7 azole drugs including had high activity vs stationary phase
Bh. Best: clotrimazole (also anti-malarial prop’s)

◼ Daptomycin: 21% residual viability (IV, expensive, SE’s)

◼ Methylene blue: 25% residual viability (used with dapsone)

◼ Gent (not IC)/?Nitrofurantoin: MIC values of 0.31–0.63 μg/mL

◼ Rifampin was the most effective against growing Bh
(doxy/zithro/quinolones also useful for growing forms)

◼ Li, T. et al. Identification of FDA-Approved Drugs with Activity against Stationary Phase Bartonella
henselae. Antibiotics 2019, 8(2), 50;

Basic Antibiotic Approaches for LD

◼ Create a personalized AB protocol:

◼ ? Allergies to any antibiotics. If sulfa sensitive, to what
extent? (most people with a sulfa sensitivity can tolerate
dapsone, as long as the reaction was not one of
anaphylaxis, or severe dermatitis, i.e., Stevens Johnson
syndrome). ? Use Zyrtec 10 mg + Zantac 150 mg before

◼ ? Are there strong Herxheimer reactions with certain
medications. A strong Herx with an intracellular drug
(tetra, macrolide, quinolone, rifampin, PZA, dapsone) or
a significant benefit, implies that the load of bacterial
inf’s making the patient sick are inside the cell

◼ Personalize treatment based on responses to medication

Lyme 101: Simply Follow the Reaction
To the AB’s, Personalize Treatment

◼ Feels better with a cell wall drug? (Amox 875 2-3

BID; Augmentin 1 g BID, Bicillin inj’s 1.2 mil U TIW, Ceftin
500 mg BID, cefdinir (Omnicef) 300 mg BID, IV Rocephin 2
g QD, IV Teflaro: then there are actively growing/log phase

◼ Can use probenecid 500 mg BID in adults to ↑ levels of
penicillins or cephalosporins for better CNS penetration,
but may ↑ levels of other medications (i.e., dapsone…)

◼ Can check peak and trough levels

◼ Can pulse cell wall drugs, ? Benefit in some patients

◼ Usually combined with Plaquenil, Zithromax, Nystatin

◼ Same logic applies to how the patient feels w/other meds

Lyme 101: Simply Follow the Reaction
To the AB’s, Personalize Therapy

◼ Feels better or worse with a cystic drug? (atypical

forms, round bodies, S-forms, L-forms, CWD forms), ie:

◼ Plaquenil, GSE: usually mild reactions if any. Plaquenil

alkalizes IC compartment (Coxiella), affects DNA Gyrase
and round bodies, modulates immunity (AI reactions). GSE
has an effect on round bodies, ? Effect on Candida

◼ Flagyl (metronidazole), Tindamax (tinidazole),
Alinia (nitoxazide): often w/ stronger reactions. ? Killing

of round body forms, flare from Candida…Flagyl and
Tindamax have excellent CNS penetration, but careful with
neuropathy/Candida! (add B complex) + no ETOH!

Lyme 101: Simply Follow the Reaction
To the AB’s, Personalize Therapy

◼ Feels better or worse with an intracellular drug? →
implies active IC inf’s (borrelia, Bartonella, Mycoplasma,
tularemia, brucella..). How to proceed?

◼ Personalize treatment: ? Good Herx or bad Herx. Good
Herx = feels better after days/weeks of ongoing ↑
symptoms. Continue med. Bad Herx= no improvement
after stopping the IC drug, back to baseline. Rotate IC med

◼ Mix IC drugs for maximum effect, ↓ any potential
resistance (not seen for borrelia, present w/ mycobact)

◼ Clues apart from clinical symptoms that an IC pathogen is
present: ↑ VEGF (Bart), ↑ 1,25/25 OH Vit D ratio, rise in
AB titers (Bart, Mycopl, Brucella), ? False + tularemia/Bruc

Lyme 101: Simply Follow the Reaction
To the Herbs, Personalize Therapy

◼ Feels better or worse with an biofilm agent? →

implies stationary forms in biofilms

◼ Biofilm agents: Commonly used at HVHAC: Work up dose:
Stevia (Nutramedix, 15 drops BID), Biocidin 2-3 pumps of
liposomal form BID, oregano oil (60 mg) ? Liposomal BID

◼ Others: Serrapeptase 1-2 BID, Lauricidin (monolaurin, up
to 1 scoop/d, rarely BID); Some MD’s use EDTA, Boluke..

◼ Also: peppermint oil, clove oil, cinnamon oil…Mix biofilm
agents & Personalize treatment: if flaring, lower dose or
use different agent? Try and push through flare

◼ Effective killing of Borrelia burgdorferi in vitro with novel herbal compounds Kati Karvonen* and Leona
Gilbert, Gen Med Open, 2018, Volume 2(6): 1-4

Dapsone Combination Therapy

◼ DDS CT: Plaquenil 200 BID, doxycycline (100-200 mg) BID,
rifampin 300 mg BID (empty stomach, or rifabutin 150 mg
BID with a full stomach), dapsone (from 25 mg QOD, to 25
mg QD, to 50/25 QOD, to 50 mg/d, max usual dose 100
mg/day), Nystatin 500,000 U tabs, 2 BID, Leucovorin 25 mg
BID, Folafy-ER (L-methylfolate) 15 mg QD or BID (increase
doses of folic acid based on anemia), triple probiotics
*(Ultraflora DF BID, Theralac BID, saccharomyces boulardii
BID) with 3 biofilm agents, including oregano oil cap’s BID,
Stevia (NutramediX) 15 drops BID, Biocidin 2 sprays BID
(work up doses of biofilm agents according to Herxing).
Future: Double dose dapsone study secondary to success

◼ Works well long term if no active co-infections (Bab, Bart)

Monitoring on Dapsone Combination
Therapy

◼ Initial G6PD levels must be normal. Rule out and treat any
underlying anemia (Fe deficiency, B12..) before treatment
with DDS CT

◼ Monitor CBC, CMP, methemoglobin levels: frequency
depends on the dose of dapsone (q wk, w/ ↑ doses)

◼ Make sure women report any unusually heavy
periods/clots where the risk of anemia rises. Stop dapsone
if any heavy bleeding, and ↑ folic acid (? > 100 mg/day)

◼ Stop dapsone if methemoglobin levels ↑> 8-10% despite
methylene blue 50 BID and 1000 mg liposomal GSH BID,
NAC 600 BID, ALA 600 mg BID, esp. if symptomatic. Lower
DDS dose to previously tolerated, helpful dose

Add on Babesia/Bartonella Therapy to
DDS CT if Symptoms/Inf’s Persist

◼ Add for Bartonella: Zithro (can be pulsed 4 days in a row

per week, i.e. Zithro BID, Mon-Thurs) + PZA (body weight),
methylene blue 50 BID (aver), clotrimazole QID. Avoid
mixing QT drugs if on a macrolide, quinolone, SSRI’s,
Coartem, Quinine…Follow Bart titers, PCR, FISH, VEGF w tx

◼ Add for Babesia: Clinda + macrolide (or quinine), +/-

Mepron (1-2 tsp BID) or malarone (2 BID) + artemisinin (?
Liposomal), cryptolepis (1 tsp BID to TID), CSA…Consider 3
day rotation of Coartem 4 BID + Daraprim 25, 2 QD,
sulfadiazine 1 g QID, followed by 11 days Primaquine 26.3
mg 2 QD X 4 cycles. Follow symptoms, titers, PCR, FISH…

What About Other Persister Drugs?

◼ IV Daptomycin: dose by body weight: based on research

by Dr Zhang at JHU. Tried his protocol at the HVHAC, using
doxycycline, Rocephin and IV Dapto in 3 patients:
Herxed+++ without significant improvement post stopping
meds

◼ Disulfuram (Antabuse) 250 mg, up to 2 day: based on

Kim Lewis’s work at Northeastern. We are presently
evaluating the effects compared to dapsone (sulfa drug
with less SE’s)

◼ Continue persister drugs/biofilm agents for adequate time

◼ Saki Miyaue et al. Bacterial Memory of Persisters: Bacterial Persister Cells Can Retain Their Phenotype
for Days or Weeks After Withdrawal From Colony–Biofilm Culture. Front. Microbiol., 26 June 2018

HVHAC Clinical Trial: Disulfiram vs
Dapsone Combination Therapy

Add Herbal/Integrative Therapies:
Solo, Combination Treatments

◼ Buhner protocol (Samento, Andrographis, J K..)

◼ Zhang protocol (TCM→Coptis, HH, Allicin, Circ P)

◼ Homeopathy: Ledum, syphilitic, malarial nosodes..

◼ Byron White protocol (A-L, A-Bab, A-Bart)

◼ Cowden protocol (Samento, Banderol, Cumunda..)

◼ Beyond Balance (MC Bab 2, Bab 1, BB-1..)

◼ Others: Biocidin, Lauricidin, Liposomal Vitamin C,
Rife, Coil machines, Bionic 880, heat therapy, stem
cells, Acupuncture, oxidative stress tx (ozone)…

◼ Silver Enhances Antibiotic Activity Against Gram-Negative Bacteria. Jose Ruben Morones-Ramirez et al.
Sci Transl Med 5, 190ra81 (2013);



V. Treat Immune Deficiency

◼ IV: Gammaguard, Gammaplex most commonly
used. Dose by body wt/level of immunoglobulins,
and response (follow small fiber nerve biopsies,
neuropsychiatric symptoms if AI encephalopathy w
o without PANS/PANDAS)

◼ Use Benadryl, other H1 and H2 blockers, fluids,
Tylenol to prevent reactions. Glutathione may help

◼ SQ: Cuvitru, Hizentra most commonly used.
◼ Follow immunoglobulin levels and subclasses,

clinical response

VI. Treat An Overstimulated Immune
System

◼ Remove and treat offending agent(s) whether infectious
(borrelia, bartonella, mycoplasma..) +/-or toxins (mold,
metals) driving AI phenomenon. Support detox pathways!

◼ Treat leaky gut, food allergies, MCAS, microbiome
imbalance, Vit D deficiency: major cause of inflammation

◼ Balance hormones (adrenal, thyroid, sex hormones, post
pituitary: VIP, MSH, ADH)

◼ Address ↑ cytokines: LDN 4.5 HS (microglial activation),
Nrf2 activators (curcuplex, Oncoplex, resveratrin, green tea
extract), Medit diet/gluten + allergen free/sugar-yeast free
DMARDS (Plaquenil + ? Mino), IVIG, SQIG, Smilax (BLT)

VII. Disrupted Sleep Patterns

◼ Differential diagnosis: Lyme, other co-inf’s (Babesia

w/sweats), LA stimulants (medication like Vyvanse,
Adderall, caffeine, chocolate), BPH, menopause, adrenal +
thyroid hormone dys(f), anxiety/depression, OSA,
narcolepsy, RLS, SWS, EMF’s, environmental noise levels

◼ Sleep study (in home: Accusom/Novasom) if resistant sx

◼ Treat underlying etiologies (as above) & treat symptoms:

◼ Get into stage III/IV non-REM sleep: avoid benzo’s,
Ambien, Lunesta when possible. Use: Tradazone (50-200
mg HS), Gabitril (4-20 mg), Remeron (7.5-15 mg),
pregabalin (Lyrica, 50-200 HS), occ gabapentin (300 mg+),
doxepin 10 HS, Flexeril 5 HS (1/3 Amrix cap), Atarax 10-25