Lyme Disease, Potential Plague of the 21st Century

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From the Townsend Letter for Doctors & Patients

January 2005

 

Lyme Disease, Potential Plague of the 21st Century

by Professor Robert W. Bradford and Henry W. Allen

 

 

Detection Problems Resolved by Imaging with the Bradford Variable

Projection High Resolution Microscope

© 2004 Bradford Research Institute

 

Introduction

In the mid-14th century, Europe was swept by a horrific catastrophe,

known variously as the Bubonic Plague, the Black Death or simply the

Pestilence. It is estimated to have killed in excess of 20 million

people, a third of the population of Europe at that time. It is

believed that half of the inhabitants of Paris died as a result of the

plague. Today we have learned to control the microorganism that caused

the great plagues of Europe and elsewhere but now we are beset by

another " plague " that is not as well known as that of 14th century

Europe. The disease was first recognized in the United States in the

small New England town of Lyme, Connecticut, and has since taken that

name. Lyme disease was first studied in 1975 by Dr. Allen Steere,

following a mysterious outbreak in that town of juvenile rheumatoid

arthritis. The relationship between rheumatoid arthritis and a disease

of another name may not at first be apparent but, as discussed more

fully below, Lyme disease has the ability to mimic many other

diseases, making diagnosis extremely difficult.

 

In 1982 the agent responsible for Lyme disease was discovered by Dr.

Willy Burgdorfer, isolating spirochetes belonging to the genus

Borrelia from the mid-guts of ticks infecting deer, other wild animals

and dogs. Spirochetes are spiral-shaped bacteria of very early origin

in the evolutionary scheme. The causative organism was named Borrelia

burgdorferi (Bb), after its discoverer. Since then, the number of

reports of Lyme disease have increased so dramatically that today,

Lyme disease is the most prevalent tick-borne illness in the United

States.

 

The Centers for Disease Control (CDC) in Atlanta, Georgia, reports

that " there is considerable under-reporting " of Lyme disease,

maintaining that the actual infection rate may be 1.8 million, 10

times higher than the 180,000 cases currently reported. Dan

Kinderleher, M.D., an expert on Lyme disease, stated that the number

of cases may be 100 times higher (18 million in the United States

alone) than reported by the CDC. It is estimated that Lyme disease may

be a contributing factor in more than 50% of chronically ill people.1

 

According to an informal study conducted by the American Lyme Disease

Alliance (ALDA), most patients diagnosed with Chronic Fatigue Syndrome

(CFS) are actually suffering from Lyme disease. In a study of 31

patients diagnosed with CFS, 28 patients, or 90.3%, were found to be

ill as a result of Lyme disease.1

 

History of Lyme and Related Spirochetal Diseases

The discovery by Burgdorfer that Lyme disease was caused by a

spirochete placed it in a category of other diseases known to be

caused by spirochetes. An example of such a disease is syphilis, the

scourge of Europe for hundreds of years. Arsenic and some of its

compounds had been known for quite some time as a highly successful

and popular means of fatally poisoning someone. Following the

discovery of the Germ Theory of Disease by Louis Pasteur (1822-1895),

it was theorized that if arsenic was toxic enough to kill, it may also

be effective in killing the organisms that cause disease. In the early

1900s, the German chemist-physician Paul Ehrlich (1854-1915) developed

a chemical treatment for syphilis. By using a " shotgun " approach of

trying hundreds of compounds in an effort to find one that worked,

Ehrlich discovered what became known as Salvarsan or " 606 " after 606

compounds had been tested. Salvarsan was an organic compound of

arsenic and may be highly toxic if not properly used. For his

monumental discovery, Ehrlich was awarded the Nobel Prize in 1908.

Salvarsan may be considered the first man-made antibiotic.2

 

Arsenic belongs to that column in the periodic table of chemical

elements known as the " Group V elements, " also including phosphorus,

antimony and bismuth. See Chart 1. (43KB .pdf)

 

Following the success of Salvarsan as a treatment for syphilis, other

compounds of antimony and bismuth were also prepared and tried against

spirochetes. Examples of these compounds include bismuth subcitrate,

bismuth subsalicylate (Pepto-Bismol), bismuth subgallate and many

others. An example of an antimony-containing antibiotic is Pentostam

(an antimonial, antimony sodium gluconate).3,4

 

A biological molecule known as ATP (adenosine triphosphate) supplies

energy to biological systems and does so through the high energy bonds

found in a chain of three terminal phosphate groups. One of the

mechanisms by which arsenic exerts its toxic effect is the

substitution of phosphorus by arsenic in ATP, since both arsenic and

phosphorus lie in the same column of the periodic table of chemical

elements and have similar chemistry. See Chart 2. (76KB .pdf)

 

When this substitution occurs, the molecule experiences immediate

hydrolysis, breaks down and is no longer functional as a source of

energy for the cell. Phosphorus, arsenic and antimony are also found

in this column of the periodic table (Group V).5,6 (106KB .pdf)

 

What may be the first case of Lyme disease was noted about 1974 in a

14-year old boy, taken to the hospital with extreme pains in the

muscles of his legs and unable to walk. This case, coupled with other

pertinent facts related to the boy and a highly classified US

Government laboratory conducting research on contagious animal

diseases in this same area is suggestive of a link between these two

events. The Government laboratory alluded to is found on Plum Island,

just north of Long Island, NY, and south of Lyme, Connecticut. Because

of its secret nature, access to the island was only by ferryboat and

restricted to the Government workers employed there. The 14-year old

boy lived near the ferryboat dock. Although not providing proof, these

considerations are highly indicative of a possible link between this

research laboratory and the subsequent outbreak in 1975 of an unknown

disease involving juveniles in Lyme, CT.29

History of Lyme Disease

1900 Effective antisyphilitic, Salvarsan, (syphilis, a spirochete

disease) discovered by Paul Ehrlich, MD

1908 Ehrlich awarded Nobel Prize for the arsenic-containing compound

to treat syphilis

1952

to date Highly classified US Government animal disease research

laboratory, Plum Island, in close proximity to Lyme, CT

1974 First Lyme symptoms, 14-year old boy, Lyme, CT

1975 Lyme disease first recognized by Allen Steere, MD, in Lyme, CT

1982 The causative Lyme spirochete was discovered by Dr. Willy Burgdorfer

1983 Borrelia burgdorferi was named after Dr. Willy Burgdorfer

2003 The Bradford Research Institute's High Resolution Microscope

imaging of Lyme spirochete and cyst forms

2004 The Bradford Research Institute (BRI) developed BismacineTM , an

injectable form of bismuth, shown effective against the spirochete

and cyst forms

 

© 2004 BRI

 

Etiology and Difficulty of Treatment

The first step in being able to treat any disease is to learn the

cause (etiology) of that disease. Once the cause of Lyme disease was

known, it would seem that a treatment modality would soon follow and

the problem would be solved. Unfortunately, as history has shown, this

was not to be the case. As more was learned about the causative agent,

namely, the spirochete Borrelia burgdorferi, it became obvious that

this organism was unlike any that had been previously studied. It is

one of the largest of spirochetes (0.25 x 25 m). Spirochetes in

general are difficult to treat for several reasons; they have the

ability to burrow into or between cells and hide, gaining protection

from the immune system. Both Bb and Treponema pallidum, the causative

agent for syphilis, have highly unusual outer membranes and the

molecular architecture of these membranes is responsible for their

ability to cause persistent infection.

 

Bb also has a three-layer cell wall, helping to determine the spiral

shape of the spirochete. This distinctive cell wall resembles those of

Gram-negative bacteria, although Bb does not stain Gram-negative but

is stained by silver stains (containing silver nitrate). This

characteristic may be related to the purported treatment of Lyme

disease by colloidal silver.

 

Another unusual structural feature is a single flagella, attached to

each end of the spirochete, running the length of the organism and

surrounded by it. This feature is significant in relation to immune

protection since most bacterial flagella are highly antigenic. Still

another difference in Bb structural architecture is a clear gel-like

coating surrounding the bacteria, giving it protection from the immune

system.28 See Photo 1. Borrelia burgdorferi Spirochete (17KB .pdf ©

BRI 2004)

 

The DNA of Bb is arranged in a different manner than in other

bacteria, lying along the inside of the inner membrane, resembling a

net just under the skin. The bacteria spelicates specific genes,

inserts them into its own cell wall and then pinches off that part of

the cell membrane, releasing it into the surrounding medium. This

fragment of the spirochete membrane with incorporated DNA is known as

a " bleb. " It is not understood why this strange event occurs or what

advantage it gives the organism but some studies suggest that the

function of blebs is to bind IgM antibodies, thereby protecting the

organism from the immune system. See Photo 9, (152KB .pdf) courtesy of

Microbiol. & Immunol. 26 (3) (1982).

 

The spirochete is typically observed in three different forms

utilizing the Bradford Variable Projection Microscope (BVPM).

 

Bradford Microscopy of a normal spiral form of spirochete, length of

approximately 25 m with evenly spaced blebs along its membrane. (62 KB

..pdf, Darkfield-Phase, 10,000X, ©BRI 2004)

 

Bradford Microscopy of the elongated bleb form described above, by

doubling back on itself, forms a circle of blebs. See Photo 3. (89KB

..pdf, Darkfield-phase, 10,000X, ©BRI 2004)

 

Bradford Microscopy of the elongated form doubled back on itself,

forming close-packed multiple clusters of figure 8s (convolutions),

typically observed inside a B-cell, but may been seen isolated. (28KB

..pdf, Phase, 18,000X, © BRI 2004)

 

Bradford Microscopy of a cyst form developed inside a B-cell, without

the clustered spiral form of the spirochete. (89KB .pdf,

Phase-Darkfield, 10,000X, © BRI 2004) With clustered spiral form of

spirochete (67KB .pdf, Phase-Darkfield,10,000X, © BRI 2004)

 

Bradford Microscopy of a cyst form inside a basophil. (74KB .pdf,

Darkfield-Phase, 12,000X, © BRI 2004)

 

Bradford Microscopy of a cyst form inside an eosinophil. (70KB .pdf,

Darkfield-Phase, 10,000X, © BRI 2004)

 

Scanning electron microscopy of blebs on spirochete membrane. (61KB

..pdf, Scanning Electron; Microscopy)

 

The cell division time of Bb is very long compared to other bacteria.

A typical cell wall reproduction time for Streptococcus or

Staphylococcus is less than 20 minutes, while the total reproduction

time of Bb is from 12-24 hours. Most antibiotics inhibit the formation

of cell walls and are effective only when the bacteria are dividing

with the formation of new cell wall. With the slow replication time of

Bb, an antibiotic would have to be present 24 hours a day for one year

and six months to be present during the cell wall reproduction period.

 

There are basically two mechanisms by which Bb can survive within the

host and remain for long periods of time, unknown by the victim.

Because of these processes, a person infected by Bb can remain

unsymptomatic for long periods of time and then suddenly, without

warning, begin to experience symptoms once again. One of these

mechanisms involves the invasion of tissues by the spirochete. The tip

of the organism has the ability to bind to cells, spin and twirl until

it stimulates the cells own enzymes to digest a part of the membrane,

finally allowing entry. Once inside, the spirochete results in either

the death of the cell or takes up residency within. It may lie dormant

for years, protected from both the immune system and the action of

antibiotics.

 

Experiments have shown that if a culture of Bb is placed under

conditions of nutrient deprivation or starvation, it senses that it

cannot survive in a metabolically active state and generates what are

known as " cysts " or small sacs attached to the organism by slender

threads. Cysts contain immature spirochetes in a metabolically

inactive form. Eventually they break off from the parent body and

either remain lodged in tissues or enter the blood where they are

sensed as foreign antigens by eosinophils (a type of WBC) and

phagocytized. Eosinophils release granules of positively charged basic

protein, attaching to the normally negative surface of cells. They

attempt to destroy the invading foreign bodies (cysts) but have little

success. See Photo 9. (152KB .pdf, Scanning electron microscopy of the

spirochete cyst form)

 

When a spirochete attacks a B-cell, it attaches the tip to the

surface, spins and twirls until it enters, then multiplies inside

until the B-cell bursts. Some of them become coated with fragments of

B-cell membrane and escape detection by the immune system by

masquerading as a B-cell. Most of the antigenic proteins in Bb (that

in other bacteria mark the microorganism for destruction by the immune

system) are found on the inside of the inner membrane where they

cannot contact those WBC that detect invaders.

Experiments have shown that Bb can rather quickly change surface

antigens so that antibodies made against one strain are effective in

killing that strain but a second strain having different surface

antigens will take up residence in a different tissue where it escapes

detection and survives. For these reasons and others it becomes

apparent that this particular spirochete has evolved guises and

biological techniques to guarantee its survival and thwart any

attempts to circumvent it.7

Distinguishing Characteristics of Borrelia burgdorferi

Internal Flagella Cyst Formation

Glycoprotein Coat Destruction of B-Cells

DNA Net Arrangement Camouflage as B-Cells

Bleb Formation Internal Antigenic Proteins

Prolonged Replication Time Surface Antigen Transformation

Cellular Invasion Ability Spiral Shape

 

© 2004 BRI

 

 

Life Cycle of Borrelia burgdorferi and Related Tick

The life cycle of Bb is related to the life cycle of the associated

tick (usually Ixodes scapularis). The tick has four stages in its

two-year life cycle: egg, larva, nymph and adult. The tick usually

acquires the spirochete during its larval stage, when it feeds on

small animals such as rodents or birds. The tick then becomes the host

for the spirochete. The bacteria resides in the digestive tract of the

host for its next nymph and adult stages during which it is passed on

to other animals and/or humans. It has been learned that Bb may also

be carried and transmitted by fleas, mosquitoes and mites.(See

illustration, Life Cycle of a Lyme Disease Tick. 48KB .pdf)

 

Signs and Symptoms of Infection

The first recognizable symptom following a tick bite is the

development of a rash at the site within 7 to 10 days. The rash

expands with an area of central clearing. Other symptoms may include

low-grade fever and/or headache. The rash and early symptoms clear

within 3 to 4 weeks. Multiple secondary rashes may occur following

this time period. Bouts of arthritis, usually involving large joints,

especially the knee, are very common. Arthritis attacks usually

resolve within 3 to 4 years with or without treatment.

Early neurological complications include Bell's palsy, meningitis and

encephalitis. Sub-acute symptoms may include cognitive deficits, mood

and sleep disturbances, persisting for more than 10 years. One of the

most common symptoms is intense fatigue. Additional symptoms may

include memory loss, poor coordination, slurred speech, poor

concentration, unusual depression, burning, stabbing pain, tremors,

anxiety, swollen glands and tinnitus.

 

Some Lyme Disease Signs and Symptoms

Intense Fatigue

Memory Loss

Burning/Stabbing Pain

Tremors

Joint Pain/Swelling/Stiffness

Shortness of Breath

Poor Coordination

Anxiety

Slurred Speech

Swollen Glands

Chills and/or Fever

Nausea/Vomiting

Rash

Muscle Cramps

Sudden Mood Swings

Headaches/Migraines

Poor Concentration

Light Sensitivity

Unusual Depression

Tinnitus

© 2004 BRI

 

Other conditions most commonly seen with Lyme disease include

Alzheimer's disease, amyotrophic lateral sclerosis (ALS), chronic

fatigue syndrome (CFS), fibromyalgia, irritable bowel syndrome, lupus,

rheumatoid arthritis, scleroderma, multiple sclerosis (MS),

Parkinson's disease and various autoimmune disorders.8

 

Most Common Diseases Associated with Lyme

Alzheimer's Disease

Polymyalgia rheumatica

ALS

Reflex sympathetic dystrophy

Bell's Palsy

Rheumatoid Arthritis

Chronic Fatigue Syndrome (CFS)

Scleroderma

Fibromyalgia

Syphilis

Irritable Bowel Syndrom

Multiple Sclerosis

Lupus

Parkinson's Disease

Depression

Autoimmune Disorders

Middle Ear Pressure

Tinnitus

Vertigo

Rheumatoid Arthritis

© 2004 BRI

 

Ticks may carry more than one infectious organism and, for this

reason, a person infected by Bb may also be infected by other

microorganisms, leading to symptoms of those diseases as well.

Examples of organisms commonly occurring with Bb include Babesia

microti,25 Ehrlichia chafeensis,26 E. equi, Mycoplasma pneumoniae,

Chlamydia pneumoniae, Bartonella henselae and Rickettsia rickettsiae.

The presence of multiple symptoms of several different diseases makes

diagnosis and treatment of Lyme disease much more difficult.8

 

Therapy for Lyme Disease

 

Antibiotics

When conditions become adverse for its survival, Bb produces cysts

containing the DNA defining the organism intended for future

generations but surviving in a metabolically inactive state. In this

state there is no cell wall generation and no way an antibiotic can

damage the organism.9

 

It has been found that tetracycline can inhibit cyst formation and

damage the envelope of cysts. It is also believed that bismuth

compounds can enter cysts through the cyst wall. In addition, the

prolonged replication rate, mentioned previously, protects the

organism from cell wall damage by most antibiotics.10

 

Antibiotics Commonly Used in Lyme Treatment

Tetracycline

Salvarsan

Amoxacillin

Cefuroxime

Doxycycline

Clarithromycin

Flagyl

Metronidazole

Cefotaxime

Ceftriaxone

Azithromycin

Penicillin

Imipenem

Benzathine Penicillin

Cefdinir

Rocephin

Tinidazole

Trimethoprim

Cipro(floxacin)

© 2004 BRI

 

Oral Salt Therapy

Certain white blood cells (WBC) display several distinct mechanisms

that may be employed for the purpose of killing invading

microorganisms. One of these deserves particular attention in relation

to killing the causative agent of Lyme disease, namely, the spirochete

Borrelia burgdorferi.

 

Neutrophils (a class of WBC) contain two essentially different types

of storage granules, peroxidase-positive granules and

peroxidase-negative granules. Peroxidase-positive granules contain

myeloperoxidase, an enzyme that uses hypochlorous acid (HOCl) in

conjunction with hydrogen peroxide, providing a source of nascent

(atomic) oxygen for the purpose of killing invading microorganisms.11

 

Peroxidase-negative granules contain a family of large polypeptides

(11 to 19 kDa) (Dalton, the unit of molecular weight) known as the

cathelicidins or, in humans, hCAP-18. A segment of this larger or

precursor protein (also known as a Bacteriacidal

Permeability-Increasing (BPI) protein) is proteolytically removed by

the enzyme elastase found in peroxidase-positive granules. The

better-known substrate of elastase is the elastic protein elastin,

found in skin and other tissues requiring elasticity. By incorporating

elastase inhibitors into skin creams, attempts are made to inhibit the

activity of this enzyme, thereby decreasing the ageing of skin. In

Lyme therapy there is an advantage (described below) to increasing the

activity of this enzyme, thereby stimulating the natural antimicrobial

system. These short peptides, ranging from 12 to 100 amino acids, have

the ability to assemble into larger units that form pores in the

membrane surrounding microorganisms, thereby increasing the

permeability of those membranes. In humans, one of these antimicrobial

peptides has been dubbed LL-37.11 See photo of a neutrophil granule

precursor antimicrobial protein and peptide, 31KB .pdf, courtesy of

Blood 96 (8) 2000.

 

Both of these proteins, the cathelicidin and elastase, meet in the

phagocytic vacuole, the cytoplasmic chamber in which resides the

phagocytized microorganism. Within this chamber, elastase removes a

short peptide capable of forming a molecular pore in the surface

membrane of the microorganism. The pore formed from a group of the

cathelicidins allows the efflux of potassium ions from the organism,

resulting in swelling and eventual lysis.12

 

Research has shown that, of all the proteins in neutrophil granules,

the only protein capable of releasing the cathelicidin active peptide

is elastase.13 It has been demonstrated that the activity of elastase

is enhanced by an increased salt concentration.14 Through oral salt

(12 g per day, see Chart 12), combined with large doses of vitamin C,

the indirect killing ability of elastase is dramatically increased.15

 

Increasing the sodium concentration surrounding the spirochete may

also facilitate cell killing by allowing sodium ions to enter the

spirochete through the pore created by the antimicrobial peptide. An

increased intracellular sodium concentration, combined with a

decreased potassium concentration, leads to spirochete death. The

exact mechanism by which the human cathelicidin LL-37 kills Bb is

unknown. See Chart 8, Oral Salt Therapy for Lyme Disease. (58KB .pdf)

 

Colloidal Silver

It is believed that colloidal silver consisting of small clusters of

silver atoms in the elemental form may be effective in eradicating Bb.

If true, this action may be explained by the known ability of the Bb

spirochete to bind silver, resulting in a brown/black stain.16

 

Bee Venom

Bee venom is a mixture of enzymes that digest most if not all of the

various kinds of biological material. Of particular value in the

treatment of Lyme are the proteolytic enzymes, those that digest

protein. It is believed that the proteolytic enzymes in bee venom are

capable of digesting the protein coating or shell of Bb cysts.17

 

Bee venom also contains a number of potent peptides, responsible for

having a strong inhibitory effect on Bb. When the spirochete is

inhibited it does not multiply and is vulnerable to the host's own

immune system and other medications.

 

Herbal Therapy

 

Cat's Claw

An herbal commonly used in the treatment of Lyme disease is Cat's Claw

(Uncaria tomentosa), native to Peru and used for centuries by that

South American culture. Traditional Cat's Claw contains chemical

antagonists to the immune system known as tetracyclic oxindole

alkaloids (TOASs). Some Cat's Claw products and preparations contain

only the pentacyclic oxindole alkaloids (POAs. superior) for

stimulating the immune system. Some are standardized for the POAs they

contain.18

 

The results of research on Cat's Claw products containing POAs

(Samento, commercially-available), demonstrate powerful immune system

modulating and stimulating properties, along with pronounced

anti-inflammatory, antioxidant, and anti-infectious effects. Cat's

Claw also contains quinovic acid glycosides—compounds with strong

natural antibiotic properties.1

 

Artemesia

A second herb that has been used in Lyme therapy is Artemesia annua,

shown effective against Babesia, one of the more common infections

accompanying Bb in Lyme patients.19

 

Bradford Research Institute/Ingles Hospital Therapy

The Bradford Research Institute (BRI)/Ingles protocols includes two

antibiotics, Ciprofloxacin and Doxycycline. Also included are one or

both of two new bismuth-containing compounds developed by BRI,

injectible Bismacine-C and Bismacine-N. These new therapeutic agents

are currently being evaluated with Lyme patients in the BRI/Ingles

Hospital, Tijuana, B.C., Mexico.

 

Oral supplementation for pain includes the following regimen:

4-5 g buffered Vitamin C, 2x/day

5 Inflazyme Forte™ (4000 IU Pancreatin) tablets 2x/day

3 Oxy-5000 Forte™ 2x/day

50 mg Magnesium Aspartate tablet one 2x/day

Basic Elemental Minerals™ 2x/day

 

Summary of Lyme Disease Therapy

Antibiotics: Includes Tetracycline, Amoxacillin, Cipro, Penicillin and

Doxycycline

Oral Salt Therapy: The enzyme elastase, found in neutrophils, is

stimulated by high salt concentrations to remove a polypeptide LL-37

from the precursor protein CAP-18. A group of the polypeptides

assemble into a pore and becomes imbedded into the outer membrane of

the infectious microorganism, allowing potassium and other ions to

escape, thereby killing the organism.

Coloidal Silver: Small clusters of elemental silver atoms that bind to

the spirochete, phagocytized by PMNs.

Bee Venom: Contains proteolytic enzymes that digest the outer coating

of cysts. Also contains polypeptides that inhibit spirochete growth

and reproduction.

Herbal Therapy: Includes fractionated Cat's Claw, an immune system

stimulant and Artemesia, effective in combattin Babesia, a disease

associated with Lyme.

Dioxychlor, SulfoximeTM, Bismacine-CTM: Bradford Research

Institute/Ingles Hospital Therapy

© 2004 BRI

 

Bradford High Resolution Microscopy

As of this writing, the Bradford Research Institute/Ingles Hospital

has 100% confirmation between Lyme morphology obtained utilizing the

Bradford High Resolution Microscope and the Bowen fluorescent antibody

test, 36 patients with positive correlation and 3 controls with

negative correlation.

 

Rheumatoid Arthritis

In Lyme patients at the Bradford Research Institute/Ingles Hospital,

it has been observed that patients with rheumatoid arthritis have

dramatically improved with the Bismacine treatment along with a

broad-based antimicrobial treatment (Sulfoxime™, Dioxychlor®).

 

In an integrative medical center, a specific treatment protocol is

tailored to the individual needs, based on the concurrent assessment

and diagnosis of functional pathology, organic pathology and the

contributory risk factors of stress and toxicities. Based on the above

assessments, an integrated treatment protocol is developed to meet the

specific patient needs.

 

Detection of Infection

 

Fluorescent Antibody Test

In this test, antibodies to selected antigens on the Lyme causative

organism (Bb) are chemically (covalently) attached to a chromophore,

an organic chemical that fluoresces when irradiated by ultraviolet

light. When the test is made, blood from the patient is mixed with the

fluorescent antibody preparation. If Lyme antigens are present (during

infection with Bb), the antibodies complex with and bind to the

antigens present in the blood. Under ultraviolet irradiation, these

molecules fluoresce, revealing the presence of Lyme antigen. This test

is superior to other tests for the presence of Lyme disease and is

more reliable for indicating an infection with Bb.20

 

PCR (Polymerase Chain Reaction) Test

The PCR test is very sensitive in revealing the presence of a minute

amount of DNA, in this case the genetic material of Bb, indicating an

infection. The test involves the amplification or multiplication of

small amounts of DNA by supplying all of the requirements for the

replication of DNA. The units of DNA (nucleotides) are provided, the

enzyme for performing the replication is provided as well as any other

required substances. If DNA from Bb is present, it will be amplified

so that it may be detected by conventional means. Known nucleotide

sequences of Bb are compared to those revealed by the sample. If

similar, a positive identification of Bb is made.21

 

ELISA (Enzyme-Linked Immuno-Sorbant Assay)

The mechanism of the ELISA test is in some ways similar to the

fluorescent antibody test described above. In the ELISA test, the

antibody made by the infected person against Bb antigens as a result

of infection is covalently bound to (labeled with) an enzyme,

typically horseradish peroxidase. The commercially prepared and

purified antigen (from Bb) as a solution is allowed to bind to the

surface of small wells formed in a plate of polystyrene (commercially

available). The wells are then contacted over a specified time and at

a specified temperature with the enzyme-labeled antibodies (made by

the patient against Bb antigens during the course of the infection and

present in serum). The plate is then gently washed to remove any

unbound proteins. The substrate for the enzyme is provided and the

plate is allowed to develop for a specified time and at a specified

temperature. If antibodies against Bb antigens are present, the

covalently attached enzyme will act on the substrate provided and

result in a color change. Following incubation, the color changes are

read and indicate the presence of antibody, and therefore Bb antigen.

This is a poor assay with marginal sensitivity for Lyme. 22

 

Western Blot Test

The Western Blot test involves two electrophoretic steps in two

different directions, followed by the application of antibody for

specificity. In a typical procedure, serum from a Lyme patient is used

as the sample protein solution in slab-gel electrophoresis on

polyacrylamide gel (PAGE). The gel slabs containing the separated

proteins are then employed in transverse electrophoresis using thick,

carbon block (graphite) or platinum foil electrodes. Sandwiched

between the gel slab and the electrodes are several layers of blotting

paper soaked in electrically-conducting buffer (salts). The proteins

are absorbed (blotted) onto a membrane of nitrocellulose for

subsequent binding by commercially-available Bb antibody. Following

the binding of specific antibody, the nitrocellulose paper is gently

washed free of extraneous protein, retaining only the insoluble

antigen-antibody complexes. These complexes are then stained by any of

a variety of protein dyes and dried. The appearance of protein bands

indicates the presence of Bb antigens in the serum. The Western Blot

test has a high percentage of false negatives and should not be used

to assess Lyme disease.23

 

The CDC Guidelines state that the ELISA test and the Western Blot test

are plagued with false negatives and are not to be used to exclude

diagnosis of Lyme disease.27

 

Detection of Borrelia burgdorferi (Bb)

Fluorescent Antibody Test: Antibodies to Bb are covalently coupled to

a fluorescent organic chemical and added to the patient's blood on a

microscope slide. Antibodies bind to antigens found on Bb (spirochete

or cyst form) and fluoresce under ultraviolet light, revealing the

presence of Bb. Most accurate.

PCR: DNA from Bb is allowed to replicate, thereby increasing the

amount present to enable a sequence determination to be made. The

sequences are compared to the known sequences of Bb. Test unreliable.

ELISAL: Antibodies to Bb are covalently coupled to a specific enzyme

and allowed to bind to Borrelia antigens in the presence of the enzyme

substrate. Enzyme activity results in a color change, revealing the

presence of Bb antigens.

Western Blot: The slab-gel electrophoresis of Lyme patient serum

separates Bb protein antigens. A second transverse electrophoresis

carries the antigens into a nitrocellulose membrane where they are

revealed by the application of specific antibody and staining. Gross

false-negatives.

Bradford High Resolution Microscopy: Both the cyst and spirochete

forms in the three different morphologies are easily identified with

resolutions less than 0.1 micron with concurrent magnification of

10,000x utilizing dark-field and phase contrast modes.

Comparison of Tests: High Resolution Microscopy is the most reliable

test. PCR, Western Blot and ELISA are the least reliable with up to

80% false-negatives (CDC Guidelines).

© 2004 BRI

 

Comparison of Detection Methods

The Centers for Disease Control (CDC) in Atlanta, Georgia, has issued

guidelines for Lyme patients, advising them of a recommended protocol

in attempting to establish whether Lyme disease is present or not.

Doctors have been instructed by these guidelines to obtain an ELISA

test first, which, under the best circumstances, identifies only

40-50% of those who actually have Lyme disease. An ELISA should NOT be

used as a screening test due to the unreliable results. The guidelines

then state that, if the ELISA test is positive, doctors are to perform

the Western Blot test. This procedure allows many cases of Lyme

disease to be missed, therefore patients are not being identified or

properly treated. The CDC guidelines also state which specific bands

on a nitrocellulose strip are to be used in considering a test

positive. When the list of bands was developed, certain bands specific

for Lyme disease were not included. When these bands are positive,

they confirm exposure to the causative organism, but it is mistakenly

reported to the doctor and patient as a " negative test. " Many

borderline tests are reported to patients as being negative and many

positive tests are reported to be " false-positive " because doctors are

not familiar with reading test results, nor with the multiple symptoms

that can occur in a person with Lyme disease.24,27 Charts 11, 12 and

12-A are typical Integrative Treatment Protocols for Lyme patients.

 

Bradford Research Institute/Ingles Hospital Protocol for Lyme Disease

 

Chart 11: Daily Intravenous Infusions

Infusion I (Nutrient, Antioxidant, Antimicrobial, 3-hour drip)

The following in 250 cc Saline:

10 cc DMSO

25 g Vitamin C

10 cc NAC

10 cc Taurine Plus™

5 cc Biorizin™

2.5 cc Multivitamin Combination

1 g EDTA

 

Infusion II in 100 cc saline, 1x/day, 10 cc Dioxychlor, over 30 minutes

Infusion III 2 cc each Bismacine-C™, Bismacine-N™, 2x/day, 1 hour

Infusion IV Sulfoxime™ (Antimicrobial) 1-3x/week, 200 cc, 20 min. drip

Infusion V Vitamin C 75 g in 250 cc saline, 2-hour drip, 1x/day

© 2004 BRI

 

Chart 12: Daily Oral Program

I. Vitamin C, 5 g 2x/day (controlled release)

II. Inflazyme™, 5 tablets, 3x/day, 30 minutes before meals

III. Oxy-5000™, 3 tablets, 3x/day

IV. Magnesium Aspartate, 50 mg, 2x/day

V. Calcium (Osteo Synergy™), 50 mg, 2x/day

VI. Potassium, 50 mg, 2x/day

VII. Glutathione, 20 mg, 2-3x/day

VIII. Beta Carotene, 25,000 IU, 2x/day; Vitamin E, 400 IU, 3x/day;

Vitamin B12 Compl., Caps., 1-3x/day; Selenium, 200 mcg, 1-3x/day;

Trace Minerals, 1-3x/day

IX. Bowel Protocol (Overview)

1. Ultra-Micro-Plex™, 4 tbs in 4 oz. water + pinch of salt, 3x/day

2. Rectal Implant, 1 tsp Ultra-Micro-Plex in 4 oz. salt water, 1-2

x/day morning and night

3. Coffee Enemas, 1x in morning

4. Chamomile Enemas, 1x in afternoon

5. HCI Protocol as Required

© 2004 BRI

 

Chart 12A

X. Liver Protector, Hepatrope, 1-3x/day

XI. Glandular Support, Thymus 1-3x/day, Adrenal 1-3x/day, Thyroid,1-3x/day

XII. Homeopathic Remedies as Indicated

XIII. NeuroRecovery™, caps., 1-3 x/day

XIV. Oral Salt Treatment (Optional) 12 grams of Salt, spaced

throughout the day

XV. Artemesia

XVI. Samento (Cat's Claw)

XVII. Homeopathic Kidney Drainage

XVIII. Homeopathic Lymphatic Drainage

XIX. Colloidal Silver

© 2004 BRI

 

The Bowen Research & Training Institute, Palm Harbor, Florida, is

FDA-licensed to perform tests in which spirochetes in various forms

can be detected and photographed from tissue and blood samples. They

are also able to identify several strains of Babesia25 and

Ehrlichiosis.26 This laboratory uses the fluorescent specific antibody

test for detecting Bb.20

 

Charts C, D, E and F summarize the basic concepts that have been

presented, including the best methods for the diagnosis and detection

of Lyme disease.

 

Chart C: Long-Standing Controversy Surrounds Lyme Disease

· There is no approved test for Lyme disease, specifically ELISA,

Western Blot and PCR.

· Fate of spirochetes after entering the human system is not totally

known with certainty.

· May enter B-cells, other WBC or a variety of tissues and organs.

· Professionals admit they do not know where the spirochete goes,

where it hides or how it may be detected.

· NOTE: The Bradford High Resolution Microscope blood imaging has

revealed the location of the spirochete and cyst form in the B-cells,

eosinophils and basophils.

· Clinical evidence has revealed the associated Lyme spirochete with

elevated PSA, rheumatoid arthritis, CFS, MS, fibromyalgia and diabetes.

© 2004 BRI

 

Chart D: Difficulties in Diagnosis and Detection

· The Centers for Disease Control (CDC) indicates that the number of

Lyme cases may be in excess of 1.8 million.

· Other experts indicate that the figure may be in excess of 18

million in the US alone.

· Lyme disease is difficult to diagnose because it mimics many other

diseases and symptoms.

· Poor detection, up to 80% false negatives using:

· ELISA (Immunological, patient's antibodies, color indicator)

· Western Blot (Electrophoresis of patient's antigens, application of

specific antibody)

· PCR (Amplification of spirochete DNA, sequence comparison)

· As a result, most Lyme patients today go untreated.

© 2004 BRI

 

Chart E: Lyme Disease Out of Control

· An estimated 18 million cases in the US alone, many more worldwide.

· With poor diagnosis and treatment, there is little hope for a

successful resolution.

· Available treatment modalities are only partially successful; the

causative organism is masked in lymphocytes, eosinophils, basophils

and tissues.

· One year ago, in the Bradford Research Institute/Ingles Hospital,

Tijuana, Mexico, 1 in 20 patients had Lyme disease. Today, the

incidence is in excess of 14 in 20.

 

Chart F: Solution to Detection Problem

· The Bradford High Resolution Blood Morphology imaging of both Lyme

spirochete and cyst forms have proven to be highly accurate.

· The various cyst forms are found in B-cells, eosinophils, basophils,

with and without the spirochete.

· The detection of Lyme disease by the Bradford High Resolution

Microscope is highly correlated with the Fluorescent Antibody Test

(FDA-licensed Bowen Laboratories, Florida)

 

Discussion

The causative organism of Lyme disease has developed the ability to

not only disguise itself but to circumvent the immune system in many

ways unparalleled by any other bacteria. Lyme disease has a reputation

of being extremely difficult to detect and diagnose with certainty,

leading many to believe they do not have the disease when, in fact,

they do. The Bradford Research Institute has made significant progress

in both the detection and treatment of Lyme disease, however, there is

at the present time no cure or " magic bullet " for Lyme disease,

implying that much additional research is greatly needed to suppress

this new alarming bacterial outbreak. The Lyme epidemic has presented

us with both a challenge as well as an opportunity to resolve not only

Lyme, but a number of associated immunological and infectious

conditions, stresses and toxicities.

 

Note: The Bradford Research Institute is seeking additional

researchers to participate in The International Metabolic Research and

Development Project (FDA-registered 1979), utilizing the Bradford

Variable Projection Microscope. The Bradford Variable Projection

Microscope blood imaging for functional assessments looks at 72 blood

morphologies correlating with 111 risk factors. To qualify, the

researcher must have a " scope of practice to diagnose and treat " in

order to comply with the established criteria. For more information we

may be contacted at: Phone: (619) 429–8200, (800) 227–4473. Fax: (619)

429–8004, email: drbradford. Websites:

www.bradfordresearchinst.org and www.americanbiologics.com.

 

The authors wish to acknowledge Ann Marie Dixon, MBA, ND, Prof. of

Medicine, Capital University of Integrative Medicine, Washington, DC,

whose invaluable contribution to this manuscript is greatly appreciated.

© 2004 Bradford Research Institute. May be reproduced with written

permission and credit.

 

Correspondence:

Robert W. Bradford

Bradford Research Institute

1180 Walnut Avenue

Chula Vista, California 91911 USA

(619) 429–8200

drbradford

http://www.americanbiologics.com

 

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Please note: All references beginning with http://www. are internet

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