Polymicrobial Infections

Ó Katherine Poehlmann, Ph.D.

 

[This article summarizes Dr. Poehlmann’s presentation at the annual CCMRF Conference

held in Windsor, Ontario, August 26-28, 2005]

 

Introduction

Bacteria span a huge range of sizes and forms. The smallest bacterial forms are almost viral-sized, and are often characterized as artifacts in microscope views. Microscopes need supplemental ultraviolet light to examine the smallest bacterial forms, since the human eye cannot see ultraviolet light.

Complete life cycle of some bacteria can take many forms such as colonies, cell wall, L-forms, cell wall deficient (CWD) forms, intracellular colonies, plasmids, macrophages, emergent “hatchlings”, and dormant stages (seed, bleb, cyst, spore, etc.). Many bacteria (some unsuspected) have the potential to develop any of these forms. At any given stage, their genes may be missing or turned off, waiting for internal or external activation by plasmids. Thus the possibilities are endless for identifying, or worse, for missing diagnosing the presence of bacteria. Physicians should remind themselves that absence of evidence is not evidence of absence.

One example of changing forms is Malaria plasmodium. Vectors and hosts range from insects to animals. Transmission is a microbe’s way of re-colonizing in a new host. Transmission can be via food, air (e.g., sneezing), water, bites, or sexual contact. The forms then replicate and transmit their genetic recipes (DNA/RNA/etc.)

Malaria plasmodium has been well studied as a pathogen that colonizes the liver and other organs. Its actions are very complex, but the same “tricks” are used by simple viruses.

 

How Chemical Recipes are Transmitted

Viruses, macrophages, and plasmids invade both host cells and large bacterial forms, changing their DNA and/or RNA. The host cells invaded are important immune system components: B-cells, T-cells, and red blood cells. T-cells (white blood cells) are monocytes, which are mononuclear phagocytes.

This invasion can either be helpful or harmful to the host. E. g., Mycoplasma kills HIV-invaded immune cells, but there is the risk of trading one pathogen for another.

Plasmids convey antibiotic recipes to bacteria so they can learn to resist future assaults. Plasmids commonly cross species in nature.  Transmission happens in shared locations such as the gut, ear, urinary tract, and in research labs. Crossing in the lab increases the odds of combination, and in turn, mutual potentiation.

 
The Role of Enzymes
Enzymes of pathogens (viruses, bacteria, and cell wall-deficient forms) cause rashes and lesions (sores), help bacteria spread, and viruses to penetrate. Because rashes have many indeterminate or unknown causes, doctors tend to consider them to be “self-limiting.” That is, the doctors provide minimum treatment and know that the rashes will usually go away in a short time. They don’t bother to look past the noticeable symptoms to diagnose what may be an infectious cause(s).
Multiple infections in turn multiply enzyme action. Viruses boost bacterial activity, as exemplified by sore throat, arthritis flare, or other symptoms. Destructive enzymes such as proteinase, hyaluronidase, collagenase lyse (i.e., disintegrate) 3-D tissues. One example of combined enzyme action is chicken pox (Varicella/Herpes zoster) plus scarlet fever can lead to an infestation of “flesh-eating bacteria” (Group A Streptococcus pyrogenes).

Dietary enzymes such as papain and bromelain are beneficial countermeasures. A traditional folk remedy for gut worms in developing countries is to eat papayas, which are rich in papain. These natural enzymes promote sports injury healing and can mitigate the effects of bee/spider venom by disabling the foreign proteins.

Vitamin C disables hyaluronidase (generated by the invading bacteria) and by doing so, indirectly stabilizes collagen, the major building block of cartilage in a matrix form. Hyaluronidase also attacks hyaluronic acid (HA, produced naturally by the body) by chopping it up. HA is made by a mass of protective “spinner” cells on the surface of the collagen matrix. If those are gone, through erosion by improper joint use or nonstop inflammation, there is nothing to chop up. Long chains are excreted and new molecules are regenerated every few days. If too many enzymes are active, too many smaller fragments are produced that can dynamically crosslink and clog the lymph system.

SYNVISC is the synthetic crosslinked form of HA engineered to have the correct viscosity for the lymph system. Treatments only last about 3-6 months, and cost $300 for a series of shots.

To do a creditable job of fighting hyaluronidase, Vitamin C must be taken daily in much larger doses than found in standard daily multivitamins, which is 100 milligrams or less, the amount needed to stave off scurvy. One-tenth gram is not nearly enough to combat destructive enzymes. The author takes 4-5 grams of Vitamin C daily. Her husband Karl’s intake is 7-8 grams.

 

Diet May Help Control Microbes

It is well known that internally, sugar(s) promote bacterial proliferation, especially yeast overgrowth. Here are the steps from overload to inflammation:

·         Candida filaments puncture the gut;

·         unfiltered food seeps through these openings and enters the blood;

·         the immune system reacts, generating food antibodies;

·         inflammation is amplified at already inflamed sites.

 

When the inflammation manifests in the joints, arthritis may be diagnosed. When the site is the stomach, a physician might label the conditions Irritable Bowel Syndrome (IBS) or a severe allergic reaction. Candida infection is often unappreciated, and its symptoms mimic other ailments. Normal gut function produces enough “good” bacteria to aid in proper digestion and to control Candida. Imbalance in good/bad bacteria leads to Candida overgrowth.

Fortunately, there are ways to suppress yeast (Candida) and restore digestive bacteria balance:

·         probiotics (acidophilus, yogurt, buttermilk, etc.);

·         cut out sugar to starve the parasites (the Atkins ketosis theory applies);

·         avoid excess estrogen (including soy products).

 

Ultimately, antibiotics are needed to control bacteria but antibiotics are not effective against dormant forms. Long-term, pulsed, low-level tetracycline antibiotics are especially effective for Rheumatoid Arthritis infections, when they attack bacteria at vulnerable stage(s) of their life cycle such as emerging “hatchlings”. The Candida suppression methods listed above are vitally important if antibiotics of any kind are used.

 

Antibiotic (AB) Protocols

I believe the medical establishment is anti-antibiotic for two main reasons: (1) physicians are adverse to prescribing long-term AB treatments and multiple ABs because they have to spend time monitoring and testing progress, and (2) doctors prefer pills, not shots, patches, or intravenous methods because writing a prescription takes less time. The convenience of gut administration leads to AB resistance.

Because antibiotics are prescribed excessively and impulsively, without determining the actual cause of the condition, and Candida countermeasures are not suggested to patients, bacteria have evolved AB-resistant strains to ensure their survival. Also, failure to advise on the importance of gut bacteria balance can lead to serious conditions such as Dysbiosis.

Improper use of certain antibiotics such as Cipro (Ciprofloxacin Hydrochloride) can be ineffective and even harmful. Doctors know that Cipro hastens the onset of Osteoarthritis, but nothing appears on the prescription label to warn consumers and patients are rarely told about this side effect. Antibiotics are routinely prescribed for children’s ear infections, although these are often viral or fungal. Antibiotics are not suitable treatment except for bacterial infections.

Intravenous AB protocols may, in some cases, be more effective, but this method is overpriced. Separate ABs may lead to antibiotic resistance because a plasmid can convey only one resistance recipe. Scientists now endorse multi-AB protocols because they are shown to work in “heroic” situations and the probability of drug resistance is much, much lower. After many years and dozens of credible studies, controlled AB protocols are slowly being acknowledged by medical schools.

 

The Marshall Protocol

This is an example of a multi-AB protocol that uses tetracycline effectively against Sarcoidosis bacteria. The Marshall Protocol is similar to the treatment for Rheumatoid Arthritis (RA) and Fibromyalgia described in Appendix II of my book, Rheumatoid Arthritis: The Infection Connection.

According to Dr. Trevor Marshall, who developed the Marshall Protocol, Benicar (a drug for lowering blood pressure) blocks the Herxheimer reaction and mitigates inflammation. He asserts that some infections are characterized by unbalanced vitamin D. His thesis is that:

 

·         macrophage/monocyte intracellular bacteria make active vitamin D;

·         high active D enhances inflammation (this explains sun sensitivity);

·         D-ratio = active / inactive vitamin D concentration ratio

 

The D-ratio is highly testable, but few labs get it right. The blood sample must be immediately frozen and kept cold until the actual test is performed. The test measures the size of bacterial colony(ies) and treatment progress. Viral and bacterial infections have different D-ratios. Specific infections with tipped D-ratios are RA, Lyme Disease, Fibromyalgia, Sarcoidosis, and many more.

Mild inflammation is beneficial, and often heals minor infections. Chronic infections lead to persistent inflammation – this is destructive.

 

Harmful Synergism

Doctors usually assume that ubiquitous microbes are harmless and not causal factors (e.g., Mycoplasma). Too often, test results that show evidence of Mycoplasma or the Epstein Barr virus are dismissed because these microbes are present in about 70% of the population.

Some combinations amplify virulence, but are undiagnosed because our knowledge of cofactor mechanisms is fragmentary. E.g., Crohn’s Disease/Irritable Bowel Syndrome can be complicated by:

·         Candida, other yeasts/fungal forms

·         Mycobacteria paratuberculosis

·         Klebsiella pneumonia

·         Escheria coli (especially the hemolytic strain, is prevalent in cattle and destroys blood cells)

·         Coxsackie virus

·         Yersinia enterocolitica

 

Co-infections lead to concurrent epidemics. Two examples are (1) Mycoplasma and Parvovirus B19 (which may have links to Lupus), and (2) Coxsackie and Yersinia (each of these attacks the pancreas, leading to diabetes). Both of these examples suppress thyroid function. Hundreds of strains capable of crosslinking means that accurate tests are impossible because tests must cover all combinations.

The following sections will show how Crohn’s Disease can be seriously complicated by any one of these infections as a cofactor: Mycobacterium paratuberculosis, Yersinia enterocolitica, and/or the Coxsackie Virus.

 

Crohn’s Link to Jonne’s Disease Through M. paratuberculosis

Jonne’s is epidemic in dairy herds at a 10-35% rate. Pasteurization of milk from infected cattle often fails because it is designed for Mycobacterium tuberculosis, not M. paratuberculosis, which is heat resistant and is present at greater than 90% levels in Crohn’s patients but not in others. This explains why not all milk drinkers get Crohn’s disease.

Here is a Catch-22: the pasteurization process should use higher temperature for a longer time, but this curdles milk, making it unmarketable.

Crohn’s symptoms include a respiratory phase followed by persistent gut inflammation. Usually, cross-species virulence decreases. One exception is the genetic predisposition of Crohn’s patients to develop the condition.

 

Crohn’s Link to Yersinia enterocolitica

Yersinia  is a very bad actor. It colonizes monocytes and disables them. Antibodies then trigger autoimmune allergies. Just as Mycoplasma has an affinity for synovial tissues, Yersinia inflames the following:

·         heart (pericardial irritation)

·         spine (arthritis, cartilage destruction)

·         nerves (central nervous system (CNS) excitation complications, autism)

·         lymph nodes (infection)

 

Many conditions like Crohn’s have symptoms that infer Yersinia but it is very hard to test accurately. The test panel for IBS covers Y. enterocolitica, Klebsiella pneumonia, and various endotoxins and exotoxins. Immunosciences Lab performs comprehensive Yersinia panel tests for about $200. This is a full test, not just Yes/No. See website www.RA-Infection-Connection.com for other test labs.

 

Crohn’s Link to Yersinia pseudotuberculosis

Similar to Y. enterocolitica, Y. pseudotuberculosis is a food-borne infection that generates a toxin which attacks nerves’ myelin sheath. It is characterized by a loss of neural transmission capability that can lead to Multiple Sclerosis.

During the Cold War, the Soviets experimented with several myelin-destructive toxins. In one of these experiments, they moved the M1 toxin gene to Y. pestis (a plague organism). Y.pestis overlaps some Y. pseudotuberculosis genes, but 13% of these are inactive (dormant). Other crosslinking could trigger activation.

This finding suggests questions about the characteristics of the many strains of Yersinia, but only a few are identified and sequenced. Which are active? Which are inactive? What happens when two or more strains are present?

 

Crohn’s Link to the Coxsackie Virus (CV)

The Coxsackie Virus is named for the city in New York where it was first discovered. It is an enterovirus similar to echovirus and poliovirus that inflames muscles (especially the heart), brain, and the CNS.

CV is a generalized disease of newborns to 3 years, characterized by high fever, rash, and sore throat. The infection can be pre-natal if the mother is infected.

About 30 strains of CV-A and CV-B lead to multiple infections and cross strain re-infections, including: conjunctivitis, Reye’s syndrome, exanthem (blooming rash), infectious lymphocytosis, myocarditis, pericarditis, pleurodynia, herpangina, and Diabetes mellitus.

 

Coxsackie Virus B (CV-B) and Chronic Fatigue Syndrome (CFS)

In 1980 UK scientists discovered an association of CV-B with CFS/Fibromyalgia. In the UK, Fibromyalgia is called “post viral muscle fatigue syndrome”, which implies multiple viruses. Researchers also found that other viruses emerge/persist when CV-B is active. The evidence is antibodies all appearing at the same time, which is a big strain on the immune system, and worse if monocytes are compromised.

The table below shows the relationship between CV-B and various conditions.

 

CV-B Serotypes             Primary Acute Condition/Disease

1                                    Hepatitis

1,2,4                               Pancreatitis

4                                    Diabetes

4,5                                 Upper respiratory tract infection and Pneumonitis

1,2,5                               Macular rash (neither raised nor indented; blotchy, discolored)

1 to 5                             Pleurodynia, Peri/Myocarditis, Myalgia

1 to 6                             Aseptic (non-bacterial) Meningitis

 

Coxsackie Virus Treatment

            This virus is very difficult to treat if well entrenched. However, quercetin and Vitamin C supplements can help alleviate symptoms.

Herbal remedies with general anti-viral properties are: Bitter Melon, St. John’s Wort, Olive Leaf extract, Licorice root, Ginger, Rosemary, Oregano, Garlic, Green Tea extracts, Shiitake and Porcini (boletus) mushrooms.

Chinese Medicine specialists suggest sophora root (kushen),  astragalus (huangqi), and ginseng (renshen).

In Germany, CV sufferers are given Pleconaril anti-viral for Picorna Viruses and anti-inflammatories. In contrast, in the U.S., the usual advice is merely to “get some rest”.

 

Future Directions

Gene Research. Clearly, with so many new threats in terms of co-infections and drug-resistant bacteria/viruses emerging, there is an important challenge to identify more bad strains and how they become pathogenic. This means a need for:

 

·         better taxonomy, gene mapping, molecule cataloging;

·         more complete gene sequencing and differential analysis;

·         developing control of genes to deactivate pathogenic ones.

 

Recent gene research has discovered siRNA (small interfering RNA) that can block an invader’s replication, metabolism, and toxin generation. Great strides in disease prevention and treatment could be made if genes could be customized to make siRNA on demand to disable intracellular forms of pathogens.

A first step to this goal is to devise better tests to span all strains/phases of pathogenic microbes. Ideally, multiple tests should be developed, perhaps on a chip, at lower cost. We need more enzyme balance tests to prove microbe activity and avoid faulty diagnoses. The tests now are simply “yes/no” and must reveal more detail if disease treatment is to be effective.

 

Pathogen Sources. Another important and necessary step it to find source reservoirs of pathogens and reduce them. This means including cleaning up all aspects of the dairy and livestock industry, e.g., feed lots and animal housing. This would result in better health for our food animals and ultimately for us.

Vector control specialists should seek to breed mosquitoes with new and different internal attachment-point shapes. The redesigned mosquitos’ gut reservoir shapes will not match pathogens’ shape, so attachment will fail and the mosquito will not be a disease carrier.

One way to attack dormant forms of pathogens is by purging/replacing infected bone marrow, the source of immune system’s infection fighters (B-cells). This method is now used against leukemia. Killed cells are repopulated with transplanted healthy cells. It should be possible to replicate B and T immune cells outside the host so infections will not deactivate or compromise them, then infuse the host with repaired immune cells. Use stem cell gene augmentation to fix host gene errors

 

Vaccines. Genetic scientists should seek ways to manufacture empty virus “shells” that can convey vaccine-like immunity. These shells would have an outer coat only (no enzymes) – like a car without an engine – to be a virus lacking the DNA that makes it harmful. The shell could contain added helpful genes, custom-made anti-toxins, or other positive results of gene manipulation.

Presently, vaccines are risky and not dependable. Adverse reactions are often a surprise in clinical trials as the vaccines trigger activation of a dormant form of a pathogen. These unintended consequences make vaccines very expensive because of liability insurance. We need to develop vaccines with alternatives to current high risk of inflammation and latent factors. To his credit, Bill Gates has given hundreds of millions of dollars to vaccine research support.

 

Improved Antibiotics. The goal is not only to block antibiotic resistance but also to enhance apoptosis (programmed death) of invaded cells. Newer antibiotics are based on other principles, including the use of ligand blockers and siRNA molecules. Natural antibiotics are being discovered in seed shell extracts, bitter foods, and mushroom extracts. With seeds, the premise is that there is natural AB protection in the shell to ensure germination.

Research is underway to model molecules based on microbes’ shapes. We are seeing more and different antivirals from outside the USA, and hopefully our medical establishment will stifle its “Not Invented Here” prejudice to make these treatments available.

Better antibiotic application protocols are being developed. Multiple antibiotics are seen to act synergistically, attacking all phases of organism at same time. This method allows better targeting of intracellular forms.

Long-term antibiotic protocols like Dr. Thomas MacPherson Brown’s or Dr. Trevor Marshall’s recommend using anti-inflammatories together with antibiotics for maximum effectiveness.

 

Resources. As we look to the future for answers to polymicrobial infections, we would do well to revisit valuable resources from the past and update them in terms of the knowledge and technology we now have. The medical establishment has over 100 years of veterinary medicine and research findings to re-examine and catalog in shared data banks. Researchers should rediscover the Materia Medica to find forgotten, effective remedies. Amazing findings in veterinary research, past and present, may hold answers to human maladies.

 

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Dr. Poehlmann is the author of Rheumatoid Arthritis: The Infection Connection, available on Amazon.com and at major bookstores, or click here to order now.

 

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