What are Mycoplasma and related infections?

Mycoplasmas are the smallest and simplest subclass of bacteria (Vojdani 1998). While they are not new, the recent discovery of certain altered forms of Mycoplasma reveals some species that have become more invasive and more difficult to find. Nicolson (1998) states that there are over 1000 different strains of Mycoplasma. The earliest reports of Mycoplasma infectious agents in humans appeared in the 1930s, 1940s and finally, in the early 1960s. It was during this initial period that the definite relationship between Mycoplasma pneumoniae and pneumonia was established.

Recent advances have identified significant varieties of these highly invasive bacteria with wide-ranging and complex effects on the systems of the human body including 'chronic pain with associated disabling symptoms and fatigue' (Nicolson 1998).

Mycoplasma has the smallest genome of any bacteria that can replicate independently of host cells (Vojdani 1998). Unlike typical bacteria, it has no cell wall, which allows it to invade virtually all bodily tissues and penetrate deep inside the white blood cells. This has a powerful cytotoxic killing effect on monocyte white blood cells, promoting suppression of the immune system. This effect including immune suppression dramatically inhibits the body’s defence in fighting disease.

'Mycoplasmas are slow-growing micro-organisms that activate the immune system and then can successfully hide from it within the immune cells. These organisms are systemic; they can go to all the tissues and organs of the body, causing complex symptoms. They generate toxic oxygenated products that damage the host cell. Damage to the cell membrane allows the Mycoplasma access to the interior of the cell. Once inside the cell wall, Mycoplasma can alter the cell structure and incorporate itself into cell division using the host cell for multiplication. This allows for prolific systemic infestation' (Nicolson 1998).

Mycoplasma has become an emerging issue in the treatment and management of chronically ill patients. Our attention was drawn to Mycoplasma and other ‘opportunistic infections’ by the fact that patients who suffer chronic debilitating illness and pain usually also suffer multiple over-lapping systemic problems. Many of these chronically ill patients may appear to have no direct connection except that they happen to present with these multi level issues (Nicolson 1998).

Our observation noted this same phenomenon with patients suffering chronic pain and with post surgical spinal operative patients. Patients presenting with complex spinal disorders suffering chronic pain also, often present with numerous multi system systemic involvement and complications.

Prof. Garth Nicolson Ph.D., of the Institute for Molecular Medicine California reports viral and bacterial infections associated with numerous overlapping illnesses and chronic pain syndromes. Nicolson identifies that many current treatment approaches are inappropriate and do not deal with the exact cause of the patient’s illness (Nicolson 1998).

Bacterial and viral infections have been identified as major co-factors with patients, involving multi-organ systemic signs and symptoms and chronic pain syndromes. The 1999 Sydney Conference on Chronic Fatigue Syndrome identified Mycoplasmas and opportunistic infections in the mechanisms of the following :

• cytotoxic effect on white blood cells (WBC): suppressing immune function

• chronic fatigue syndrome (CFS and ME)

• gulf war syndrome

• polyarthralgia (arthritis): damaging connective tissue and synovial lining

• fibromyalgia syndrome (musculoskeletal pain)

• chronic migratory joint related pain

• short-term memory loss

• sleep difficulties

• chronic headaches

• vision problems

• nausea

• intermittent fevers and skin rashes

• breathing disturbances and shortness of breath

• respiratory disorders

• wasting syndrome (a physical syndrome similar to late stage AIDS patients)

• liver infection (mimicking chronic alcoholism and cirrhosis)

• unexplained diarrhea

• pelvic floor inflammatory disorders

• urinary disorders including nongonococcal urethritis

• peritonitis

• chorioamniontitis, transferred via the placenta

• non specific chest and heart problems

• unrelated neurological disorders with disruption nerve impulse transmission

Frustration can push a doctor towards one of several responses, the most damaging being denial of the patient’s complex clinical presentation. Commonly these patients will tell you that they were told that their problem was ‘in their head’ or that they had to learn to ‘live with the condition and cope with the pain’. On the other hand, continued clinical investigation due to dissatisfaction with the easy option compels the clinician towards a diagnostic explanation, identifying the cause hopefully resulting in an improvement in the patient and their condition.  

How can it be detected?

Because Mycoplasma is one of the few major pathogens that are not be easily cultivated, conventional antibody tests cannot identify these organisms, and they can go undetected for years, resulting in complex illnesses. Many conservative treatments may in fact contribute to further compromise of the immune capabilities, which fosters and accelerates this opportunistic disorder.

A new, very sensitive testing method involving DNA based technology has been developed that can detect and identify Mycoplasma in the blood. In fact, 'Polymerase Chain Reaction (PCR) analysis can be performed with virtually all fluids and tissue biopsy samples' (Dussurget 1994).

Blood is collected and packed with predetermined temperature at 4°C. The sample must be processed immediately for Nucleoprotein Gene Tracking (NPGT) after isolation of blood leukocyte nuclei (Nicolson 1996, 1998) or Polymerase Chain Reaction (PCR) after purification of blood leukocyte DNA using a Chelex procedure (Nicolson 2000, Nasralla 1999). These procedures are very sensitive and specific and can detect down to a few copies of intracellular bacteria in a blood sample. Results of Mycoplasma quantification are expressed as the number of copies of Mycoplasma DNA per ml of blood. The PCR test results are expressed as a number, which allows researchers and clinicians to monitor disease progression and evaluate the effect of drug therapy.

Routine PCR testing can prove problematic in detecting chronic intracellular infections due to protein-DNA complexion and the presence of inhibitors in clinical specimens. Nicolson (1998) has developed methods to overcome these complex problems, such as the use of Chelex to remove inhibitors and chemotropic agents to remove proteins from DNA complexes that can block the Polymerase chain reaction.  Nicolson reports that 'unless PCR testing is performed correctly with specificity, many infections and multi-infections affecting numerous tissue sites will be undetected'.

The difficulty with this highly sophisticated form of analysis is both commercial availability and cost. Until recently, complex serum analysis had to be sent to the United States of America, costing hundreds or even thousands of dollars, depending upon the extent of sensitivity and differentiation. Currently, limited laboratory PCR DNA Chelex based analysis is offered in Australia. The current testing methods are considerably lower than those readily available in the USA.

In Australia, typically samples being directed for mycoplasma commercial testing are limited to evaluating only the presence of ‘antibody response’ as an indicator of diagnosis. Nicolson reports that antibody response should be found to be at a higher frequency in diseased patients than in those without disease. However, Nicolson states that this ‘response is usually not found until the disease has progressed’. According to Lo et al (1989, 1991, 1993) M. fermentans 'hides inside cells and does not elicit a strong immune response until near death'. 

Basically this interprets that a significant number of pathologies remain undetected because of ‘apparent PCR methods’ unless the broad based treatment approach offered to the patient has been 'lucky enough' to kill the infectious agent.

Inconjunction to systemic evaluation, Nicolson employs 'biopsy methods of the targeted tissue using PCR and Chelax methods proving to be extremely accurate is the establishment of the exact destructive agents and more accurate treatments in the disease process'. Unfortunately, Australian patients remain disadvantaged because of these investigative techniques are not commercially available.

Our frustration is the fact that we are not able to commercially biopsy chronic spinal patients  evaluating the presence of underlying opportunistic pathogens, however our evidence clearly demonstrates that we are influencing these potentials based upon pre and post MRI evidence.

Mycoplasma and Chronic Fatigue Related Syndromes

During the past two years PCR based DNA technology has been used to determine the prevalence of Mycoplasma fermentans (incognitus) in blood samples of CFS patients (n=250). Vojdani (1998) reports 30% of CFS patients tested positive to M. fermentans and a further 52% of the CFS group tested positive to some form of Mycoplasma infection. In a normal healthy population, only 4-8% of health controls carry the M. fermentans genome. The researchers emphasize that these results should not be construed to mean that Mycoplasma infection causes Chronic Fatigue Syndrome. It may however, be a cofactor in compromising the immune system and allowing other agents to produce symptoms of CFS. As the reader will observe, Mycoplasma through a cofactor relationship is implicated in numerous disease processes and clinical conditions.

Mycoplasma and Gulf War Veterans

In addition, military forces returning from Operation Desert Storm and Desert Shield have reported a variety of complex health problems and issues. A disorder now referred to as Gulf War Syndrome or Gulf War Illness (GWI) has afflicted approximately 150,000 veterans and their families. Prof. Garth Nicolson and other researchers and physicians have noted the similarity between the symptoms of Chronic Fatigue Syndrome, Fibromyalgic Syndrome and those of Gulf War Illness (Nicolson 1998).

Studies using the PCR methodology have found a sizeable number (45%) of Mycoplasma fermentans infections among GWI sufferers. This evidence indicates that M. fermentans may also be an important cofactor in the illness of Persian Gulf War veterans.

Mycoplasma and Rheumatoid Arthritis

Many experts have suggested that Rheumatoid Arthritis (RA) and other forms of chronic arthritic related conditions may be caused by an infectious agent including Mycoplasma. Reports confirm that RA is about 30% genetic. However medical evidence demonstrates that the autoimmune manifestations of RA are virtually identical to those seen in slow growing bacterial infections like chronic Mycobacterium.

Vojdani (1998) has applied the PCR DNA-based technology to determine the prevalence of M. incognitus in blood samples of RA patients (n=250). 'In 40% of patients, Mycoplasma gene sequences were detected'. When specific primers for M. incognitus were used, 24% of Mycoplasma positive RA patients tested positive, indicating that other Mycoplasma species are definitely involved in arthritis (Nicolson 1998).

In the initial stage of RA produced by Mycoplasmas, living bacteria may release toxic radical substances, which may cause tissue damage. The destruction of host cells promotes the growth of Mycoplasma by liberating cellular material that can be used as nutrients by the micro-organisms. Vojdani (1998) reports that Mycoplasma infections in their chronic phase can induce many new genes that lead to the production of ‘superantigen and heat-shock proteins’, accelerating tissue destruction.

The occurrence of Mycoplasma and plasma species in the joint tissues of patients with rheumatoid arthritis and other forms of arthritis can no longer be ignored. M. fermentans was suggested more than 20 years ago as a cause of RA on the basis of its presence in the synovial fluids of a few patients.

Advances with PCR methodology have enabled both researchers and clinicians to study the effects and impact of Mycoplasma in arthritic related conditions. The Mycoplasma fermentans genome has been confirmed in over 40% of synovial biopsy specimens with differing forms of arthritis, and specifically in 21% of joints of patients with rheumatoid arthritis (Nicolson 1998).

In addition to the presence of the mycoplasma group of infection, 'Epstein-Barr (EB) virus (Fox 1992) and Cytomegalovirus (CMV) (Tsai 1995) have been identified in the cells of the synovial lining in RA patients suggested their involvement in RA, possibly as cofactors'.

Degenerative Motor Neuron disorders

Rare and insidious degenerative motor neuron disorders including Multiple Sclerosis (MS), Amyotrophic Lateral Sclerosis (ALS), Lupus, Graves’ Disease and many other complex autoimmune diseases are also being linked with ‘opportunistic’ infections. Autoimmune responses are consistent with certain chronic infections, such as mycoplasmal infections, that actually penetrate into nerve cells, synovial cells and other cell types and stimulate autoimmune responses by their own or host antigens. It is reported that the autoimmune signs and symptoms in these patients could be the result of intracellular pathogens, such as Mycoplasmas, escaping from cellular compartments and incorporating into their own structures pieces of host cell membranes that contain important host antigens that can trigger autoimmune responses. 

Alternatively, mycoplasma surface components, sometimes called ‘superantigens,’ may directly stimulate autoimmune responses (Kaneoka 1997). Perhaps the most important event, the molecular mimicry of host antigens by mycoplasma surface components, may explain, in part, their ability to stimulate autoimmune responses (Baseman 1996).

Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic Lateral Sclerosis (ALS) is an adult-onset, idiopathic, progressive degenerative disease. Although the cause of ALS remains unknown, there have been several hypotheses. Of these, the role of chronic infections has attracted recent attention with the finding of enterovirus (EV) sequences in 15 of 17 spinal cord samples (Nicolson 2000). The possibility that two or more infectious agents could interact to produce ALS remains a distinct possibility. Our recent findings indicate that 28 of 31 patients tested also have mycoplasmal infections.

Patients with ALS show gradual progressive weakness and paralysis of muscles due to destruction of upper motor neurons in the motor cortex and lower motor neurons in the brain stem and spinal cord, ultimately resulting in death, usually by respiratory failure (Williams 1991, Swash 1992, Walling 1999). The overall clinical picture of ALS can vary, depending on the location and progression of pathological changes found in nervous tissue.

In addition to muscle weakness and wasting, the ALS clinical presentation includes (Rothstein 1992, Lo 1993, Brahic 1985, Nicolson 1996 Nicolson 2000, Berger 2000, Woodall 1994, Swanson 1995, Muir 1996, Rawadi 1996) 

• disabling fatigue

• mental impairments, loss of short-term memory, confusion

• headaches

• photophobia, transient visual scotomata

• irritability and depression

• sleep problems

• nausea

• speech and swallowing problems

• dental problems

• intermittent fevers

• history of asthma, bronchitis or pneumonia

• chronic bronchitis

• chronic allergies

• skin rashes

• night sweats

• fasciculation

• cramping

• arthralgia, myalgia, rheumatoid arthritis signs/symptoms

• intermittent diarrhea

• digestive problems, abdominal bloating

• chronic infections

Nicolson reports that many patients with clinical signs and symptoms unrelated to ALS diagnosis are similar to those usually found in FMS and CFS patients (Nicolson 2000). These symptoms are not localized to any one organ with symptoms systemic and infection multi faceted and not consistent with a single, specific disease. The Nicolson study has identified the presence of systemic microbial infections, M. fermentans in a number of ALS patients (Nicolson 2000).

Chronic enterovirus (EV) infections have also been identified in ALS patients (Nicolson 2000). 15 of 17 ALS patients were found to be positive for EV infections (Berger 2000). This virus was found in the motor neurons that degenerate in ALS.

Nicolson and his team have designed specific PCR probes to detect this virus in blood and tissue samples from ALS patients. Studies (10 out of 11) confirm that a significant high percentage of ALS sufferers test positive for EV in their blood. According to Nicolson, the presence of EV in ALS patients has not received attention because of inappropriate testing (Swanson 1995). Nicolson claims EV and related infections require extremely sensitive and specific methods including removing inhibitors of the PCR reaction using the Chelex method to establish diagnosis (Nicolson 2000).

Heavy metal contamination has also been demonstrated in ALS and many patients with neurological or degenerative diseases, some having a history of heavy metal exposure. Some metals, such as mercury, may result in high levels of oxidative stress or reactive oxygen species (Hussain 1997, Tan 1998), which have been implicated in neurological diseases (Spencer 1998, Jenner 1998).

Mercury can also form conjugates with thiol compounds, such as glutathione and cysteine and cause depletion of glutathione, a necessary metabolite to counter or mitigate reactive damage. Eggleston (1984,1987) found that mercury amalgam fillings or nickel dental materials caused suppression of T-lymphocytes and impaired T4/T8 ratios. In one study 12 out of 13 ALS patients tested showed positive lymphocytes to heavy metals in vitro (Stejskal 1994). There are case reports of patients with severe signs and symptoms similar or the same as ALS improving after treatment for mercury poisoning (Iyer 1976). Although these reports are not compelling or conclusive, they do point to one possible complication in motor neuron disorders including ALS.  

Heart complications

Cardiopathies can be caused by chronic Mycoplasma species (Prattichizzo 1997) and Chlamydia species (Fairley 1996) infections, resulting in myocarditis, endocarditis, pericarditis and other types of infections. These cardiac infections are often due to Mycoplasma species, Chlamydia  species and possibly other intracellular bacteria and other infectious agents, and they are emerging agents in coronary diseases.

• All patients with chronic symptoms including neurodegenerative signs should be investigated for mycoplasma complexes and associated cofactors.  

Can Mycoplasma be treated?

In order to eliminate the pathogenic Mycoplasmas and related bacterial and viral infections, the human body needs a functional immune system, which most patients with chronic illnesses do not have. Therefore strategies to enhance the immune system along with prolonged drug therapy may help. Many patients infected with Mycoplasma have realized dramatic improvement with long-term cycles of specific antibiotics. Since the organism resides deep in the cells and has a long life cycle, antibiotic treatment can take several months, or for that matter, years (Nicolson 1998).

For most patients, antibiotic treatments must be continuous for at least 6-months, followed by additional 6-week cycles of antibiotics, if necessary. Some practitioners treat chronic infections by administration of antibiotics every other day, and some recommend daily dosing. Due to poor gastrointestinal absorption in certain patients or the acuteness of signs and symptoms, intravenous therapy has been used for a few weeks, followed by oral antibiotics. Nicolson reports that most patients cannot tolerate intravenous antibiotics for more than a few weeks or complications can then occur, so follow-on therapy with oral antibiotics is necessary.

Can antibiotic therapy be part of a successful regime of management that deals with the underlying intracellular bacterial infections often found in chronic illness patients?  Yes, but antibiotics should not be used solely or exclusively to treat intracellular bacterial infections.  The vast majority of patients do not recover within several weeks or for that matter a 6-month period of antibiotic therapy. Nicolson considers an initial 6-month period is essential to commence the recovery process (Nicolson 1999). Those that recovered earlier were relatively young patients (most <25 years of age) that were healthy before their illness, and this could have played a role in their higher response rates compared to civilians with chronic illnesses which tend to be on the average older and not as healthy.

Antibiotics used to treat Mycoplasma

There are several antibiotics that researchers and specialists recommend to treat Mycoplasma, but treatment commonly begins with Doxycycline (Nicolson 1998). Taking the medication orally works well for most patients, but a few highly sensitive patients may need to have antibiotics given intravenously at first.

It is not yet known whether antibiotics are a cure for Mycoplasma infections. Since M. fermentans has the ability to change its cellular makeup with every cell division, it may be difficult for readily available antibiotics to completely eliminate this organism from the body.

Doxycycline (aka Vibramycin, Monodox, Doxychel, Doxy-D, Doryx). Doxycycline is a broad-spectrum tetracycline with good lipid solubility and ability to penetrate the blood-brain-barrier. This antibiotic acts by inhibiting micro-organism protein synthesis; it is readily absorbed by the (normal) gut, and peak blood concentrations are maintained between 2-18 hours (half-life, 18-22 hrs) after an oral dose of the drug. Food, calcium, magnesium, antacids and some drugs reduce absorption, and alcohol, phenytoin [Dilantin] or barbiturates reduce blood half-life or suppress the immune system.

Minocycline (Minocin) can be substituted, and for some illnesses such as RA it is preferred. For chronic fatigue and fibromyalgic and polyarthritis symptoms (Nicolson 1998), the recommended oral dose is 200-300 mg/day (2-3X 100 mg capsules, 2 in morning) for 6 months. After 6 months, 6 week cycles are suggested. Initially, doxycycline exacerbates signs/ symptoms (Herxheimer reactions or adverse responses, such as transient fever, skin or gut discomfort, etc.) but these are generally gone within 2 weeks or so. Patients usually start feeling better with alleviation of most major signs and symptoms within 12 weeks, but in some patients major symptoms are not alleviated until after 12 weeks.

Adverse Reactions: The recovery is usually slow and gradual after an initial period of Herxheimer and other adverse reactions that make patients temporarily more symptomatic. This Herxheimer period can last for several weeks with the patient feeling worse and obviously doubtful of the treatment process. Practitioner guidance is essential. Doxycycline causes gastrointestinal irritation, anorexia, vomiting, nausea, diarrhea, rashes, mouth dryness, hoarseness and in rare cases hypersensitivity reactions, haemolytic anemia, skin hypersensitivity and reduced white blood cell counts. In general, doxycycline is considered a safe drug, in that there are few adverse reactions reported in the literature.  

Minocycline in Rheumatoid arthritis

In two recently published independent randomised trials, rheumatoid arthritis patients were treated with 100 mg of oral Minocycline twice daily, or a placebo for a period of 26 weeks. In the Minocycline group, more Minocycline-treated patients than placebo showed greater than 75% improvement in swollen joint count, tender joint count and in clinical parameters such as serum C-reactive protein (CRP) level and erythrocyte sedimentation rate (ESR). In these studies (Nicolson), the inter-group differences were statistically significant for these findings and the mean changes over time revealed continual improvement in the Minocycline-treated patients during the entire period of both studies (Nicolson 1998).

This and other presently available data on Minocycline therapy in rheumatoid arthritis suggest that such treatment may be considered, along with disease-modifying anti-rheumatic drugs such as methotrexate, sulfasalazine, gold salts and hydroxychloroquine. However, additional clinical research is necessary to document the long-term efficacy of Minocycline in the decreased progression of joint destruction.

Nicolson states that long-term study regarding the efficacy of Minocycline should be conducted on patients who are positive for both the Mycoplasma and Chlamydia genome, since we detect the Chlamydia trachomatis genome in the blood and joint fluid of 20% of patients with rheumatoid arthritis.

The eradication of the pathogenic Mycoplasmas from the blood and various tissue sites requires an intact functional immune system, which most patients with chronic illnesses do not possess. Therefore immune enhancement strategies along with prolonged drug therapy may help to eliminate Mycoplasma from the human body.

Hyperbaric Oxygen Therapy and 'Opportunistic Chronic Infections': Mycoplasma, Chlamydia, Cytomegalovirus, Epstein Barr Virus

Hyperbaric oxygenation of the blood elevates the amount of dissolved oxygen (reported 20-30 fold increase in oxygen content in the target tissue) and results in the correction of tissue hypoxia. This significantly enhances and mobilizes immune function and response. HBOT accelerates wound healing, promotes systemic infection control, alleviates tissue ischemia and the dissociation of carboxyhemoglobin, which provides excellent host-sites for opportunistic infections.

• HBOT enhances fibroblast migration and mitosis. High lactate levels and hyperoxia also combine to induce greater collagen synthesis

• Increased fibroblasts collagen synthesis enhances capillary growth, which further raises the partial pressure of oxygen as neovascularization (new capillary formation within ischemic zones) progresses

• HBOT significantly enhances white blood cell (WBC) function, killing phagocytized bacteria. Elevated oxygen increases the oxygen free radicals and hydrogen peroxide formation in the white cell lysosomes, improving antimicrobial activity

• HBOT leads to the constriction of blood flow in inflamed and oedematous tissue, reversing cellular leakage and fluid loss into surrounding tissue. HBOT reinstates normal lymphatic drainage, reducing painful inflammation and swelling

• Selected prescribed drugs and immune stimulating vitamins (injectable) are enhanced with increased tissue oxygenation and at higher partial pressure of oxygen

• Increased oxygen partial pressure increases the nitrogen gradient, boosting nitrogen elimination from the body. Increased oxygen partial pressure also directly reduces carbon monoxide effects on tissue

Nutritional and Lifestyle considerations

Most chronically ill patients including those with Mycoplasma infestation, are often immune suppressed and susceptible to opportunistic infections, so proper nutrition is vital.

The patient is advised not to smoke or drink alcohol or take caffeinated products. The patient is instructed to drink as much fresh fluid as they can, fruit juices or pure water are best. High sugar and high fat and junk foods, fast foods and acid-forming foods should also be avoided. The patient’s intake of fresh vegetables, fruits and grains should be increased and they need to decrease their intake of fats and simple or refined sugars, because these can suppress the patient’s immune system. To build the immune system, plenty of fresh vegetables must be eaten, and also soluble fibre foods including prunes, bran, wheat germ, yoghurt, fish and whole grains. In some patients exclusive use of 'organic' foods and the avoidance of gluten related products has also proved to be beneficial.

Vitamins and Minerals

Chronically suppressed immune patients are often depleted in essential vitamins and minerals because they suffer inadequate absorption from the gut. High doses of antioxidant vitamins and mineral are therefore recommended. Injectable vitamins including B group and C vitamins have also proved beneficial. Oral dosage high potency B group, amino acids and minerals including zinc, magnesium, chromium and selenium are also reported to be effective. Minerals should not be taken at the same time of day as antibiotics, because the minerals can affect the absorption of the antibiotics.

A number of other natural remedies including ginseng root, echinacea-C, bioflavonoids, herbs and herbal teas, lemon/olive drink and olive leaf extract with antioxidants are also reported to be useful, especially during or after antibiotic therapy. These products appear to be useful during antibiotic therapy as they boost the immune system. Utilized in a maintenance program, antioxidants can help prevent or minimize recurrence of the illness.

Replacement of Natural Gut Flora with Lactobacillus

Patients undergoing treatment with antibiotics and other substances risk destruction of normal gut flora (Nicolson). Antibiotic use that depletes normal gut bacteria can result in the over-production of less desirable bacteria. To supplement beneficial bacteria in the gastrointestinal system, yoghurt, especially Lactobacillus acidophilus powder is recommended. Mixtures of Lactobacillus acidophilus, L. bifidus, B. bifidum, L. bulgaricus and FOS (fructoologosaccharides) promote growth of these ‘friendly’ bacteria in the gut. Numerous products are available: acidophilus mixtures above 3 billion live organisms should be taken 2-3 times per day.

Yeast/Fungal or Bacterial Overproduction

Nicolson reports yeast and fungal related over-production that can occur with antibiotic therapy, especially in females (vaginal infections). Gynaecologists recommend Nizoral, Diflucan, Mycelex, or anti-yeast creams. Metronidazole (Flagyl, Prostat) has been used to prevent fungal or parasite overgrowth or other antifungals (Nystatin, Amphotericin B, Fluconazole, Diflucan) have been administered for fungal infections occurring whilst on antibiotics. As mentioned above, complex spectrum L. acidophilus mixtures are used to restore gut flora. Bacterial over-production can also occur, for example, in between cycles of antibiotics or after antibiotics have been stopped. This can be controlled with 2-week courses of Augmentin (3-500 mg/day) in between cycles or concurrently with other antibiotics.

• Mycoplasma and related opportunistic infections are proving to be major factors in the treatment of degenerative neurovascular disorders. Early detection, together with appropriate treatment implementation, will enable a more rapid resolution of these potentially debilitating conditions and hopefully stop the cycle of degenerative effects.