[Fwd: Chemtrails and MYCOPLASMAL INFECTIONS]

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StevenPowersMD

Chemtrails and MYCOPLASMAL INFECTIONS

 

Chemtrail activity MYCOPLASMAL INFECTIONS appear to go hand in

hand.

 

 

http://www.geocities.com/canadianchemtrails/

 

 

Antimicrobics and Infectious Disease Newsletter (Elsevier

Science)

 

THE PATHOGENESIS AND TREATMENT OF MYCOPLASMAL INFECTIONS

Garth L. Nicolson

The Institute for Molecular Medicine, Huntington Beach,

California

 

Marwan Y. Nasralla

International Molecular Diagnostics Inc., Huntington Beach,

California

 

Nancy L. Nicolson

The Institute for Molecular Medicine, Huntington Beach,

California

 

Summary

 

Pathogenic mycoplasmas have been found in the blood or other

specimens of patients with a variety of chronic clinical conditions,

including respiratory, oral cavity, genital and other infections,

autoimmune, inflammatory and immunosuppressive diseases and fatigue

syndromes of unknown origin. These small bacterial microorganisms are

possible causative agents, cofactors or opportunistic infections in

these and other illnesses. Evidence for their association or possible

role in various clinical conditions is suggested by their

significantly higher incidence or degree of infection in symptomatic

patients than in non-symptomatic controls and their gradual

suppression by the appropriate antibiotics resulting in gradual

patient recovery from clinical signs and symptoms. Although they are

not widely appreciated for their pathogenic properties, certain

Mycoplasma species and certain other species of bacteria (Chlamydia,

Borrelia, etc.) appear to play a role in disease progression or

patient morbidity in rather large subsets of chronic illness

patients.

 

Introduction

 

Certain Mycoplasma species, the smallest and simplest, free-

living, bacteria that lack a rigid cell wall, are important pathogens

in animal, plant and insect species. In humans mycoplasmal infections

have only recently been associated with certain acute and chronic

illnesses where they may function as causative agents, cofactors or

opportunistic infections that cause patient morbidity. Although

various Mycoplasma species are commonly found as commensals in the

oral cavity and at other superficial sites, certain species appear to

cause morbidity when they penetrate into the blood and spread to and

colonize various tissues. For example, M. hominis and Ureaplasma

urealyticum are common inhabitants of the human genital tract but

they can play an etiologic role in pyelonephritis, pelvic

inflammatory diseases and post-abortion and post-partum fevers. Some

reports claim that some Mycoplasma species cause serious systemic

infections, such as septicemia, septic arthritis, neonatal meningitis

and encephalitis, and this has been confirmed in animal models. For

example, M. fermentans can cause severe, fatal neurological and

respiratory signs and symptoms after injection into the cerebral

fluid of rats. Although sometimes questioned, several pathogenic

Mycoplasma species have been proposed to be etiologic agents in

various acute and chronic diseases in man. Less appreciated is the

possibility that multiple chronic infections, including Mycoplasma

species, play an important role in various chronic illnesses and

their progression.

 

Mycoplasma genomes are the smallest among bacteria

 

The genomes of most Mycoplasma species encode about 600

proteins. For example, The M. genitalium and M. pneumoniae genomes

contain 470 and 677 protein-coding gene sequences, respectively,

compared with 1,703 protein genes in Haemophilus influenzae and about

4,000 genes in E. Coli. The genomes of M. genitalium and M.

pneumoniae have lost the genes involved in certain biosynthetic

pathways, such as the genes for amino and fatty acid and vitamin

synthesis. Since they are cell wall-deficient bacteria, there is a

major reduction in genetic information needed for cell wall

biosynthesis. Although Mycoplasma species carry a minimal set of

genes involved in energy metabolism and biosynthesis, they still have

the essential genes for DNA replication, transcription, translation,

and the minimal number of rRNA and tRNA genes. The reduction in

mycoplasmal genomes explains their need for host nutritional

molecules. A significant number of mycoplasmal genes appear to be

devoted to cell adhesion and attachment organelles as well as

variable membrane surface antigens to maintain parasitism and evade

host immune and nonimmune surveillance systems.

 

Mycoplasma species variably express structurally heterogeneous

cell surface antigens. Variations in the genes encoding cell surface

adherence molecules reveal distinct patterns of mutations capable of

generating changes in mycoplasma cell surface molecular size and

antigenic diversity. Variable surface antigenic structures and rapid

changes in their expression are thought to play important roles in

the pathogenesis of mycoplasmal infections by providing altered

structures for escape from immune responses and protein structures

that enhance cell and tissue colonization and penetration of the

mucosal barrier.

 

Mycoplasma interactions with host immune systems

 

Certain Mycoplasma species can either activate or suppress host

immune systems, and they may use these activities to evade host

immune responses. For example, some mycoplasmas can inhibit or

stimulate the proliferation of normal lymphocyte subsets, induce B-

cell differentiation and trigger the secretion of cytokines,

including interleukin-1 (IL-1), IL-2, IL-4, IL-6, tumor necrosis

factor-a (TNFa), interferons, and granulocyte macrophage-colony

stimulating factor (GM-CSF) from B-cells as well as other cell types.

Moreover, it was also found that M. fermentans-derived lipids can

interfere with the interferon (IFN)-g-dependent expression of MHC

class II molecules on macrophages. This suppression results in

impaired antigen presentation to helper T-cells in an experimental

animal model. Also, mycoplasmas are able to secret soluble factors

that can stimulate proliferation or inhibit the growth and

differentiation of immune competent cells.

 

Mycoplasma species are known to secrete immune-modulating

substances. For example, immune cells are affected by spiralin, a

well-characterized mycoplasmal lipoprotein that can stimulate the in

vitro proliferation of human peripheral blood mononuclear cells and

murine splenocytes. This stimulation of immune cells results in

secretion of proinflammatory cytokines (TNFa, IL-1 or -6). Spiralin

can also induce the maturation of murine B-cells.

 

As described above, mycoplasmas can evade immune recognition by

undergoing surface antigenic variations thus rapidly altering their

cell surface structures. Such antigenic variability, the ability to

suppress host immune responses, slow growth rates and intracellular

locations may explain the chronic nature of mycoplasmal infections

and the common inability of a host to suppress mycoplasmal infections

with host immune and nonimmune responses.

 

Rapid adaptation to host microenvironments by mycoplasmas is

usually accompanied by rapid changes in cell surface adhesion

receptors for more successful cell binding and entry as well as rapid

structural protein changes to mimic host antigenic structures

(antigen mimicry). For example, during chronic, active arthritis the

size and antigenic diversity of the surface lipoprotein Vaa antigen

changes in structure and expression in vivo. Antigenic divergence of

Vaa can affect the adherence properties of M. hominis and enhance

evasion of host-mediated immunity. Variations in the Vaa genes reveal

a distinct pattern of mutations that generate mycoplasma surface

variations and thus avoid host immune responses.

 

Mycoplasmas Can Induce Programmed Cell Death and Necrosis

 

Mycoplasmas can directly suppress host immune responses by

initiating or enhancing apoptosis. For example, M. fermentans, an

AIDS-associated mycoplasma, can initiate or enhance concanavalin A-

induced apoptosis of T-cells. Relatively large amounts of nucleases

are also expressed by Mycoplasma species, and these can be released

intracellularly to cause degradation of host DNA. Mycoplasmal

nucleases may also be involved in secondary necrosis seen in advanced

mycoplasmal infections, as indicated by the occurrence of

morphological characteristics of apoptosis (chromatin condensation)

and necrosis (loss of membrane integrity and organelle swelling).

Although mycoplasmas can release activated oxygen species that may be

involved in initiating apoptosis, some Mycoplasma species, such as M.

fermentans, express a novel cytolytic activity in a nonlipid protein

fraction that has a cytocidal effect not mediated by the known

mycoplasmal cytokines like TNFa.

 

In addition to apoptosis, mycoplasmas can also release growth

inhibitory molecules into their surroundings, such as arginine

deaminase. This enzyme can act as a growth-inhibitory substance that

suppresses IL-2 production and receptor expression in T?cells

stimulated by non-specific mitogens, and it can induce the

morphologic features of dying cells and DNA fragmentation indicative

of apoptosis.

 

Clinical Testing for Mycoplasmal Infections

 

Until recently one of the most difficult problems in detecting

mycoplasmal infections was that the available techniques, serological

and culturing procedures, were relatively insensitive for detecting

intracellular infections. Mycoplasma culture techniques can be highly

specific for detection of some mycoplasmal infections, but they are

relatively insensitive because of difficulty culturing various

Mycoplasma species. Conventional serological detection of mycoplasmal

infections is quite difficult due to the lack of humoral immune

responses in most patients. Also, detection methods that use

antibodies against mycoplasma antigens are not very reliable, because

mycoplasmas are able to hide inside cells. This can result in rather

normal antibody titers during active mycoplasmal infections.

 

The most reliable clinical testing for mycoplasmal infections

uses whole blood, blood leukocytes or tissue biopsies and polymerase

chain reaction (PCR). Even with this approach it is necessary to

insure that intracellular Mycoplasma species are being detected at

high sensitivity. Another research technique that has been used for

intracellular infections is nucleoprotein gene tracking. This

approach detects mycoplasmal genes directly in nucleoprotein

complexes isolated directly from cell nuclear fractions. Although

highly specific, it is not as sensitive as PCR.

 

Persistence of Mycoplasmal Infections and Various Clinical

Conditions

 

Mycoplasmas have been found at significantly higher incidence

in blood and tissue specimens obtained from patients with various

chronic illnesses compared to healthy controls. Since little is known

about the involvement of mycoplasmas in the pathogenesis of chronic

illnesses, it remains uncertain whether these findings indicate that

some Mycoplasma species are causal agents, cofactors, or

opportunistic (superinfections) in patients with immundisturbances.

Since mycoplasmas can be found at superficial sites, such as normal

flora in the genitourinary tract, oral cavity and gut where they are

thought to be nonpathogenic. The distinguishing characteristic in

pathogenic infections may be the penetration of Mycoplasma species

into the blood circulation and especially into cells in various

tissues. This may explain the finding of pathogenic Mycoplasma

species in genitourinary tract, oral cavity, gut and the blood in a

few percent of asymptomatic subjects. Unless mycoplasmas penetrate

into tissues and cells, it is unlikely that they can exert their

pathogenic effects, but in some individuals the presence of

mycoplasmas is not associated with any clinical condition. In such

cases it is not apparent whether this represents a superficial

infection, an early nonsymptomatic or dormant phase of the illness

process or a carrier phenomenon.

 

The persistence of mycoplasmal infections has many similarities

with Chlamydial persistance. Certain Chlamydia species infections can

remain dormant and do not always progress to replication and host

cell lysis, and similarly certain Mycoplasma species can remain

inside cells for long periods without initiating apoptosis and

eventual cell lysis. Unlike Chlamydia species where much is known

about the dormant or cryptic intracellular phase of their life

cycles, little is known about the mechanism of persistence of

mycoplasmal infections. Both of these bacteria (at least their

pathogenic strains) are considered obligatory intracellular parasites

because they are dependent on host cell intermediary metabolites and

biosynthetic precursors, and they are thought to cause much of their

pathogenic effects during their intracellular persistance phase.

Alternatively, when intracellular pathogens, such as certain

Mycoplasma species, are released from cells without cell lysis, they

can carry host cell surface antigens with them, eventually resulting

in autoimmune host responses against the infected tissues.

 

Mycoplasmal Infections and Respiratory Illnesses

 

Various respiratory illnesses, such as chronic asthma, airway

inflammation, chronic pneumonia and other respiratory diseases, are

known to be associated with mycoplasmal infections. For example, M.

pneumoniae is a common cause of upper respiratory infections, and

severe asthma is commonly associated with mycoplasmal infections.

Recent evidence has shown that certain mycoplasmas, such as M.

fermentans (incognitus strain), are unusually invasive and found

within respiratory epithelial cells. Similar to certain Chlamydia

species, pulmonary macrophages appear unable to kill pathogenic

Mycoplasma species.

 

Although mycoplasmal infections are often associated with

chronic asthma, the exact role of mycoplasmas in the pathogenesis of

asthma remains unclear. Certain Mycoplasma species are involved in

respiratory tract infections associated with airway inflammations,

induction of bronchial hyperresponsiveness (BHR) and asthmatic

attacks. At a minimum, M. pneumoniae infections can cause worsening

of conditions in asthmatic patients, whose attacks are associated

with significant and specific IgA and IgE responses. Specific

antibodies of these subclasses for M. pneumoniae protein antigens

were found in a majority of patients with M. pneumoniae infections.

Mycoplasmas are only one of many agents that can trigger BHR, and

other infectious or chemical agents may contribute to the complex

disease process.

 

Mycoplasmal Infections in Urogenital Diseases

 

Mycoplasma species are commonly found in urogenital infections.

For example, M. hominis was detected in more than 12% of females who

presented at gynecological services, and M. genitalium has been

associated with acute and nonspecific non-gonococcal urethritis in

males but not in asymptomatic controls. This organism is also a

common cause of genital infections in women, and it was detectable in

7% of women with sexually transmitted diseases. M. hominis and U.

urealyticum have been implicated in a wide variety of urogenital

diseases, such as pelvic inflammatory disease, infertility, non-

gonococcal urethritis (NGU) and other genital infections,

pyelonephritis, Reiter's syndrome, and peritonitis. The appearance of

various bacterial species in bacterial vaginosis may be a result of

pathophysiological alterations of the vaginal ecosystem, and

mycoplasmas appear to play an important role in this process.

Mycoplasmas are also known to interfere in pregnancy, For example, U.

urealyticum was found to be involved in 11% of patients with

fertility problems.

 

Mycoplasmal Infections in Immunosuppressive Diseases

 

Some Mycoplasma species, M. fermentans, M. penetrans, and M.

pirum, have been implicated as infectious cofactors in HIV-AIDS.

Using relatively insensitive techniques all three mycoplasmas have

been detected in up to 20% of patients with HIV infections, and

serological studies have suggested that the presence of M. penetrans

is also associated with HIV infection. Moreover, the incidence of

systemic mycoplasmal infections in HIV-AIDS patients could be much

higher than previously thought. Most of the analyses were performed

using relatively insensitive techniques, such as serological

analysis. Pathogenic Mycoplasma species may influence HIV

pathogenesis by specific and direct activation or suppression of the

immune system, the production of superantigens with subsequent

alterations in immune responses, or their contribution to the

oxidative stress observed in HIV-positive patients. Also, the

development of AIDS may increase the susceptibility of HIV-infected

patients for coinfection with various Mycoplasma species, such as M.

fermentans. This species is able to bind HIV capsid protein gp120

permitting adhesion of HIV virions to the mycoplasma surface.

Subsequently the HIV viruses could be transported directly to cells

expressing CD4 receptors. After binding to target cells, mycoplasmas

can stimulate host cell activation by IL-1 and TNFa, which are known

effectors for virus reproduction. In addition, oligosaccharides of

the mycoplasmal glycocalyx may protect bound HIV-1 virons from host

immune responses.

 

Antigen similarities between the surface components of

mycoplasmas and HIV-1 have led to speculation that they use similar

mechanisms for cell entry. For example, the HIV?1 gp120 envelope

glycoprotein and M. genitalium adhesion proteins share sequence

homology and also have significant similarity with the CD4-binding

site of the class II major histocompatibility complex (MHC) proteins.

The interactions of microorganisms with MHC-related antigens on host

cells could contribute to a number of possible outcomes, including T-

cell dysfunction, T-cell depletion, T-cell shift, B-cell

proliferation, hyperglobulinemia and antigen-presenting cell

dysfunction. Interestingly, all of these have been observed during

the development of HIV-AIDS.

 

Mycoplasmal Infections in Rheumatic Diseases

 

Although the underlying causes of rheumatic diseases are not

known, rheumatoid arthritis (RA) and other rheumatic illnesses may

involve, at least in part, infectious agents. In addition, the

progression of rheumatic diseases may also be related to infectious

processes. The remarkable clinical and pathological similarities

between certain infectious diseases in some animal species and those

of some human rheumatic illnesses, such as RA, have encouraged the

search for microbial etiologies for these syndromes. A long list of

microorganisms, including aerobic and anaerobic intestinal bacteria,

several viruses and Mycoplasma species have been proposed as

important in these illnesses. We recently found multiple mycoplasma

species in about one-half of the blood samples from RA patients using

PCR. All multiple infections occurred as combinations of M.

fermentans with other species.

 

Mycoplasma species are known to be able to induce

immundysfunction and autoimmune reactions that could be related to

the development of RA. In animal models of RA, M. arthritidis-related

superantigens were found to compromise T-cells, and they can trigger

and exacerbate autoimmune arthritis. Furthermore, M. arthritidis can

release substances that can act on polymorphnuclear granulocytes,

such as oxygen radicals and chemotactic and aggregating substances.

Also, the isolated membranes of M. arthritidis possessed toxic

effects when injected into various animals.

 

Mycoplasmal Infections in Cardiac Diseases

 

Mycoplasmal infections of the heart have been reported in

patients with different types of carditis. The most common

association was with M. pneumoniae infection. Endocarditis and

myocarditis associated with M. pneumoniae infections appear to be an

important cause of death in M. pneumoniae infections. Direct

bacterial invasion of M. pneumoniae into pericardial tissue appears

to be more likely to cause pericarditis than autoimmune phenomena.

Viral and bacterial (Mycoplasma, Chlamydia and Mycobacterium

tuberculosis) infections appear to be common causes of myocarditis

and/or pericarditis, and this is just beginning to be appreciated by

infectious diesase specialists.

 

Mycoplasmal Infections in Autoimmune Diseases

 

Although pathogenic mechanisms have not been established in

autoimmune diseases, mycoplasmal infections seem to play an important

but not well understood role in these diseases. Several

characteristics of mycoplasmas make them attractive as agents that

may be responsible for triggering autoimmune responses. First, during

their intracellular replication and release from host cells

mycoplasmas can capture antigens from the host cell surface and

incorporate them into their cell membranes. This can lead to immune

responses against these antigens and possibly autoimmune reactions.

Second, mycoplasmal antigens can mimic host antigens and trigger

immune responses against these antigens with resulting cross

reactivity against host antigens. Third, mycoplasmas can cause

apoptosis of host cells with subsequent release of normal host

antigens.

 

Superantigens are potent immunomodulators derived from

microorganisms, such as bacteria, viruses and mycoplasmas. Their

effects on immune systems are the result of their binding both to MHC-

binding sites on antigen presenting cells and binding to structures

within hypervariable regions of T?cell antigen receptors. The

contributions of microbial superantigens to the pathogenesis of

autoimmune diseases have been investigated in experimental animal

models where a superantigen, the mycoplasma arthritis T?cell mitogen,

was arthritogenic in mice. When injected into mice, M. arthritidis

causes a chronic arthritis that resembles RA in its pathology and

pathogenesis. Mycoplasmal infections have also been implicated in the

progression of Kawasaki disease, Graves' disease, Hashimoto's

disease, Sjögren's syndrome, systemic lupus erythematosis (SLE) and

multiple sclerosis (MS).

 

Mycoplasmal Infections in Fatigue Illnesses

 

Chronic fatigue is the most commonly reported medical complaint

of all patients seeking medical care. However, the fatigue syndromes,

such as chronic fatigue syndrome (CFS, sometimes called myalgic

encephalomyelitis), fibromyalgia syndrome (FMS) and Gulf War

illnesses (GWI) are distinguishable as separate syndromes that have

muscle and overall fatigue as major characteristics, among many other

multiorgan signs and symptoms, including immune system abnormalities.

Because of the complex nature of these illnesses, many patients are

often diagnosed with multiple syndromes. We and others have examined

the presence of mycoplasmal blood infections in CFS, FMS and GWI

patients and have found that the majority of patients have blood

mycoplasmal infections.

 

Patients with CFS or FMS often have multiple mycoplasmal

infections and probably other chronic infections as well. When we

examined CFS/FMS patients for the presence of M. fermentans, M.

pneumoniae, M. penetrans, M. hominis infections, multiple infections

were found in over one-half of 93 patients. CFS/FMS patients had

double (>30%) or triple (>20%) mycoplasmal infections, but only when

one of the species was M. fermentans or M. pneumoniae (17). We also

found higher score values for increases in the severity of signs and

symptoms in CFS/FMS patients with multiple infections. CFS/FMS

patients with multiple mycoplasmal infections generally had a longer

history of illness, suggesting that patients may have contracted

additional infections during their chronic illnesses.

 

Antimicrobial Therapy for Mycoplasmal Infections

 

Once mycoplasmal infections have been identified in subsets of

chronic illness patients, they can be successfully treated, if the

therapy continues for some time to eliminate or suppress dormant

forms of the microorganism. Using this strategy appropriate treatment

with antibiotics can result in patient improvement and even recovery.

The recommended treatments for diagnosed mycoplasmal blood infections

require long-term antibiotic therapy, usually multiple 6-week cycles

of doxycycline (200-300 mg/day), ciprofloxacin (1,500 mg/day),

azithromycin (500 mg/day) or clarithromycin (750-1,000 mg/day).

Multiple cycles are required, because few patients recover after only

a few cycles, possibly because of the intracellular locations of

mycoplasmas like M. fermentans and M. penetrans, the slow-growing

nature of these microorganisms and their ability to exhibit

persistence as dormant forms and their relative drug sensitivities.

For example, of 87 GWI patients that tested positive for mycoplasmal

infections, all patients relapsed after the first 6-week cycle of

antibiotic therapy, but after up to 6 cycles of therapy 69/87

patients recovered and returned to active duty. The clinical

responses that were seen were not due to placebo effects, because

administration of some antibiotics, such as penicillins, resulted in

patients becoming more not less symptomatic, and they were not due to

immunosuppressive effects that can occur with some of the recommended

antibiotics.

 

Chronic illness patients often have nutritional and vitamin

deficiencies that must be corrected. These patients are often

depleted in vitamins B, C and E and certain minerals. Unfortunately,

patients with these chronic illnesses often have poor absorption.

Therefore, high doses of some vitamins must be used, and others, such

as vitamin B complex, must be given sublingual. Antibiotics that

deplete normal gut bacteria can result in over-growth of less

desirable flora, so Lactobacillus acidophillus supplementation is

recommended. In addition, a number of natural remedies that boost the

immune system are available and are potentially useful, especially

during antibiotic therapy or after therapy has been completed. They

appear to be useful during therapy to boost the immune system or

after antibiotic therapy in a maintenance program to prevent relapses.

 

Conclusions

 

Why aren't physicians successfully treating mycoplasmal,

chlamydial and other chronic infections? In many cases they are

treating these infections, but they are often not taking into account

the intracellular persistent phases of these infections. And it has

been only recently that such infections have been found in so many

unexplained chronic illnesses. These infections cannot be

successfully treated with the usual short courses of antibiotics due

to their intracellular locations, slow proliferation rates,

persistence and inherent insensitivity to most antibiotics. In

addition, a fully functional immune system may be essential to

overcoming these infections, and this is why vitamin and nutritional

supplements are important in the therapy. Finally, chronic illness

patients must be weaned off antidepressants and other potentially

immune suppressing drugs before they can fully recover from their

illnesses