The diverse biofilms of Borrelia……
the majority of bacteria in nature exist attached to a substratum.

Psoriasis :
Several studies have examined the responses of psoriasis patients to Malassezia. One of the early studies (375) noted that if dense suspensions of Malassezia were applied to the shaved skin of rabbits, lesions similar to psoriasis resulted. The lesions persisted as long as Malassezia continued to be applied but otherwise resolved within 3 to 4 days. Further work by the same group used patch testing with Malassezia to study the response in 10 patients with psoriasis and 10 controls (259). All of the patients developed psoriatic lesions when challenged with Malassezia, and biopsy specimens showed features consistent with psoriasis. Therefore, Malassezia was able to elicit psoriasiform lesions in both animals and humans.

Additional support for the role of Malassezia in psoriasis comes from successful use of ketoconazole in patients (374). Although ketoconazole may act by a direct antifungal mode of action, it has also been shown to suppress Malassezia-induced proliferation of lymphocytes from psoriatic patients (13), thus reducing the response to antigenic stimulation in lesions.

The first study to characterize the humoral immune response to Malassezia in patients with psoriasis was carried out by Squiquera et al. (417). This study included 15 patients, of whom 8 had active disease, and 10 healthy controls. SDS-PAGE of Malassezia extracts was performed, and the test sera were immunoblotted. The sera from psoriatic patients bound to a 120-kDa band (11 of 15) and a 100-kDa band (7 of 15), but none of the control sera recognized these bands. Consequently, the authors suggested that antibodies to the 100- and 120-kDa proteins were specific serologic markers for psoriasis. These antibodies were subsequently shown to recognize the N-acetylglucosamine terminals of glycoproteins present in Malassezia (276). However, both of these proteins are recognized by sera from patients with AD (256, 312), and so they are not specific markers for psoriasis.

Neutrophils form part of the inflammatory infiltrate in the dermis of psoriatic lesions (90). A study examining the chemotaxis of neutrophils from psoriatic patients and controls demonstrated that Malassezia induced significantly more chemotaxis in neutrophils from psoriatics than other groups (75). The effect was specific, since Staphylococcus epidermidis did not affect chemotaxis, and was due to a protein. Psoriatic lesions often develop at sites of trauma (the Koebner phenomenon [294]), and the increased chemotactic response of neutrophils to Malassezia was suggested to play a role in this event.

Only one study has examined the cellular immune responses to Malassezia in patients with psoriasis (36). All the psoriatic patients included (n = 13) had lesions on the scalp, with disease durations ranging from 2 months to 20 years. Proliferation of PBMC was seen in response to Malassezia in all of the patients tested. However, since no healthy controls were included in the study, it is not possible to determine whether the responses differed from those of normal individuals. The response of PBMC was due to CD4+ T lymphocytes and required antigen presentation by HLA-DR+ cells, and so it was not mitogenic stimulation. T-lymphocyte lines were established from psoriatic and nonpsoriatic patients and were stimulated with Malassezia. Similar patterns of response were obtained whether the patient had psoriasis or not, and the authors concluded that Malassezia-specific T lymphocytes were not involved in psoriasis.

Consequently, the role that Malassezia plays in psoriasis is, as yet, undetermined. Although it may contribute to the inflammation associated with the disease, via complement activation and neutrophil recruitment, convincing evidence that it is of prime importance in the pathogenesis of the disease is still lacking.

Overall, it is difficult to rationalize and explain the wide range of results documented for humoral and cellular immune responses to Malassezia in patients with PV, SD, folliculitis, AD, and other superficial diseases. The use of different techniques, different antigenic preparations, and organisms from different classifications makes comparison of results unreliable and may partly explain the disparity in the findings. However, many of these limitations can now be overcome. The characterization of several antigens from Malassezia and the ability to produce them in vitro should provide a reliable source of defined antigen for use in future immunological studies. The unification of different classifications of Malassezia into one scheme should removed the uncertainty about whether similar strains or species are being studied. Lastly, the finding that, at least in AD, there is significant cross-reactivity between mannans of different yeasts may encourage the use of protein antigens in immunological assays used to define the response specific to Malassezia. Although our understanding of the immune response to Malassezia in superficial diseases has advanced significantly over the last 10 years, there are still many interesting questions awaiting an answer.

Most patients showed serologic evidence of infection (antibodies) with one or more unexpected potentially pathogenic microorganisms despite testing for only a few species.

There are six particle types that are consistently recovered from the skin surface of those suffering from Morgellons disease, 1) ribbon-like fibers, 2) rounded fibers, 3) capsule-like particles, 4) black flakes/grains, 5) worm-like particles, and 6) stellate-shaped (“starfish-shaped”) particles. The fibers are often pigmented and may luminesce under ultraviolet light.

Current Morgellons research at a laboratory in Massachusetts shows that individuals affected by Morgellons disease have been in contact with soil and/or water containing cyanobacteria (blue-green algae), algae, aquatic fungi, water molds and lichen (algae and fungi). This assemblage of organisms, and associated bacterial populations, is common in soil and aquatic environments where cryptobiotic soils are present and/or in environments where nutrient rich conditions promote the development of algae blooms.

Dermal contact with a water source and/or inhalation of aerial dust containing cyanobacteria and algae may lead to the progressive colonization of organisms that are capable of feeding on or consuming these photosynthetic producers, thus contributing to the wide range of symptoms reported by Morgellons sufferers. Incidental growth of these opportunistic populations, such as actinomyces, aquatic fungi and true fungi, are known to promote disease in humans, as they consist of species capable of degrading either cellulose or keratin (skin/hair). Evidence for the presence of opportunistic micro- organisms in samples is indicated by the occurrence of capsule-like Morgellons particles that have been identified as parasitized pine pollen grains. Chytrid populations are obligate parasites of frogs, nematodes, algae, cyanobacteria, plants, and pine pollen (see photo below).

These findings serve as a focus for further understanding the ecological significance of the organisms identified in this study and the role they may play as causative agents of Morgellons disease.

From Here :

The human oral cavity is a highly diversed ecosytem conatining more than 500 species of bacteria, including both cultivable and non-cultivable species. It is believed that infection with a select few Gram-negative anaerobes, called the ‘red-complex’, is responsible for causing periodontitis or ‘gum-disease’, which if not treated leads to tooth loss. My lab focuses on pathogenic mechanisms of the red-complex bacteria by utilizing molecular-genetic and biochemical approaches; the bacteria of the red-complex include Porhyromonas gingivalis, Tannerella forsythia (formerly Bacteroides forsythus) and Treponema denticola (a spirochete). My overall objectives are to gain a better understanding of how these pathogenic bacteria initiate colonization, form biofilms and initiate tissue destructive host immune responses critical for disease progression. The research focuses on identifying the virulence factors these bacteria produce and host-cell receptors involved in recognition of virulence factors. Once these virulence factors and host cell receptors have been identified, the logical next step would be to develop intervention strategies, such as vaccines, against these bacteria. In this regard, we have developed genetic systems in non-pathogenic oral streptococci (Streptococci gordonii) for expression and delivery of vaccine antigens of choice as vectors for oral immunization.

Trepenoma dentricola. Image by Joe Dixon, 2007. From here :

B.forsythus

More on P.Gingivalis pathogenesis.From Here :

Genetic associations with disease may result from alleles that increase protection from one pathogen but increase vulnerability to another.

The genetic variation responsible for these associations may persist indefinitely, because the success of a variant is negatively related to its frequency.

As a pathogen variant increases, it favors increased frequency of a host variant that controls it; as this host variant becomes more prevalent, it increasingly disfavors the pathogen variant. “Dynamical polymorphisms” of resistance genes may thus persist by this process of nonprogressive seething.
If underlying infectious causes are not recognized, the reduced success of some host variants (due to the inherent costs of the particular genetic defense or to the increased vulnerability to the existing mix of pathogens) could be misconstrued as a genetic disease.

Variations in human leukocyte antigens (HLA) appear to be a particularly important example of this process, because different HLA alleles are associated with differences in recognition and presentation of foreign antigens, or with differences in vulnerability to autoimmune disease as a consequence of cross reactivity between pathogen and host antigens.

HLA variants are associated with vulnerability to infectious diseases such as malaria and tuberculosis, and infection has been causally linked to HLAassociated autoimmune diseases such as herpes stromal keratitis and Reiter’s syndrome. The high degree of polymorphism of such alleles implicates a role for infection in many diseases that exhibit moderate heritibilities.

HLA variants are associated with many chronic diseases, such as juvenile diabetes, rheumatoid arthritis, systemic lupus erythematosus, scleroderma, Crohn’s disease, myasthenia gravis, Hodgkin’s disease, multiple sclerosis, Grave’s disease, narcolepsy, and pernicious anemia.

Individuals with HLA B-27, for example, comprise about 5 percent of the population and are about 80 times more likely to have ankylosing spondylitis, which is often manifested by severe arthritis-like conditions. The monozygotic twin concordance for most of these HLA-associated diseases is less than 50 percent—something other than host genetics is therefore making a major contribution. Infectious causation has not been investigated for some of these HLA associations; for others there is suggestive evidence.

Juvenile diabetes, for example, is due to the gradual disappearance of insulin production. Its temporal association with infection, the similarity of viral antigens with autoimmune-associated HLA antigens, and regional and seasonal patterns, implicate infectious causation. Coxsackie virus is a
leading suspect.

The reasons for the presence and maintenance of trinucleotide repeatdiseases such as fragile X and myotonic dystrophy are largely unknown.
These diseases occur after a small, “subclinical” length of trinucleotide repeats lengthens rapidly over several generations as a result of errors associated with a hairpin transcriptional structure. The lineages of these people then tends to dwindle to extinction. Individuals with subclinical repeat
lengths are virtually absent in some regions and too widespread in other regions to be attributed solely to founder effects. The low frequency of new haplotypes among such individuals suggests that the low repeat numbers are generated too rarely by new mutations to be maintained solely by mutation.
This set of characteristics is consistent with the subclinical repeats being a defense against infectious agents and are difficult to explain without invoking such a benefit; we therefore suggest that the possibility of a defensive function of subclinical repeat lengths warrants investigation.

Psychological Phenomena

The fitness load approach also applies to psychological phenomena.

Psychological and behavioral alterations among infected individuals may represent manipulations of hosts for the spread of pathogens, defenses against the pathogen, or side effects of infection that benefit neither host nor pathogen. Rabies is a dramatic example of a manipulation: the pathological rage induced by the virus increases the chance of biting and hence transmission of the virus in the saliva. Syphilitic insanity appears to be an example of a side effect. These examples could be dismissed because they are so extreme, but it is the extreme examples that are the most conspicuous
and that therefore will tend to be discovered without a concerted research effort.

Just as it was inappropriate to reject infectious causation of human cancers on the basis of the conspicuous progression of Rous’s sarcoma in chickens, it would be inappropriate to reject the idea that pathogens could cause subtle changes in human behavior on the basis of
the conspicuous psychological effects of rabies and syphilis.

Had Treponema pallidum been a less conspicuous organism, causing less conspicuous mental illness, and less conspicuous links between early symptomatic infection and mental illness we might not recognize even today that this spirochaete can cause mental illness.
The intricacies of neuronal circuitry suggest that behavioral changes may result from slight changes in brain structure; and such slight changes may be more difficult to link to infectious organisms than the gross pathological changes found in other less intricate tissues, such as the changes in
the lungs caused by M. tuberculosis.

Moreover, generating appropriate animal models for testing of infectious causation often may be very difficult or even impossible because of the intellectual complexity of human behavior, the subtleties of variations in human behavior, and the difficulties of understanding the thought processes of nonhuman subjects.

Considering these problems, we cannot use the absence of conspicuous evidence of infection-induced behavioral alterations as evidence of the absence of such alterations.
In spite of these limitations, a combination of comparative study and animal experimentation are already proving useful for investigations of some psychiatric disorders. Borna disease virus, for example, has a tropism for the limbic system and is known to cause mood disorders in sheep, horses,
and rats. It has been isolated from human brain tissue, and infections in humans are significantly associated with schizophrenia and clinical depression (i.e. bipolar disorder).
Evidence also implicates infectious causation of some obsessive compulsive disorders by
streptococcal infections.

Some of what I do know (or at least what I think if a philosopher argues with the word “know):

Morgellons is a physical pathology. It is not a simple subset of a psychiatric disorder Multiple forensic tests (FTIR, mass-spec, etc) at multiple locations have confirmed that the Morgellons fibers are not identifiable as a known compound. The fibers are a fairly pure organic compound containing: carbon (single & double bonds), hydrogen, nitrogen, oxygen, at least one methyl group, maybe a sulfur group and a few unclear FTIR peaks. They are quite heat resistant and not dissolvable in lab-type solvents or detergents. The red & blue colors of the analyzed fibers are neither dyes nor pigments in any conventional sense.

Attempts to use fixatives for EM analysis have been ongoing for months ( have not been trivial lab exercises) and will hopefully yield results in the near future. Thanks to a large donation outside commercial labs will be doing analyses that we cannot do “inhouse” as soon as non-trivial details can be worked out. We are looking at a possible connection with Agro-bacterium. Multiple physicians are participating in this.

Morgellons is not a skin disease. It is a systemic condition affecting multiple organs. It does not seem to be highly contagious. People who “fight Morgellons” seem to do better than those who isolate themselves and resign themselves to a downward spiral. This is true of most chronic conditions. Just an observation.

Cure is a word I am hesitant to use, but I have met one person who has been symptom free for about 3 years after discontinuing treatment. That person reported that they did a long-term course of high-dose antibiotic, anti-fungal and anti-helmenthic meds. Several people have claimed to be cured, but this is the only one I have personally met that has remained symptom-free for multiple years after discontinuing all treatments. I am not a physician and can give no recommendations for treatment. This person was not seen or treated by any physicians at OSU-CHS. I am merely passing this information on as a personal observation. I will keep working to try to identify the cause of Morgellons. At the moment I have no research-based, front-runners for the cause.

With respect,

RSW

Randy S. Wymore, Ph.D.
Director, OSU-CHS Center for the Investigation of Morgellons Disease
Associate Professor of Pharmacology
Oklahoma State University
Center for Health Sciences

From Here :
Dermatophilosis is an exudative dermatitis that affects mainly ruminants, but also other species including humans.
The aetiological agent of dermatophilosis is the branching filamentous actinomycete bacterium Dermatophilus congolensis.
Various forms of the disease are recognized in different species, and there is considerable variation in the clinical appearance of the disease and in the affected areas of the body.
AND
Dermatophilus congolensis itself is not highly pathogenic; combinations of factors predispose animals to infection. For example, malnutrition at the start of the rainy season can affect the course of infection, and infection is initiated at sites where the skin’s defensive barriers, comprising sebum, skin surface antibodies and stratum corneum, have been damaged by intense rainfall and/or by mechanical trauma.
Rainfall also has a role in dispersal of the organism from crusts to healthy skin and it triggers activity in arthropod populations.
Haematophagous flies cause skin damage and initiate inflammation at feeding sites.
The resulting exudate attracts flies that act as mechanical vectors for D. congolensis, and provides a growth medium for the bacterium.
The bacterium proliferates by growth of hyphae that undergo transverse and longitudinal division
to produce filaments containing cocci (see Poster, this issue).
Motile, flagellate cocci are released from wet crusts and these establish new sites of infection on the
same animal or are transmitted to new hosts.
Dermatophilosis crusts characteristically comprise alternating layers of keratinocytes, vesicles of serous exudate and infiltrates of neutrophils, giving a palisaded appearance in stained sections. This suggests that crusts are formed by repeated cycles of epidermal proliferation, bacterial invasion, release of exudate into vesicles and influx of neutrophils.

The dermis underlying chronically infected epidermis contains accumulations of neutrophilis, mononuclear cells and plasma cells (Fig. 2). The density of the cellular infiltrate correlates with lesion severity. This infection provides unique opportunities to examine immune responses in the skin and the influence of tick infestation on immune responses to a second pathogen.

A SILENT FOREST: The Growing Threat of Genetically Engineered Trees (GE/GMO).

This award winning documentary film explores the growing global threat of genetically engineered trees to our environment and to human health.
The film features renowned geneticist and host of PBS’ The Nature of Things David Suzuki, who explores the unknown and possibly disastrous consequences of improperly tested GE methods.
Many scientists and activists are interviewed in the film, which serves as an effective and succinct tool for understanding the complex issue of GE trees.
The film includes the testimony of many experts on the subject and serves as a valuable tool to inform students and those interested in environmental issues.
The film has been well used in public forums, government as well as college and high school classrooms. The film includes an interview with Percy Schmeiser, who lost the rights to his own crops to Monsanto, when Monsanto seeds contaminated his fields.
As Schmeiser says in the film: “It doesn’t matter how it gets there, destroying your crop. All of your crop, becomes Monsanto’s ownership and they can lay a lawsuit on top of it against you. Even if the contamination rate is 1%, all your other 99% of your crop goes to Monsanto. And that’s what startled the world, how farmers can lose their rights overnight, an organic farmer can lose his seeds and his rights overnight, and get subject to a lawsuit.”
The film shows how farmers like Schmeiser and indigenous people may lose their way of life and belongings in the face of new biotech friendly science and legislation.
A Silent Forest won first place in the EarthVision Environmental Film Festival and a First Place in the Wild and Scenic Environmental Film Festival. The film is created by award-winning director Ed Schehl who has been making and promoting documentaries on environmentalism and social justice for 15 years. As new crucial forms of legislation and urgent needs for action arise, this film makes information available to the general public.

You can order the “A Silent Forest” video from: http://www.CreateSpace.com
Thank you.

The scleroderma bacterial took a long time to grow and could not be diagnosed as a TB germ or other definite “atypical” mycobacteria.
The microbe was highly pleomorphic (various forms). There were round staphylococccal forms, as well as typical acid-fast rod forms. Eventually this isolate became fungal-like and “actinomycete- like.” Despite expert opinion, it was impossible to classify the microbe into a specific species.

This case of scleroderma was reported in The Archives of Dermatology in 1966.

Please follow this link to an extraordinary pdf file with images of Borrelia and other Spirochaetal Biofilms, which is titled “Biofilms of Borrelia Burgdorferi and clinical implications for chronic Borreliosis” by Alan Macdonald MD and dated July 7 2008 from the University of New Haven, Lyme Disease Symposium, New Haven Connecticut

and this link to many more images which may be interesting for Alzheimer’s sufferers in adddition to Lyme Borreliosis patients.

They are then referred to as L-form or cell wall deficient (CWD) bacteria. Although researchers have known about L-form bacteria for over a century, up until recently they have not fully understood their connection to chronic disease.

It is now known that these bacteria are responsible for causing a wide array of chronic diseases including rheumatoid arthritis, Chronic Fatigue Syndrome, Lyme disease, and sarcoidosis.

Pathogenic spirochetes are bacteria that cause a number of emerging and re-emerging diseases worldwide, including syphilis, leptospirosis, relapsing fever, and Lyme borreliosis. They navigate efficiently through dense extracellular matrix and cross the blood–brain barrier by unknown mechanisms. Due to their slender morphology, spirochetes are difficult to visualize by standard light microscopy, impeding studies of their behavior in situ. We engineered a fluorescent infectious strain of Borrelia burgdorferi, the Lyme disease pathogen, which expressed green fluorescent protein (GFP). Real-time 3D and 4D quantitative analysis of fluorescent spirochete dissemination from the microvasculature of living mice at high resolution revealed that dissemination was a multi-stage process that included transient tethering-type associations, short-term dragging interactions, and stationary adhesion. Stationary adhesions and extravasating spirochetes were most commonly observed at endothelial junctions, and translational motility of spirochetes appeared to play an integral role in transendothelial migration. To our knowledge, this is the first report of high resolution 3D and 4D visualization of dissemination of a bacterial pathogen in a living mammalian host, and provides the first direct insight into spirochete dissemination in vivo.

These images are very familiar.

From Here :

AND extracted from the lesions on my scalp ……

From Here :

For more info go Here : and then to Phase 1 on the left sidebar menu.

The descriptive information below is a phase I summary report presenting the findings of an investigative research study. This work is supported through a grant from the Morgellons Research Foundation (MRF). Phase I is the first of three phases proposed in this research project. Phase I is a “look-see” initial study to determine what, if any, organisms, pathogens and/or materials in household water samples may be associated with Morgellons Disease. Phase I is only a findings presentation and no conclusions as to association and/or cause of Morgellons Disease are drawn. This initial phase lays the ground work for phases II and III as well as future research projects.

It is hoped that this information will encourage other researchers and scholars with knowledge in this field, to contribute to the present information base by becoming involved in this and additional research studies related to Morgellons disease.

A time lapse video under the microscope has been developed which demonstrates the cultured growth pattern and behavior of a primary pathogenic form that is in direct association with the so-called “Morgellons” condition.

The general public appears to be subject to the conditions that are shown in this report.