Nov
25
The diverse biofilms of the Borrelia species
November 25, 2009 | Comments Off
The diverse biofilms of Borrelia……
the majority of bacteria in nature exist attached to a substratum.
Nov
18
Immunology of Diseases Associated with Malassezia Species
November 18, 2009 | Comments Off
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.
Oct
2
Important New Website
October 2, 2009 | Comments Off
From Here :
On September 24, 2009, CDC convened an external review panel made up of experts from the fields of dermatology, infectious diseases, public health, and mental health which examined the study activities to date and provided advice on future activities. The panel provided recommendations and guidance to CDC about analyses they think should be conducted on the data. A summary of the findings of the peer review panel will be presented to CDC’s CCID Board of Scientific Counselors in November 2009 and will be made available on this website.
Sep
8
Micro-Myiasis
September 8, 2009 | Comments Off
From Here :
Micro-Myiasis is a term coined by the authors of this research. It describes an affliction of myiasis, but focuses on small, primitive fly species, that cause the infestation of small fly larvae, causing generalized, chronic myiasis. This research leads to the possibility that cases of Morgellons disease, are forms of myiasis described above. It discusses the possibility that the unusual entities leached from morgellon sufferer’s skin and their symptoms, can be explained via the anatomy, physiology and secretions from these small fly larvae.
Aug
12
New Case Study—Morgellons disease, illuminating an undefined illness.
August 12, 2009 | Comments Off
Most patients showed serologic evidence of infection (antibodies) with one or more unexpected potentially pathogenic microorganisms despite testing for only a few species.
Jun
9
Some Research Findings
June 9, 2009 | Comments Off
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.
May
24
Oral Spirochetes
May 24, 2009 | Comments Off
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 :
May
24
Infectious Causes of Disease: An Evolutionary Perspective
May 24, 2009 | Comments Off
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.
May
12
Morgellons – A Response from Randy S. Wymore, Ph.D.
May 12, 2009 | Comments Off
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
Apr
17
Dermatophilosis - Tick Borne
April 17, 2009 | Comments Off
The description of the disease in this article has a strange familiarity.
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.
Mar
6
GM Trees, Paper, Our Health
March 6, 2009 | Comments Off
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.
Feb
25
Scleroderma
February 25, 2009 | Comments Off
From Here :
………. At the time my dermatology professor was J. Walter Wilson, who was also a world famous mycologist, an expert in fungal diseases. He was somewhat skeptical about my findings of acid-fast bacteria in all these four patients and he suggested I use a scleroderma patient as a “control.” Scleroderma is a so-called “collagen disease” where the skin becomes hardened. The disease can affect the internal organs and is sometimes fatal. The cause is unknown, and bacteria were never thought to cause this disease. Dr. Wilson said I should check a scleroderma skin biopsy because that would serve as a negative “control” case. I was astonished when Eugenia Craggs called me from the TB lab and told me the skin tissue grindings of the scleroderma sample were positive for acid-fast bacteria, the kind of bacteria found in tuberculosis. She would try and grow the germ in a TB culture. After much searching I was also able to find a few acid-fast rod forms of bacteria in the scleroderma skin biopsy microscopic sections prepared by the pathologist.
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.
Feb
7
Images - Borrelia and Spirochaete Biofilms
February 7, 2009 | Comments Off
The majority of bacteria exist in nature attached to a substratum.
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.
Jan
19
L - Form Bacteria
January 19, 2009 | Comments Off
From Here :
A wide body of research has shown that classical forms of bacteria often transform into tiny variants of the same species, losing their cell walls in the process.
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.
Jan
3
3D Imaging of the Lyme Disease Spirochete Adhering to and Escaping from the Vasculature of a Living Host
January 3, 2009 | Comments Off
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.
Sep
7
Morgellons - A Short film from Silentsuperbug
September 7, 2008 | Comments Off
Sep
6
Morgellons Phase I study - Primary Organisms Of Interest
September 6, 2008 | Comments Off
The Morgellons Research Foundation lists the suspect organisms…and supplies images too.
These images are very familiar.
AND extracted from the lesions on my scalp ……
For more info go Here : and then to Phase 1 on the left sidebar menu.
Sep
6
Phase 1: Recovery of Morgellons-Related Particles from Water Samples
September 6, 2008 | Comments Off
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.
Sep
4
Trichophyton eboreum sp. nov. Isolated from Human Skin
September 4, 2008 | Comments Off
From Here :
An unusual dermatophyte was isolated from the plantar scales of a human immunodeficiency virus-positive man with tinea pedis. Morphology, physiology, and molecular data provided evidence to support the new species Trichophyton eboreum. This dermatophyte is characterized by rapid growth on common mycological media, a flat powdery off-white colony, formation of clavate microconidia, smooth- and thin-walled cylindrical or club-shaped macroconidia with two to nine cells, the presence of hook-shaped hyphae, the production of cleistothecium-like structures and spiral hyphae in older cultures, positive hair perforation, the absence of pigmentation on potato glucose agar, the absence of a requirement for vitamins, a weak positive urease reaction, no growth at 37°C, resistance to 5% NaCl, resistance to fluconazole, good growth on human epidermal keratin, and the production of various enzymes on different media by the API-ZYM test. More than 5% divergence from any known species of dermatophyte was revealed by sequence analysis of the internal transcribed spacer of the rRNA gene.
Aug
24
Morgellons: Growth Captured
August 24, 2008 | Comments Off
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.
Aug
20
Lifestyle and Genome evolution in vector borne Bacteria
August 20, 2008 | Comments Off
Lifestyle Evolution in Alpha-Proteobacteria
Interestingly, species from a group called Ochrobactrum, which is most closely related to Brucella has been isolated from an astonishing number of different sources…..For example, Ochrobactrum is frequently isolated from Humans for which it is considered an opportunistic pathogen.
Moreover, two species have been shown to form associations with the nematode pathogen and insect - symbiont P. Luminescens in its nematode host…and another is a nitrogen fixing symbiont of Anaplasma……Ochrobactrum species have been described as free living, but since the majority of isolates are from patients, and since most environmental strains are from the Rhizosphere, this description may not be entirely correct…
Other related species of Alpha-Proteobacteria include :
Bartonella, Brucella, Ochrobactrum, Mesorhizobium, Agrobacterium, Sinorhizobium, Rhodopseudomonas, Bradyrhizobium, Gaulobacter, Rickettsia, Wolbachia, Anaplasma and Erlichia
Aug
19
Ochrobactrum anthropi pseudobacteraemias
August 19, 2008 | Comments Off
Ochrobactrum anthropi pseudobacteraemias
About 95 blood isolates of Ochrobactrum anthropi have been referred for identification and/or typing over the past two years, originating from 30 hospitals in England and Wales.
Ochrobactrum anthropi is an oxidase-positive, motile, non-lactose fermenting Gram-negative bacillus, formerly known as Achromobacter sp.
It is normally found in the natural environment, sometimes acting as an opportunist pathogen in humans. About 40 of the isolates from nine of the referring hospitals were indistinguishable on pulsed-field gel electrophoresis (PFGE). No other PFGE profile was seen in more than one hospital, although there were 20 different distinguishable patterns for the other isolates of O. anthropi. Most, if not all, of the indistinguishable isolates were of doubtful clinical significance and appear to be pseudobacteraemias, often occurring in patients who were otherwise very ill.
This can clearly have an impact on the management of these patients. More than one blood culture system has been involved.
The Communicable Disease Surveillance Centre (CDSC) and Central Public Health Laboratory (CPHL) have been asked to investigate these apparent pseudobacteraemia incidents in order to identify any potential source of contamination. It would be helpful if microbiologists could discuss any further testing for possible O. anthropi pseudobacteraemia isolates with Polly Kaufmann from the Laboratory of Hospital Infection, Central Public Health Laboratory, Colindale (tel 020 8200 4400 ext 4205 email PKaufmann@phls.org.uk).
In some instances these organisms have been mis-identified as Pseudomonas stutzeri or Stenotrophomonas maltophilia, and they have also sometimes been found in mixed culture with S. maltophilia.
Aug
19
Ochrobactrum was found to be closely related to Brucella
August 19, 2008 | Comments Off
AFLP was used to analyze the genetic diversity among Ochrobactrum strains. AFLP patterns showed a great genomic variability that separated the samples into three distinct clusters.
Ochrobactrum intermedium was found to be closely related to Brucella abortus S99.
Ochrobactrum spp. are potential human pathogens. Ochrobactrum anthropi bacteremia is usually associated with contaminated intravenous lines in immunocompromised human patients, water sources, and environmental conditions in hospitals (1, 5, 8, 10, 11). O. anthropi isolates have also recently been obtained from other sources such as water, concrete, soils, termites, feces, activated sludges, oil spills, etc. Many of these isolates present interesting degradative properties not only towards multiple antibiotics but also towards herbicides, hemicellulose, anthracene, and other complex organic molecules including crude oil (2-5, 8, 12, 15, 17, 19, 25), displaying an opportunism that allows them to succeed in a wide range of environments.
Aug
19
Ochrobactrum spp. are human opportunist pathogens
August 19, 2008 | Comments Off
Bacteria naturally associated with the symbiont Photorhabdus luminescens subsp. akhurstii were isolated from the entomopathogenic nematode Heterorhabditis indica. Bacterial isolates distinct from P. luminescens subsp. akhurstii were obtained from 33% of the samples. Fourteen bacterial isolates, from nematodes collected from three different Caribbean islands, were characterized by conventional phenotypic tests, restriction fragment length polymorphism and sequence analyses of PCR-amplified 16S rRNA genes (16SrDNAs).
Isolates were grouped into three genotypes, each one being associated with one Caribbean island. Phenotypic characteristics and 16S rDNA analysis showed that the Photorhabdus-associated bacteria were closely related to Ochrobactrum anthropi for the group from Guadeloupe, and to Ochrobactrum intermedium for the two groups from the Dominican Republic and Puerto Rico. No pathogenicity of the Ochrobactrum spp. to the insects Galleria mellonella and Spodoptera littoralis (Lepidoptera) was detected.
Since Ochrobactrum spp. are considered as human opportunist pathogens, the mass production of entomopathogenic nematodes for biological control requires strict vigilance.
Aug
19
The genome sequence of Bacillus anthracis Ames and comparison to closely related bacteria
August 19, 2008 | Comments Off
Bacillus anthracis is an endospore-forming bacterium that causes inhalational anthrax. Key virulence genes are found on plasmids (extra-chromosomal, circular, double-stranded DNA molecules) pXO1 (ref. 2) and pXO2 (ref. 3). To identify additional genes that might contribute to virulence, we analysed the complete sequence of the chromosome of B. anthracis Ames (about 5.23 megabases). We found several chromosomally encoded proteins that may contribute to pathogenicity–including haemolysins, phospholipases and iron acquisition functions–and identified numerous surface proteins that might be important targets for vaccines and drugs. Almost all these putative chromosomal virulence and surface proteins have homologues in Bacillus cereus, highlighting the similarity of B. anthracis to near-neighbours that are not associated with anthrax. By performing a comparative genome hybridization of 19 B. cereus and Bacillus thuringiensis strains against a B. anthracis DNA microarray, we confirmed the general similarity of chromosomal genes among this group of close relatives. However, we found that the gene sequences of pXO1 and pXO2 were more variable between strains, suggesting plasmid mobility in the group. The complete sequence of B. anthracis is a step towards a better understanding of anthrax pathogenesis.
Aug
19
Glowing Insect Bug - Harms Humans
August 19, 2008 | Comments Off
A new disease has been identified caused by a luminous bug that has evolved in insects, scientists say.
There have been about a dozen cases of the bug - Photorhabdus asymbiotica - in the US and Australia, which causes pustulant sores to appear on the body.
In insects, the disease leaves the bodies glowing, the University of Bath and London School of Hygiene and Tropical Medicine scientists said.
They are now warning more insect bugs may mutate to threaten humans.
Aug
19
Nematode Symbiont for Photorhabdus asymbiotica
August 19, 2008 | Comments Off
Photorhabdus asymbiotica is an emerging bacterial pathogen that causes locally invasive soft tissue and disseminated bacteremic infections in the United States and Australia.
Although the source of infection was previously unknown, we report that the bacterium is found in a symbiotic association with an insect-pathogenic soil nematode of the genus Heterorhabditis.
From Here :
Photorhabdus are the only known terrestrial bioluminescent bacteria. Most members of the Photorhabdus are however insect pathogens that live in a strict symbiotic relationship within the guts entomopathogenic Heterorhabditid nematodes. Infective juvenile nematodes search in the soil for insect prey until they encounter a suitable host. They then scratch their way into the insect’s hemocoel (an “open” blood system ) and “vomit” up Photorhabdus cells directly into the blood. The Photorhabdus then set up a lethal septicemia, secreting toxins and virulence factors that rapidly kill the insect host. The bacteria replicate rapidly and bio-convert the insect tissues into more bacteria that serve as a food source for the reproducing nematodes. It is around the time of insect death that the bioluminescence of the insect corpse can be seen.
Aug
18
Bacillus cereus can cause local skin and wound infections
August 18, 2008 | Comments Off
From Here :
Bacillus cereus also can cause local skin and wound infections, ocular infections, fulminant liver failure, and invasive disease, including bacteremia, endocarditis, osteomyelitis, pneumonia, brain abscess, and meningitis.
Ocular involvement includes panophthalmitis, endophthalmitis, and keratitis.
Aug
18
Outbreak of Cutaneous Bacillus Cereus Infections
August 18, 2008 | Comments Off
The findings in this report indicate that immunocompetent persons can be vulnerable to cutaneous B. cereus infections when skin is compromised. Isolation of three indistinguishable B. cereus isolates from three patients on two separate days suggested that this was a common-source outbreak and not a laboratory contaminant, even though the environmental source of B. cereus was not identified during the investigation. All but five cases were diagnosed on two concurrent days, making person-to-person transmission unlikely. Transmission most likely occurred from an exposure at the beginning of the orientation week. The short haircut likely caused microabrasions, compromising the protective effect of scalp epidermis. Exposure to mud, sun, and sunscreen further provided an environment suitable for bacterial growth.
Aug
18
Bacillus Cereus
August 18, 2008 | Comments Off
Bacillus cereus is a Gram-positive, facultatively aerobic sporeformer whose cells are large rods and whose spores do not swell the sporangium. These and other characteristics, including biochemical features, are used to differentiate and confirm the presence B. cereus, although these characteristics are shared with B. cereus var. mycoides, B. thuringiensis and B. anthracis. Differentiation of these organisms depends upon determination of motility (most B. cereus are motile), presence of toxin crystals (B. thuringiensis), hemolytic activity (B. cereus and others are beta hemolytic whereas B. anthracis is usually nonhemolytic), and rhizoid growth which is characteristic of B. cereus var. mycoides.
In the past decade, outbreaks of human illness associated with the consumption of raw vegetables and fruits (or unpasteurized products produced from them) have increased in the United States. Pathogens such as Listeria monocytogenes, Clostridium botulinum, and Bacillus cereus are naturally present in some soil, and their presence on fresh produce is not rare. Salmonella, Escherichia coli O157:H7, Campylobacter jejuni, Vibrio cholerae, parasites, and viruses are more likely to contaminate fresh produce through vehicles such as raw or improperly composted manure, irrigation water containing untreated sewage, or contaminated wash water. Treatment of produce with chlorinated water reduces populations of pathogenic and other microorganisms on fresh produce but cannot eliminate them. Reduction of risk for human illness associated with raw produce can be better achieved through controlling points of potential contamination in the field; during harvesting; during processing or distribution; or in retail markets, food-service facilities, or the home
Aug
17
Alcohols in skin disinfectants increase biofilm expression of S.epidermidis
August 17, 2008 | Comments Off
The pathogenesis of Staphylococcus epidermidis is correlated with biofilm formation. We investigated the effect of three common alcoholic skin disinfectants, ethanol, n-propanol and isopropanol, on the biofilm formation of 37 clinical, icaADBC-positive S. epidermidis isolates. In alcohol-supplemented media 18 strains displayed increased biofilm expression. Sixteen of 19 strains were generally incapable of biofilm formation. In three representative isolates, the increase in biofilm formation was paralleled by increased polysaccharide intercellular adhesin synthesis. Regarding the widespread use of alcoholic skin disinfectants, it is possible that the alcohol-inducible biofilm phenotype of S. epidermidis could add to the development of foreign body-related infections
Aug
15
Cercarial Dermatitis
August 15, 2008 | Comments Off
From Here :
Avian schistosomes are the primary causative agent of cercarial dermatitis in humans, but despite its worldwide occurrence, little is known of the immune mechanism of this disease. Using a murine model, hosts were exposed to primary (1x) and multiple (4x) infections of Trichobilharzia regenti via the pinna. Penetration of larvae into the skin evoked immediate edema, thickening of the exposure site, and an influx of leukocytes, including neutrophils, macrophages, CD4+ lymphocytes, and mast cells.
More research from the Czech Republic indicating that this problem may be more widespread and damaging to humans and other mammals than at first thought.
Horák P, Kolárová L, Adema CM.
Department of Parasitology, Charles University, Vinicná 7, CZ-12844 Prague 2, Czech Republic.
Trichobilharzia is the largest genus within the family Schistosomatidae, covering over 40 species of avian parasites. To clarify the existing confusion in the systematics of the genus, we recommend combining knowledge of life cycles and developmental stages, snail/bird hosts, cytogenetical and molecular data together with morphological criteria for the characterization of particular species. The high specificity of Trichobilharzia for the intermediate host is a likely reflection of the ability to avoid the internal defence of specific snails. The spectrum of final hosts (birds) seems to be much wider. The infection of birds–trichobilharziasis–may lead to considerable tissue injuries, caused by eggs of the parasite or migration of immature/mature worms through the body. Most Trichobilharzia (visceral species) migrate through the viscera of the host, but nasal species display a neurotropic mode of migration. Due to a low specificity of penetrating cercariae, mammals (including humans) can be attacked. This leads to cercarial dermatitis, predominantly in sensitized hosts. Experimental infections indicate that Trichobilharzia never mature in an incompatible (mammalian) host. However, not all cercariae and schistosomula are necessarily trapped and eliminated in the skin, and parasites may migrate throughout the viscera and the nervous system of mammals. These findings suggest that the pathogenicity of Trichobilharzia may have been underestimated in the past and health risks associated with trichobilharziasis need to be studied further.
Aug
7
Bacillus Subtilis Macrofibers
August 7, 2008 | Comments Off
Abstract : From Here
Growing Bacillus subtilis macrofibers use twist and supercoiling to: power their own selfassembly, join fibers together into multiclonal aggregates, move themselves over solid surfaces, and to drag 2 other structures (cargo) over solid surfaces.
The dragging of multiclonal aggregates attached to the ends of growing macrofibers is analyzed here. The linkage between fibers and cargo arose naturally in macrofiber cultures. Dragging was triggered when growing macrofibers became linked to cargo at both of their ends.
Such macrofibers supercoiled, reduced their length, and dragged the cargo toward one another. In parallel experiments immobile wire was used in place of cargo at one end of macrofibers that were linked to cargo at the other. The cargo was dragged toward the wire when these fibers supercoiled. To estimate the force required for dragging we determined the dimensions of the cargo, the buoyant density of macrofibers in the growth medium where dragging occurred, the rate and distance over which the aggregate structures were dragged, and the viscosity of the growth medium. Friction resulting from contact with the solid surface over which the structures were dragged was estimated using the measured parameters. The results indicate that the supercoiling tension required to overcome limiting friction must have been approximately 10 nN, while that needed to overcome fluid drag was of the order of 1 nN. These values suggest that only a small fraction of the total power available from macrofiber supercoiling was needed to drive this new form of multicellular bacterial movement.
Keywords: Macrofibers; Supercoiling forces; Dragging over surfaces; Bacillus subtilis
Jul
30
Antimicrobics and Infectious Disease Newsletter (Elsevier Science) 1999; 17(11): 81-88.
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.
Bibliography
Ainsworth JG, Katseni V, Hourshid S; et al.: Mycoplasma fermentans and HIV-associated nephropathy. J Infect 29:323-326, 1994.
Baseman JB, Lange M, Criscimagna NL, Giron JA, Thomas CA: Interplay between mycoplasmas and host target cells. Micro Pathogenes 19:105-116, 1995.
Baseman JB, Reddy SP, Dallo SF: Interplay between mycoplasma surface proteins, airway cells, and the protean manifestations of mycoplasma-mediated human infections. Am J Resp Crit Care Med 154:S137-144, 1996.
Baseman JB, Tully JG: Mycoplasmas: Sophisticated, reemerging, and burdened by their notoriety. Emerg Infect Dis 3:21-32, 1997.
Binder A, Runge M, Meier B, Jacobs R, Busche K: Pathogenic mechanisms in the Mycoplasma arthritidis polyarthritis of rats. Rheumatol Int 9:193-196, 1989.
Blanchard A, Hamrick W, Duffy L, Baldus K, Cassell GH: Use of the polymerase chain reaction for detection of Mycoplasma fermentans and Mycoplasma genitalium in the urogenital tract and amniotic fluid. Clin Infect Dis 17:S272-S279, 1993.
Blanchard A, Montagnier L: Blanchard A, Montagnier L: AIDS-associated mycoplasmas. Ann Rev Microbiol 48:687-712, 1994.
Bonilla HF, Chenoweth CE, Tully JG, et al.: Mycoplasma felis septic arthritis in a patient with hypogammaglobulinemia. Clin Infect Dis 24:222-225, 1997.
Brenner C, Wróblewski H, Le Henaff M, Montagnier L, Blanchard A: Spiralin, a mycoplasmal membrane lipoprotein, induces T-cell-independent B-cell blastogenesis and secretion of proinflammatory cytokines. Infect Immun 65:4322-4329, 1997.
Busolo F, Camposampiero D, Bordignon G, Bertollo G: Detection of Mycoplasma genitalium and Chlamydia trachomatis DNAs in male patients with urethritis using the polymerase chain reaction. New Microbiol 20:325-332, 1997.
Cassell GH: Infectious causes of chronic inflammatory diseases and cancer. Emerg Infect Dis 4:475-487, 1998.
Cimolai N, Wensley D, Seear M, Thomas ET: Mycoplasma pneumoniae as a cofactor in severe respiratory infections. Clin Infect Dis 21:1182-1185, 1995.
Citti C, Rosengarten R: Mycoplasma genetic variation and its implication for pathogenesis. Wien Klin Wochenschr 109:562-568, 1997.
Fairley CK, Ryan M, Wall PG, Weinberg J: The organisms reported to cause infective myocarditis and pericarditis in England and Wales. J Infection 32:223-225, 1996.
Fernandez C, Alvarez K, Muy L, Martinez M: Detection using molecular biology techniques of Mycoplasma hominis and Ureaplasma urealyticum in urogenital samples. Rev Argent Microbiol 30:53-58, 1998.
Frisch M, Gradehandt G, Muhlradt PF: Mycoplasma fermentans-derived lipid inhibits class II major histocompatibility complex expression without mediation by interleukin-6, interleukin-10, tumor necrosis factor, transforming growth factor-beta, type I interferon, prostaglandins or nitric oxide. Eur J Immunol 26:1050-1057, 1996.
Furr PM, Taylor-Robinson D. Webster ADB: Mycoplasmas and ureaplasmas in patients with hypogamaglobulinemia and their roll in arthritis: microbiological observation over twenty years. Ann Rheum Dis 53:183-187, 1994.
Gendrel D, Raymond J, Moulin F, et al.: Etiology and response to antibiotic therapy of community-acquired pneumonia in French children. Eur J Clin Microbiol Infect Dis 16:388-391, 1997.
Gil JC, Cedillo RL, Mayagoitia BG, Paz MD: Isolation of Mycoplasma pneumoniae from asthmatic patients. Ann Allergy 70:23-25, 1993.
Gogate A, Deodhar LP, Shah PK, Vaidya P: Detection of Chlamydia trachomatis antigen and Toxoplasma gondii (IgM) and Mycoplasma hominis (IgG) antibodies by ELISA in women with bad obstetric history. Indian J Med Res 100:19-22, 1994.
Grau O, Slizewicz B, Tuppin P, et al.: Association of Mycoplasma penetrans with human immunodeficiency virus infection. J Infect Dis 172: 672-681, 1995.
Gray GC, Duffy LB, Paver RJ, Putnam SD, Reynolds RJ, Cassell GH: Mycoplasma pneumoniae: A frequent cause of pneumonia among U.S. marines in southern California. Mil Med 162:524-526, 1997.
Haier J, Nasralla M, Franco AR, Nicolson GL: Detection of mycoplasmal infections in blood of patients with rheumatoid arthritis. Rheumatol 38:504-509, 1999.
Himmelreich R, Plagens H, Hilbert H, Reiner B, Herrmann R: Comparative analysis of the genomes of the bacteria Mycoplasma pneumoniae and Mycoplasma genitalium. Nucl Acids Res 25:701-712, 1997.
Jacobs E: Mycoplasma infections of the human respiratory tract. Wien Klin Wochenschr 109:574-577, 1997.
Jacobs E: Mycoplasma pneumoniae virulence factors and the immune response. Rev Infect Dis 12:338-353, 1991.
Kaneoka H, Naito S: Superantigens and autoimmune diseases. Japan. J Clin Med 6:1363-1369, 1997.
Kok T, Higgins G: Prevalence of respiratory viruses and Mycoplasma pneumoniae in sputum samples from unselected adult patients. Pathology 29:300-302, 1997.
Komada Y, Zhang XL, Zhou YW, Ido M, Azuma E: Apoptotic cell death of human T lymphoblastoid cells induced by arginine deiminase. Int J Hematol 65:129-141, 1997.
Kraft M, Cassell GH, Henson JE, Watson H, Williamson J, Marmion BP: Detection of Mycoplasma pneumonia in the airways of adults with chronic asthma. Am J Resp Crit Care Med 158:998-1001, 1998.
Kusunoki S, Chiba A, Hitoshi S, Takizawa H, Kanazawa I: Anti-Gal-C antibody in autoimmune neuropathies subsequent to mycoplasma infection. Muscle Nerve 18:409-413, 1995.
Levi N, Prag J, Jensen JS, Schroeder TV, Lorenzten JE: Surgical infections with Mycoplasma: a brief review. J Royal College Surg Edinburgh 42:107-109, 1997.
Mardh PA, Elshibly S, Kallings I, Hellberg D: Vaginal flora changes associated with Mycoplasma hominis. Am J Obstet Gynecol 176:173-178, 1997.
Montagnier L, Blanchard A: Mycoplasmas as cofactors in infection due to the immunodeficiency virus. Clin Infect Dis 17:S309-315, 1993.
Muhlradt PF, Kiess M, Meyer H, Sussmuth R, Jung G: Isolation, structure elucidation, and synthesis of a macrophage stimulatory lipopeptide from Mycoplasma fermentans acting at picomolar concentration. J Exp Med 185:1951-1958, 1997.
Nasralla M, Haier J, Nicolson GL: Multiple mycoplasmal infections detected in blood of Chronic Fatigue and Fibromyalgia Syndrome patients. Eur J Clin Microbiol Infect Dis 18:359-365, 1999.
Nicolson GL, Nicolson NL: Diagnosis and treatment of mycoplasmal infections in Persian Gulf War Illness-CFIDS patients. Int J Occup Med Tox 5:69-78, 1996.
Nicolson GL: Considerations when undergoing treatment for chronic infections found in Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Gulf War Illnesses. (Part 1). Antibiotics Recommended when indicated for treatment of Gulf War Illness/ CFIDS/FMS (Part 2). Intern J Med 1:115-117, 123-128, 1998.
Nicolson GL: The role of microorganism infections in chronic illnesses: support for antibiotic regimens. CFIDS Chron 12(3):19-21, 1999.
Nicolson GL, Nasralla M, Franco AR, De Meirlier K, Nicolson NL, Ngwenya R, Haier J: Mycoplasmal infections in chronic diseases. J Chronic Fatigue Syndr 6:in press, 1999.
Nicolson GL, Nasralla MY, Haier J, Erwin R, Nicolson NL, Ngwenya R: Mycoplasmal infections in chronic illnesses: Fibromyalgia and chronic fatigue syndromes, Gulf War illness, HIV-AIDS and rheumatoid arthritis. Med Sentinal 4:172-176, 1999.
Nicolson GL, Nasralla M, Haier J, Nicolson NL: Diagnosis and treatment of chronic mycoplasmal infections in fibromyalgia and chronic fatigue syndromes: Relationship to gulf war illness. Biomed Therapy 16:266-271, 1998.
Paddenberg R, Wulf S, Weber A, Heimann P, Beck LA, Mannherz HG: Internucleosomal DNA fragmentation in cultured cells under conditions reported to induce apoptosis may be caused by mycoplasma endonucleases. Eur J Cell Biol 71:105-119, 1996.
Pollack JD, Williams MV, McElhaney RN: The comparative metabolism of the Mollicutes (Mycoplasmas): the utility for taxonomic classification and the relationship of putative gene annotation and phylogeny to enzymatic function in the smallest free-living cells. Crit Rev Microbiol 23:269-354, 1997.
Posnett DN, Hodtsev AS, Kabak S, et al.: Interaction of Mycoplasma arthritidis superantigen with human T cells. Clin Infect Dis 17:S170-175, 1993.
Prattichizzo FA, Simonetti I, Galetta F: Carditis associated with Mycoplasma pneumoniae infection. Clinical aspects and therapeutic problems. Minerva Cardioangiol 45:447-450, 1997.
Rawadi G, Roman-Roman S, Castedo M, et al: Effects of Mycoplasma fermentans on the myelomonocytic lineage. Different molecular entities with cytokine-inducing and cytocidal potential. J Immunol 156:670-678, 1996.
Razin S: Comparative genomics of mycoplasmas. Wien Klin Wochenschr 109:551-556, 1997.
Razin S: Molecular biology and genetics of mycoplasmas (Mollicutes) Microbiol Rev 49:419-455, 1985.
Rossi OV, Kinnula VL, Tuokko H, Huhti E: Respiratory viral and mycoplasma infections in patients hospitalized for acute asthma. Monaldi Arch Chest Dis 49:107-111, 1994.
Schaeverbeke T, Renaudin H, Clerc M, et al.: Systematic detection of mycoplasmas by culture and polymerase chain reaction (PCR) procedures in 209 synovial fluid samples. Brit J Rheumatol 36:310-314, 1997.
d arthritis. Rev Rheum Engl Ed 64:120-128, 1997.
Sharma S, Brousseau R, Kasatiya S: Detection and confirmation of Mycoplasma pneumoniae in urogenital specimens by PCR. J Clin Microbiol 36:277-280, 1998.
Shibata K, Hasebe A, Sasaki T, Watanabe T: Mycoplasma salivarium induces interleukin-6 and interleukin-8 in human gingival fibroblasts. FEMS Immunol Med Microbiol 19:275-283, 1997.
Shibata K, Watanabe T: Mycoplasma fermentans enhances concanavalin A-induced apoptosis of mouse splenic T cells. FEMS Immunol Med Microbiol 17:103-109, 1997.
Stadtlander CTKH, Watson HL, Simecka WJ, Cassell GH: Cytopathogenicity of Mycoplasma fermentans (including strain incognitus). Clin Infect Dis 17:S289-301, 1993.
Stratton CW, Mitchell WM: The pathogenesis of Chlamydia species. Antimicrob Infect Dis Newsl 15:83-88, 1996.
Taylor-Robinson D; Furr PM: Genital mycoplasma infections. Wien Klin Wochenschr 109:578-583, 1997.
Wise KS: Adaptive surface variation in mycoplasmas. Trends Microbiol 1:59-63, 1993.
Wohlman A, Gallily R, Yirmiya R, Weidenfeld J: Characterization of the effect of Mycoplasma fermentans on the hypothalamo-pituitary-adrenal axis. Neuroendocrinol 66:221-228, 1997.
Zhang Q, Wise KS: Molecular basis of size and antigenic variation of a Mycoplasma hominis adhesin encoded by divergent vaa genes. Infect Immun 64:2737-2744, 1996.
Jul
28
Capnine - Bio-Film’s Dirty Little Secret
July 28, 2008 | Leave a Comment
I immediately knew we had something very important here, and when I researched these special “gliding” bacteria, which move by gliding, perhaps like a snail, rather than by whipping flagella like the common blood-borne bacterial species, I realised we had hit mother-lobe.
Associated with the gliding motion is a unique lipid called capnine, a highly charged lipid, and one which is a strong inhibitor (antagonist) of VDR transcriptional activity.
It really doesn’t matter whether these gliding bacteria harm the body in any other way, by shutting down the AMPs they create an environment where a plethora of other bacteria and viral pathogens can weave their nasty ways upon the host.
Jul
27
C.Pneumoniae & Eye Infections
July 27, 2008 | Leave a Comment
Similarly, researchers at the Massachusetts Eye and Ear Infirmary found Chlamydia pneumoniae present in the diseased eye tissue of five out of nine people with age-related macular degeneration (AMD) - a disease in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thinning, atrophy, and in some cases bleeding. However, the bacterium was not found in the eyes of more than 20 individuals without AMD.
Jul
27
Understanding L-form Bacteria
July 27, 2008 | Leave a Comment
In a 2006 the Centers for Disease Control and Prevention (CDC) released a paper stating, “Infectious agents have emerged as notable determinants, not just complications, of chronic diseases. To capitalize on these opportunities, clinicians, public health practitioners, and policymakers must recognize that many chronic diseases may indeed have infectious origins.”
According to the CDC, infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated. In fact, they argue that the potential to avoid or minimize chronic disease by preventing or treating infections may yet be substantially underestimated. Those of us familiar with the Marshall Protocol know that they are absolutely correct.
Jul
13
Wound Healing - Manuka Honey
July 13, 2008 | Leave a Comment
From Here :
and on video here :
Jul
8
Biofilm Image showing Diatoms & Bacteria
July 8, 2008 | Leave a Comment
Jun
28
A certain clone of Borrelia burgdorferi….
June 28, 2008 | Leave a Comment
Newswise — Benjamin Luft, M.D., Professor of Medicine, Stony Brook University Medical Center, and colleagues discovered that a certain clone of Borrelia burgdorferi, the spirochete that causes Lyme disease, appears to be the most common strain causing Lyme disease in North America and Europe, and may account for the increase in cases for the past 20 years. Their investigation and findings of the ospC-A clone are reported in the July 2008 issue of Emerging Infectious Diseases, which is currently available on line Here :
According to Dr. Luft, Lyme disease is the most common vector-borne disease in the United States with more than 20,000 cases reported annually. While B. burgdorferi is the primary pathogen in the United States, clones of the pathogen are known to cause major disease. The ospC-A clone was one of the first strains ever identified.
In “Wide Distribution of a High-Virulence Borrelia burgdorferi Clone in Europe and North America,” Dr. Luft and colleagues detail various methods of genetic testing of 68 B. burgdorferi isolates from Europe and North America. Based on the findings of their tests, the researchers concluded that the ospC-A clone dispersed rapidly and widely in the recent past and in both regions of the world.
“I believe this discovery will make an important contribution since it identifies an identical and high virulence clone of Borrelia in both Europe and North America,” said Dr. Luft. “This may explain the recent spread of Lyme disease in North America.”
Jun
20
National Pure Water Association
June 20, 2008 | Leave a Comment
UK campaign for clean drinking water.
Jun
20
Flouride - Poison in our water
June 20, 2008 | Leave a Comment
Artificial fluoridation involves increasing the fluoride level in water supplies to one part per million (ppm). Fluoride’s toxicity lies somewhere between that of lead and arsenic, and, like lead and arsenic, it’s a cumulative poison. Only half of all the fluoride we ingest is excreted. Our bodies retain the other half. It is stored, mainly in bone but also in some soft tissues, such as the pineal gland.
Naturally occurring fluoride is commonly bound to calcium and is less bioavailable than the fluoride added by water companies to treat their customers, which comes from fluorosilicic acid. The fluorosilicic acid used in the UK and Ireland is believed to originate from phosphate fertiliser operations in continental Europe. The UK Department of the Environment will not name the producers.
Worldwide, some 350 million people receive artificially fluoridated water, representing just six per cent of the global population. Of this global total, 171 million are Americans; only two per cent of Europeans receive fluorosilicic acid on tap, comprising around 5.7 million in Britain and around 2.4 million in Ireland. In addition, World Health Organization figures show that dental health has improved as much in countries without fluoridation as in those with fluoridation.
The US Centers for Disease Control stated in 1999 that fluoride’s anti-caries effect was topical, not systemic, confirming that we do not need to ingest fluoride.
Jun
16
More Important to the Body than MMS
June 16, 2008 | Leave a Comment
Interesting Site.
From Here :
Even though there are common threads to all disease pathologies, in no way would I want any reader to think that MMS is a “one-stop” wonder with respect to helping mitigate and ameliorate said conditions. It is, however, an indispensable component that should be part of anyone’s health and well-being “tool box.”
Jun
9
Hydrogels
June 9, 2008 | Leave a Comment
Hydrogels are three-dimensional, hydrophilic, polymeric networks capable of imbibing large amounts of water or biological fluids. The networks are composed of homopolymers or copolymers, and are insoluble due to the presence of chemical crosslinks (tie-points, junctions), or physical crosslinks, such as entanglements or crystallites. Hydrogels exhibit a thermodynamic compatibility with water, which allows them to swell in aqueous media. They are used to regulate drug release in reservoir-based, controlled release systems or as carriers in swellable and swelling-controlled release devices. On the forefront of controlled drug delivery, hydrogels as enviro-intelligent and stimuli-sensitive gel systems modulate release in response to pH, temperature, ionic strength, electric field, or specific analyte concentration differences. In these systems, release can be designed to occur within specific areas of the body (e.g., within a certain pH of the digestive tract) or also via specific sites (adhesive or cell-receptor specific gels via tethered chains from the hydrogel surface). Hydrogels as drug delivery systems can be very promising materials if combined with the technique of molecular imprinting.
Jun
7
Image - Red & Blue Fibres
June 7, 2008 | Leave a Comment
From my Eye :
Jun
6
Treat Lyme Disease with Chinese Herbal Medicines
June 6, 2008 | Leave a Comment
A silent epidemic is ravaging our people, inflicting a large and harrowingly complex group of symptoms including arthritic conditions, autoimmune conditions, cognitive problems, and many more. This quiet, nearly undetectable bacterial pathogen has infected millions, and most of them don’t even know it. This disease has been identified as the fastest-growing infectious disease in the US, as well as the number-one insect-borne pathogen in the US. Yet this only represents the known cases of a disease that is known to be dramatically under-reported, under-diagnosed, and very difficult to both detect and treat. Up to one-half the population may have been exposed to this disease, according to Lyme disease expert Dietrich Klinghardt, MD, of Seattle, WA.
and more here :
Jun
4
Under our Skin
June 4, 2008 | Leave a Comment
A dramatic tale of microbes, medicine and money, this eye-opening film investigates the untold story of Lyme disease, an emerging epidemic larger than AIDS. Each year thousands go undiagnosed or misdiagnosed, told that their symptoms are “all in their head.” Following the stories of patients and physicians as they battle for their lives and livelihoods, the film brings into focus a haunting picture of our health care system and its ability to cope with a silent terror under our skin.
Jun
3
Breakspear Hospital
June 3, 2008 | Leave a Comment
Unfortunately the many common symptoms lead to many cases of borreliosis being undiagnosed or misdiagnosed. Many undiagnosed sufferers have been told that the symptoms are just in their heads.
The standard investigations at Breakspear Hospital for borreliosis are:
Borrelia antibody evaluation by ELISA technique, which measures antibodies to the organism.
Polymerase Chain Reaction test for Borrelia burgdorferi, which measures the presence of the DNA – the chromosomes of the organism from the patient.
Lymphocyte Transformation Test for Borrelia burgdorferi (LTT MELISA), which, if the results are positive, demonstrates current active infection with the organism.
Borrelia burgdorferi IgG and IgM antibody evaluation by the Immunoblot/Western Blot technique, which detects portions of the Lyme disease organism.
Bowen test, which provides rapid identification of Borrelia burgdorferi (RIBb) and is a research test being undertaken in a laboratory in the United States.
There are other investigations that may be undertaken. Tests of specific Lyme related lymphocyte reactions can be performed. The outer surface peptides often camouflage the organisms and reactions to these may be evaluated. We can also measure co-factor infections of Borrelia.
Jun
3
Toxicity of Titanium
June 3, 2008 | Leave a Comment
Titanium may not be the inert, harmless metal that it was once thought to be.
Titanium has historically maintained the reputation of being an inert, and relatively biocompatible metal, suitable for use as both a medical and dental prosthesis. There are many articles supporting these beliefs, but more recently, there is scientific evidence that titanium, or its corrosion by-products, may cause harmful reactions after traveling through the circulatory, or lymphatic systems. These corrosion by-products can cause reactions in the blood, fibrotic tissue, and in the osteogenic cells.
Jun
1
New UK site
June 1, 2008 | Leave a Comment
A Promising looking site for UK and world wide sufferers of Morgellons…
They are especially keen to hear from:
Members of the public that are personally affected by Morgellons.
General Practioners and other Health care professionals.
Consultants; Dermotologists, Infectious disease specialists.
Scientists of various disciplines, involved in research; Microbiologists, Parasitologists etc.
Department of Health and DEFRA officials.
Politicians (Councillors/Members of Parliment).
Vets.
Environmental Health officers, inc. pollution control and Pest control professionals.
Water Authorities, dealing with wastewater and sewage.
Go Here Please.
| M | T | W | T | F | S | S |
|---|---|---|---|---|---|---|
| « Nov | ||||||
| 1 | 2 | 3 | 4 | 5 | ||
| 6 | 7 | 8 | 9 | 10 | 11 | 12 |
| 13 | 14 | 15 | 16 | 17 | 18 | 19 |
| 20 | 21 | 22 | 23 | 24 | 25 | 26 |
| 27 | 28 | 29 | 30 | |||
Links
- Alliance for Natural Health
- Andy Coyle UK
- Carnicom
- CCID
- Center for Disease Control USA
- Charles E. Holman Foundation
- Chlamydia Pneumoniae Info
- Cliff Mikelson’s Forum
- DSP
- GMContaminationRegister
- Health Protection Agency UK
- ISIS
- LDA - UK Lyme Information
- Lymebusters
- LymeNet
- LymePhotos
- MMS
- Morgellons - Canada
- Morgellons Exposed
- Morgellons Research Foundation
- Morgellons Sanctum
- Morgellons UK
- Morgellons-Research
- Morphborgs
- National Geographic
- Natural News
- Neuro-Cutaneous Syndrome
- New Morgellons Order
- Oklahoma State University
- SilentSuperbug
- The Sunshine Project
- Union of Concerned Scientists