May

24

Oral Spirochetes

May 24, 2009 | Comments Off

p_gingivalis.jpg

From Here :

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

mouthspirochete.jpg
Trepenoma dentricola. Image by Joe Dixon, 2007. From here :
bforsythus.jpg
B.forsythus

More on P.Gingivalis pathogenesis.From Here :

May

24

From Here :

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

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

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

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

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

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

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

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

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

Psychological Phenomena

The fitness load approach also applies to psychological phenomena.

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

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

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

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

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

May

12

From Here :

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

May 2009
M T W T F S S
« Apr   Jun »
 123
45678910
11121314151617
18192021222324
25262728293031

Links