--> Cancer, Stealth Microbe

Mark Peters gquest at nol.net
Sun Nov 17 23:22:24 EST 1996


STEALTH MICROBE CAUSES CANER


There are two basic forms of carcinogens (cancer causers):

EPIGENETIC -   carcinogens that  do not directly damage DNA but cause
alterations such as hormonal derangements, immunosuppression or chronic
tissue injury that in turn predisposes to cancer.

GENOTOXIC  -   Carcinogens that react directly with DNA or with
macromolucles that then react with DNA.

     The Stealth Microbe damages tissue by its presence, and alters
hormone balance, and causes immunosuppression .   The Stealth Microbe
can cause the formation of the carcinogen NMBA  by cell-mediated
catalysis. 
Also he Stealth Microbe secretes organic acids during carbohydrate
metabolism that can result in spontaneous nitrosation of the carcinogen
NMBA..  The Stealth Microbe is EPIGENETICALLY AND GENOTOXICALLY
CARCINOGENIC.


The rest of this document will be dedicated to medical research
that supports the statement that the stealth microbe causes
Cancer.


1980    Studies of a population with a high incidence of esophageal
carcinoma
showed that Stealth Microbe invasion was common in the esophageal
epithelium of patients with either premalignant changes or early
esophageal
carcinoma.  Nitrate and Nitrite were present in high concentrations in
the
water and staple grains.  This study established the ability of the
Stealth
Microbe to augment the nitrosative formation of the esophagus - specific
carcinogen benzylmethylnitrosamine (NBMA; N-nitroso-N-
methylbenzylamine).  Results showed that when there were more microbes
there was also more NBMA. Spontaneous nitrosation of BMA  was enhanced
under the acidic condidtions resulting from the acids secreted by the
Stealth
Microbe during Carbohydrate Metabolism.  Thus, the Stealth Microbe
invasion
into the epithelium could cause local formation of NBMA by both cell-
mediated catalysis and extracellular decreases in pH.

1987    From twelve cases of precancerous lesions, 21 strains of the
Stealth
Microbe were isolated belonging to 15 different biotypes.  Stealth
Microbes
obtained via biopsy were accessed for their ability to catalyze N-
nitrosobenzylmethylamine (NBMA) N-benylmethylamine and nitrite.  Strains
with the higher niltrosation potential were generally isolated from
lesions with
the more advanced precancerous changes.  This evidence supports the
hypothesis that the Stealth Microbe plays a causal role in the
development of
cancer, by means of endogenous nitrosamine production.  The microbe is
able to secrete organic acids during carbohydrate metabolism which
decreases the local pH and this results in a considerable increase in
the
microbes production of the carcinogen NBMA.

1994   "The study was aimed at determination of possible connection
between
co-existing S.M. infection in patients with lungcarcinoma with course of
neoplastic disease and ability to achieveremission by application of
different
methods of treatment. Thestudy involved 25 patients with histologically
confirmed lung carcinoma. Their sputum and bronchial rinsings were
tested.
The tests were performed at the moment of diagnosisof the
diseases, during and after treatment. In all patients so occurrence and
type of
S.M. infections was investigated  .Dynamics of  S.M.  infection was
measured by a scale from minimal to very severe. In about 1/3 of
patients at
the moment of diagnosisof the disease, severe or very severe infection
was
seen which was dependent of stage of the disease advancement. These
preliminary studies seem to indicate that presence of severe or very
severe S.M  infection is not favorable prognostically and frequently
correlates
with a progress of neoplastic changes and worse responseto treatment."


1994  Patients with malignancies are at high risk to develop systemic
non bacterial
infections. Stealth Microbe  accounts for approximately 80% of these
isolates.
The vast majority of these infections are of endogenous origin."

HOST DEFENSES AND HOW Stealth Microbe DEFEATS THEM  
     The skin and mucous membranes are primary
defenses                    
          Stealth Microbe attacks and eats the skin 
     The mucous membranes are primary
defense                              
          Proteinase attacks secretory IgA of mucous membranes 
          Gliotoxin attacks mucociliary action 
     Macrophages protect the respiratory
tract                             
          Gliotoxin inhibits macrophage phagocytosis 
     Cell mediated immunity protects us from Stealth
Microbe               
            Antigen processing 
            Macrophage activation 
          (3a) Inhibited lymphokine production 
          (3b) Inhibited activation of T lymphocytes 
     Myeloperoxidase enzyme protects against
mycoses                       
          Mannan inhibits myeloperoxidase release 
     Phagocytic cells are the mainstay of cellular
immunity                
          Stealth Microbe  grows from phagocytic cells 
          Antiphagocytic compound 
                           
     Humoral immunity: opsonization helps protect us           
          Proteinase reduces opsonizing activity 
    
     Humoral immunity: complement C3 role in host
defense                  
          Proteinase degradation of complement C3 
     Nonimmune serum factors: transferins bind
iron                        
          Stealth Microbe siderophores sequester iron  
     Lactobacillus produces potent S.M.  growth
inhibitor                 
 
MORE ON Stealth Microbe PROTEINASE  
     Cleavage of immunoglobulins including
IgA                             
      FC Portion of immunoglobulin g
degraded                               
     REDUCED BACTERICIDAL ACTIVITY AGAINST ESCHERICHIA
         
COLI                                                             
     Alpha 2 macroglobulin & alpha 1
proteinase                            

MORE ON MANNANS AND POLYSACCHARIDES 
     Multiple inhibition of proliferative
response                         
     Mannan inhibits
lymphoproliferation                                   
     Stealth Microbe specific inhibition proliferative
response            
     Glycoprotein & mannan suppress
lymphoproliferation                    
     Mannan increases hydrogen peroxide
production                         
     Polysaccharide antigens inhibit lymphocyte
proliferation              
     Polysaccharide depression of cellular
function                        

MORE ON GLIOTOXIN 
     Gliotoxin present in vaginal
samples                                  
     Cultured cell growth
blocked                                          
     Gliotoxin reduces B lymphocytes
count                                 
     Irradiation increased gliotoxin
toxicity                              
    
Apoptosis                                                             
          DNA fragmentation in macrophages - apoptosis  
          Apoptosis of mouse L929 fibroblast cells 
          Apoptosis in concanavalin a-stimulated t blasts 
          Apoptosis of T blasts and macrophages 
          80-95% inhibition of protein synthesis 
          Lymphoid organ apoptosis 
          Cytoskeletal structure damage & adhesion loss 
          Kills non-hematopoietic cells 
     TISSUE
DAMAGE                                                         
          Extensive tissue damage 
          Cytoskeletal microfilament/detachment/vacuolation 
          Modification of microfilaments or plasma membranes 
               Induction of microvilli loss  
               Reorganization of cortical cytoplasm  
               Altered bile acid uptake   
               Afflux   
               Modified hormone responsiveness  
(Stealth Microbe DIABETES will have much on hormones)
"Incubation of Stealth Microbe cells with human luteinizing hormone
(hLH),
human chorionic gonadotrophin(hCG) Or glucagon  produced a significant
rise in cAMP total levels."

Mice treated with cortisone were susceptible to intratracheal challenge
with
10-100 x less  Stealth Microbe than were untreated mice. 

"Stealth Microbe also possesses enzymes that can reduce steroids at the
3-
,17-and 20-oxo-groups.

          Altered morphology and plasma membrane function 
          Tumor-like lesions on major organs  

     DNA
CHANGES                                                           
          Drastic DNA changes & precancerous tissue damage 
          Raised inositol triphosphate & DNA fragmentation 
          30 ng/ml prevents T & B cell DNA synthesis 
          DNA fragmentation of T and B cells 
               Genome severely damaged  
               Alloreactive cytotoxic T cells  
     DAMAGE BELOW THE GENERALIZED TOXICITY
THRESHOLD                       
          Significant DNA damage in thymocytes at  um  
          Glucose metabolism selectively affected 
          Macromolecular synthesis selectively affected 
          Basal rate of H2O2 production inhibited 
          Macrophage activity abrogated 
    
LYMPHOPROLIFERATION                                                   
          T-cell proliferation inhibition 
          Mitogen or interleukin induced b & t proliferation 
          Leukocytes as stimulator cells disabled 
          Depletion of murine epidermal Langerhans  
               Major histocompatibility complex   
               (nm) concentration ultrastructural damage to lc   
               Immune response and contact sensitivity   
          Increased suppressor cell activity of B-lymphocytes 
               Phytohemagglutinin-induced mitogen response
                    suppressed  
               Anti-sheep erythrocyte antibody response
                    suppressed  
               Anti-thy 1 antibody and complement    
               Not plastic-adherent or mac-1 antigen-positive    
          Cytotoxic T cells production failure 
    
MACROPHAGES                                                           
          Macrophage phagocytosis irreversibly inhibited  
          Microvilli loss and chromatin condensation 
          In vivo macrophage & T cell dependent mechanisms 
     Stealth Microbe
TOXINS                                                
          High molecular weight toxins 
               Glycoprotein toxins  
               SMtoxin  
          Low molecular-weight toxins 
          Stealth Microbe toxin investigation results 
          Pathogenic enzymes 
               Proteinase  
               Phospholipases  
               Lysophospholipase-transacylase  

WHAT Stealth Microbe IS 
     Stealth Microbe - the most pervasive S.M. pathogen                  
     A facultative pathogen - masquerading
marauder                        
     Pathogenic
trickery                                                   
     Pathogenesis and phenotypic
switching                                 
          Differential expression of virulence factors  
          Rapid alteration of phenotype 
          9 distinct colony phenotypes 
          Colony morphology 
          Constraints on the ___ __ _____ transition 
          Cellular phenotype 
          Patterns of gene expression 
          Resistance to anti-S. M. agents 
          Antigenicity 
     Stealth Microbe has amphotericin b
resistance                         
     Pathologic states are extremely
varied                                
     Invasive potential increases with
quantity                            

MORE ON WHAT Stealth Microbe DOES 
     Gut colony may impair cell mediated
immunity                          
     Stealth Microbe is a cause of
immunodeficiency                        
     Increased susceptibility to bacterial
infection                       
          Suppressed DTH and bacterial sepsis 
          Elevated Stealth Microbe antigen titers & bacterial sepsis 
     World wide plague - often
refractory                                  
     Stealth Microbe infections are increasing in
incidence                

How it isn't detected 
     Molecular
mimicry                                                     
     Antigenic
variability                                                 
     Topographical variation dependent on carbon
source                    
     Diagnostic skin test
failure                                          

How it is diagnosed 
     Successful post autopsy
diagnosis                                     
     Antemortem diagnosis is
difficult                                     
     Clinician's
uncertainty                                               
     Difficulty in differentiation - colony or
invasion                    
     Invasive biopsy
required                                              
     Therapy by
suspicion



More information about the Biochrom mailing list