Mark Peters gquest at
Thu Nov 14 01:23:58 EST 1996

between the microbe and the human immune system.  Microbes that can
remain undetected have a much greater chance of survival agianst modern
drugs and technologies.  Microbes that feed upon and benefit from
standard medical procedures have a great advantage over the other lesser
fortunate hungry microbeasts.


They know that it is there but they can't figure out how  use it as an
offensive weapon.  They claim it to be generally harmless and say they
have no idea what triggers it into its lethal deadly action.

	Isolation of the microbe from lab samples tends to obfuscate rather
than clarify the diagnosis.  The clinicians uncertainty as to the
significance of the microbe cultured from skin lesions, blood or
cerebrospinal fluid and other internal foci will often prevent or delay
specific therapy.

	1966		Despite ample evidence to the contrary many text books and
articles perpetrate the disinformation that the microbe is
saprophytically common on normal skin.   As a result, the microbe is
shrugged off as a simple contaminant.  The delay in therapy will result
in the death of the target.

	1988		The microbe is one of the more common infections in the human
oral cavity.  doctors continue to view the microbe as a minor and self
limiting ailment.

	1989		ELISA serologic diagnosis of the microbe yields a large
percentage of false-positive reactions.

	1989		Tests for the detection of circulating antigens and metabolic
products have shown variable and inconsistent results.

	1989		Sensitive , specific and timely diagnostic tests are just not

	1989		Definitive diagnosis is often difficult to establish and usually
requires an invasive biopsy.  Lengthy culture tests contribute to poor
results of therapy.

	1989		Antemortem diagnosis of the lethal infection is a difficult and
significant obstacle to the successful treatment of the stealth microbe.

	1989		"Unfortunately, sensitive, specific, and timely diagnostic tests
for candidiasis are not available, and therapy may often be indicated
solely by a high level of suspicion of a systemic fungal infection."

	1989		This microbe has several attack mechanisms which allow it to
attack and invade the targets tissues.

	199			This review clearly shows that the virulence of the microbe is a
function of a multiplicity of factors (triggers)  working jointly to
overcome host defenses.  Failure to properly trigger one or of these
virulence factors will result in the microbe maintaining its commensal
status on the human population.

	1991		The microbe has an impressive variability potential in its method
of attack.  In vivo experiments and clinical observations of the active
virulence factors ar scant.

	1991 		The Genomic variability hypothesis represents an attempt  by the
medical establishment to explain why, "despite intense searching," no
one attack mechanism of the microbe has been identified as "THE"main
cause of death.

	199			"Considerable difficulty surrounds the differentiation of the
microbes colonization from microbes  invasion.  Although the microbes
colonization is relatively harmless, invasive stealth microbe 
infections carry an ominous prognosis even when appropriate
antimicrobial therapy has been instituted".

	1992		Despite the presence of many virulence factors the host's defense
mechanisms will generally keep the stealth microbe in check.

The doctors can't see it when it is right under their noses and it goes
right on causing cancer and killing cancer patients.  The stealth
microbe is the perfect biological weapon.  The target will die and the
autopsy shows the cause of death to be a common lethal disease.

		1)	Exploit errant status of simple commensal
		2)	Impose aversions to healthy foods
		3)	Enlist iatrogenic and nosocomial as ally
		4)	Evade quantitative analysis
		5)	Engage propaganda to deter lab testing
		6)	Disable detection via delayed type 	 			hypersensitivity 
			reaction tests
		7)	Hibernate past culture test duration of 30 			days
		8)	Effect 9 morphologies to addle lab tech's
		9)	Dodge discern by high frequency 	 			phenotypic switching
		10)	Use gene pattern array to alter antigenicity
		11)	Camouflage counter attack as drug 	 			hypersensitivity 
		12)	Debase therapeutics impersonating 	 		herxheimer's reaction
		13)	Camouflage infiltration with molecular 			mimicry
		14)	Synergies bacteria to be the scape-goat
		15)	Create diversions with deviant 		 			symptomatologies
		16)	Infiltrate host habitat to promote reinfection
		17)	Disrupt synaptic report with beta-blockers
		18)	Steel host nutrients to produce 		 			carcinogenic biotoxins
		19)	Muffle inflammation respon...... truncated.

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