OVERVIEW:
Spirochetes are their own phylum.
The nature of the phylum in persistence
and extensive preservation mechanisms to
environmental stresses of temperature,
gases, moisture, and chemicals, is
demonstrated across genera.
From the PBS "Life on Earth" Series
interview with Eugene Shapiro, Yale
Pediatrician, "They would have you
believe
that form of the disease, somehow this
is, the bacteria knows to act
differently and it doesn't respond to
antibiotics in this sense. It really
doesn't make any sense."
In fact, spirochetes *do* behave
differently from other bacteria, as will
be demonstrated below. One must
study
nature to become familar with human
disease. The answers to the
persistance of Lyme disease come from
the
characteristics of the phylum.
Simply put, the spheroplast is not the
"end stage". When that
morphological variant is observed in
vitro, with exposure to various
antibiotics, it should not be
concluded that the organism has been
killed.
The argument that the observation that
spirochetes persist, empirically, in
patients' symptoms is
necessary to be understood per the
politics of Lyme:
http://www.faim.org/Lyme%20hearing.htm
To understand the controversy, one must
understand that the CDC says "Lyme
disease" is 5 of 10 bands on a Western
Blot, but they say this with no proof.
A physician may be paid to testify
against a patients' right to treatment
by saying they don't have "Lyme disease"
(5 of 10 bands) and then in that sense,
they are correct. Most Lyme-
infected patients do not have 5 of 10
bands. It has not been published,
how many people who have been
*treated* have 5 of 10 bands, although
it is known, as this data was collected
by Mark Klempner, formerly of
Tufts, with his $4.7 million research
grant. The anecdotal evidence (Dr.
Klempner's comment in a
public talk, among others) is that that
range is 0.5 to 3.9% of all treated Lyme
patients. Treatment abrogates
antibody response and many patients are
completely seronegative. Treatment
does not always entirely wipe
out the infection *or* symptoms, as is
the case in animal and human spirochetal
infections. It will be shown how
this is so, below.
THE NATURE OF THE PHYLUM- Defies Managed
Care
What can Spirochetes do?
Morphological changes- the spheroplast
or "cyst"
Dessication
Antimicrobial resistance genes sharing
Lateral gene tranfser
Intracellular persistence- immune and
antibiotic evasion
Antigenic variation- immune evasion
Freezing- Lyme patients cannot donate
blood, per the Red Cross
Porins- resistance to antimicrobials
Other, dessication
US army document (aerosolized)
http://www.google.com/search?q=cache:WpRbE1BgHKM:www.afpmb.org/pubs/dveps/haiti.pdf+US+Army,+Leptospira,+Haiti&hl=en
Haiti, 1994, Armed Forces Pest
Management Board, Defense Pest
Management Analysis Center, Forest Glen
Section,
WRAMC, Washington, DC, 20301-5001
"INFECTIOUS AGENT : Leptospira
interrogans, over 200 serovars are known
to exist. EPIDEMIOLOGY : This
disease
occurs in both rural and urban
environments, and it is particularly
common among people who work outdoors.
The
case fatality rate is usually less than
20%. Reservoirs include numerous
wild and domestic animals, reptiles and
amphibians. Transmission is effected
through pathogen contact with skin and
mucous mem branes (especially if
these are cut or abraded) via
contaminated food or water, moist soil,
vegetation, the urine or tissues of
infected
animals or, rarely, aerosols."
"Spherical bodies"- Oral Spirochetes
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10895696&dopt=Abstract
Oral Microbiol Immunol 1999
Dec;14(6):384-6, Factors affecting the
formation of spherical bodies in the
spirochete Treponema denticola., De
Ciccio A, McLaughlin R, Chan EC.,
Faculty of Dentistry, McGill University,
Montreal, Quebec, Canada.
"The oral spirochete Treponema denticola
typically is a helically shaped, motile
bacterial cell. However,
morphological variations of T. denticola
cells in the.form of "spherical bodies"
are sometimes seen. Little
is known about the environmental factors
that cause their formation. The effects
of oxygen, growth temperature,
nutrient depletion and the addition of
metabolic end- products were tested to
determine their role in the
morphogenesis of the spherical bodies.
It was found that the age of the
culture, the omission of individual
components (yeast extract, rabbit serum,
volatile fatty acids or thiamine
pyrophosphate) from the medium and
the addition of the metabolic end
product lactic acid enhanced the
formation of these bodies. However,
their
formation was decreased upon omission of
the medium components asparagine and
sodium bicarbonate."
PMID: 10895696
PHAGE TRANSDUCTION; TRANSFER of
ANTIBIOTIC RESISTENCE GENES
Bacteriophage transduction of
Brachyspira (swine dysentery)
http://www.nps.ars.usda.gov/publications/publications.htm?lognum=0000091627
Online publication of the United States
Department of Agricultural Research
Service, Identification And
Detection Of Genes Of Vsh-1, An Unusual
Bacteriophage (host Genome Packaging
Agent) Of Serpulina Hyodysenteriae
"Interpretive Summary: We recently
reported the transfer of antibiotic
resistance genes between cells of
Serpulina
hyodysenteriae. This spiral-shaped
bacterium causes swine dysentery, a
worldwide disease estimated to cost the
U.S.
pork industry $100 million per year.
This was the first report of gene
transfer between S. hyodysenteriae
cells.
We discovered that the genes were
transferred by a previously unknown gene
transfer agent that we named
VSH-1. In the present studies, we
identified several VSH-1 genes. We found
VSH-1 genes in every known species
of Serpulina which cause intestinal
disease in chickens, pigs, and possibly
in humans. These pioneering studies
suggest the gene transfer agent, VSH-1,
is common among Serpulina species. As a
result, VSH-1 and similar agents
should be evaluated for bacteria in the
intestinal tract to trade genes. ***The
importance of these results is
that we have described a new method by
which genes such as antibiotic
resistance genes can be spread among
bacteria.*** The resistance of bacterial
pathogens to antibiotics is anemerging
and serious problem in human
and veterinary medicine."
LEPTOSPIRA BACTERIOPHAGE REPLICATES AS A
PLASMID
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11004167&dopt=Abstract
J Bacteriol 2000 Oct;182(20):5700-5705,
The LE1 bacteriophage replicates as a
plasmid within Leptospira
biflexa: construction of an L. biflexa-Escherichia
coli shuttle vector., Girons IS, Bourhy
P, Ottone C, Picardeau
M, Yelton D, Hendrix RW, Glaser P,
Charon N., Unite de Bacteriologie
Moleculaire et Medicale, Institut
Pasteur,
75724 Paris Cedex 15, France.
isgirons@pasteur.fr
SWINE LAGOONS AND RESISTANCE TO THE
TETRACYCLINES
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11282596&dopt=Abstract
Appl Environ Microbiol 2001,
Apr;67(4):1494-1502, Occurrence and
diversity of tetracycline resistance
genes in lagoons and groundwater
underlying two swine production
facilities., Chee-Sanford JC, Aminov RI,
Krapac IJ, Garrigues-Jeanjean N, Mackie
RI., Department of Animal Sciences,
University of Illinois at
Urbana-Champaign,Urbana, IL 61801, USA.
PHAGE TRANSDUCTION/BACTERIOPHAGES OF
BORRELIA burgdorferi
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11466280&dopt=Abstract
J Bacteriol 2001 Aug;183(16):4771-4778,
Transduction by phiBB-1, a Bacteriophage
of Borrelia burgdorferi.,
Eggers CH, Kimmel BJ, Bono JL, Elias AF,
Rosa P, Samuels DS., Division of
Biological Sciences, The University of
Montana, Missoula, Montana 59812. "The
kan cassette recombined into a resident
cp32 and was stably maintained.
The cp32 containing the kan cassette was
packaged by phiBB-1 released from this
B. burgdorferi strain. phiBB-1
has been used to transduce this
antibiotic resistance marker into naive
CA-11.2A cells, as well as two other
strains of B. burgdorferi. This is the
first direct evidence of a mechanism for
lateral gene transfer in B.
burgdorferi."
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6853449&dopt=Abstract
J Bacteriol 1983 Jun;154(3):1436-1439,
Bacteriophage in the Ixodes dammini
spirochete, etiological agent
of Lyme disease., Hayes SF,
Burgdorfer W, Barbour AG. "A
bacteriophage with a B-3 morphology was
detected by
electron microscopy in a spirochete
isolated from the tick Ixodes dammini.
It has a 40- to 50-nm elongated
head and a tail 50 to 70 nm in length.
It appears devoid of collars or
kite-tail structure. The
spirochete has been identified as the
causative agent of Lyme disease."
ANTIGENIC VARIATION IN BRACHYSPIRA
Brachyspira Antigenic variation
http://www.nps.ars.usda.gov/publications/publications.htm?lognum=0000114138
The Search For Brachyspira Outer
Membrane Proteins That Interact With The
Host "Technical Abstract:
Little is known about the outer membrane
structure of Brachyspira hyodysenteriae
and Brachyspira
pilosicoli or the role of outer membrane
proteins (OMPs) in host colonization and
the development of
disease. The isolation of outer membrane
vesicles from B. hyodysenteriae has
confirmed that cholesterol
is a significant outer membrane
constituent and that it may impart
unique characteristics to the lipid
bilayer structure including a reduced
density. Unique proteins that have been
identified in the B.
hyodysenteriae outer membrane include
the variable surface (Vsp) proteins and
lipoproteins such as SmpA
and BmpB. While the function of
these proteins remains to be determined,
there is evidence to
suggest that they may be involved in
immune evasion. These data may explain
the ability of the organism
to initiate chronic infection."
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10510046&dopt=Abstract
Vet Microbiol 1999 Aug
31;68(3-4):273-283, Sequence
characterization of two new members of a
multi-gene
family in Serpulina hyodysenteriae
(B204) with homology to a 39 kDa surface
exposed protein: vspC and
D., McCaman MT, Auer K, Foley W, Gabe
JD., Berlex Biosciences, Process
Development Department, Richmond,
CA, USA.
"Previous cloning and sequencing of
clones from a genomic library
constructed from Serpulina
hyodysenteriae
B204 had identified a tandem pair of
open reading frames, identified as vspA
and vspB (variable surface protein)
expected to encode proteins with
homology to (but not identical with) a
39 kDa surface exposed membrane protein
from this animal pathogen. Additional
screening of the genomic library was
performed to retrieve the remainder of
the vspB gene using new oligonucleotide
probes based upon the cloned gene
sequences. Not only was this goal
met but we also discovered two more
adjacent and related vsp genes (vspC and
vspD) and have completely sequenced
them.."
ANTIGENIC VARIATION IN THE OTHER
BORRELIA
http://www.cdc.gov/ncidod/eid/vol6no5/barbour.htm
Emerging Infectious Diseases, Vol. 6,
No. 5, Sep-Oct 2000, Synopsis
Antigenic Variation in Vector-Borne
Pathogens, Alan G. Barbour* and
Blanca I. Restrepo, *University of
California Irvine, Irvine, California;
and Corporación para Investigaciones
Biológicas, Medellín, Colombia
"Several pathogens of humans and
domestic animals depend on hematophagous
arthropods to transmit them
from one vertebrate reservoir host to
another and maintain them in an
environment. These pathogens
use antigenic variation to prolong their
circulation in the blood and thus
increase the likelihood of
transmission. By convergent
evolution, bacterial and protozoal
vector-borne pathogens have acquired
similar genetic mechanisms for
successful antigenic variation. Borrelia
spp. and Anaplasma marginale
(among bacteria) and African
trypanosomes, Plasmodium falciparum, and
Babesia bovis (among parasites) are
examples of pathogens using these
mechanisms. Antigenic variation
poses a challenge in the development
of vaccines against vector-borne
pathogens.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8486939&dopt=Abstract
J Infect Dis 1993 May;167(5):1074-1081,
Invasion of human skin fibroblasts by
the Lyme disease spirochete,
Borrelia burgdorferi., Klempner MS,
Noring R, Rogers RA., Division of
Geographic Medicine and Infectious
Diseases,
New England Medical Center, Tufts
University School of Medicine, Boston,
Massachusetts 02111.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8240439&dopt=Abstract
Arthritis Rheum 1993
Nov;36(11):1621-1626, Persistence of
Borrelia burgdorferi in ligamentous
tissue from a
patient with chronic Lyme borreliosis.,
Haupl T, Hahn G, Rittig M, Krause A,
Schoerner C, Schonherr U, Kalden
JR, Burmester GR., Department of
Medicine III, University of Erlangen-Nuremberg,
Germany. [In this study, the
patient was treated for 6 weeks with
oral doxy 200 mgs/ day and then 2 weeks
IV ceftriaxone, and then 3 weeks
of roxithromycin, sulfatmethoxazole and
trimethoprim, and then surgery was
performed.-KMD]
PERSISTENCE OF LEPTOSPIRA (Immune
evasion)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9009336&dopt=Abstract
Infect Immun 1997 Feb;65(2):729-38,
Invasion of Vero cells and induction of
apoptosis in macrophages by
pathogenic Leptospira interrogans are
correlated with virulence., Merien F,
Baranton G, Perolat P.,
Laboratoire des Leptospires,
Institut Pasteur, Noumea, New Caledonia,
France. "...Invasion of epithelial
cells and induction of apoptosis in
macrophages may be related to the
pathogenicity of Leptospira, and
both could contribute to its ability to
survive in the host and to escape from
the immune response."
PERSISTENCE OF BORRELIA burgfdorferi
PAST TREATMENT IN ANIMALS
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10048169&dopt=Abstract
Wien Klin Wochenschr 1998 Dec,
23;110(24):874-81,
Clinical manifestations, pathogenesis,
and effect of antibiotic treatment on
Lyme borreliosis in dogs.
Straubinger RK, Straubinger AF, Summers
BA, Jacobson RH, Erb HN., James A. Baker
Institute for Animal
Health, Ithaca, New York, USA.
rks4@cornell.edu
"CONCLUSIONS: B. burgdorferi
disseminates through tissue by migration
following tick inoculation,
produces episodes of acute arthritis,
and establishes persistent infection.
The spirochete survives antibiotic
treatment and disease can be reactivated
in immunosuppressed animals."
VIABILITY AFTER FREEZING
LEPTOSPIRA
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3804861&dopt=Abstract
J Appl Bacteriol 1986 Nov;61(5):407-11,
Storage of pathogenic leptospires in
liquid nitrogen., Palit A,
Haylock LM, Cox JC. [to minus 70
C-KMD] "The viability of nine strains
has so far been
observed over a period of 8-22 months
storage in liquid nitrogen and full
viability of all strains
has been preserved over this period.
Virulence of strains of serovars pomona
and hardjo was well
preserved, as demonstrated by challenge
tests in guinea pigs and domestic pigs."
B. burgdorferi AND FREEZING
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2773025&dopt=Abstract
Transfusion 1989 Sep;29(7):581-3,
Survival of Borrelia burgdorferi in
blood products., Badon SJ,
Fister RD, Cable RG. American Red Cross
Blood Services, Farmington, Connecticut.
"The organism was shown to
survive ***in RBCs*** (4 degrees C) and
FFP (below -18 degrees C) for 45 days
and in PCs (20-24 degrees C)
for 6 days. The results of this study do
not exclude the possibility of
transmission of Lyme disease through
blood transfusion."
So, in conclusion, spirochetes do not
behave like other bacteria. They behave
like spirochetes. They
are persistent, environmentally
resistant, undergo morphological changes
and revert, can be intracellular,
resistant to antibiotics, can acquire
virulence via phage-vector.
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