Marshall Protocol Knowledge Base

L-form bacteria


As a part of their natural life cycle, bacteria can transform into a variety of forms. One of those phases is the L-formL-form bacteria, also known as cell wall deficientbacteria, are a phase of bacteria that are very small and lack cell walls.

Though the subject of a great deal of research over the last 100 years and implicated in a variety of diseases, L-forms remain largely misunderstood - or at the very least, underappreciated - by the medical research community. According to the Marshall PathogenesisL-forms are part of a metagenomic microbiota responsible for chronic disease.

Species capable of L-form transformation


Thus far, researchers have identified over 50 different species of bacteria capable of transforming into the L-form and it is likely that more species will be found in the coming years. “Probably most bacterial species can be converted into L-forms if treated with the antibiotics that inhibit cell wall synthesis,” states researcher Josep Casadesus.1

Some of the species of L-form bacteria that have been implicated in chronic disease include Bacillus anthracis, Treponema pallidum, Mycobacterium tuberculosis, Helicobacter pylori, Rickettsia prowazekii, and Borrelia burgdorgeri. Not all species cause disease.

Size and shape


L-form bacteria are pleomorphic, that is, they can change size and shape. During much of their lifetimes they are tiny, about 0.01 microns in diameter.

Since they are smaller than viruses or fungal particles, they cannot be seen with a normal optical microscope. The small, individual forms of L-form bacteria are often referred to as coccoid bodies. Coccoid bodies sometimes group together, assuming the appearance of a string of pearls

Occasionally L-form bacteria break out of the cells. In the lab they can grow into long, thin biofilmA structured community of microorganisms encapsulated within a self-developed protective matrix and living together. filaments that can reach 60-70 microns in length. The biofilm filaments are composed of L-form bacteria and a protective protein sheath. For reasons still unknown, L-forms can also grow into large “giant” bodies.

L-form bacteria lack flagella, long slender appendages that allow some forms ofbacteria to propel themselves forward by using a whip-like motion. Instead they glide to their destinations in a snail-like fashion.

Groups of L-form bacteria are often encased inside tubules. They are also separated from the environment inside the cell by a membrane or exoskeleton that keeps them from being digested by the cell.

Resistance to certain antibiotics


Cell wall deficient variants of bacteria cannot be killed by many commonly used antibiotics. Multiple studies have also shown that when one of the Beta-lactam antibiotics, a class of antibiotics that includes penicillin, are applied to wild-type bacteriain a Petri dish, small colonies of L-form bacteria form on the edges of the plate. According to Casadesus: 2

Treatment with penicillin does not merely select for L-forms (which are penicillin resistant) but actually induces L-form growth.

Josep Casadesus

Replication and reproduction


L-form bacteria replicate in various ways, including budding, filamentous growth and binary fission. Some species of L-forms such as Proteus can form large bodies that replicate by division. In other instances, granules bud from the body of the bacterium and give rise to small L-form colonies.

Survival mechanisms


Classical forms of most bacterial species can be found in the bloodstream. However L-form bacteria have figured out how to successfully infect and live inside the very cells of the immune system whose role is to kill bacteria. Once inside these cells, they can no longer be detected by the immune system and are able to persist in the body over long periods of time. L-form bacteria can infect many types of cells but prefer to infect white blood cells called macrophages.

Several very recent studies have confirmed the fact that bacteria can live inside the cells of the immune system. In a paper published in the Journal of Immunology by a team at the University of Michigan Medical School, Gabreil Nunez, senior author of the paper, stated “In our study, the presence of bacterial microbes inside the cell is what triggers the immune response.” 3

Similarly, a team of researchers at the Bacterienne Institute in France released a paper detailing how the bacteria E. coli is able to live inside the cells of the immune system.

[ E. coli are] true invasive pathogens, able to invade intestinal epithelial cells and replicate intracellularly. Strains also survive and replicate within the macrophages.

Nathalie Rolhion et al. 4

Markova has provided evidence that E. coli can survive lethal treatments such as boiling or autoclaving (subjecting equipment to high pressure steam at 121 °C or more) by transitioning into the L-form5


Culturing and detection


Once bacteria have transformed into the L-form they can no longer be detected by many standard laboratory procedures. Although scientists have known about L-formbacteria for over a century, many of them have not detected them in tissue and blood samples because they are very difficult to culture.

Forms of bacteria with cell walls can be easily grown outside the body (grown in vitro). However L-form bacteria have great difficulty surviving in a foreign environment. In order to grow them successfully in the lab, conditions must be similar to those in the human body (grown in vivo). Consequently they can be cultured on a medium called blood agar at very specific temperatures and at a certain pH.

The concept that some bacteria cannot grow in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory. is not new. Scientists have known for decades that neither ( Syphilis Treponema pallidum ) nor leprosy ( Mycobacterium leprae) cannot be easily cultivated outside the body.

L-form bacteria take several measures to ensure they can survive for as long as possible inside a cell. They are able to infect all types of white blood cells, but seem to prefer to infect macrophages, the type of white blood cell, which at 45 days, has the longest life span.

Several studies have shown that once inside a macrophage, L-form bacteria are able to delay the process of apoptosis, or programmed cell death, allowing them to thrive inside the cell for a period of time even longer than 45 days.

PCR testing


Classical bacterial forms can be detected by a lab test called Polymerase Chain Reaction (PCR). PCR identifies and amplifies the proteins and DNA of bacteria that have been killed. However since L-form bacteria are able to persist inside the macrophages for such extended periods of time, few of them die and only tiny amounts of L-formbacterial proteins and genetic material reach the bloodstream at any given time; an amount so small that the PCR test cannot pick them up.

Even if a few small fragments from L-forms that have been killed are identified by PCR testing, the remains are often not from the bacterial species causing the most harm to the patient. This is because the most well adapted, persistent bacterial species are the ones who have developed the most effective survival mechanisms and are consequently least likely to die.

Antibody testing


L-forms can also not be detected with antibody testing. Antibodies are Y-shaped proteins that are found in blood. They are used by the immune system to identify and neutralize foreign objects including bacteria.

However, antibodies only form in response to bacteria that have died. Since L-formbacteria are able to persist for such long periods of time inside the cells, very few antibodies are created in response to their presence.

Challenge of studying l-forms


Scientists such as Lida Mattman at Wayne State University, Gerald Domingue, and Nadya Markova have worked extensively with the L-form and figured out new ways to grow and view the pathogens. These techniques include a variety of special staining techniques. Nevertheless, many doctors and researchers still question whether the L-forms actually exist.

Mattman and others have spent decades figuring out how to correctly culture the L-form. Applying their techniques correctly requires rigorous adherence to specific guidelines. Mattman has said that, over and over again, researchers misinterpreted just one of the steps required to correctly grow the bacteria. They then report to the medical community that no L-forms appear in their samples.

Unfortunately, in the area of L-form or cell wall-defective bacteriology, too often there have been conclusions (anecdotal) drawn without supporting scientific data. In my opinion, many of these studies have hampered progress in the field and especially the role of these cryptic organisms in bacterial persistence and expression of disease.

Gerald Domingue, professor emeritus, Tulane University School of Medicine

“Features of a number of important but poorly explained human clinical syndromes strongly indicate a microbial etiology,” states Relman. “In these syndromes, the failure of cultivation-dependent microbial detection methods reveals our ignorance of microbial growth requirements.” 6

Koch's postulates


Another problem with fully understanding the role of L-forms rests with the fact that many researchers rely on a series of rules called Koch’s postulates when interpreting research data. The postulates state that only one pathogen can cause a given disease. But research has shown each chronic disease is the result of infection with multiple species of L-forms.

This means that separate teams of researchers often detect different L-forms in patients with the same disease. For example both Borrelia burgdorferi and Rickettsia helvetica have been detected in patients with sarcoidosis. These findings make little sense to researchers still bent on adhering to Koch’s postulates.

Infection with L-form bacteria


People are exposed to L-form bacteria in many places. Because they cannot be killed by pasteurization or chlorination, L-form bacteria can be found in milk, food, and water. They can be transmitted via sperm, intimate contact, and can be passed from mother to child during childbirth. Since they are too small to be filtered during the purification processes used in pharmaceutical manufacturing procedures, they can be transmitted through injectable medicines. They have even been cultured from dry soil.

One 2007 trial for an AIDS vaccine had to be abruptly discontinued when scientists realized that the vaccine somehow raised the risk of infection. The researchers administering the trial stressed that the vaccine could not itself cause the infection. Although it was not mentioned in the news story about the incident, one very plausible hypothesis is that the vaccines were infected with L-form bacteria.

Once macrophages and other cells have been infected with L-form bacteria, thebacteria circulate in the blood and tissues. In some cases they cluster together in clumps called granulomas. In other cases, they accumulate in regions such as the joints.

After L-form bacteria have successfully invaded a cell, they begin to use the nutrients inside the cell to their own advantage, disturbing the cell’s delicate chemical balance. They are also able to take control of the host’s genetic material, which allows them to create proteins that enhance their ability to survive.

Inflammation as evidence of infection


L-form bacteria cause inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. and painful symptoms by taking control of the protein known as Nuclear Factor Kappa B. They are able to activate proteins that increase the activity of Nuclear Factor Kappa B, which subsequently moves to the nucleus or center of the cell. Once there, it turns on a variety of genes that cause the release of inflammatory cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system., proteins that generate pain and/or fatigue. These cytokines include interferon gamma and TNF alpha.

In this way, an inflammatory response is correlated with diseases caused by L-formbacteria.

An inflammatory immune response—one of the body’s primary means to protect against infection—defines multiple established infectious causes of chronic diseases, including some cancers.

David Relman, MD

Inflammation also drives many chronic conditions that are still classified as (noninfectious) autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body or immune-mediated (e.g., systemic lupus erythematosusrheumatoid arthritis, Crohn’s disease). Both [the innate and adaptive immune systems] play critical roles in the pathogenesis of these inflammatory syndromes. Therefore, inflammation is a clear potential link between infectious agents and chronic diseases.

Siobhán M. O'Connor of the Centers for Disease Control and Prevention concurs, stating, “The epidemiologic, clinical, and pathologic features of many chronic inflammatory diseases are consistent with a microbial cause.”

Future research


There seems to be little incentive for scientists to study the L-form. Since the bacteriacan be killed by simple low-dose antibiotic therapy, drug companies have little interest in investing money into related research. Researchers studying the L-form often find themselves with very little grant money but must still work long, tedious hours in the lab.

It is generally agreed among scientists that L-form bacteria are extraordinarily intriguing, interesting tools for biological study, yet the most neglected area of research has been on the role of these organisms in disease, particularly in host-pathogen interactions.

Gerald Domingue, PhD

Notes and comments



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These guys are looking at the same stuff Andy Wright was:

Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11358-63. Epub 2006 Jul 18. Electrically conductive bacterial nanowires produced by Shewanella oneidensis strain MR-1 and other microorganisms. Gorby YA, Yanina S, McLean JS, Rosso KM, Moyles D, Dohnalkova A, Beveridge TJ, Chang IS, Kim BH, Kim KS, Culley DE, Reed SB, Romine MF, Saffarini DA, Hill EA, Shi L, Elias DA, Kennedy DW, Pinchuk G, Watanabe K, Ishii S, Logan B, Nealson KH, Fredrickson JK.

Pacific Northwest National Laboratory, Richland, WA 99352, USA. Abstract Shewanella oneidensis MR-1 produced electrically conductive pilus-like appendages called bacterial nanowires in direct response to electron-acceptor limitation. Mutants deficient in genes for c-type decaheme cytochromes MtrC and OmcA, and those that lacked a functional Type II secretion pathway displayed nanowires that were poorly conductive. These mutants were also deficient in their ability to reduce hydrous ferric oxide and in their ability to generate current in a microbial fuel cell. Nanowires produced by the oxygenic phototrophic cyanobacterium Synechocystis PCC6803 and the thermophilic, fermentative bacterium Pelotomaculum thermopropionicum reveal that electrically conductive appendages are not exclusive to dissimilatory metal-reducing bacteria and may, in fact, represent a common bacterial strategy for efficient electron transfer and energy distribution.

PMID: 16849424

The Foundation has now put Lida Mattman's second-to-last presentation on YouTube. This was filmed at our 2005 Chicago conference.

PLoS One. 2009 Oct 6;4(10):e7316. Insights into the molecular basis of L-formformation and survival in Escherichia coli. 7

Glover WA, Yang Y, Zhang Y. Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, United States of America. Abstract L-forms have been shown to occur among many species of bacteria and are suspected to be involved in persistent infections. Since their discovery in 1935, numerous studies characterizing L-form morphology, growth, and pathogenic potential have been conducted. However, the molecular mechanisms underlying the formation and survival of L-forms remain unknown. Using unstable L-form colonies of Escherichia coli as a model, we performed genome-wide transcriptome analysis and screened a deletion mutant library to study the molecular mechanisms involved in formation and survival of L-forms. Microarray analysis of L-form versus classical colonies revealed many up-regulated genes of unknown function as well as multiple over-expressed stress pathways shared in common with persister cells and biofilms. Mutant screens identified three groups of mutants which displayed varying degrees of defects in L-form colony formation. Group 1 mutants, which showed the strongest defect in L-form colony formation, belonged to pathways involved in cell envelope stress, DNA repair, iron homeostasis, outer membrane biogenesis, and drug efflux/ABC transporters. Four (Group 1) mutants, rcsB, a positive response regulator of colanic acid capsule synthesis, ruvA, a recombinational junction binding protein, fur, a ferric uptake regulator and smpA a small membrane lipoprotein were selected for complementation. Complementation of the mutants using a high-copy overexpression vector failed, while utilization of a low-copy inducible vector successfully restored L-form formation. This work represents the first systematic genetic evaluation of genes and pathways involved in the formation and survival of unstable L-form bacteria. Our findings provide new insights into the molecular mechanisms underlying L-formformation and survival and have implications for understanding the emergence of antibiotic resistance, bacterial persistence and latent infections and designing novel drugs and vaccines. PMID: 19806199


1) , 2) Casadesús J BacteriaL-forms require peptidoglycan synthesis for cell division.Bioessays. 2007;29:1189-91.
3) Kanneganti TD, Lamkanfi M, Kim YG, Chen G, Park JH, Franchi L, Vandenabeele P, Núñez G Pannexin-1-mediated recognition of bacterial molecules activates the cryopyrin inflammasome independent of Toll-like receptor signaling. Immunity. 2007;26:433-43.
4) Rolhion N, Darfeuille-Michaud A Adherent-invasive Escherichia coli in inflammatory bowel disease. Inflamm Bowel Dis. 2007;13:1277-83.
5) Markova N, Slavchev G, Michailova L, Jourdanova M. Survival of Escherichia coli under lethal heat stress by L-form conversion. Int J Biol Sci 2010; 6:303-315.
Last modified: 11.20.2010
© 2010, Autoimmunity Research Foundation. All Rights Reserved.
Brat mi poslal hromadu roznych clankov na lymsku boreliozu a rozne sprevadzajuce choroby s nou. Tiez ako na liecenie zhladiska roznych lekarov, vcitane pouzitia doplnkov.
Co ma tam zaujalo(zbezne som cez to presiel) bola tato zmienka

"BORRELIA NEUROTOXIN (With thanks to Dr. Shoemaker)
Two groups have reported evidence that Borrelia, like several other bacteria, produce neurotoxins. "

Tj borelioza a mnohe sprevadzajuce infekcie tak isto produkuju neurotoxiny, nielen nase oportunisticke virusy, ktore pri oslabenej viralnej imunite tak isto napadaju nervy a nervove obaly, o com viem uz davnejsie.
Poslal som ti to na adresu ako dva subory

Druhe, co ma zarazilo je vyskyt boreliozy, v USA jej dnes odhaduju az 25% a viem ze na Slovensku a Rakusku bola epidemia nakazenych kliestov(az 90%!!!!) a ze sa borelioza prenasa aj komarmi, muchami, dokonca slinami a potom, samozrejme sa da dostat od matky pri narodeni a dokonca aj pri kojeni.
Este pred 4 rokmi sa oficialne priznavalo v state Illinois len 46 novych pripadov, predminuly rok pisali v periodiku JAMA(lekarske, najvacsie na svete) ze je v USA najmenej 400 tisic novych pripadov rocne a teraz hovoria o 1/4 vsetkych Americanov?To by bolo 75 milionov???

Ako je mozne taka nezrovnalost v statistike nakazenia?
Nuz L-formy sa daju velmi tazko diagnozovat a rozne bakterie, ktore su tu spominane s Boreliozou  produkuju L-formy, vcitane boreliozy a chlamidii pneumoniae.

Inac tieto rozne bakterie a ich ine formy su na zemi zrejme stamilionov rokov, len teraz su alebo "vyslachtene"(geneticke modifikacie) alebo nejak prudko poklesla nasa imunita celkove z roznych dovodov(zamorenie, viralne epidemie, priemyselne pripravovane jedla, ziarenie(EMF), lieky a ockovania...), lebo inac si neviem vysvetlit to prudke narastanie roznych problemov.
Reuma bola aj pred tym , ale Parkinson, MS, ALS lupus, a ine dodnes nazyvane tzv "autoimunne", to sa velmi prudko naraz zvysuje. A to plati aj na depresie a ine neurologicke problemy.
Prudky narast je aj crevnych zapalov(IBS, Crohn), tiez zatial lekarmi dostatocne nevysvetleny.

Moj brat si uz odomna objednal hromadu Samenta , lebo sa stazoval na bolesti klbov, celkovu slabost a nizke horucky napriek braniu roznych antimikrobialnych(GSE, oreganovy olej, extrakt z olivovych listov) 
Samozrejme lekari mu dali "zelenu", nenasli nic beznymi testami.....

Tu je zopar clankov na tu temu

tento je vyborny, popularny s obrazkami

zase tento je trochu odbornejsi

V kazdom pripade lyme disease=borelioza je velmi rozsirena a siri sa nielen postipanim kliestom, ako sa to v literature dosial pise, nielen inym bodavym hmyzom, ale spirochety nasli aj v pote, slinach a vykaslanych kvapockach. Na stastie tak male davky obvykle nesposobia chorobu, na to treba masivnejsia davka, ale aj tak sa zrejme niektore bakterie premenia v tele na mykoplazicke formy a tak v tele zostavaju nepozorovane nasou obranou a "potichucky" skodia.

V tejto forme ich bezne testy nedetekuju, prave dr Jo Ann Whittaker ma ovela citlivejsi a presny test na ne.

Citricidal je silne baktericidny, davka je 35 az 70 kvapiek za den, do litra vody, pit po malickych glgoch cely den, nie naraz!

Samento ma sice napisane davkovanie 2x10 kvapiek ale ja som pouzil az 3x20 kvapiek, ked som mal zapal stredneho ucha, a zabralo to za 2 dni vyborne.

Samento je ucinne najma na mykoplazmicku formu boreliozy, menej na bakterialnu.

Na mykoplazmy je znacne ucinny aj extrakt z olivovych listov

davka 3x750 mg +(20% oleuropein, co je aktivna latka)

Inac s olivovym listom mam aj ucinne doliecovane boreliozy v rodine(3 pripady, ktorym sa to vracalo spat aj po dlhsich davkach doxycyklinu, ktory zialbohu neadresuje mykoplazmy, len bakterie boreliozy), brali mensiu, udrzobnyu davku, 2x500 mg (15% oleuropein), samozrejme hodne dlho, aspon 1/2 roka ba i viac.

Samozrejme kombinacia vsaetkych troch by mala byt najucinnejsia, kde citricidal by mal byt brany aspon 3 tyzdne, Samento 6 tyzdnov a extrakt z olivovych listov aspon pol roka v udrzobnych davkach minimalne.

Neviem, co za produkt mali v Cechach, ale prave Samento a NAC vyliecilo aj napr dr Whittakerovu(nie je pribuzna dr Juliana Whittakera, na ktoreho sa tu casto odvolavam), ktora bola vo vozicku vyse 15 rokov a skusala vselico a za Samentom stoji, lebo jej pomohlo znova chodit.

Je to reakcia na tento film:

Je tam hromada pre mna novych informacii, nie vsetky som "kupil", najma ta kontraverzna teoria o vitamine D a jeho skodlivom metabolite 1.25D a rady, ze treba znizit prisun vitaminu D a vystrihat sa dokonca hojivych rybacich olejov pre ich obsah vitaminu D.
Ale tvrdia, ze tato bakterie(borelioza burkdorferi) nema len formu spirochety a bunecneho parazitu bez bunkovych stien, ale aj sporu, podobne ako sa zistilo na Chlamidii pneumoniae. To definitivne "kupujem", lebo mnozstvo bakterii vytvara spory a tieto sa n4edaju diagnozovat ziadnymi lekarskymi skuskami, tie su viditelne len elektronkovym mikroskopom a najst ich je naozaj fuska.
Ja poznam na tie formy bez bunecnych stien(mykoplazmicke) niekolko ucinnych prirodnych doplnkov, najma extrakt z olivovych listov(to mam vyskusane na viacerych ludoch v rodine) a vacsie davky uncarie tometosy a tiez vytazku z nich pod menom Samento.
Tie bezplastove vnutrobunecne parazity tiez prinutia bunky vytvarat na bunecnych stenach akoby maskovacie hlieny, cez ktore telesna obrana "nevidi"
Daju sa ciastocne odstranit napr NAC a tiez roznymi enzymami.Tym sa telesna obrana znacne posilni.
Spory by vysvetlili, preco sa borelioza vracia aj po rokoch, na spory totiz prakticky nic neposobi, snad to "odmaskovanie" a enzymi ich mozu poskodit.
To by tiez vysvetlilo, preco aj dlhsie brane antibiotika zlyhaju, hoci tie povodne bakterialne formy, spirochety velmi ucinne nicia.Preto sa predpisuju atb na roky brania, kde by som si trufal radsej odporucat prirodne latky s antimikrobialnymi vlastnostami, najma take, co adresuju nielen bakterie, ale aj mykoplazmicke formy, ako uz uvedeny extrakt z olivovych listov a uncaria tometosa a jej vytazok, Samento.
Pri akomkolvek zamoreni tela, hlavne roznymi mikrobialnymi toxinami aj tak odporucam cistenie tela enzymami a absorbentmi

Co by som tym clankom vycital je, ze neuvadzaju fakt, ze boreliozne bakterie, ich formy bez bunkovych stien (a pravdepodobne aj spory) sa pozitivne nasli v semene, slinach a dokonca v pote, takze ich prenos nie je limitovany na klieste a iny bodavy hmyz, ale prenos je mozny aj telesnym a dokonca mimotelesnym stykom, co by vysvetlovalo tie miliony infikovanych na svete, co doteraz lekari maskovali a ignorovali.
Samozrejme to iste plati aj na podobnu epidemiu chlamidii pneumoniae, ktore sa prenasaju tak isto napr kvapockovou infekciou pri kaslani, o com sa uz nepochybuje.

Na Slovensku a v Cechach je mimoriadne vysoky vyskyt tohoto ochorenia, co by som usudil z predminulorocnej spravy, ktora zistila, ze az 90% kliestov je tam infikovanych B.b bakteriami.
Ine zdroje krvneho prenosu, ako stipajuce muchy, ovady a komare sa tam pri bakteriologickom vyskume zatial ignoruju ako nosice tychto nakaz.

Zialbohu, nemam cas si to dokonalejsie prestudovat, hlavne podklady na ten vitamin D, ci to nie je len vedecky vyzerajuca rozpravka, ktore sa zialbohu v medicine siria velmi casto aj proponentmi, aj odporcami alternativ za roznymi ucelami.

Inac obe spomenute choroby znizuju imunitu proti roznym inym chorobam, ktore casto maskuju povodnu infekciu v tele.
Medzi inymi su to rozne viralne, ktore mame cely cas v tele a preto, ked sa navonok neprewjavuju, lekari ich vobec nediagnozuju a specialisti prehlasuju za "spiace"=dormant a neskodlive. Ale rozne herpesove a ine virusy vedia velmi rychlo poskodit nervovu izolaciu(myelin) co by vysvetlilo tie velmi rychle pripady paralyzacie.
Bakterie boreliozy sa totiz rozmnozuju extremne pomaly a vnutrobunecne "mykoplazmicke" formy este radove pomalsie.
Preto vsade zdoraznujem zvysovanie viralnej imunity, lebo podla roznych virologov zijeme v obdobi prudko narastajucich viralnych nakaz, ktore zostavaju v tele casto do smrti.

Inac po prezreti toho 13.5 minutoveho vytazku z filmu a znovaopakovani, ako choroby zvysuju obraty a zisky medickeho priemyslu a ako jednotlivi lekari a lekarske spolocnosti na tom bohatnu sa mi zda ta teoria o geneticky vypestovanej novej viac odolnej forme B.b coraz viac pravdepodobna...Lebo borelioz je vyse 30 a su tu zrejme uz starocia a nikdy neboli tak nebezpecne a odolne proti prirodzenej obrane tela a dostupnym liekom.
Some older data is on this page:
Since then there vas much higher number cases admited by JAMA, possibly over 400 thousand a year in USA and transmission was also admitted possible by any biting bug, including horse flies, dear flies and moskitoes. Borelia was found in sweat, saliva and semen, so transmition is much more available than only tick bites.
At the same time was admitted, that borelia is capable of discarding its outer walls and parasite inside cells as micoplasma. There has very low activity, but is practically invisible to human imunity systems.
By its influence it will make cell to produce materials(similar to mucus) on cell walls thus mask its presence for body imune mechanizm.
Some demasking elements were mentioned by various dostors as usefull, as NAC and uncaria tometosa(cats claw and its patented extract Samento)
I had personally very good results with using extract from olive leafs, which is known to be usefull on various mycoplasmic infections as well.
Or visit this link or this one