Joachim Gruber, editor
Abstract, links, additions in [ ] or small print and search forms by Joachim Gruber.
Abstract
Lyme disease research is testing new working hypotheses. The ones presented here point in the direction of a paradigm shift: Borreliae burgdorferi (Bb) could be compared with people: acute Bb infection is like people staying overnight in a hotel, whereas chronic Bb infection means people living in their home and garden, having shaped their environment according to their needs and -vice versa- being subject to the limitations of their environment.
Expressed in terms of this paradigm
[Review in RB Stricker, Pathophysiology of Lyme Disease in "Counterpoint: Long-Term Antibiotic Therapy Improves Persistent Symptoms Associated with Lyme Disease", 2007]
Borrelia burgdorferi (Bb)
[Alitalo et al., 2001; Hartmann et al., 2006; McDowell et al., 2003; Bykowski et al., 2007; Güner, 1996; Kraiczy et al., 2002, 2004; Liang et al., 2004]
[Cruz et al., 2008, see also Iliopoulou and Huber, 2011],
and["cytokine modulation lyme": NCBI Result].
A lot more research needs to be done.
Chronic Lyme Disease, or better termed Chronic Tick Borne Complex, has no different or confounding problems in proving the disease than any other chronic, stealth infection with parasitic features:
[stealth pathology of Bb in: Stricker, 2007; "parasitic": LymeRick Result]
[for stealth pathology see
One can find the germ
["(PCR + DNA) + lyme + detection": NCBI Result],
["culture-confirmed + lyme + test": NCBI Result],
["xenodiagnosis + lyme": NCBI Result],
["(antigen detection) + lyme": NCBI Result]
["(Brunner OR Coyle OR Schutzer) + ("immune complex" + lyme)": NCBI Result, "immune complex dissociation" + lyme": NCBI Result; Schutzer et al. (1994, 1990); Brunner and Sigal, 2000].
All of these test methods have been used in research studies demonstrating presence of the microbe. Antigen detection and DNA testing are unfortunately the only direct tests available to practicing health care members and their patients.
Since tick borne microbes are very complex there will likely never be a single one test standard demonstrating directly the presence of the germ for practical cost effective patient use.
As Dr. Stricker and Lorraine Johnson Esq. reviewed, future proteomics may offer better evidence by demonstrating specific metabolic products from non dormant Borrelia.
[Review: Stricker and Johnson, 2011];
[Barbour, 2008, Xu, 2008; "Stricker + Johnson": NCBI Result].
There is a multitude of results to mark how the microbe(s) are making the patient sick. Some samples:
["CD 57": Lymenet.de; CD = Cluster of Differentiation]
["immune + dysfunction": Lymenet.de].
["peripheral neuropathy": Lymenet.de, "autonomic + neuropathy": Lymenet.de]
These are just a few markers of how the microbe(s) is making the patient sick. All or nearly all chronic tick borne complex is an immune-neuro-endocrine disease and these manifestations can be treated and followed to connect the presence of the germ with the clinical manifestations.
["immune + neuroendocrine": LymeRick Result, neuroendocrine: Lymenet Europe Result]
Culturing a germ was a necessity as the gold standard in proving infection per Dr. Robert Koch
Members of the Infectious Diseases Society of America (IDSA) will often state that it is the gold standard to prove infection.
["Lyme": IDSA]
It was gold in the early 1900s and tarnished now by other advanced testing and recognition of the complexity of parasitic acting infections.
... Regardless of the test (culture, antigen etc.) which establishes presence of the microbe, another test/finding is required to demonstrate secondary illness i.e. brain spect scan, ATP production, cytokine panel flares etc. [see also here]
The work by Barthold and Hodzic [Hodzic et al., 2008] demonstrates persistence of live Borrelia after 30 days of antibiotic treatment in mice. The authors cultured many tissue samples but using DNA testing they found DNA most often in the tibiotarsal tissues after treatment.
Earlier work by them showed some of this was live spirochete DNA after culture since they could culture if they immune suppressed or influenced the mice immunologically.
["Barthold + live + spirochetes": LymeRick Result]
A few points:
"intracellular": LymeRick Result]
["biofilm + lyme": NCBI Result; Sapi, 2011; Parveen et al., 2011; biofilms blog by Alan MacDonald]
Overall, however, it is another study demonstrating persistent infection with secondary seeding sites after courses of ceftriaxone.
[Christ: "Hormones", "Lyme and Hormones": Yvonne's blog, "hormones": Lymeinfo.net]
Streeten et al., 1984, Arafah, 2006,
Comprehensive Melatonin Profile, 2008 (in cache, melatonin is the primary substance secreted by the pineal gland, which modulates the hypothalamic-pituitary-adrenal (HPA) axis during clinical illness, the serotonergic system in psychiatric disease, as well as the body's general response to stress.)
"comprehensive + melatonin + profile": Google Search on Genova Diagnostics,
Tjemberg et al., "Mapping of hormones and cortisol responses in patients after Lyme neuroborreliosis", 2010]
Wikipedia, "Lyme disease":
"A developing hypothesis is that the chronic secretion of stress hormones as a result of Borrelia infection may reduce the effect of neurotransmitters, or other receptors in the brain by cell-mediated proinflammatory pathways, thereby leading to the dysregulation of neurohormones, specifically glucocorticoids and catecholamines, the major stress hormones [Elenkov et al., 2005, Calcagni and Elenkov, 2006].
This process is mediated via the hypothalamic-pituitary-adrenal axis. Additionally tryptophan, a precursor to serotonin, appears to be reduced within the central nervous system (CNS) in a number of infectious diseases that affect the brain, including Lyme [Gasse et al., 1994]. Researchers are investigating if this neurohormone secretion is the cause of neuropsychiatric disorders developing in some patients with borreliosis [Zajkowska et al., 2006]."
Blunted hormone responses could be one of the methods persistent microbes utilize to maintain persistence.
These are not bandaids as the best description- more like getting the train back on track or replacing a flat tire.
The hormonal defect appears to be focused on impaired
Published studies have demonstrated hypothalamic-pituitary dysregulation in the other two spirochetal infections - syphilis and leptospirosis. Thus, Borrelia burgdorferi similar effect would not be a random thought without association due to common features.
[Schäfer et al., 2008, Hypothalamic-pituitary insufficiency following infectious diseases of the central nervous system, assays and pituitary insufficiency: data]
["pituitary": LymeRick Result]
This means the defect could be at one of multiple sites such as
["cross reacting antibodies": LymeRick Result, "cross reaction + autoimmune": LymeRick Result, "endocrine + receptor + lyme": Google Result]
["hypothalamic pituitary": ILADS Result, "vascular": LymeRick Result],
["cytokine downregulation + (lyme or borrelia)": NCBI Result, "cytokine + downregulation": LymeRick Result]
[thyroid: LymeRick Result]
One approach is
Review in R.B. Stricker, Immunosuppression in "Counterpoint: Long-Term Antibiotic Therapy Improves Persistent Symptoms Associated with Lyme Disease"
Elenkov et al., Cytokine Dysregulation, Inflammation and Well-Being, 2005
... hypotheses about late autumn and early spring relapses matching an ecosystem drive between the spirochetes, the life cycles of ticks and the seasons: which notes again how opportunistic these microbes are.
There may be more complex reasons beyond relative immune control for the cyclical times when symptoms and signs of illness abate.
Quiet times, as in the disappearance of the bulls eye rash while spirochetes are seeding elsewhere, can also be due to control of [in contradistinction to "by"] the immune system or dysregulation of the immune system
["("immune dysregulation" OR "host-pathogen interaction") + lyme": NCBI Result)
by the
[e.g. Liang et al., 2002]
of the spirochetes.
Also, for many patients, the specific organ manifestations are not synchronous and what is a relief in one system can simultaneously be a flare up time in other organs.
Patients may be doing well for many months (before relapse) despite opportunities for positive signals to the Borrelia. When a relapse occurs, and then clears spontaneoulsy, it may be a mistake to conclude that the clearance of symptoms weighs in favor of immune control of infection over infection control of the immune response. Fortunately, advanced lab culturing and Kellerman lab cytokine testing can add a lot to our ability to distinguish one from the other.
Chronic infections that continue to drive autoimmune illness are one of the leading directions in investigation.
The immune dysfunction spin off effects on
["immune activation + coagulation": "Google, Berg et al., 1990],
are all ways that chronic tick borne illness makes one sick.
Separating the mechanisms of illness induced by chronic infections as though these are independent of an ongoing infection is certainly one of the biggest assumptions. [When an infection is chronic, infection mechanisms and host environment need to be considered as being interdependent.]
Actually HOW tick borne microbes make one sick, whether acutely or chronically, is critical to understanding chronic tick borne infections- but rarely if ever investigated by mainstream research.
J. Clin. Invest. 2012 Jul; 122(7): 2652-60.
Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy.
Bockenstedt LK, Gonzalez DG, Haberman AM, Belperron AA
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
DOI: 10.1172/JCI58813
Abstract:
An enigmatic feature of Lyme disease is the slow resolution of musculoskeletal symptoms that can continue after treatment, with some patients developing an inflammatory arthritis that becomes refractory to antibiotic therapy. Using intravital microscopy and the mouse model of Lyme borreliosis, we observed that Borrelia burgdorferi antigens, but not infectious spirochetes, can remain adjacent to cartilage for extended periods after antibiotic treatment. B. burgdorferi was not recovered by culture or xenodiagnosis with ticks after antibiotic treatment of WT mice and all but one of the immunodeficient mice with heightened pathogen burden due to impaired TLR responsiveness. Amorphous GFP+ deposits were visualized by intravital microscopy in the entheses of antibiotic-treated mice infected with GFP-expressing spirochetes and on the ear cartilage surface in sites where immunofluorescence staining detected spirochete antigens. Naive mice were not infected by tissue transplants from antibiotic-treated mice even though transplants contained spirochete DNA. Tissue homogenates from antibiotic-treated mice induced IgG reactive with B. burgdorferi antigens after immunization of naive mice and stimulated TNF-α production from macrophages in vitro. This is the first direct demonstration that inflammatory B. burgdorferi components can persist near cartilaginous tissue after treatment for Lyme disease. We propose that these deposits could contribute to the development of antibiotic-refractory Lyme arthritis.
The persisting dna is foreign enough to stimulate a continued inflammatory response- in the absence of viable spirochetes at the articular tissue sites according to the authors.
Two interesting questions arise:
able to return and cause inflammation again and the failure of signaling and recruitment of pus cells [leukocytes] to the tissue sites?
... the results of this study combine with many other studies to build a paradigm of chronic tick borne complex disease. E.g. the Embers study of chronic infected rhesus monkeys [Embers et al., 2012] demonstrated
Elizabeth Aberer's ["Aberer": NCBI Result] work and Embers' [Embers et al., 2012] support the paradigm that longer rx leads to lower, but persistent, bacterial load.
At what point does the number and variant forms of Bb (even if not/never fully eradicated) no longer cause immune system dysfunction and all the other spin-off effects on
Obviously at some much lower number and variant forms.
How Bb causes illness related to
needs to be summarized from the many international studies so far and hypothesized and further studied.
Until then, it is a very narrow concept, overgeneralized from limited data and concepts, that smaller numbers of Borrelia in patients after
that these smaller numbers are no longer somehow contributing to/causing illness.
This hypothesis [the irrelevance of smaller numbers] sounds perhaps like a manufactured model for future directed entrepreneurial grants/patents and excuses for serious past mistakes rather than well established pathophysiology. At the grant level, funds are directed at a pre-planned and conceived model of illness that is chosen to lock arms with the Bayh-Dole Act of 1980. Evidence that is opposed is discarded/ignored. Or not published for years.
... Elizabeth Aberer in Graz, Austria, many years ago did sequential deep core needle biopsies of connective tissue in and around joints of patients with persistent symptoms.
[Aberer, 1996;
see also "Lyme borreliosis - an update", Aberer, 2007]
Elizabeth concluded the forms were not simply debris because these forms ingested acridine orange and this is evidence of metabolic activity - not dead debris or simply protein products. She did not rely on synovial fluid but went to the home of persistent forms.
Probably
Alginate (major component of pseudomonas biofilms and suspected to be present in Borrelia biofilms) production by pseudomonas is stimulated by estrogens [Chotimall et al, 2012]. Apparently in females with cystic fibrosis, exacerbations of bronchitis are significantly more common in the perimenstrual period [time span around menses]. It is interesting to speculate whether this happens in Bb as well.
Here are some factors that likely can activate dormant or very slowly triggered replicating Borrelia burgdorferi:
["dormant": LymeRick Result]
This works
["inflammatory + cytokines": LymeRick Result], [Norman, 2008, "From vitamin D to hormone D: fundamentals of the vitamin D endocrine system essential for good health"]
["prednisone": LymeRick Result]
[e.g. Gasse et al., 1994]
["coinfections": LymeRick Result]
- to name some starters to explore.
Vet Med Nauki. 1987;24(4):50-4. PMID: 3629949
[Effect of ultrasound-disintegrated spirochetes on blood coagulation and hemodynamics in chickens].
Abstract:
Blood coagulation tests and histopathologic investigations of birds were carried out following the injection of a suspension of spirochaetes destroyed with ultrasound. It was found that the suspension acted as thromboplastin, causing disseminated intravascular clotting of blood after intravenous injection.
It is engaging to ask how tick borne microbes make us sick. And with this knowledge ask what mechanisms lead us to believe about the likely success or matching efficacy of a 2 or 4 week arbitrary duration of antibiotic treatment of tbds [tick bite diseases].
Immune activation of coagulation, as in above study, is described in CFS [Chronic Fatigue Syndrome] in the Hemex lab results and coagulation study special tests at Hemex. Rx is heparin. Large numbers are not needed to activate the domino effect of coagulation factors and complete clot formation is not necessary for down stream hypoperfusion.
Other examples:
["molecular mimicry autoimmune Lyme": NCBI Result; "cross reaction + autoimmune": LymeRick Result; Rashid and Ebringer, 2012]
These are some mechanisms, that are not dependent on large numbers of spirochetes, functioning to drive a serious disease state.
Consequently, finding small numbers of Borrelia in rhesus monkeys after 4 weeks of antibiotic rx, small numbers which can continue to drive an illness via these mechanisms, and can repopulate- small numbers can be as significant as larger numbers.
The mechanism of illness must be fundamentally addressed to answer- are the patients better/cured after a particular duration of treatment?
Syphilis cannot be lab cultured and no one holds the position that therefore it is not present, is not causing disease, and that small numbers mean the microbe is benign.
There have been many critiques of the original Valhalla center study on the prevention or effectiveness of single dose treatment for tick bites [Wormser, 2005]. Probably one of the greatest is simply that the study conclusion makes no sense at all when weighed against what is known about the microbiology of tick borne diseases and the ecosystem of tick/borrelia/host.
... Regardless of the test (culture, antigen etc.) which establishes presence of the microbe, another test/finding is required to demonstrate secondary illness i.e. brain spect scan, ATP production, cytokine panel flares etc. [see also here]
J Vet Diagn Invest. 2011 Jul;23(4):757-63. Epub 2011 Jun 13.
Krimer PM, Miller AD, Li Q, Grosenbaugh DA, Susta L, Schatzberg SJ.
Abstract:
Although neurological signs have been reported sporadically in dogs with systemic Lyme disease, it is unknown if neuroborreliosis occurs in dogs. The current study systematically evaluates canine brains for evidence of Borrelia burgdorferi infection. Twelve Beagles were experimentally challenged with B. burgdorferi-infected ticks at 18 weeks of age, and 2 unexposed dogs served as controls. One of the uninfected dogs and 6 infected dogs were each given 5 daily immunosuppressive doses of dexamethasone starting at 153 days post-infection. Eleven dogs were confirmed as infected by skin punch biopsy polymerase chain reaction (PCR) and serology. Neurological signs were not seen in any dogs through the end of the 190-day study. Whole blood, serum, cerebrospinal fluid (CSF), and brains from all dogs were collected. DNA was extracted from blood, CSF, and brain and evaluated by PCR for B. burgdorferi. Formalin-fixed brain tissue was examined by histopathology, immunohistochemistry, and PCR. Immunohistochemical staining for B. burgdorferi antigen was negative in all cases. The CSF analysis was normal, and PCR was uniformly negative for B. burgdorferi in all dogs. Six of the 11 (45%) infected dogs had mild to moderate lymphoplasmacytic choroid plexitis, which was more pronounced in the immunosuppressed dogs. The lack of B. burgdorferi DNA and immunohistochemical evidence of organisms, including within the choroid plexus lesions, suggests that B. burgdorferi does not have a direct role in the etiopathogenesis of canine central nervous system pathology.
Comments:
This is a fairly interesting article for several reasons:
Immunity. 2012 February 24; 36(2): 251-261
The circadian clock controls toll-like receptor 9-mediated innate and adaptive immunity
Adam C. Silver, Alvaro Arjona, Wendy E. Walker, and Erol Fikrig
Abstract
Circadian rhythms refer to biologic processes that oscillate with a period of approximately 24
hours. These rhythms are sustained by a molecular clock and provide a temporal matrix that
ensures the coordination of homeostatic processes with the periodicity of environmental
challenges. We demonstrate the circadian molecular clock controls the expression and function of
toll like receptor 9 (TLR9). In a vaccination model using TLR9 ligand as adjuvant, mice
immunized at the time of enhanced TLR9 responsiveness presented weeks later with an improved
adaptive immune response. In a TLR9-dependent mouse model of sepsis, we found that disease
severity was dependent on the timing of sepsis induction, coinciding with the daily changes in
TLR9 expression and function. These findings unveil a direct molecular link between the circadian
and innate immune systems with important implications for immunoprophylaxis and
immunotherapy.
Nearly all organisms have developed mechanisms for anticipating environmental changes in
order to optimize their survival. Circadian rhythms are autonomous, self-sustained, ~24 h
oscillations in biologic processes entrained by environmental cues, most notably the daily
changes in light intensity.
Body clock 'alters' immune system
By James Gallagher, health and science reporter, BBC News
The time of the day could be an important factor in the risk of getting an infection, according to researchers in the US.
They showed how a protein in the immune system was affected by changes in the chemistry of the body through the day.
The findings, published [February 2012] in the journal Immunity, showed the time of an infection changed its severity.
An expert said drugs were likely to take advantage of the body clock in the near future.
Plants, animals and even bacteria go through a daily 24-hour routine, known as a circadian rhythm. Jet lag is what happens when the body gets out of sync with its surroundings after crossing time zones.
It has been known that there are variations in the immune system throughout the day. Researchers are now drilling down into the details.
The immune system needs to detect an infection before it can begin to fight it off. Researchers at Yale University School of Medicine were investigating one of the proteins involved in the detection process - Toll-like receptor nine (TLR9), which can spot DNA from bacteria and viruses.
In experiments on mice, the scientists showed that the amount of TLR9 produced and the way it functioned was controlled by the body clock and varied through the day.
Immunising mice at the peak of TLR9 activity improved the immune response, the researchers said.
They said humans with sepsis, blood poisoning, were known to be at a greater risk of death between 02:00 and 06:00.
Time link
When testing mice, the severity of sepsis depended on the time of day infection started and coincided with changes in TLR9 activity.
Prof. Erol Fikrig, who conducted the study at Yale University, said they had found a "direct molecular link between circadian rhythms and the immune system", which could have "important implications for the prevention and treatment of disease".
He added: "It does appear that disruptions of the circadian clock influence our susceptibility to pathogens."
Dr Akhilesh Reddy, who is researching circadian rhythms at the University of Cambridge, said it was "known long ago" that timing had an impact on the immune system, but this was "one of the first forays" into the reasons why.
The implications for healthcare could mean that drugs need to be given at certain times of day in order to make them more effective, or drugs could be made which actually target the body clock to put the immune system into its most active phase.
Dr Reddy said drug companies were "all switching onto this" and were "now screening drugs at different times of the day".
He could see the body clock impacting medicine "within 10 years".
Comments:
In many patients the very low AM [before noon] cortisol levels are not due to adrenal fatigue i.e. lack of production burn out- but due to immune interaction with microbial night cycles that cause consumption of stress hormones at night as they are being produced.
These patients can have very high metabolite quantities in the urine of cortisol over 24 hrs and a reversal of the saliva level zenith/nadirs. Low in the AM and gradually rising during the day with peaking at the normal sleep phase when it should be low.
The Cyclical growth concept of Bb in the human body, as mentioned by Dr. Joe Burrascano, may (and I'm not sure of the details because I'm getting old) date back to the halcyion days of the late 1980s when Joe and I worked together in Southampton, New York, in our joint study of patients with my technique to culture Bb from blood.
I don't have my notebooks so I can't quote details about the clinical histories of individual patients. If there was a cyclical yield of positive and negative blood cultures Dr. B would have the details.
There is also the model of relapsing fever borrelia (Borrelia hermsii) which is famous for its cycles of spirochetemia alternating with no febrile intervals (and borrelia seen in blood during the afebrile intervals) and then successive episodes of fever (+ spirochetemia) and no fever (- spirochetemia).
The mystery in NON FEVER intervals in B. hermsii infection or B. duttoni infection in Africa is the so called Negative Phase.
The NEGATIVE PHASE really pertains to the studies of the tick vector, and translated into plain Anglo Saxon English... during the NEGATIVE PHASE, no spirochetes can be seen in the vector tick, but after a period of time has passed, spirochetes are again visible in the vector tick.
I personally blame the negative phase on the formation of granular forms of the spirochete. Granular forms live inside cells (intracellular residence) and from time to time break out of the cells and re-form spiral spirochetes.
Only two living pathologists on the planet believe in the granular form of borrelia (Dr. Marie Kroun of Denmark, and me). All of our predecessors who had big names in their time (Balfour, Fantham, Levaditi, Coutts, Dutton etc.) lived and died in the early 20th century.
As to cystic forms reverting to spiral forms, the hard data comes entirely from laboratory studies of Dr. Oystein Brorson and by Dr. Eva Sapi, and me.
Cysts can be stratified into two types:
Therefore Brorson has shown that borrelia cysts have an independent "life of their own" - No spiral borrelia need apply.
Now to the biofilm paper (in cache). Dr. Eva Sapi is first author. It has passed its first critical peer review. The reviewers have asked that some sentences in the paper be rewritten. Dr. Sapi has done the required re-writes. No reviewer generated objection to any of the scientific methodology in the paper has come up. I am one of several coauthors. The final paper is expected to be approved for publication in a first rate highly academic journal, probably before September [2012].
Other distinguished colleagues, such as Dr. Klaus Eisendle, Prof. Bernhard Zelger have already written accepted peer reviewed manuscripts which allude to the concept of biofilms of borrelia [Eisendle and Zelger, 2009], a concept which Dr. Eva Sapi conceived and an idea which I lectured on later. My full PDF of the biofilms of borrelia lecture at the University of New Haven (in cache) is freely available on multiple sites on the web.
It is important to realize that accepted categories of biofilm formation are already in the scientific literature for the following spirochetal genera:
The Leptospiral biofilms have only been proven to exist in laboratory models and in water supplies. As of right now there is no proven animal model for the formation of Leptospira biofilms in a warm blooded animal, although studies are underway to search in the kidney of dogs for leprospire biofilms in the proximal convoluted tubules of the kidney. [Leptospirosis is frequently shed into the environment via animal urine.] Whenever you take your dog to the veterinarian the dog will be eligible for a "lepto" immunization, if not up to date.
[By the way:] I believe in neuroendocrine dysfunction in LB [Lyme Borreliosis].
Literature
Abstract
Borrelia burgdorferi has long been known to be capable of forming aggregates and colonies. It was recently demonstrated that Borrelia burgdorferi aggregate formation dramatically changes the in vitro response to hostile environments by this pathogen. ... In this study, we investigated the hypothesis that these aggregates are indeed biofilms, structures whose resistance to unfavorable conditions are well documented. Biofilm formation by Borrelia species might play an important role in their survival in diverse environmental conditions by providing refuge to individual cells.
Results:
- Doxycycline reduced spirochetal structures approx. 90% but increased the number of round body forms about twofold.
- Amoxicillin reduced spirochetal forms by approx. 85% - 90% and round body forms by approx. 68%, while treatment with
- metronidazole led to reduction of spirochetal structures by approx. 90% and round body forms by approx. 80%.
- Tigecycline and tinidazole treatment reduced both spirochetal and round body forms by approx. 80% - 90%.
When quantitative effects on biofilm-like colonies were evaluated,
- the five antibiotics reduced formation of these colonies by only 30% - 55%.
- In terms of qualitative effects, only tinidazole reduced viable organisms by approx. 90%.
- Following treatment with the other antibiotics, viable organisms were detected in 70% - 85% of the biofilm-like colonies.
Conclusions:
Antibiotics have varying effects on the different morphological forms of B. burgdorferi. Persistence of viable organisms in round body forms and biofilm-like colonies may explain treatment failure and persistent symptoms following antibiotic therapy of Lyme disease.
Videos
more on lymenetEurope.
The following remarks (#14 and #15) will be included in this minireview once permission by the author is obtained.
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chronic persistent infection despite intensive antibiotic treatment
Version: 29 February 2016