COMMON LYME DISEASE MISUNDERSTANDINGS
AND THE DELUSION OF A FAST CURE
Dr. Stephen Phillips is a doctor's doctor and a man who has served both ill children and adults by serving with great sacrifice in the elite clinical organization of ILADS. Some physicians in ILADS have treated more Lyme and other tick-borne illness patients successfully than entire hospital complexes. Below is just one more example of Dr. Phillips trying to reason clearly about the serious magnitude of Lyme disease. He does so with no benefit other than to serve the citizens of Connecticut and the US. I offer his pearls below with great pride and permission.
Written Testimony of Steven Phillips, MD
Attorney General's Hearing on Lyme Disease
Lyme disease is perfectly positioned to engender controversy. The bacteria that causes the illness, B. burgdorferi, has been exceedingly difficult to grow from Lyme patients with disseminated disease, regardless of their antibiotic treatment status. As a result, there has been no definite laboratory diagnostic test and no concrete definition of cure. If B. burgdorferi could not be cultured from a patient before antibiotic therapy, then there is no reference point with which to compare to indicate whether that individual is cured of the infection after therapy. As such, questions regarding diagnosis, treatment efficacy, and definition of cure, although still lingering problems, were virtual black holes for many years. Because of this prior void of knowledge, early researchers made a series of blind assumptions, many of which, sadly, have proven to be patently invalid. Fortunately, now decades later, there is a wealth of solidly peer reviewed scientific data debunking the prior dogma that Lyme disease is an easily diagnosed and cured illness. Yet, for unknown reasons some of the initial researchers in the field have refused to change their old paradigm in response to the accumulating storehouse of scientific fact, and this has led to a bitter divide in the medical community.
There has been considerable criticism as to the accuracy of currently available antibody blood testing for Lyme disease.1 Seronegative Lyme disease (Lyme with a negative antibody blood test) has been widely reported.2,3,4,5,6,7,8,9,10,11 Analogously, studies demonstrate central nervous system (CNS) infection with B. burgdorferi (the Lyme bacteria) by polymerase chain reaction (PCR) (a DNA test), 10,12,13 antigen capture (a test for Lyme protein),2,3 and culture,10,14,15,16 despite negative cerebrospinal fluid (CSF) by routine Lyme antibody, cell count and chemistries. As such, the absence of antibodies against B. burgdorferi in CSF cannot be relied upon to rule out CNS infection with this organism. Despite these findings, some factions of the scientific community astonishingly continue to place inappropriate emphasis on these obsolete antibody tests for unclear reasons.
Regarding the treatment of Lyme disease, some researchers claim that 30 day courses of antibiotic therapy are curative for even later stage Lyme disease, but it has been impossible for them to prove their claim without a high yield method for culturing B. burgdorferi. However, as difficult as it is to isolate B. burgdorferi from patients with disseminated disease, the reverse can be proven. It has been proven by various methods that 30 day courses of antibiotics are not curative for disseminated Lyme disease in both animal and human clinical trials.
For instance, studies document that 30 day courses of antibiotics do not eradicate disseminated B. burgdorferi infection from dogs.17,18 Unfortunately, and not surprisingly, many humans with late stage Lyme disease do not get cured of their symptoms with 30 day courses of antibiotics. Indeed, there are also many volumes of peer reviewed medical studies demonstrating persistent infection with B. burgdorferi in humans despite multiple and extended courses of aggressive antibiotic therapy. In fact, chronic infection with B. burgdorferi despite both "adequate" and even extensive antibiotic therapy has been demonstrated time and again by both PCR,7,19,20,21,22,23 visualization of the organism by histopathology specimens, 11,23,24,25,26,27,28,29 and despite the well-known difficulties in culturing B. burgdorferi from Lyme patients, by culturing the organism alive from these patients with chronic Lyme disease, most of whom have been seronegative. 15,30,31,32,33,34,35,36,37,38
As a group, pathogenic spirochetes are unusual bacteria. From the infamous Treponema pallidum, which causes syphilis, to the more recently recognized B. burgdorferi, for years they have stimulated debate not only for their breadth of clinical spectrum, but also for a variety of microbiologic incongruities. One such curiosity involves the difficulty in culturing these organisms from infected hosts, yet this may be readily explained once the fundamental life cycles of these bacteria are more fully elucidated, as the following will attempt to achieve in regard to B. burgdorferi.
B. burgdorferi, is frequently described as gram negative (a type of stain for microbiology analysis), microaerophilic (growing best in small amounts of oxygen), spiral in shape, and ranging from 9-32 microns in length, but this narrow definition of the organism cannot logically explain its ability to survive in the divergent conditions existing in the mammal vs. within the tick. If the spiral form was the only rendering in which the bacterium could exist, this relatively large Borrelia should be readily detectable in blood smears of human Lyme disease patients and susceptible infected host animals, yet it is not. As a corollary to this, ticks fed from infected hosts result in very high rates of infected ticks, despite the inability to culture B. burgdorferi routinely from their blood with standard media used to culture the organism from the tick. A logical explanation for these observations is that B. burgdorferi exists in the blood of infected hosts, but in altered states that are quite different from the familiar spiral forms. Logic further dictates that these other forms of the bacteria must not only have different appearances, but also must have unique nutritional and environmental requirements for growth than the archetypal helical forms.
Indeed, B. burgdorferi can exist in a variety of forms, which are ultra-structurally and metabolically distinct. Even in the tick, altered morphological forms of B. burgdorferi are present,39 but selective pressure within the mammal by its immune system results in these altered forms becoming far more common. These "host adapted" forms, referred to collectively as L-forms or spheroplasts, are generally lacking of a cell wall to varying degrees. B. burgdorferi spheroplasts, of which cystic forms and granules are sub-types, have been extensively documented both in vitro (in the test tube),40,41,42,43,44,45 46,47,48,49 and in vivo (in the body) both outside of and within cells.43,50,51,52,53,54 Further to this, their ability to revert from host adapted forms back to helical forms under appropriate conditions has been well documented in vitro. 43,55,56 Since energy expenditure in the way of protein synthesis is required for the conversion into spheroplasts40, the theory that these are merely end stage degenerative forms is implausible. A starving bacterium on its "deathbed" could not expend precious energy on major structural and metabolic changes, unless of course, such action was to ultimately enhance its survival.
Indeed, it has been unequivocally proven that B. burgdorferi cystic forms are virulent and infectious. The infectivity of B. burgdorferi cystic forms, their survival under extreme environmental conditions, and their ability to revert back to helical forms in vivo has been demonstrated by mice inoculation of B. burgdorferi cysts and subsequent recovery of spiral forms from the animals.57 As such, host adapted forms of B. burgdorferi are thought to be critical to the relapsing and chronic nature of the illness.58,59,62
Just as B. burgdorferi spheroplasts have altered metabolic requirements for growth, so too do they have unique antibiotic sensitivities, altered surface protein expression, dramatically reduced surface area presented for immune surveillance, and the ability to cause multiple potential problems for PCR analysis, all as compared to the helical form, respectively, and as such, all of the foregoing helps to explain the observations of antibiotic resistance, seronegativity, and PCR negativity in active disease.47,51,56, 60,61 To elaborate specifically as it pertains to problems with seronegativity, surface proteins of spheroplasts are different than surface proteins of helical forms of B. burgdorferi. Since the current antibody tests are designed to detect reactions to surface proteins of helical forms, these tests are, unfortunately, looking for the wrong targets. This helps to explain the high rates of seronegativity in Lyme disease. To reiterate specifically in regard to B. burgdorferi spheroplasts and altered antibiotic resistance, one very clear example is of cystic forms demonstrating sensitivity to metronidazole (an antibiotic), while their helical kin are resistant.62
As a general rule, chronic bacterial infections must find sanctuary within cells in order to maintain persistence. As such, B. burgdorferi has been documented within a variety of cell types, including but not limited to endothelium (a type of skin cell),63 fibroblasts (connective tissue cells),64 lymphocytes (type of white blood cell),65 macrophages (another type of white blood cell), and keratinocytes (another type of skin cell),47,66 as well as synovium (joint tissue cell).51,67 Such localization within a variety of cells68,69 affords protection against antibiotic destruction and in combination with its ability to convert into spheroplasts, provides B. burgdorferi with a protective arsenal with which it may establish a chronic and persisting infection despite antibiotic therapy.
In light of overwhelming scientific evidence that the B. burgdorferi persists in patients despite extensive treatment, insurance companies and some initial researchers still, without verifiable basis, proclaim patients cured and in no further need of therapy. The real need is to find a definite cure for this illness. However, since many of these researchers are rather occupied in the denial of its existence, the very institutions which are most in a position to find a cure, are, ironically, not looking.
However in the absence of a definite cure, antibiotic therapy can be helpful. In fact, they can mean the difference between disability and good health. It has already been shown that longer treatment durations, although certainly not necessarily curative, may be more effective than shorter durations.70,71 In light of the foregoing totality of objective peer reviewed data, any medical professional who declares a persistently symptomatic Lyme patient cured simply because 4 weeks of antibiotic therapy has been completed, is, at best, sadly and grossly misinformed.
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