Paradigm shift

My patients with chronic Lyme disease may suddenly relapse after years of feeling well.

A new mouse study shows not just persistence of Lyme bacteria after 30 days of antibiotic treatment with ceftriaxone but “resurgence” of infection. The authors of the study tell us their findings are controversial and caution us not to change the way we treat patients based on these findings. Of course not.

The study is published in PLOS January 2014.  The levels of bacteria in experimentally treated mice were found to decrease at months 2, 4 and 8 but surge to pretreatment levels at 12 months. The DNA load of bacteria in in the group treated with salt water and the group treated with 30 days of antibiotics was the same at 12 months.  As seen in other studies, the post-treatment spirochetes were “non-cultivable.” They can cannot be cultured in laboratory media. These spirochetes were clearly different from their pre-antibiotic forbearers.  Other mouse studies have demonstrated non-cultivable organisms. It has been suggested that these bacteria are attenuated and do not cause disease. Various metrics performed in this study do not support this thesis. Although these spirochetes do not culture, they transfer to other mice via ticks used in xenodiagnoses. Intact, viable spirochetes were microscopically observed in the same tissues; joints, heart and blood vessels. 

A study published March 11, 2014 looked at stored serum from Lyme patients. PCR for Lyme in patient serum has always been a low yield test.  In 1/12 post treatment blood samples a genetically novel Lyme variant was found; and, in 20 pretreatment samples one Borrelia miyamotoi and two B. burgdorferi were found. These findings are surprising. Perhaps we do not have a good handle on the genetic spectrum of Borrelia species causing Lyme disease syndromes.

According to standard bearers of the disease like Steere, as described in his paper “Diagnosis of Lyme Borreliosis,” --  the 2 tier CDC test is essentially always positive in patients with disseminated disease after 4 weeks;  PCR of synovial fluid in patients with negative serology should not be performed because positive results will be false positives; and usually, patients with objective evidence of dissemination have one or more of the following:  EM rash, atrioventricular cardiac conduction delays, myopericarditis, facial palsy, meningitis and meningioradioradiculoneuritis (Bannsworth’s syndrome).

I think maybe we are talking about two completely different diseases.

In our patients (with Lyme disease) Western Blot testing is neither accurate nor dependable. In our experience IgG bands, especially the 5/10 discussed by Steere are almost never seen. Positive Western Blot responses are primarily IgM in all stages of the disease.  ( Regarding the Steere/CDC two tier test for Lyme It is fascinating to read that the IgM bands are based on Engstrom’s work using B. burgdorferi strain 297, that the IgG bands are based on Dressler’s work with Bb strain N40 and that the antigens in standard FDA approved kits come from yet a third strain of Lyme, Bb B31).  These studies were pre- 1994 and presented at the Dearborne conference.

When I find a positive PCR for Lyme in joint or body fluid it is essentially always a true positive result. The fault with PCR is low sensitivity. 

Aside from different sero-reactions, my patients with late, disseminated disease have: constitutional symptoms like fatigue; neurocognitive and neuropsychological problems; arthralgia (joint pain) with arthritis (inflamed swollen joints) rare; peripheral neuropathy and autonomic neuropathy and usually have none of the above manifestations.  Of course my patients do have arthritis, meningitis, radiculitis, EM and carditis, but these are exceptions, not the rule.  

I think I explain the split personality of the disease. The characterization of the disease from the perspective of academic medicine is based on inherent biases and the need to have something concrete which can be easily characterized and defined.  The other personality of the disease stems from a patient-centered clinical process. Medical practitioners know that disease is frequently not black and white and that it usually forgets to read the text books. 

Those on the academic side are interested in having a debate. They are by nature competitive and feel they have to prove they are correct.  Recently Barbour described the 3 decades long debate and compared the two sides, one his side: all of academia, science, public health authorities – on the other side: a few non-academic practitioners and patient advocacy groups. This is not a valid debate point. Many famous persons and institutions have been wrong throughout history.  And important medical academics like Fallon do in fact disagree with the main view. 

I think biases within the academic world are very important. For example:  “Germs are killed by antibiotics – end of story.”  Barbour elicits the image from “The Terminator” movie where a robot is turned to molten metal and magically resurrects itself as analogous to our thinking about Lyme bacteria suggesting we are imbuing the spirochetes with supernatural properties.  He proffers the concept that the remains of dead Lyme bacteria may trigger a post-Lyme syndrome. The science is saying something else. 

I suspect Lyme spirochetes are not entirely unique in their response to antibiotics. Many microbes are never completely destroyed by antibiotics and may contribute to chronic illness in some manner. This may apply to mycoplasmas and chlamydias for example. 

Academic medicine should take notice. Something unique and very significant is going on when patient groups are able to get laws changed in opposition to their unyielding views. The prevailing paradigm is changing.  New thinking requires the experts to set aside their egos and preconceived notions and take a fresh look at the problem with new eyes.

Babesia only

This 53-year-old male, formerly a serious athlete, has been sidelined since 2000 with a primary diagnosis of chronic fatigue syndrome. He suffered dehydration and hyponatremia, low sodium, after running a marathon, and has never been well since. His symptoms have included: severe fatigue, muscle pains, tendinitis and joint pains. Over many years he experienced significant ups and downs with reliable exacerbation every 4 to 6 weeks. During these episodes he had more fatigue and achiness, and felt more flu-like. He has never had any significant fevers, night sweats or air hunger.

He lives in an area were Lyme disease is endemic and spends much time outdoors. He has no recollection of any tick bites or EM rash. Testing for Lyme disease has been negative.  Co-infection testing has been negative except for a blood smear examination which showed the presence of intra-erythrocytic organisms compatible with Babesia species.

He has been treated specifically for Babesia and has improved dramatically over a 7 month course. Recently hyperbaric oxygen therapy was added and he has done even better. Of course antibiotics in Babesia programs also kill Lyme. 

People sometimes ask me: can you just have Babesia? In theory yes.   Infected Ixodes scapularis ticks can pick up an unpredictable “grab bag” of germs.  Any one tick will be infected with varied combinations of:  Babesia, Anaplasma, Rickettsia species, Mycoplasma species, Bartonella species, Lyme – a variety of strains, others?  Some ticks will be infected only with Babesia.  

Some suggest that hyperbaric therapy “feeds” Babesia, making it worse. This is not true. 

Recurring flu-like symptoms, ostensibly the calling card of Babesia have been gone for months. The cyclical exacerbations are gone.  He still suffers with fatigue but his pain is almost completely gone. He was recently able to participate in a sporting event without the severe consequences (utter exhaustion and horrible muscle pains) he has become accustomed to – and this is great.  

An inconvenient truth

The CDC has replaced the term post Lyme disease with post treatment Lyme disease syndrome and admit on its website that the cause of the syndrome is not known. The CDC says the cause of the syndrome is unknown but acknowledges research shows persistence in animals. The CDC claims that studies show no benefit from prolonged antibiotic therapy and that patients with this syndrome eventually get better without further care; both of these statements are wrong. Substantial, contemporary literature disputes the first claim and nothing supports the latter claim. The piece (CDC web page) dredges up the notion that patients who do not get better with 2-4 weeks of therapy have an "autoimmune" disease comparable to three other bacteria which cause the same sort of thing. Strep throat - rheumatic fever; chlamydia - the STD variety- Reiter's syndrome; and Campylobacter, a gut bug- Guillain-Barre syndrome. None of these other germs is anything like Lyme disease: the analogies are poorly drawn. These other bacteria cause localized infection: throat, genitals, colon: Lyme is a widely disseminating multisystem bacteria. Reiter's syndrome is an obsolete term now replaced with reactive arthritis.(at least use the correct mainstream terminology). I do not dispute that a variety of microorganisms cause autoimmune disease. But the existence of an autoimmune phenomenon does not preclude the role of chronic, persisting infection. Chlamydias are small intracellular organisms which do not clear easily. Latest research, 2010:

Controversial Treatment Approach Could Lead to a Cure

Keywords for this press release: reactive arthritis, Chlamydia-induced reactive arthritis, Reiter's syndrome, chronic ReA, Chlamydia trachomatis bacterium, antibiotic treatment, chlamydial gene transcription, heat-shock proteins, chlamydial protein synthesis, antibiotic combinations, doxycycline, azithromycin, rifampin

Researchers from University of South Florida College of Medicine found a combination of antibiotics to be an effective treatment for Chlamydia-induced reactive arthritis, a major step forward in the management, and possibly cure, of this disease. Results of this study are published in the May issue of Arthritis & Rheumatism, a journal of the American College of Rheumatology.

Strep throat. An aerobic gram positive cocci which replicates every 20 minutes and infects superficial throat structures and tonsils is very different from an anerobic, pleomorphic, blood-brain crossing spirochete. Thankfully we rarely see rheumatic fever anymore, but patients with recurring disease were frequently treated with long term penicillin therapy including Bicillin injections. A significant percent of the population is permanently colonized with strep and remain so no matter how many courses of amoxicillin they take.  PANDAS is a more contemporary issue in this same vein. 

Guillain-Barre. An awful syndrome. Can be caused by flu vaccines, Lyme disease and many other infections. This is apples and oranges.

Patients with post-treatment Lyme have a disease so complex and varied that it can make your brain stop working or cause your heart to stop.

Nothing else is like this.  Lyme spirochetes disseminate widely, easily cross into the brain and infect a host of tissues. These other syndromes are not comparable. The CDC piece is dismissive, essentially saying: autoimmune disorders occur in the aftermath of other infections so there is nothing special about this post-treatment Lyme syndrome which is relatively rare and gets better by itself anyhow.

Assertions that a few weeks of doxycycline kill all Lyme spirochetes have no basis in fact or science.

Antibiotics are not that effective. If they were we would die every time we took them. It is impossible to eradicate all the flora in our gut with any course of antibiotics, thankfully. Otherwise our immune systems would be fatally wounded.  I do not believe we ever eradicate all dental spirochetes protected by biofilms with courses of antibiotics. How then are we going to eradicate Borrelia spirochetes, demonstrating the best survival skills of any organism on the planet.  Spirochetes persist in mice, dogs, monkeys and people. It is an inconvenient truth.

Bile acid sequestrants, mold, toxins and Lyme

My patient after 5 years of antibiotic treatment had been in a fairly remitted state. And then she was exposed to toxic mold and the entire Lyme syndrome became activated.  She experienced recurrent fatigue, pains, cognitive dysfunction, mood swings with emotional ups and downs, along with night sweats and other symptoms had taken multiple naturopathic therapies for detoxification which had not helped much.  We started Welchol, which had been helpful in the past and which was very effective right away. A urine test sent to Realtime laboratories showed the presence of mycotoxins. The concept is that even though the home mold issue had been remediated, mold persisted in her sinuses elaborating toxins. The treatment for this was intranasal antifungal therapy, intraconazole, combined with BEG, to treat bacteria and also break down biofilms. Topically EDTA works here to degrade biofilms mucopolysaccharide strands held together by calcium which is in turn chelated by this agent. Other aspects of her illness, including:   neuro-Lyme, Babesia and Bartonella were also addressed independently.  The addition of glutathione and methy b12 and methylfolate may promote detoxification and seem to be helpful.

Bile acid sequestrants, (BAS) primarily cholestyramine and Welchol have become popularized for their putative role in the removal of toxins. In the past, I implied, or stated that these agents remove neurotoxins. This statement cannot be supported. I do not believe they remove quinolinic acid.

QUIN, quinolinic acid is the major neurotoxin associated with Lyme neuroborreliosis and possibly many other neuro-inflammatory diseases: HIV dementia, Parkinson’s disease, motor neuron diseases, Huntinington’s disease, MS and psychiatric disorders.  It is produced and released by infiltrating macrophages and activated by glial cells. The concentration of QUIN in cerebrospinal fluid may correlate with the severity of these illnesses. QUIN serum concentration was recently shown to be associated with increased hepatic encephalopathy seen in patients with cirrhosis of the liver.  QUIN, an NMDA agonist, acts as a neurotoxin, gliotoxin,, proinflammatory mediator, prooxidant molecule and may alter the integrity of the BBB.

Many exogenous toxins have negative effects on the brain and central nervous system.

BAS have been shown to help removal of toxins from mold and some bacteria. There is no narrative to support the contention that Lyme is a biotoxin disease or that BAS removes these unsubstantiated toxins. 

BASs remove stuff. 

Bile acids are produced by the liver and circulated through the small bowel to assist in the digestion of fat, emulsification. BAS remove these substances – and other things. For example, thyroid hormone. Recent studies point to the usefulness of these agents for thyrotoxicosis. BAS also remove toxins associated with C. diff colitis. BAS have other effects which are not well understood. Their primary purpose is to lower cholesterol. Bile acids are derived from cholesterol; when they are taken away -  the liver makes new bile acids from circulating serum cholesterol therefore lowering serum cholesterol levels.  For reasons not understood, BAS also lower blood sugar. The BAS, as previously stated, has been shown to lower CRP levels, an indicator of lowered inflammation by way of complement activation. 

BAS may cause decreased adsorption of some drugs, (not most). Penicillin and tetracycline are on the list. There is a concern about fat soluble vitamins, not proved. 

Activated charcoal is also reported to remove mycotoxins. Charcoal is known as the universal antidote for poisoning; I am afraid it also indiscreetly removes drugs you want to keep on board.

As more adverse information about statin drugs comes out:  raise blood sugar, cause cognitive difficulties, cause muscle inflammation and liver inflammation --  in general, I would argue that BAS should be considered in lieu of the more toxic agents. Pharmaceutical representatives quickly point out that “data” only supports the use of statins to prevent cardiovascular disease. Older studies with cholestyramine showed similar results: new studies will never be done with these drugs because of economics. But I digress.