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Sunday, March 16, 2014

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.

Tuesday, March 4, 2014

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.