Monday, October 14, 2019

Unecessary suffering and beating a dead horse

My new 40 year old patient is besides herself.  She has struggled with a tickborne illness for 5 years.  She has managed to keep her job, but barely. She cries uncontrollably.  She is very irritable and angry. She complains of anxiety and panic attacks.  Mostly, she is depressed. She admits to night sweats.  She denies air hunger.  Ongoing symptoms include exhaustion, chills, poor sleep, tinnitus, painful lymph nodes, abdominal pain and nausea, GERD, irregular menses, joint pain, headache, dizziness and vertigo and feeling off balance, dysesthesias and crawling sensations, panic attacks, suicidal ideation (no plan or intent), brain fog, trouble with with focus and concentration and thinking clearly. She has had a lot of unexplained abdominal pain over the years.

She has seen 2 "Lyme"  doctors off and on over the last 5 years. She has also seen many "regular" doctors.  The first Lyme doctor diagnosed Bartonella and treated her extensively with minocycline, azithromycin and rifampin.She didn't get better.   A second Lyme doctor confirmed the diagnosis of Bartonella.  Laboratory tests were negative but the physician was certain on clinical grounds the diagnosis was correct.   After all, what else causes severe GI symptoms and abdominal pain?  Anxiety and irritability are typical symptoms, almost diagnostic - she heard somewhere.

The "regular" doctors diagnosed depression, fibromyalgia, chronic fatigue syndrome and hypochondriasis.

One Lyme doctor treated her with ivermectin for one year.   She states she thinks she had a Herxheimer reaction but does not know why this drug was prescribed. The treatment did not help.

The same doctor prescribed Biaxin and rifampin.  The dose of rifampin was increased to 1200 mg daily.  After 9 months of this therapy she has gotten worse.  The doctor told her she has not been treated long enough. She decided she has waited long enough.  She thinks she had Herxheimer reactions but never got better.

She has never been treated for Babesia or even Lyme. A course of doxycycline with other Lyme drugs was never prescribed -- or anti-Babesia therapy.

A LymeWestern Blot was equivocal by MDL standards, IgG only.
Serologial tests demonstrated a low positier titer for Rickettsia species.
All other serological tests, inclusive of  Bartonella and Babesia were negative.
CRP was elevateed at 10.

I am able to offer another test in my CLIA certified blood parasitology lab.

Her an image taken from her Giemsa smear:



If a patient doesn't respond to a therapy the clinician is obligated to go back to the blackboard and take another look.

The slide shows marked infection with the malaria-like red blood cell parasite: Babesia. Few things are black and white in Lyme's orbit. This is an exception.

This CDC endorsed standard malaria/Babesia smear is a gold standard.    Many tests circulating in the Lyme-osphere are questionable.

Even without this piece of dramatic evidence, the patient should have been treated for Lyme, e.g. Doxycycline/Ceftin (Tindamax, Flagyl, disulfiram and others) and also treated for Babesia.

This poor long-suffering patient went  5 years, with night sweats and profuse tearfulness (depression) and Babesia was never considered or treated.

Hundreds of things can cause abdominal pain other than Bartonella, etc, etc. The symptoms of Lyme and common coinfections overlap. No one symptom should be attributed to  a particular tickborne pathogen.

Babesia treatment includes Zithromax and high doses of Mepron plus Coartem plus Krintafel. It is important to completely knock out Babesia when first encountered.  Otherwise, the parasites relapse and return mean and drug resistant.  *Please don't use Malarone because Mepron, the yellow paint is hard to stomach. Two malarone twice daily provides a daily Atovaquone dose of 1000 mg.  Two tsp of Mepron twice daily provides 3000 mgs of atovaquone, three times the dose. This dose falls within FDA approved, manufacturer guidelines. This high initial dose must be used to avoid drug resistance and years of misery. If its virgin Babesia you have one change to hit it hard and fast. Don't miss.

I am optimistic. We will get her better and sooner rather than later.

Tuesday, September 3, 2019

Lyme germ warfare?


Complex subjects, like the provenance of Lyme, are oversimplified into a soundbite and the truth is lost in the noise. The Washington Post does us a disservice.

Sam Telford, in the Washington Post told us that Lyme is not an escaped military bioweapon. The headline is  an implicit smirk at the alternative Lyme community said to be steeped in unfounded conspiracy theories. Ant-science. Fits right into the IDSA narrative.

Dr. Telford is a smart guy, a professor of Biowarfare at Tufts University, who has researched the topic for decades. Largely, he is telling the truth. Largely.

Let's listen to his truth. It speaks volumes.

Lyme is an old disease, even ancient.   Lyme was found in the 5300-year-old ice man dug up from the permafrost in the Alps – previously published in National Geographic.  Lyme infected ticks were found from 1945 and 1896 in the northeast US. Facts.

Ticks (Lyme carrying ticks) were studied during the cold war as a means of transmitting germ warfare.  Fact.

Deadly agents, including Tularemia and Q fever – transmitted by the same Ixodes ticks were studied (and continue to be an area of research -- other source).

The double helix of DNA was discovered in 1953.  Scientists during the cold war (1950s - 1980ish) lacked technology to modify germs and make them more deadly. Now it can be done.

Germ warfare research was done at Fort Dietrich and Plum Island. Modern Biocontainment procedures were unknown. (Animals and Ixodes ticks were allowed to roam free on the Island, with the belief they could not leave the island -- other sources). It was unknown that seabirds could ferry ticks to the mainland.

Lyme and the coming epidemic was something military researches could not have imagined.  The Lyme Bacteria was not discovered until 1981.

The Lyme epidemic cannot be entirely sourced to Plum Island since the epidemic broke out in the Midwest and West Coast at around the same time as Lyme Connecticut. The author does not say that Plum Island didn't contribute to the epidemic. 

Willie Burgdorfer participated in tickborne biowarfare research for the US Department of Defense.

Dr. Telford says a few dumb and obviously incorrect things: Willie was just joking with the interviewer about his role in germ warfare research.  Plum Island was repurposed for agriculture research in 1954 -- during the height of the cold war. (not a cover story).
And -- the US stopped bioweapon research in 1969 because Nixon said so. 

These are the clearly established facts.

In summary:  Our government was involved in germ warfare research for years. Some of the research involved ticks and tickborne disease (Q fever, Tularemia). Willie Burgdorfer, whose names is attached to the Lyme agent, B. burgdorferi worked for the government and  some of this research was with the same ticks that transmit Lyme disease. Biocontainment procedures were unknown and government scientist did not know the ticks and the unknown pathogen (Lyme) could easily jump across the Long Island Sound to Lyme Connecticut. 

It is easy to conjecture the Government unwittingly helped spread the epidemic of Lyme disease to New England as an unexpected consequence of secret germ warfare research. And, it is widely known the Government has a habit of not admitting wrong doing and covering its tracks. 

When we say Lyme was not an escaped bioweapon the statement is both true and false. There was no conspiracy to infect Americans with a horrible disease. But is seems likely that an unexpected consequence of tickborne disease bioweapon research on Plum Island was the spread of some Lyme infected ticks to the mainland. 

The law of unintended consequences applies and there is much we will never know.

Congress can investigate and it will be a waste of time.

Thursday, July 18, 2019

Novel drugs for Lyme


The dry spell is over. We have some promising new therapies.

Investigators have been used a method to screen large numbers of drugs which might treat Lyme. Dr. Lewis has apparently found that disulfiram, Antabuse, used to treat alcoholics and makes them vomit if they drink alcohol seems to kill Lyme. Apparently, he has discussed his findings at lectures. Practicing doctors don’t get the low down until findings are published in a journal. A recent case report of 3 patients showed efficacy of the drug.  Antabuse is something I have used throughout a 37-year career in medicine. It is generally safe, but liver tests need to be monitored. Repurposing the drug empirically seems quite reasonable. Dr. Fallon, Columbia University, is doing a clinical study. 

The fact that Antabuse is not an antibiotic is exciting.

The combination of Rocephin, doxycycline and daptomycin may be effective in humans. A clinical question is how long do the drugs need to be given?  Will we see durable benefits in 30 days, 60 days etc.?  Can an intensive IV therapy circumvent months, even years of other complex and perhaps less effective therapies? Let’s find out.

Controlled clinical trials are important. Placebos are incredibly effective. Personal interactions influence outcomes as do other confounding variables.  Studying a complex disease like Lyme is challenging; coinfections are not accounted for and a million other variables are not and perhaps cannot be taken into account.. Study results must be interpreted with care, nuance and ample discussion. The limitations of the study must be addressed. And I hope investigators will not be strong armed by politically motivated institutions to parse words when stating conclusions.  These few words have been misinterpreted, willfully with far reaching ramifications. The IDSA drew incorrect and absurd conclusions from Fallon's last Lyme study. And here we go with another set of IDSA recommendations.

Tafenoquine in the form of Krintafel is being used for treatment resistant Babesia. Looks good so far.

Friday, June 28, 2019

Bartonella persisters and daptomycin: two for the price of one?


While Lyme persistence I denied for political reasons the persistence of other human zoonotic pathogens is recognized. 

I have seen two cases of brucellosis recently and Brucella is recognized as a persistent bacterium, perhaps impossible to eradicate, at least with currently used and/or recommended therapy.

B. abortus is one of several well-known human pathogens of the genus, the one which may be acquired via tick bites.

Brucellosis can be acquired by consumption of uncooked meat and raw milk. I don’t understand the fad of drinking unpasteurized milk, a potentially deadly fad.

Brucellosis may cause numerous untoward clinical syndromes many of which similar to those seen with chronic Lyme.

Bartonella, especially B. henselae is a well known tickborne pathogen also known to exhibit persistence. The bacteria, a fastidious (difficult to culture) gram negative rod is an obligate (facultative) intracellular gram-negative bacteria associated with well described clinical syndromes, discussed elsewhere. Spotty medical literature supports the notion that Bartonella infection is clinically persistent.

Biologically, Bartonella are the only bacteria which may reside in red blood cells. The only other RBC pathogens are malaria and babesia species. Specific biological features, a protected niche and the discovery of stationary forms provide an ample narrative of fact and biological plausibility for persistence. 

The primary home for these bacteria is not RBCs but the endothelial cells that line blood vessels. This is why bartonellosis causes well known vasculitis syndromes. 

Zhang, a prolific publisher, should now be a star at JHH published about Bartonella persisters in antibiotics April. Again, daptomycin is the star.   Daptomycin has the best activity against stationary (persister) forms. Only aminoglycosides, e.g gentamycin are competitive.  In my experience, gentamycin may eradicate clinical infection, but not consistently. Complex multidrug regimens are frequently recommended for Bartonellosis, perhaps this is unnecessary.

This study added to others vis-à-vis Lyme raises the clinical (preclinical) question. Should patients with chronic illness caused by Lyme and Bartonella be treated with combination IV therapy, Rocephin, Doxycycline and Daptomycin earlier rather than later in the course of treatment?

From an Evidenced Based Medicine approach this is anathema,  such therapies can only be recommended after randomized clinical trials, peer reviewed and published.

Such studies are perhaps decades away.  Currently the political divide make diagnosis of Lyme nearly impossible, let alone coinfections.

The preclinical approach allows for empiric use of the therapy without waiting for IDSA approval, which may or may not ever come.

This concept of applying preclinical data (translational medicine) is well developed and well used in the field of oncology. Of course, cancer is considered a serious disease (and Lyme isn’t?).

Those of us in the alternative universe of Lyme disease are accustomed to very long-term antibiotics, including IV ones.  In this world, the use of these 3 IV drugs sounds reasonable. In the other world we are no strangers to cocktail therapy and IV therapy.  In the IDSA/CDC world of doxy for 3 weeks even discussion of this idea is heresy or treasonous, if such things apply in medicine (apparently, they do).

Treating chronic Lyme through the other world approach is very complicated, lengthy and expensive. This sort of preclinical information should be considered in lengthy, informed consent discussions with patients.  

Monday, June 24, 2019

Lyme arthritis, peptidoglycans and political correctness




Medical science and other branches of science are biased and political.  A researcher, an investigator(s) has to walk on eggshells when their findings bump up against beliefs of mainstream beliefs espoused by the experts. They have to fall in line with political correctness if they hope to see their research published, and if they want to keep their jobs as academic researchers. .  

The research findings published in the PNAS, Proceedings of the National Academy of Science this month entitled Borrelia burgdorferi peptidoglycan is a persistent antigen in patients with Lyme arthritis appears to be excellent science.

The research moves the ball forward in our understanding of chronic inflammation associated with Lyme disease. Political correctness and conformity with mainstream thinking corrupts the paper from the start seriously damaging the credibility of the authors.  Immediately the terms postinfectious Lyme arthritis and posttreatment Lyme disease are used and they poison the broth.

The preponderance of scientific evidence, overwhelming and mounting evidence supports the understanding that Lyme bacteria persist in the face of the standard antibiotic therapies discussed.

The finding that peptidoglycan (PPG), the crosslinking molecules which comprise cell walls in gram-negative and gram-positive bacteria are a major determinant of persistent Lyme arthritis is new information that moves the ball forward.

Borrelia spirochetes have a double outer membrane and lack PG cell walls. However, PG molecules are present internally, inside the outer membrane (cell envelope) providing support to the spirochetes.

The fragments of PG are call muropeptides.

We learn Bb, Lyme processes a unique PG structure. And we learn these fragments are highly immunogenic – incite an excessive immune response or cytokine response likely responsible for clinical manifestations of Lyme arthritis.

Perhaps the peptide fragments do cause an autoimmune response. Although the theory is discussed at length this is not what the research shows. Lyme related joint inflammation is directly caused by unique Lyme PGs.  


A variety of experiments, controlled experiments using a variety of bacteria with different PGs, a variety of clinical diagnoses, mice, humans, joint fluid and serum support the findings. The findings are based on a great deal of animal and human research.

Antibodies were developed against Lyme specific PGs. These antibodies could be the basis for a new, more accurate diagnostic test.

From recent research we know that Lyme biofilms and planktonic round forms cause more inflammation than spirochete forms. We know these are the most antibiotic tolerant forms or resistant forms.

The article at length discusses issues related to diminished bacterial recycling of PGs compared with gram negative bacteria.

Two theories are proffered as to how Lyme PG persists after “curative therapy” with a short course of doxycycline or Rocephin. The authors suggest that these mechanisms account for the persistence of symptoms lasting weeks or months.

But Lyme arthritis lasts for years. Biofilm forms are impervious to standard antibiotic therapies.

Somehow the authors suggest that immune suppressive therapy should be considered rather than additional antibiotics.

We have heard catchy phrases like “persistence of evidence or evidence of persistence." The issue has prevsiously be settled.

Good science can easily self-destruct with the unforced errors all for the sake of political correctness.

To bad.

Thursday, June 6, 2019

Lyme, Alzheimer's, Enbrel -- new potential treatment

I have learned that most people want a simple sound bite answer or conclusion. The edges of medicine always operate in the grey and nuanced.

It has long been dogma in Lyme circles that immune suppressing drugs, e.g. Enbrel are very dangerous and should not be used.  The same is true with prednisone.

I have patients who get the occasional injection by their rheumatologist; joint pain gets better and they are no worse for the wear.

The drug is used for psoriasis amongst other many other conditions. The drug has serious side effects: its use should not be taken lightly.

A study suppressed by Pfizer, brought to light be the Washington Post, was based on insurance company data considering outcomes of  hundreds of thousands of patients and found those taking Enbrel had a 64% decrease in the incidence of Alzheimer's disease. 

Enbrel impairs the function of TNF alpha, a master cytokine responsible for trafficking immune cells.

Pfizer did not make the disclosure because: a generic version will be  available.  A shiny new, me-too drug promoted heavily by pharm reps costing obscene amounts of money will take its place. Doctors will be given shiny data, along with lunch, proving equivalency? with the old drug.

The myth that generics are poor (dangerous) and lack quality control may be resurrected.

Watch out for first year generic prices: cute trick. For the first year a single company is given a monopoly and only required to reduce the price by 20%.  "See, the generic is almost as cheap as the brand," the rep will inform a doctor. This is a bad pro big-pharma rule passed by Congress decades ago I'm sure) by the way. Cheap is a relative term.

The pharmaceutical giant, Pizer has excuses, reasons why it withheld the data, for example, they  claimed the data is wrong because of biological plausibility: the molecule is too large to cross the blood brain barrier.

Really? I care if the molecule gets into the brain; maybe it's an advantage.  The brain has its own immune system which needs to be tweaked lightly. Ask anyone who has had a brain Herxheimer reaction knows. The Cytokine storm which may make you crazy results from peripheral cytokine reactions/overproduction primarily.  And there is no data the molecule cannot get into the brain. Cytokines get in the brain.

Alzheimer's is in part motivated by inflammation. Other major factors are: production of amyloid beta protein (AB) (plaques and tangles), genetic factors and multiple external factors.

It is thought that AB protein is a naturally occurring antibiotic which responds to inflammation. Discussed elsewhere. Lyme resides in the brain along with many  bacteria, viruses, protozoans. It is true that spirochetes have been reported to aid in the transportation of AB into the brain.  Infection (or colonization) may be omnipresent and therefore not the whole story -- or the most critical piece.

The vast majority of my patients present with cognitive complaints. Many or most Lyme patients, at one time or another fit the criteria for a disorder call MCI, minimal cognitive impairment. The mainstream medical community considers this a pre-Alzheimer's condition, often.

What's a Lyme patient to do?

First off, if symptoms completely resolve with usual therapy do nothing.

If you are a patient who has had very aggressive therapy, e.g. months of IV antibiotics and cognitive symptoms persist, look up MCI and consider the following:

Get an AB PET. The tests measures metabolic activity in the brain and the presence of early AB protein deposition. IF the test is positive you are at very high risk for developing Alzheimer's.

Prednisone and Enbrel have largely been dangerous seen as because patients are misdiagnosed and not also treated for Lyme. Enbrel is likely tolerably safe, in many cases, considering benefit to risk ratio.

A lot of money has been spent searching for an Alzheimer's cure. To no avail. Nothing very promising in the literature.

I for one am very angry with Pfizer. I suppose it is typical behavior in the industry. We still need big pharma. Don't throw out the baby with bathwater. Hold them accountable. But, do not  conclude big pharma is corrupt therefore all drugs developed through the system are fruit of a poisoned tree and are therefore inherently untrustworthy and dangerous -- in addition to being immorally overpriced.

It's a bad syllogism. Drug companies are a very necessary evil.

Getting back to Enbrel Is this a silver bullet?.  More comment, biostatistics and analysis are required as well as prospective RCT medical studies. Since the drug will be generic soon big pharma will not finance the research. Fortunately, Alzheimer's, a burgeoning epidemic as our population ages, is well funded through private sources.

Ideal prospective studies, which will likely be done make observations moving forward starting with a baseline current population. The process is slow.

Retrospective, population studies, primarily manipulation of data already there will not take long. These studies are never as good as prospective studies but perhaps good enough.

If you want my  bottom line: don't run out and get Enbrel-- YET.

I am not endorsing the use of the drug for any medical condition, including Alzheimer's,
This site is for informational purposes only.  Medical care can only be delivered by a certified medical practioner who properly evaluates your particular issues. Please don't diagnose or treat yourself. 





Monday, May 20, 2019

Posttreatment Lyme disease case


A 52-year-old female was seen in my office several months ago.  She has a history of tick bite and bull’s-eye rash treated with recommend "standard" doxycycline for 3 weeks and she felt well -- until she didn't.  Symptoms appeared gradually.  Eighteen months later18 months later she complained of: incapacitating fatigue, poor sleep, diffuse pain, weakness, numbness and tingling, headaches, cognitive impairments–trouble remembering words, impaired focus and attention and memory loss, to the point of disability. She was hanging onto her job by a thread.

She also experienced severe night sweats but had chalked it up to menopause. The  sweats however,  were new and drenching, occurred several days weekly and  were qualitatively different from previous night sweats -- primarily hot flashes. 

With further question she stated she had been experiencing gasping mid-sentence and thought  she had developed a tic. 

Lab testing was positive for Lyme (CDC, IgM and IgG) and Anaplasma.

Lyme was initially treated with a triple regimen, doxycycline, rifampin and Tindamax. Also covers Anaplasma. 

Within 4 months she reported getting her life back and regaining a high level of function. Babesia symptoms, well described above (night sweats, air hinger) persisted.

The treatment was changed.  Rifampin was discontinued.  Doxycycline, Zithromax and Mepron were prescribed. 

Notes:  Typical  posttreatment Lyme disease, relatively early presentation (in my practice). The role of coinfection has been ignored in clinical studies.  Lyme as sole infection, absent coinfection is rare. Coinfections may be difficult to diagnose because of poor diagnostic testing.
Human trials have used only doxycycline and Rocephin. In mice, triple IV therapy: daptomycin, doxycycline and Rocephin (ceftriaxone) was shown to eradicate Lyme spirochetes.  

Medical literature suggests that about 20% of early patients treated by CDC standards will have chronic symptoms.
Many reasons have been suggested, Including:

Tick inoculates human host with antibiotic resistant biofilms.
Coinfections.
Strain specific virulence factors.
Host specific immune responses. 
Host already infected but asymptomatic.

Standard therapy ineffective -- high failure rate unacceptable, leads to chronic illness and/or serious sequalae.

Clinical approaches may include: 

More aggressive cocktail therapy early
Careful monitoring of patient for persistent symptoms and symptoms suggesting coinfection and early treatment
Not telling patients: don't worry, symptoms will clear.