Monday, February 27, 2017

Bicillin LA


 My patient today is a 53-year-old woman who I have known for several years.  She has been disabled with Lyme and tickborne disease for the last decade and a half.  When she came to my office a few years ago, things had taken a turn for the worse. When she came to my office for the first time she had a clear agenda. She wanted IV antibiotics, the only thing that works she said.
Her saga dates back to 1995, in Silver Spring, Maryland.  She remembers finding a tiny tick attached to her abdominal wall. She recalls that 2 weeks later a large circular rash appeared on her abdominal wall.  She recalls being barraged with symptoms soon thereafter. She experienced fevers and had trouble walking and talking. Her doctor at the time ordered an array of tests, which were negative and the physician offered no diagnosis or treatment.  An ID doctor offered nothing. A neurologist ruled out MS. Other doctors suggested her symptoms were psychosomatic and she was left to suffer, without answers or help.  

After a few years, she developed burning sensations, tremors, leg pain, weakness, muscle twitching and jerking and progressive joint pain. She developed migratory pains in her shoulders, knees, wrists, ankles, fingers and toes.  Brain symptoms were insidious.  Her thinking felt clouded. She starting getting lost. She experienced disoriented episodic confusion.  Other strange neurological symptoms seemed to mimic strokes or seizures she thought.

Finally, in 1998, she diagnosed herself.  She convinced an ID doctor to treat her.  With 6 weeks of IV antibiotics and she began to improve.  They were taken away and she crashed.  She garnered a glimmer of hope.  She began looking for help elsewhere and saw many doctors.  She ultimately found a New Jersey physician who aggressively treated her with IV antibiotics for 12 months.  She regained a quality of life, did OK for a while – a couple of years. Gradually symptoms reappeared.  She called the same doctor only to discover she was no longer in business, courtesy of the State Medical Board.
She found other doctors who were loath to prescribe IVs. Lot of doctors, lots of oral meds.  Her stomach was a mess and she was no better.  She recalls that she tested positive for Lyme, Babesia and RMSF.  She remembered a yellow paint-like medicine which made her sick and no better.

When we first met, she was desperate for help.  Mostly bedridden, getting out of bed and getting dressed was a heroic action.

A partial list of symptoms included:  exhaustion, fevers, chills, night sweats, insomnia, double vision, flashing lights, blurred vision, tinnitus, trouble speaking, trouble swallowing, swollen lymph nodes, rapid and irregular heartbeats, abdominal and pelvic pain, generalized muscle and joint pain (severe), back pain, stiffness, headache, migraine, vertigo, numbness and tingling, weakness, loss of balance, trouble walking with falls, brain fog, forgetfulness, confusion, disorientation, depression, anxiety and panic attacks.

She knew what she wanted: IV antibiotics. I wasn’t a hard sell.

Laboratory testing was positive for Bartonella antibodies.  A Lyme Western Blot at LabCorp was negative across the board.  A Stony Brook Western Blot revealed a single nonspecific IgG band (64) and 9 IgM bands: 18,25,28,31,37,41,58,64,93.
I found other abnormal laboratory values from the start.  She had a very low B12 level. A parietal cell antibody test was positive. Folic acid and vitamin D were also very low.

IV therapy didn’t work.  First there was a DVT and we had to pull the line. We tried therapy through a peripheral line and she had an adverse reaction to Rocephin. 
She became discouraged and fell off the radar.

Doing poorly, after some months, she came back to try something else:  intramuscular penicillin.  This has worked beautifully – as well as Rocephin worked, she states. All major symptoms are melting away and after a couple of months she is functioning quite well.  I give her the shots. We warm up the syringe to room temperature, and slowly inject, (deep IM, lateral aspect of iliac crest)– based on tolerance. The injection site is “rubbed in.”  She tells me the pain is relatively minor and doable, especially once weekly.

Bicillin LA is used.  It is a depot form of the drug and stays in the tissues for 2-4 weeks. I understand some patients are injecting 1.2 million units 2-3X per week.  I have found that 2.4 million units weekly works fine.  The larger volume of the higher dose is tolerated when injected slowly.

She is also treated with complementary oral drugs for Lyme and Babesia. We have found effective options which she tolerates.  She receives various supportive therapies.  And B12 injections are key.

I don’t know why the pernicious anemia (PA) diagnosis had been missed.  B12 deficiency can mimic many Lyme symptoms and B12 levels should routinely be checked.  PA is an autoimmune disorder. Autoimmune issues are prevalent amongst Lyme patients, for example, thyroid disorders. I can’t say I routinely see cases of PA, but I think the prevalence in my patient population is greater than the general population which is around 0.1%.
Bicillin LA is very expensive and insurance doesn’t cover it.  I checked on goodrx.com.  A 10 pack goes for 2,700 dollars. The monthly out of packet cost is about 1,000 dollars which isn’t horrible for a Lyme treatment.  A brief google search finds several outfits advertising a fraction of the cost.

The history that 12 months of IV Rocephin in the past imparted temporary relief would seem to augur poorly for the future. But I optimistic that a better understanding of cocktail therapy and coinfection therapy is changing this trajectory.  

An aside – let me digress.
Like many of the sickest, her positive Western Blots show a predominance of IgM responses.  In his research, Dr. Aucott incidentally discovered that about 20-25% of the populace, genetically, appears to be incapable of mounting an IgG response and may show only a weak IgM response.  This finding was predictive of a poor long term disease.  ID doctors still call IgM only “false positive” backed by the IDSA/CDC emphatically insisting that all chronic Lyme patients have the touted 5/10 IgG responses.

“You are entitled to your own opinion, but not your own facts.”  The erroneous version of reality stems from peer reviewed literature. Of course, it does.  Virtually all academic peer reviewed studies use the 5/10 IgG criteria for acceptance into clinical studies.  The conclusion that all chronic Lyme patients have these findings is silly. These criteria are used for study inclusion only. There is no clear academic peer reviewed literature that supports the notion that the criteria can be reliably used for diagnosis. Opinion papers, not research papers make this claim frequently, by incorrectly citing literature that uses the study inclusion criteria.  The first of 4 off cited academic, NIH sponsored studies (Krupp), specifically states that he included seronegative patients in his study.
The incorrect syllogistic reasoning used by the experts goes something like this:  In Lyme studies all chronic Lyme patients have CDC criteria:  patients have chronic Lyme; therefore, all chronic Lyme patients must have positive CDC findings.  And “experts” say it’s true – by fiat.

My 16-year-old daughter sees the erroneous logic and conclusion in about 30 seconds.
Everything about this case is all too familiar and horrible. Thankfully, this survivor of an odyssey of insanity and cruelty is headed for happier times.

Friday, February 17, 2017

Bartonella Madness and PANS



There exists a pernicious conspiracy between Borrelia species and Bartonella species with the intention of making us humans mad.  (This as close as I will get to conspiracy theories and politics in this BLOG).


One young man may have PANS as well (pediatric autoimmune neurological syndrome).  The teenager in question developed OCD, correctible anorexia with rapid weight loss and an aversion to one family member, for no apparent reason. The patient has no explanation or insight into this unusual change in his personality.  He is somewhat irritable, angry and rageful with other family members but not out of control, and, he does reasonably well at school, interacting well with teachers and peers.
The diagnosis of PANDAS was made because a particular expert who blames Strep.  Evidence for Strep is scant. The ASO titer and anti-DNase B were minimally elevated (Strep antibodies).  Lyme antibodies and Bartonella antibodies are present. Everyone in the family has tickborne disease.
The Cunningham panel was essentially normal.  This test is frequently relied upon for the diagnosis of PANS/PANDAS.  I ordered a GAD 65 auto-antibody which was elevated. This is a nonspecific marker but it can be associated with autoimmune encephalopathy.  
The hallmark of PANDAS is that symptoms seem to come on overnight.  In other patients, this has been the case and I have characteristically seen tics, including Tourette’s and more typical OCD manifestations. In my experience, the Cunningham panel is reliably positive.  This   patient’s symptoms came on over a short period of time, but not overnight.  The Cunningham panel is comprised a group autoantibodies directed against the brain that can be measured in a peripheral blood test. The test is supported by peer reviewed literature.
In this patient, the SPECT scan was dramatically abnormal.  This tends to confirm the diagnosis of encephalopathy but does not impute a cause.  
The patient was treated with a single dose of IVig and there was no response. The treating physician recommended waiting 6 months before retreating.  (Not what I would do).
Encephalopathy in patients with Lyme/Bartonella may be multifactorial. There may be an inflammatory component as well as an autoimmune component.  And there may be something else, far less understood.
Mysteriously, brain infectious, may induce specific effects. For example, Bartonella reliably causes, anxiety, irritability, rage (Lyme rage) in many patients. Patients may also suffer with virtually every other conceivable psychiatric symptom.
One can explain this case without consideration of PANS, or any autoimmune encephalopathy. But there is the GAD antibody, suggesting something autoimmune is going on.
Dreaded steroids (overly maligned in my opinion) are very helpful in these cases. Steroids may be administered on a one-time basis. A response to a burst of steroids is predictive of response to IVig.
If neuropsychiatric symptoms do not budge with steroids, IVig will likely fail. Steroids did not help the patient in question. This is important. IVig is prohibitively expensive. And even though tertiary academic centers recommend its use, insurance companies will not cover the therapy for PANDAS/PANS. 
If there is a dramatic response to steroids IVig can be life saver. In my experience, IVig, like antibiotics, must be given on a regular, consistent basis over a long period of time. And PANS requires high doses, 1.5 – 2 gm/kg. I have a patient who developed acute symptoms in early childhood with no evidence of strep and with 10/10 IgG Lyme WB bands and with a positive Cunningham test, who is maintained, a decade later, on IVig every 4 weeks. She has done beautifully. When IVig was withdrawn a few years ago, OCD symptoms emerged immediately.
If Bartonella is suspected to be the major culprit, specific therapy is indicated.  Combinations such as Biaxin, Rifampin and doxycycline have been used by some. This is not my favored approach. Biaxin crosses the blood brain barrier poorly (brain the target).  I like Doxycycline and Rifampin, both pass the BBB well and are active against Bartonella species. I like to add a third drug in the sulfa class. These drugs are active against Bartonella species and cross the BBB well, especially at higher doses.
This approach is not always highly effective.
The addition of low pressure hyperbaric oxygen therapy, good for all encephalopathies, may be a great adjunct.
If this isn’t working, I will go with IV therapy, preferably gentamycin and others. In lieu of IV, I have had good luck giving gentamycin as a once daily intramuscular shot. Never alone.
I stay away from quinolones which are riskier and less effective in my experience.
Gentamycin can be given as a single daily dose and relatively low doses can be clinically effective. Ear and kidney toxicity are minimized with lower doses. Gentamycin, like rifampin, is never given as solo therapy, it must be given in a cocktail with other drugs.
With these steps, I have successfully treated many cases.
I was asked recently by another physician what I do when patients don't get better.  My answer is go back to the drawing board, reconsider the diagnosis and options. Try a different approach. Sometimes you have to get creative. This is all unchartered water.
It may be necessary to juggle: IVig, hyperbaric oxygen therapy, IV gentamycin and other IV drugs while covering Lyme and sometimes Babesia species. 
A word about doxycycline.  A little bit of knowledge is dangerous and it is easy for a lay person to misinterpret things read on the internet.  Doxycycline does not kill only a small percent of Lyme bacteria and doxycycline is not a “cyst generator.” 
Doxycycline remains one of the very best drugs.  It is highly active against rapidly growing spirochete forms of Borrelia – perhaps the most active of any known drug.  It gets into tissues well when taken orally, including the brain. And, it may be given IV.  As is the case with two drugs mentioned above, rifampin and gentamycin, I don’t order doxycycline as solo therapy. It is part of a cocktail. If you look at Zhang’s work on in vitro eradication of Borrelia burdorferi, doxycycline is always a key component of successful three drug regimens. Doxycycline is also a primary component of many anti-Bartonella cocktails.
I have good success treating patients with therapies that are rational and can be explained within the context of available scientific facts.  My BLOGs and medical approaches to tick borne illness, are also based on empirical experience garnered over many years of trial and error practice.

A word about Bartonella testing. This patient tested positive for B. henselae.  Commercial antibody testing is unreliable. There are another 15 or so species and subspecies that may be clinically relevant for which no such test exists.  We got lucky here. I always tell patients: positive results are helpful, negative results are not. Clinical diagnosis is required in most cases.

The presence of darkly colored parallel stretch marks are hugely helpful, as in this case, but this is not a reliable sign.









Monday, January 30, 2017

Chronic Lyme disease: an approach to treatment


THIS POST IS NOT INTENDED FOR MEDICAL ADVICE.  IT IS FOR GENERAL INFORMATION PURPOSES ONLY. 
I will talk a little about treatment approaches.
BACKGROUND
No one knows the best way to treat chronic Lyme disease; and what works best for one patient may not work well for another.  In a sense, each patient is his/her own “experiment.”
Treatment of chronic Lyme (and associated infections) is based on:  A new paradigm regarding the role of tickborne infections and its connection to chronic illness. Scientific information; empiric evidence from the collective experience of a large cohort of physicians over many years; the clinical acumen of the treating physician; and, parallel models which can be drawn from Mainstream Medicine comprise the basis for treatment.
Tuberculosis on one level offers clues as to the management of chronic Lyme disease.  Lyme and TB both bacterial illnesses which are difficult to treat due to the presence of Persister organisms.  Experience with TB may offer clues as to how best treat Lyme, and  -- offer proof of concept regarding the “cocktail” approach used to treat Lyme.
Lyme persisters are thought to largely be comprised of round body forms and biofilms colonies. Let’s correct the record.  No L-forms have been found.   The Lyme spirochete is pleomorphic. This means it can change its form.  Bacteria do not form cysts. Round forms of the spirochete may be referred to as pleomorphic variants or round body forms.
Antipersister drugs:  Persisters and their appropriate therapy is mysterious.  The drug pyrazinamide (Z/Pza) is a key part of the therapy for tuberculosis. The drug was discovered in the 1920s and first used for TB in the early 1950s. It is an essential, highly effective antipersister drug for TB.
With today's science the drug would never have been discovered.  The drug was not initially tested in a test tube (in-vitro). The drug was first test in a mouse model (in-vivo) and was found to be highly effective.  The drug has no activity whatsoever in a test tube. The modern scientific approach would have screened out and discarded the drug forever.
Initial therapy for TB consists of 4 drugs given together in a “cocktail.”  There are many other examples of bacteria which are treated with combination therapy, for example H. pylori, but TB provides a good template.  TB infection may be systemic, but is generally limited to a single organ – the lung.
Late stage Lyme is always disseminated, infecting many organs. TB is generally treated for 6 months. It makes sense that Lyme may require long term as well.
In test tube experiments Zhang found eradication of Lyme bacteria required a cocktail of three powerful antibiotics.  This is also provides proof of concept.
APPROACH TO THERAPY
I typically treat Lyme with a cocktail of 3 drugs, as tolerated.  Choices are based on the answers to certain questions:  Has the drug been shown to have good activity against the organism, even at low serum concentrations?  Does the drug offer synergy when combined with others? Does the drug have good tissue penetration and can it pass through the blood brain barrier (BBB)?  Does the drug also hit coinfections? How will that impact choices?  Does the proposed "cocktail kill spirochetes and persisters well? Are drug to drug interactions a concern? Should the drug be given by mouth or by IV, or even IM?  Are side effects tolerable?  On balance, do the benefits outweigh the risks?
DRUGS I LIKE (ORAL AGENTS)

Doxycycline: always first line -  most effective against spirochete form of Borrelia organisms, usually well tolerated; may be given by mouth or IV -  either way, good systemic adsorption and good penetration into brain. Kills Lyme better than minocycline. Draw back:  no effect on persister forms. That’s OK. That’s why we use a cocktail.  The bonus of hitting coinfections cannot be understated.
Second drug choice(s) Rifampin is a good choice. By a synergistic mechanism, confers antpersister properties to doxycycline; achieves good tissue and brain levels; it is an antipersister with a proven track record, used for TB and used to eradicate Strep bacteria carriage.  Drawback:  Highly active against Bartonella sp.  Herxheimer reactions can be intolerable.
Another choice could be Bactrim, effective only at higher doses, unlike doxycycline which can be effective at lower doses, also hits Bartonella sp. Herxheimer response less drastic than that seen with Rifampin. Still can be a no starter. Kills persisters and penetrates BBB.
Another option could be Tindamax.  Well tolerated, good blood and tissue levels and highly active against Lyme organisms. Sapi’s research says it is excellent against persisters. Zhang's research says it is only slightly better than Flagyl (which he surprisingly found has little or no activity against persisters.  All I can say is it works.
Another option could be Amoxicillin or Ceftin.  I typically use these drugs when doxycycline is not tolerated or not an option.  Amoxicillin does not penetrate the blood brain barrier unless given in high doses but may be an excellent choice because of low toxicity and it is hightly active against spirochete forms.  Ceftin is the only oral cephalorsporin said to penetrate the BBB; It also shows activity against all forms of Lyme (spirochetes and persisters).  Not my first choice because it may be too hard on the gut and I it s more likely than others on this list to cause C. diff. Good option when tolerated.
The worst offenders for C. diff are quinolones such as Levaquin.  Drugs of this class can also cause tendon rupture. They penetrate well into the brain but can cause odd brain side effects that are not Herxheimer responses. I recommend avoiding these drugs if possible and using low doses when necessary.

Biaxin and Zithromax may be good choices but are not usually first line.
Why use 3 drugs?  There is no scientific basis for this. Zhang's test tube results are a weak argument, at best.  I have used to use 2 agents in the past and have found 3 works better.  I don't use 4 because I worry about the increased risk of toxicity, and -- 3 works.
There is no consensus on how best to treat the disease.  This approach has evolved over years and may be quite different from recommendations seen elsewhere. In general, treatment is long-term: The length of therapy  may be much more important than specific choices of therapy.  Again, what works for one patient may not work well for another.   Coinfections need to be considered and may alter the clinician's approach to the patient dramatically, even at the start. The use of IV antibiotics or IM (penicillin) vs oral agents needs to be sorted out. There are many other drugs which may be considered, not discussed here.  The duration of therapy is unpredictable and different for every patient.
Continuous therapy vs pulsed therapy is a complex discussion, not covered here.
Drugs are never started all at once. They are gradually added incrementally, watching for toxicity and/or side effects.   


NOTHING HERE SHOULD BE CONSTRUED AS MEDICAL ADVICE. IF YOU ARE ILL WITH ANY DISEASE OR SYMPTOMS, SEEK HELP FROM A KNOWLEDGEBLE PHYSICIAN.

Monday, November 7, 2016

Lyme disease tests: New and Old


Diagnostic testing



Testing may be difficult when the standard diagnostic test fails. The gold standard, the identification of the organism by DNA or culture is frequently not feasible or available. Several antibody tests have been developed which may be helpful, but these tests have a low sensitivity, missing many cases. As an adjunct, a newer technology involves lymphocyte stimulation.  When cells (T lymphocytes) are exposed to proteins derived from the pathogen, cell mediated responses such as the release of gamma interferon can be measured indicating prior exposure to the pathogen. This test may have limitations and likely should only be used adjunctively.
Of course, we are talking about diagnostic procedures for Mycobacterium (tuberculosis).
Let’s talk about Lyme.

Testing for Lyme remains problematic.  Tests have been inaccurate, unreliable and at times and prohibitively expensive. 
We depend on clinical diagnosis. But sometimes we are not sure.
All currently available tests have pros and cons.
A lot of labs are suddenly getting into the Lyme testing business.  Many tests are in development.
The Western Blot remains the first line test.  It is important that a Western Blot be ordered, not just an ELISA with reflex to Western Blot. The ELISA is not dependable. An alternative ELISA, the C6 peptide may be ordered. Usually negative, sometimes it is positive when other tests are not.   A C6 from LabCorp/Quest is not adequate, a numerical value, available from various reference laboratories is needed. (MDL, IgeneX, many others).  In my experience, values under the lab recommended positive cutoff may indicate exposure to Lyme.
PCR (polymerase chain reaction) is a test which measures the presence of specific DNA.  Most consider this the gold standard.  DNA testing for Lyme also has a low sensitivity and misses most cases. The only specimen available to test is usually blood. Lyme is a tissue pathogen and may be present in the blood in very small numbers. This is different from viral illnesses such as HIV and Hepatitis C where large numbers of viral particles are present in the blood.  Many clinical labs are working on ways to improve the sensitivity of the test.  Urine may be a better place to look.  Lyme lives in the bladder and is shed in urine. One such test is offered by Quest. So far I have not found any positives. Other clinical labs may have better results.
This is not to be confused with the antigen capture test or the nanotechnology test, which also looks at urine samples.
The Nanotrap captures tiny amounts of proteins found on the surface of the Lyme bacteria. The test so far only measures outer surface protein A, or OspA.  This protein corresponds with the 31 band of the Western Blot.  Remember, Lyme is a clever “shape shifter.” This protein is expressed when the spirochete is attached to the gut of the tick. After infection, this protein disappears (downregulated) and Osp C (upregulated) takes its place. So, the current test is really only helpful for acute Lyme and -- maybe late-stage Lyme. After many months of infection, this protein (OspA) may reappear. The test as it sits is not clinically useful for most patients.
The scientists at the Center for Applied Proteonomics and Molecular Medicine, George Mason University, new to the field, were shocked that the so-called experts in the field insisted that chronic Lyme is not real.  To get "proof of concept" and the blessing of the IDSA, ILADS and the CDC, the new test was designed to detect only acute Lyme. The CDC admits that current testing (two tier test) for acute Lyme is flawed, and THERE IS AN X-PRIZE award for the first lab to develop an accurate acute Lyme test!  
Now there is general proof of concept. An improved test, said to come out soon, will look for many proteins, including OspC.   The improved test may be extremely helpful for the diagnosis of all stages of Lyme disease.  
A culture test from ALS is available. After being slammed by the CDC, the lab is actively engaged in studies to achieve FDA clearance.  The blood culture test has two drawbacks: cost and the patient must be off antibiotics for 2 months before the test is performed. Otherwise, it may be a very good test. At first I was concerned that the test found Borrelia species rather than B. burgdorferi. This may be an advantage rather than a disadvantage because Lyme disease is a borreliosis comprised of an expanding menu of species and strains.
Another test, Lymphocyte transformation test, is available from Pharmasan and others. This test measures a different kind of immune response.  It is based on FDA approved, commercially available TB tests.  The test measures the innate immune response. An initial response which predates acquired immune responses which lead to antibody production. Immune cells patrolling our blood and tissues have the ability to recognize patterns which shouldn't be there (Pattern Recognition Receptors). Killer T cell lymphocytes are the first line of defense. Killer T cells attack offending antigen (Lyme) and turn on other immune responses including the production of cytokines, modulators of immune regulation.  When this reaction occurs it leaves behind permanent T memory cells. These memory cells, when exposed to Lyme antigens react by releasing gamma interferon, a potent cytokine.  This reaction can be measured.  This test may be considered a complement to other tests, such as the Western Blot test. It is somewhat costly.
From a cost perspective, in my experience, it is best to start with a Western Blot (MDL) which provides images and alternative diagnostic criteria.
A fair question might be: since the Western Blot only shows exposure to Lyme, not the presence of actual infection, shouldn’t a test that directly measures Lyme infection be done, to prove that Lyme is there?
Here is my answer:  Since Lyme persists in mice, dogs and monkeys and test tubes and the test subject has symptoms compatible with Lyme disease, it is reasonable to conclude active infection is present. Further testing is not needed.  Additional tests may have false negative results only adding a layer of unneeded confusion. The goal of therapy is remission of symptoms, not eradication of organisms.

At the end of the day, in many cases, the diagnosis of Lyme disease is clinical and the role of lab testing adjunctive only.

Tuesday, October 18, 2016

Alpha gal allergy (meat allergy) and lone star ticks


A 40-year-old patient developed a meat allergy after a tick bite.  This condition has been reported in association of lone star tick bites.  She previously lived in a rural part of South Eastern Virginia and actively engaged in gardening and she had two dogs. Over a period of years, she had numerous tick bites. On one occasion she developed a bull’s eye rash after a tick bite and was treated for Lyme disease. It was after this she noticed a reaction to dairy products, causing hives. She had acquired the tick-bite meat allergy syndrome.  She was a long time vegan. One would have thought “meat allergy” wouldn’t be a problem. It was. Dairy was surprisingly an issue. She found that she was sensitive to trace amounts of meat. For example, she reacted to vegan food prepared in restaurants that also served meat. She became sensitive to leather shoes and leather belts. She began to have hives daily. Nothing could control the reactions.  She became progressively sensitive to a wide array of inciting agents. Chemicals, other foods, environmental changes (change in temperature), non-specific scents would cause reactions. Hives were a daily affair, recurring several times. The hives were severe covering large swaths of skin, itching like mad. The hives were minimally controlled with high doses of antihistamines. She had several scary anaphylactic reactions and carried an epi-pen at all times. The illness was progressive and frightening. In addition to allergic manifestations she suffered with: chronic fatigue, migratory joint pain, numbness and tingling and brain fog.  
She tested positive for alpha gal antibodies.  Alpha gal is short of galactose-alpha-1,3 galactose. Alpha gal is a carbohydrate not found in our bodies but present in other mammals we ingest, i.e. cows and pigs.  A protein in lone star tick saliva promotes the production of antibodies against the foreign carbohydrate leading to the disorder.

Alpha gal allergy is not a benign disorder.  Despite claims to the contrary, patients may become sensitive to many other foods, including dairy, eggs and poultry.  In the case of this patient, she became reactive to foods high in histamine and histamine promoters (such as tomatoes, eggplants, strawberries etc.).  She developed a generalized, systemic mast cell disorder. To the best of my knowledge, this has not been described in literature.

When I first met her, several months ago, she had acquiesced to the notion that hives would always be with her.
But we got her better.  

Treatment has included: therapy for mast cell activation disorder and long-term antibiotics. The former daily hives now occur once monthly at most.
Mast cell programs have previously been described.  A low histamine or mastocytosis diet is required.  In addition, high doses of antihistamines: H1 and H2 blockers, Singulair (leukotriene blocker) and cromolyn (mast cell inhibitor) have effectively controlled her symptoms.

Long-term antibiotics have been very helpful, controlling fatigue, numbness and tingling, joint pain and brain fog.  We she came to see me she was only worried about alpha gal not realizing how much persistent Lyme was affected her.

This disorder is associated only with bites from lone star ticks (perhaps chiggers) but not deer ticks.

Yet another reason to avoid tick bites at all (reasonable) costs.

Friday, October 14, 2016

Unsuspected high level parasitemia (babesiosis)

 Everything I said in the last post needs to be taken with a grain of salt. 

A 40 year old patient from Texas recently presented to my office with:  fatigue, headache, crawling sensations, shooting ear pain, feeling hot, hearing loss, lack of endurance, poor sleep, sound sensitivity, brain fog, swelling of lymph nodes, irritability and other strange sounding symptoms.

She denies ever experiencing: night sweats, air hunger, fevers, depression, mood changes or tearfulness.

She had previously tested positive for Lyme antibodies.

This patient's Giemsa stained blood smear shows a high level of parasitemia. (High levels of Babesia in the blood).


 

Babesia antibodies were not present. Only B. microti and B. duncani tests are available.  LabCorp is offering the B. duncani or WA1 antibody test again.  Direct examination of freshly prepared stained blood smear remains the gold standard for the identification of the organisms. Other, high tech modalities may be limited, especially when the particular species is unknown. These other tests may include: PCR and FISH.

Some patterns of disease are frequently observed, but the disease as a whole, remains quite unpredictable.

A coinfection cannot be excluded based on history alone. On the flip side, a negative blood test does not exclude the presence of coinfection. In this case Babesia. All available Babesia tests are imperfect.

One of the many challenges.


Thursday, October 13, 2016

The Swiss Agent




From STAT we learn that Willie Burgdorfer, the Swiss microbiologist who discovered the Lyme bacterium also discovered a long discarded something else. The mysterious sounding Swiss Agent. Sleuthing the mysteries and controversies surrounding Lyme, modern day researchers have uncovered 40-year-old papers which denote the discovery of the Swiss Agent bacterium. In a note to himself, Burgdorfer asked himself: “I wondered why somebody didn’t do something.”  “Then I realized that I am somebody.”  The agent is known by science to be Rickettsia Helvetica. The organism is purported to cause a Lyme-like illness. The primary investigator at the CDC told the author that molecular biology methods will uncover the germ but the process will take several years. * (Their priorities are clear).  Infection with the agent and associated illness is better known in Europe. It is said to cause debilitating symptoms including: fatigue, headaches, muscle weakness, meningitis, facial paralysis and (sarcoidosis?). I am not vouching for the veracity of this statement.
The paper lays bare, in the starkest terms, the gist of the issues central to the Lyme wars, naming names.
Rickettsia are a genus of tiny, gram negative, obligate intracellular bacteria. Intracellular bacteria are notoriously difficult to eradicate. The best known disease caused by Rickettsia is the redundant sounding Rickettsia rickettsii which causes Rocky Mountain Spotted Fever. RMSF is one of the most severe and potentially devastating tickborne illnesses and thankfully is rare. Many of my patients test borderline positive for RMSF and I have long considered this evidence an unknown cross-reacting species of Rickettsia.
These germs are primarily treated with doxycycline. This is another reason why doxycycline should always be incorporated into the treatment of patients with tickborne illness, at least early on, unless there is a compelling reason not to do so.
I suspect this exotic sounding germ: The Swiss Agent – is a relatively minor and fairly benign coinfection. 
We do not need another explanation for the chronicity of Lyme. The evidence, both clinically and in the laboratory is clear.
The article states the IDSA position is that Lyme is characterized by a bull’s eye rash and “pinpoint” lab test and cured with 2-4 weeks of antibiotics. Really?
The Lyme syndrome is consistently a product of Lyme (borreliosis), babesiosis and bartonellosis. The exact species of which is more often than not, an unknown.
A simple categorization based on stereotypic symptoms is more common than I would have once thought.
Babesiosis: recurring flulike symptoms, night sweats (or day sweats), air hunger, low grade fevers – usually in the late afternoon and depression with inexplicable sudden tearfulness (even in macho men).
Bartonellosis: Pain in non-joint regions (tendons, muscles, plantar fascia or bottom of feet, “shin splints,” neck pain, headaches and occasion characteristic rash. Other symptoms such as those of interstitial cystitis are also relatively common.  Rather than depression, these patients complain of anxiety, irritability, anger, (Lyme rage) and other psychiatric symptoms.
Lyme: Everything else.  Fatigue (all 3), Exhaustion, poor sleep, migratory joint pain, cognitive dysfunction with brain fog, trouble finding words, trouble thinking clearly, episodic confusion, getting lost etc., weakness, numbness and tingling and usually others symptoms suggesting broader multisystem connections, for example: floaters, ringing in the ears, racing heart, change in bowel/bladder function and others.
Sound familiar?
Patients will have visited many doctors and been told: they don’t have Lyme, they have fibromyalgia or chronic fatigue, they need to see a psychiatrist.
Optimal treatment options are becoming clearer over time.  I know longer write about the details of therapy.  Treatment needs to ultimately cover Lyme and Lyme persisters and the two other prominent coinfections, comprising the “nuclear triad.”

Appointments in my office are currently available. Our hyperbaric oxygen therapy at 1.6 ATA (20 feet underwater) is currently underutilized and “on sale.”