Suspected Bartonella Psychiatric Herx

A 32 year old woman came to see me one month ago. She was diagnosed with LD in 2003.
At that time she presented with EM rash, stiff neck, and flu like symptoms. She tested positive by ELISA and WB criteria. She was treated with 29 days of Doxycyline.
Over the last 6 years she has experienced a progressive illness. At presentation she complained of: joint pains, muscle pains, head and neck pain, memory loss, anxiety, depression, light sensitivity, and sound sensitivity. Additional symptoms included: intermittent facial rash, dizzy spells, loss of balance, profound fatigue, and irritable bowel symptoms. There was also a history of an elevated rheumatoid factor. The neurological exam was normal save sensory loss of sensation of the lower extremities. Initial Labcorp testing, done at this time showed Lyme WB positive IgM 39 and 41 bands. Her rheumatoid factor and other autoimmune parameters were normal.

She was started on therapy with Omnicef, Mincin and Plaquenil.

Four weeks later she was unexpectedly profoundly depressed. She had increased irritability with mood swings and personality changes. All antibiotics were stopped and she began psychotherapy. She deferred the use of psychotropic medications.

One month later she was feeling much better. Not exactly following my instructions, she had stopped the Minocin and Plaquenil and resumed the Omnicef as solo therapy.
Pains and fatigue were essentially gone. Her mood improved. She still had some mood swings, but the major depression was gone. Her prominent complaints were: persistent dizzy spells, night sweats, neck pain and only right hip pain. Other joint pains had vanished. She noted that bowel changes- constipation and diarrhea had abated but she had increased heartburn.

What had happened?

The patient thought the psychiatric exacerbation was due to Plaquenil. I thought not.

Brain Herx: But- she was fine on Omnicef.

Based on her symptoms it seemed likely that she had Babesia. I had not prescribed any medications that would be active against this parasite- so this shouldn't be the issue.

The question then became: Why the Minocin pych herx but no reaction to Omnicef? Omnicef attacks cell wall synthesis of spirochetes, in this case Lyme. It is relatively ineffective against Bartonella and it has no affect on intracellular L-form disease. Bartonella, according to Psych/LLMD literature is frequently associated with pyschiatric disturbances.

My hypothesis then became: Minocin killed Bartonella, perhaps in the brain leading to this peculiar reaction.

With this in mind, I decided to give all drugs with known activity against Bartonella a wide berth for the time being. These drugs do include- Minocin, Doxycyline, Zithromax, Biaxin, Cipro, Levaquin and perhaps a few others including Bactrim.

Given the night sweats and neck pain I decided to approach the suspected Babesia. My inclination was to start with low doses Artemesin while continuing the Omnicef.
The patient told me should could not afford medications that would not be covered by her insurance drug plan-

With a little more trepidation, I decided to test the waters of Babesia and prescribed a low doses of Malarone.

Another option would have been to continue Omnicef alone. My experience tells me to treat Lyme first.

Side bar: The bowel symptoms were worse but there was increased GERD- heartburn symptoms. The most likely explanation is drug induced gastric irritation of the stomach, although this is not common with Omnicef. I am becoming more convinced that Lyme frequently inhabits the GI tract and can cause symptoms there. Perhaps acid blockers which decrease stomach acidity may help kill gastric Lyme; and, regarding a somewhat related issue, it certainly appears that Asacol, a bowel anti-inflammatory, helps colon related symptoms. I prescribed Prevacid- a proton pump inhibitor which decreases stomach acidity. This should improve symptoms and perhaps aid in killing Lyme in her stomach.

Bartonella psychiatric Herx? Perhaps. We shall see.

Documented gastric Lyme

An 18 year old female with an 11 year history of complex multisystem Lyme disease recently had an upper endoscopy for the evaluation of persistent unexplained gastrointestinal symptoms.

Biopsy samples taken from the stomach and duodenum were sent to Clongen labs for PCR analysis. The samples were tested for Mycoplasma fermentans, Borrelia burdorferi, Babesia microti and Bartonella henselae. These specific tests were chosen by Dr. Ray Jones. This patient is new to me and has recently requested that I contribute to her case.

THE STOMACH TISSUE PCR TESTED POSITIVE FOR BORRELIA BURDORFERI!

Looking for Lyme by PCR has been difficult because it has not been clear which tissue should be biopsied. Here is a case demonstrating the persistence of the Lyme bacteria in gastric mucosal tissues after 5 years of continuous antibiotic therapy.

This begs the question: Should gastric Lyme be treated differently. Perhaps the acid environment enhances survival of the organism. Drawing from the H. pylori experience, it may be helpful to treat with high dose proton pump inhibitor therapy in addition to combination antibiotics.

Here we are sailing on uncharted waters.

Pregnancy and Lyme

Sitting at my desk today is a delightful 25 year old woman -- she is also 12 weeks pregnant. She lives in a rural wooded area. . Two and one half  years ago she developed an acute, multi-system disease.  She had myriad symptoms, to numerous to list: fatigue, swelling of lymph nodes, headaches, loss of balance, numbness and tingling, weakness with inability to walk associated with a severe loss of balance, painful and swollen joints, spontaneous lactation, depression, OCD, ADD like illness treated with Adderall, severe headaches.
 
Numerous doctors had been of no help. A friend referred her to me.

Her treatment has been aggressive:  she was on IV antibiotics for more than six months. At some point we treated her for adrenal fatigue and this made a tremendous difference.

 Now, 12 weeks pregnant.she has been hospitalized three times, not for Lyme disease but for hyperemesis gravida. Now resolved.

We had discussed the management of chronic Lyme disease vis-à-vis pregnancy. We had decided to use dual therapy Amoxil and Flagy which took for a short time and had to drop the Flagyl because of GI intolerance. Her gastrointestinal system is still very touchy. At this point we will use mono-therapy with amox.


Depression has been a serious issue: a year ago expressed suicidal ideation without plan or intent.  She still has a modicum of depression
She is on Zoloft. When she lowered the dose from 50mg to 25mg depression worsened: We are titrating the dose  We discussed the pros and cons -- of the medice, I think depression is worse for the fetus than potential risks associated with SSRI therapy. And post-partum depression is expected to be severe.


Did I mention -- today, all the Lyme symptoms are gone: including headache and  knee pain and swelling.

But we know this temporary.

During pregnancy the immune system is tamped down to protect the fetus from inflammation.  After the baby is borne the immune system is turned back on and a Lyme relapse may rage.

Then, we discussed breast feeding.  Lyme has been found in breast mild ---- but a new-born is immune suppressed,  a baby less than 8 weeks can die from herpes sepsis.

Not all babies acquire trans-placenta Lyme.  Cord blood can  be tested at a reference lab  like Clongen, 

Irrespective of the test result, I still recommend breast feeding.  Lyme is transmitted by a tick bite or perhaps an exchange of blood. The critical colostrum and  should not have contact with blood as its goes down the back of the throat; down a tube- the esophagus, and into the cauldron of acid in the stomach. Even when the baby spits up, the milk has already been in contact with stomach contents: and we will have antibiotics on board. Lyme is associated with autism:  lets get a head start with treatment.

I know that many in the Lyme community disagree with my approach; I can only make recommendations based on my understanding of the science and common sense.

From a wheelchair to asking for a note to go back to work today, I am delighted, and so is she.

History lessons

I appreciate the comments of my readers. No, I am not suffering like Semmelweis. And I am not fighting the struggle alone.

In 1847 Viennese Physician Semmelweis was ridiculed for suggesting that attending OB physicians wash their hands between patients. He was subsequently called the "Savior of mothers," when deaths from "childbed fever" plummeted.

In 1862 Pasteur suggested the germ theory of disease. His ideas were met with ridicule for years to come.

In 1979 and 1981 Warren and Marshall discovered a bacteria in the stomach. They suggested that the bacteria (Helicobacter pylori) was pathogenic- and that it was associated with peptic ulcers amongst other things. Colleagues, who knew better, dismissed these ideas as nonsense.

Of course, all of these paradigm shattering physicians and scientists, who advanced our knowledge and medical practice in quantum leaps, are now highly revered heroes of history.

After years of rebuke, Warren and Marshall were given long overdue credit; they were awarded the Nobel Prize for Medicine in 2005.

The question is: Are the "Lyme Wars" just another iteration of the paradigm wars described by Thomas Kuhn in his famous essay "The Structure of Scientific Revolutions?" Or, is this particular process different, in some fundamental- perhaps Orwellian way? This is a debate I will not enter.

Many others have vivisected the Klempner study and other purported pillars of the IDSA view point. The notion that this single- highly flawed study should be allowed to discredit the work of hundreds of scientists and physicians is mind boggling, to say the least. As I have noted in the past, it is difficult to wed medicine and science. The practice of medicine has always given equal weight to the art and the science of medicine. Bench top, basic science research is clear. The basic scientific facts as they have been uncovered, offer unwavering support for our contentions. Clinical science is murky at best and is always open to criticism.
This blog is not science. It is a collection of fact, theory and clinical vignettes sent out into the ether of cyberspace, perhaps the equivalent of a modern day message in a bottle. I suppose my motive is similar to that of any other author who scribbles a note on a piece of paper and then sends it out adrift in the sea; perhaps by chance, It will be found, read by the right person- and make a difference.

It seems clear to me that documentaries, books and scientific assemblies offering compelling, and at times horrifying information, have thus far failed to scratch the armor coat of the other side.

I do believe that history is critical. We must never forget its lessons, as we move forward each day, with the knowledge that we are doing the best that we can.

I will veer off the subject of my blog for a moment. I am awestruck and brought to tears of joy at this incomprehensible moment in history. I could never imagined that I would live to see the prophetic vision of one of my personal heroes, Martin Luther King, become reality, as I now watch a black American take the highest office in the land, perhaps the world.

As always, the people can make a difference. The medical community will not accept the truths of Lyme disease until it is forced down their throats by a grass roots movement coming not from doctors like myself, but from ordinary people- like you.

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.

Lyme disease symptoms, or not?

A young man came into my office with a hodgepodge of odd symptoms. He wanted to know if he had chronic Lyme disease. In fact, there was nothing to suggest this diagnosis.
His presentation was consistent with what we used to call "the worried well."

Please note that what follows are my opinions. This is my Blog after all.
I have the utmost respect for the accomplishments of Dr. Burrascano. Nonetheless, I have concerns about some Lyme disease symptoms included in his guidelines.

The ILADS guidelines are quite circumspect and are the product of a committee of interested physicians and scientist. I feel that these guidelines are excellent. The ILADS web page links to Dr. Burrascano's guidelines. Dr. B's guidelines represent his opinions only, but I am not sure that this is made clear to the public.

Here is my concern: Medical Boards, the IDSA and members of the lay public read these guidelines. I am concerned that such entities may interpret small parts of the guidelines in ways which could have a deleterious effect.

A large menu of expanded symptoms is said to be associated with Lyme disease. A point system based on the presence of symptoms is suggested. While I agree that many listed symptoms suggest Lyme disease in its various manifestations, there are many symptoms on the list which I find questionable. I address these below. Again, let me make this clear. I think that the majority of Dr. B's symptoms are right on target. I am only addressing the small number of symptoms on the list which concern me.

Dental Pain: There are numerous reasons for this, I personally do not believe it correlates with Lyme disease. It certainly lacks specificity.

Neck stiffness: This is a common symptom. It is usually due to muscle spasms, cervical arthritis and other common orthopedic disorders. It is thought by many to be a symptom of Babesiosis. However, by itself, it lacks specificity for Lyme and related disorders. I am here not discussing neck pain in the context of pain/complex disorders including fibromyalgia. I am only discussing it as an isolated symptom.

Weight loss or weight gain: Well, which one is it? Appetite and weight changes are commonly seen. I again feel this symptoms is very non-specific.

Irregular menses: Their are numerous reasons for this. Dysfunctional uterine bleeding can be benign but it can also be linked to serious disorders like cervical cancer. This is not a typical symptom of Lyme disease. I understand that abnormal bleeding can be seen in the context of endocrine dysfunction related to Lyme disease. In and of itself this symptom is not specific for Lyme disease.

Bladder dysfunction: This is common and has many causes. Certainly it can be seen in patients with systemic Lyme disease, but it lacks specificity. I do see many patients with bladder issues but I would be hesitant to include this with a list of common Lyme symptoms.

Erectile dysfunction and loss of libido: These are common complaints. When I hear them from my patients I do not think of Lyme. There are many other causes.

Nausea and Heart burn: H. pylori is common. Lyme is fairly far down on the list of possible diagnoses. Patients may have ulcers, Barretts disease or even cancer. I have now seen evidence of Lyme infection of the stomach, as I recently reported. It has not been my experience that this is a common symptom in patients with Lyme disease.

Constipation and Diarrhea: This is a common complaint. It is usually associated with irritable bowel syndrome. It may be associated with celiac disease or even occasionally colorectal cancer. Lyme colitis is probably relatively common. Nonetheless, I would be hesitant to list this symptom.

Heart murmur and valve prolapse: Lyme typically causes arrhythmia, heart block and pericarditis. I have not seen it cause the mentioned syndromes/symptoms.

Head congestion, cough, sore throat: These are common complaints and usually due to upper respiratory infection, GERD or asthma. Air hunger may be seen in Babesia infection. Lyme may cause pleurisy. These symptoms seem to lack specificity for Lyme disease.

Hair loss: Male pattern balding is normal. Hypothyroidism may be considered. Not specific for Lyme disease. Alopecia areata is an autoimmune disease. It may be associated with Lyme disease. This symptom is non-specific.

Swollen glands: This is non-specific. I have seen Lyme present with this finding. Certainly it may be associated with Bartonella. Doctors must first exclude serious disorders like malignancy. It is a fairly non-specific symptom.

Back pain: This is generally due to a variety of common orthopedic disorders. Lyme is typically associated with large and small joint pain. It is rarely associated with back pain unless the sacroiliac joints are inflamed. Non-specific.

Headaches: Non-specific. Most common causes are migraines and tension headache. Headaches are commonly seen in patients with Lyme disease. However, the vast majority of patients with headaches do not have Lyme disease. This is a non-specific symptom.

Seizures and psychosis: Lyme is unlikely. Doctors must exclude brain tumors. Recently we have heard about Lyme rage and associated psychotic behavior. More frequently Lyme is associated with anxiety, depression, mood swings, ADD like symptoms and combinations of the above. Lyme as a cause of psychosis would seem to be quite rare.

Milk production: This may be due to a pituitary growth called a prolactinoma. Not
specific for Lyme disease. It may been seen in disorders of the hypothalmic pituitary axis which have been described in Lyme disease, but its association with Lyme disease is still low on the list of possible causes.

These symptom lists are published on the world wide web and linked to the ILADS web site.

Lyme disease is frequently a multisystem disease. It can be associated with a surprising list of symptoms. Patients cannot self diagnose. Only a physician, after carefully weighing all the clinical data can make the diagnosis. Patients may look at expanded symptom lists and reach unwarranted conclusion, as is the case with the patient I alluded to at the beginning of this Blog.

Such all inclusive symptom lists may create the erroneous impression that LLMDS think that everything is caused by Lyme disease. And this is simply not true.
I am a member of ILADS. My comments here should not be construed as an effort to disparage ILADS or Dr. Burrascano. Lyme disease and associated guidelines are in a state of flux and refinement. To the extent that my comments may seen as critical, my intent is to provide only constructive criticism.

Continuous or pulsed

Two patients yesterday with neuropsychiatric symptoms responsive to amoxicillin. One patient claimed that Moxatag, a long acting drug, was more effective than traditional short acting amoxicillin. The other adamantly claimed the opposite.

The question about continuous therapy versus pulse therapy is controversial and unsettled.

At least one(Lyme)study showed that continuous exposure to drug, even at lower concentration was more effective(had better killing kinetics).

Test tube study.

Clinical support: Long acting Bicillin (penicillin) works very well despite low blood/tissue concentration of drug.

Amoxicillin reaches a peak blood level without hours and is rapidly excreted with preferential penetration to some tissues. In-vivo(you), tissue concentration may be higher than shown with in-vitro(test tubes). Don't know.

IV antibiotics with long half lifes - Rocephin and Zithromax can be very effective.

Oral antibiotics behave differntly in the body than IV for a number of reasons.

I currently prescribe amoxicillin as 500 mg, two twice daily. Perhaps one four times per day would work better. There are practical limitations: better adsorption on an empty stomach, scheduling doses.

My impression: continuous better than pulsed.

Lyme and biliary disease

Most readers have some familiarity with the liver and gallbladder.  The biliary (bile duct) system includes the gallbladder and a collection of ducts coming from the liver which join to enter the first part of the small intestines, the duodenum, the first part of the small intestines (bowel) just below the stomach. 


The liver is best known as our body’s detoxification organ (along with kidneys). The liver “metabolizes,” alters and excretes medicines and other substances. 


The liver makes bile, a yellow viscous fluid stored in the gallbladder, located directed under the liver. The gallbladder contracts with meals. Bile made of bile acids, from cholesterol, aid in the digestion of fat (an emulsifier) but has many other functions.  


The liver detoxifies medications and toxins through a system of enzymes with names like cytokine P450. Toxins and medications may end up in bile. 

Adsorption of medications may be dependent on something called the enterohepatic recirculation of bile.

Most bile is recycled from the gut which is considered 95% efficient. A particular bile acid molecule may be used 20 times before it is replaced. This is not necessarily a bad thing. The process of repeated cycling may enhance the function of therapeutic drugs and delay their excretion. For liver toxins this works the other way.  Proper functioning of the enterohepatic system depends in part on a healthy gut flora and specific bacterial enzymes.  Higher doses of antibiotics may be required because disruption of normal flora and necessary enzymes caused by the antibiotic(s). 

The use of bile acid sequestrants to remove unknown toxins like cholestyramine is not supported by scientific evidence. 

Some antibiotics promote the production of biliary cholesterol sludge and gall stones, primarily Rocephin, the popular intravenous drug used to treat Lyme disease.  Cholecystitis (gall bladder attacks) with or without the presence of gall stones is a common occurrence. 

Lyme anecdotally can attack the biliary system. Cases of positive Lyme PCR/DNA from gallbladder tissues are known to me but there are no published reports to date. 

Published reports have established Lyme liver disease in the form of granulomatous hepatitis. 
Tests like sonogram, HIDA/CCK scan and others may be used diagnostically for problems with gallbladder and bile ducts.  Negative test results do not rule out gallbladder/biliary disease. 

I am treating a patient with primary biliary cholangitis (PBC). Generally, the disorder is considered autoimmune, “idiopathic,” which of course means the patient is pathological and the doctor is an idiot. Some European literature (this patient is European) connects Lyme with this enigmatic illness. The patient has a clear history of Lyme. No such connection is made in the U.S. PBC is now a treatable disease. 

Bile via an array of ducts ultimately empties into the common bile duct. Bile the empties into the duodenum into a structure called the Ampulla of Vater. The flow of bile is regulated by a muscle called the sphincter of Oddi. 

After cholecystectomy, (surgical removal of the gallbladder), prior gallbladder pain may seem to recur. The bile ducts may become dilated. When a medical workup excludes a left-over stone stuck in bile duct, liver disease, pancreatic disease and other rare diseases, the diagnosis may be post-cholecystectomy syndrome or sphincter of Oddi dysfunction.

These syndromes are more common in Lyme patients, many of whom suffer with gallbladder disease and biliary tract disease and have had their gallbladders removed. 

The diagnosis is commonly missed or not taken seriously. The disorder can be disabling. Effective medical therapy, in my recent experience, is available but overlooked.

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.

Lyme, Babesia, Bartonella - images - seeing an old friend

This 20 year old female has spent her life in particular town in outer suburbia where everyone sees to have Lyme disease. Over a period of many years, with many symptoms, she has asked for Lyme tests - which have always been negative, until now, September, 2013. The Lyme EIA titer was positive at 1.36 and 2/3 IgM bands were positive. Her doctors prescribed 21 days of doxycycline which has offered no help. She came to my office with her father and her boyfriend asking for my help.

Seven years ago a 14 year old boy was brought into my office. He had a distant, far off gaze. This former sports star and honor's student could no longer participate in sports and his grades went from straight As to Ds. This is a case I'll never forget.
He had a quiet, almost eerie "zombie-like" affect. His eyes were blank and vacant.  Early on I decided he had profound Lyme encephalopathy and aggressive therapy was called for. I started him on IV Rocephin. One, then two months later, he returned for follow-up care, unchanged. I remember feeling nervous about the case. In the third month I added IV Zithromax. He returned a month later: no change. With butterflies in my stomach I added Flagyl. He returned to the office a month later, month 5 of intravenous treatment. I was amazed. A switched had been flipped:  he was back. His eyes were bright and clear. This case left an indelible imprint on my psyche. But after the PICC line was removed I never saw him back. We doctors say he was "lost to follow-up."

My new patient's 21 year old boyfriend said: "Hey doctor do you remember me." It took me a minute, but then I recognized him, my 14 year old now grown up. The bright eyes were still there; he had now referred his girlfriend to me.

His girlfriend is very ill. She limped into my office with a cane. She was suffering with severe daily headaches. A neurologist had prescribed Topomax which seemed to make things worse. Of critical concern at the moment: she had lost 30 percent of her peripheral vision in both eyes over the last three months and the neurologist and eye specialist could not figure out why.

She had been sick for a long time, years. She had a plethora of symptoms. Some of the highlights include: severe fatigue, numbness, weakness, shooting pains, a diffuse chronic pain syndrome, night sweats, shortness of breath, air hunger, back, neck and joint  pains, loss of coordination, dropping things, loss of balance, confusion, memory loss, global cognitive dysfunction. Psychiatric symptoms including anger, rage, irritability, visual and auditory hallucinations. She also complains of sudden episodes of paralysis of her face and extremities.

Her neurological examination showed evidence of severe neuropathy and also a loss of proprioception. When I manipulated her big toes she could not tell if the toes were pointed up or down. This is an unusual finding only seen in cases of complex neuropathy.

Another word about her headaches. The pain was throbbing or band-like, behind an eye or across her entire head. The headaches typically occur twice daily lasting 4-6 hours rendering her non-functional. She had dropped out of college and also quit her part-time job. Daily headaches were fairly new over the previous 3 months.

Laboratory tests were remarkable for a positive antibody against B. duncani. Here are some images of her blood smear Giemsa stains. The slides show ample evidence of active Babesia infection. In the third slide below a small bacteria can be seen at the periphery of a red blood cell. This is characteristic of a Bartonella-like organism.

Chronic daily headache syndrome is a relatively new entity on the scene. At least some is due to tick borne disease. It is frequently written that Bartonella causes "ice pick" headaches behind an eye and that Babesia causes posterior headaches with muscle pain. Lyme can cause headaches as well.  I think it is usually not possible to tease out the exact cause of headaches in persons suffering with tick borne disease.

My approach to this patient is to treat Babesia but also start intravenous antibiotics. I think Bartonella will need to be addressed at a later point.

PS:  The boyfriend doesn't remember a lot about the time he had severe Lyme disease. He does recall walking in and out of rooms not knowing why.

Plaquenil alone?

A 70 year old male patient was diagnosed with Lyme disease 6 or 7 months ago. He reported a history of tick bite and rash in 2002. He received a short course of antibiotics at that time. When I saw him initially he complained of knee pain and swelling, fatigue, generalized arthralgia (joint pain), numbness and tingling and an irregular heart beat. He was seropositive by Western Blot. He was treated with Amoxil, Biaxin and Plaquenil. After two weeks he reported that the antibiotics were causing nightmares and insomnia. He attributed this to Biaxin. The regimen was changed to Amoxil and Minocin. The knee pain and other symptoms rapidly improved over the next two weeks. Then one week later he complained of confusion and unsteadiness. I diagnosed a "brain Herx." I added Plaquenil back, as well as Welchol, presumptively to remove "neurotoxins." I also reduced the dose of Amoxicillin and Minocin. He continued to improve rapidly once more with a cessation of neurocognitive symptoms. However three weeks later he had a bout of gastroenteritis and the antibiotics were held for a few days. Like many of my patients, he was "lost to follow up" for a couple of months. The patient stopped the Amoxil and Plaquenil and took only Minocin, on his own which he increased back to the full dose, without consulting with me. He returned to my office after a total of 4 months of treatment stating that he was 85% better. I scolding him for non-compliance: it didn't do any good. I added Flagyl only 250mg twice daily. When he returned a month later he told me that the Flagyl had made him "spacey" so he stopped it after a few days. He was feeling close to normal. Call me! I tried him on Zithromax and Plaquenil about 6 weeks ago. I made the change because he was also complaining of sinusitis. It seemed that there may have been problems with Amoxil, Biaxin and other antibiotics. He came back to see me today. He felt perfectly fine: back to normal for the past four weeks. And by the way, he had only taken the Zithromax for a few days because it upset his stomach. Everything was fine he was taking only Plaquenil. To review: Brain symptoms, joint pain, neuropathy symptoms, palpitations and fatigue were gone. He Had been treated for a little more than 6 months. This was the best he had felt in years. So far the symptoms were not returning.

This is not my typical patient. Most actually do what I say; they take medicines as prescribed and return for follow up as instructed. In his defense, his wife had major surgery during this time frame; personal mitigating circumstances interfered with our process.

When patients go into remission it is unlikely that the Lyme bacteria have been eliminated. Let me insert an additional piece of information. This patient had a fairly strong IgG response on the standard Western Blot: 4/10 bands were reactive.

Patients with IgG responses may have some blocking immunity for intact spirochetes.
Per the immunology text book: symptoms related to intracellular infection relate mostly to the immunologic response to the infection- not the presence of the germs in and of themselves.

One could postulate that 1) The patient had a blocking IgG response to keep the spirochetes in check and 2) The immunomodulating effects of Plaquenil were keeping the lid on a potentially toxic T cell response to the intracellular component. The fact that he responded so favorably with primarily Minocin supports the hypothesis that the main issue in his case related to intracellular disease.

It was clear that cystic forms of the bacteria were still present. However, if they converted to spirochetes or L-forms the above two mechanisms would be in place to keep the disease quiescent.

I decided to leave him on just Plaquenil for the time being to see if this would foster a long term clinical remission. Sure, it doesn't follow any standard paradigm. But I can't argue with success.

Interstital Cystitis and Lyme- preliminay report

I would like to comment briefly about this disorder and its potential relationship to Lyme disease. I have been treating at least one patient who has reported an excellent response to treatment. Willie burdorferf, the microbiologist who discovered the Lyme spirochete reported in 1988 that Borrelia burdorferi, the bacteria which bears his name was found consistently in the urinary bladders of mice.
A great deal of research has supported the notion that Bb widely disseminates into many organs. The co-existence of urinary tract disorders in patients with Lyme disease is well documented. There is evidence that Lyme has been found in stomach, colon and gallbladder biopsy samples. To the best of My knowledge no studies have been undertaken to examine bladder tissue samples for the presence of Lyme. At least one study has demonstrated positive Lyme PCR in genital secretions. This may represent contamination from the urinary tract. PCR tests for genitourinary STDs, Chlamydia and gonorrhea, from urine samples have existed for years(this demonstrates that urine contamination from other sources is frequently present). Positive Lyme PCRs have been obtained from urine specimens. Overall, a body of evidence suggests that Lyme can- may reside in the urinary bladder.

Interstitial cystitis is a fairly common disorder. It occurs more commonly in women. It's name is derived from the minimal pathological changes seen in bladder biopsies.
It is associated with symptoms which at times are crippling. Such symptoms may include: pain in various locations, frequency, pelvic pain, bloating and other related symptoms. IC(interstitial cystitis) patients are thought to have a higher incidence of fibromyalgia and chronic fatigue syndrome.
The standard thinking is that the cause is unknown; although it is said not be due to infection and not respond to antibiotics.

These symptoms overlap with several other disorders: chronic pelvic pain of unknown cause, chronic prostatis or prostatosis in men and chronic urethral or para-urethral syndrome seen in women.

Standard urinary tract infections are caused by bacteria that normally live in the colon. Examples include: E. coli and enterococcus. These are classic gram negative and gram positive bacteria. They can be easily grown in standard culture medium. standard antibiotics only treat gram negative bacteria- such as Bactrim.

Lyme is very difficult to grow in culture media, even by expert hands. And- if it is found only in the bladder wall, such cultures will be useless.
Other L-form bacteria have also been implicated in these syndromes, including: Chlamydia and Mycoplasm species. These too are very difficult to culture.

Physicians typically prescribe antibiotics for 7 to 14 days for urinary tract infections. Experience with Lyme disease shows that short courses of antibiotics are not effective. Only in prostate infections have longer courses of antibiotics been used. Physicians are aware of the prostate-blood barrier and bacterial sequestration within the gland. Antibiotic courses up to 90 days have been used- with some success and frequent relapse.

My patient has established IC. She also tests positive for LD by Western Blot and has a variety of other symptom commonly associated with Lyme disease. She had been miserable for two years with a horrendous quality of life. Experts in IC had been unable to help her.

She has been treated with the usual Lyme antibiotic combinations. The combination of Biaxin with Plaquenil was incredibly effective for the IC symptoms and life altering.

My thoughts are that IC and related conditions are caused by L-form infection of perhaps Bb and other L-form bacteria. Biaxin is not an antibiotic used for urinary tract infections in the typical sense. Minocin has also shown some promise. Cipro has been used for both Lyme and urinary tract infections, but I have noticed a very significant "bladder herx" when patients have been treated with it. Perhaps it can be tolerated later in the course of therapy.

I have seen evidence that IC and related syndromes respond to antibiotics. Long term antibiotics are required- patients need to realized that symptoms will not improve over-night.

Lyme disease should be considered in these patients. This is a work in progress. I cannot claim a lot of experience here. However- my patient has reported that other IC patients, with whom she communicates, have also experienced improvement with the combination of Biaxin and Plaquenil.

Morgellons: case closed

I thought --  rather unexpectedly --  that a young graduate student working with Dr. Eva Sapi presented some ground-breaking results from her research looking into Morgellons disease. As she first pointed out, the disease is discounted by mainstream medicine and the CDC who call it delusional parasitosis. The mainstream belief in short is that patients with this illness are not physically sick but rather suffer from a psychiatric ailment. The young student (I apologize that I cannot recall her name) said her research delved into the Lyme-Morgellons connection. Essentially "scab" material  obtained from patients suffering with the disease, some of whom were sero-positive for Lyme disease, most of whom were not, was ground up and analyzed via molecular biology techniques looking for the presence of Lyme DNA. In all cases Lyme, B. burdorferi was found to be present. Specifically Bb sensu stricto, the North American version of the disease was present in samples taken from each patient diagnosed with Morgellons disease. In some cases, surprisingly, H. pylori, the bacteria associated with stomach ulcers and other related conditions was also found.

Perhaps of even greater significance was the finding that normal skin flora were essentially absent except for sparse S. epidermitis.

In some corners Morgellons  was already known to be Lyme associated (not previously proved) but connected to some yet undiscovered pathogen(s). The nature of the peculiar fibers has not yet been determined. The absence of other, usual bacteria in the affected skin would seem to indicate that another organism was secreting an antibiotic substance capable of eradicating normal skin bacteria. Another possibility is that another organism, whose DNA is unknown, assumes the niche inhabited by normal skin flora. The molecular techniques used in the study would not uncover fungal/mold or protozoal DNA.

Organisms that produce powerful antibiotics typically belong to the mold family as seen with penicillin. Anecdotally, there is evidence that the disease responds to agents used to kill protozoa, not mold. The mystery remains.

What I think is clear is that Morgellons is linked to Lyme infection in the skin; that is a distinct disease, not another presentation of Lyme like erythema migrans; that it is not a tick-borne co-infection; that although strange and mysterious, is not a disease from outer space as some have suggested; and most importantly, is not a delusion or hallucination on the part of the sufferer and/or treating physician.

One can only hope that these findings will be replicated in other research and put before authorities like the CDC who will then be forced to take this disease seriously, and perhaps Lyme as well (wishful thinking).

So we have one important piece of the puzzle, given to us (or at least me) unexpectedly, in a rather poorly attended seminar, from a young, somewhat diffident (and brilliant) graduate student, while most attendees were in another seminar.

OK -  the case is not closed. But we have a piece of the puzzle. This research will be published in a peer reviewed journal (probably PLOS) and this is very exciting news.

MCAS, mast cell activtion syndrome, nuts and bolts

Mast cell activation syndrome – MCAS – a stand-alone theory of everything.  The disorder is not accepted by mainstream medicine.  Hematologist deal with a set of serious disorders which may involve tumors but that’s is not what we are going to discuss--not to say mast cell activation syndrome is not a serious disorder. It can be deadly serious.  MCAS is a novel way of looking at disease and is used to explain many diseases, symptoms and syndromes. 

What is a mast cell? Mast cells are important actors within the immune system. Stained, under the microscope, they are plump purple cells. They are like other cells found in the blood (eosinophils, basophils) But these cells are located in tissues, various organs, outside the blood stream and around blood vessels. Mast cells have a role in allergies and killing certain parasitic worms. Not the topic of the day. We are interested in inappropriate action of the cells.  

The granules inside the cells contain various substances which cause inflammation. These granules contain things like:  enzymes, histamine, leukotrienes and prostaglandins. 

Activation:  These caustic immune cells release many inflammatory substances causing severe swelling, immune responses and local tissue injury.  Instead of killing parasitic worms or attacking an allergen mast cells are attacking us and damaging our tissues. Mast cells are omnipresent and symptoms vary depending on which tissues are attacked.   For example, if mast cells activate in the intestinal tract symptoms may include bloating, diarrhea, GERD and other dysfunction. Mast cell activation in muscles and joints causes joint pain and swelling. Mast cells activating in the brain may cause brain fog, headaches and neuropsychiatric symptoms.  Diffuse mast cell activation can cause a “multisystem” presentation: fatigue, brain fog, joint pain, muscle pain, bowel and bladder dysfunction, neurological dysfunction, change in mood, confusion and many others. 

Patients may experience one mysterious problem after the next.  Symptoms may come and go over many years. Doctors scratch their heads or diagnose a psychosomatic disorder. Doctors will not think: MCAS.  MCAS is a new paradigm on the edge of medical practice and medical science. Doctors don’t know about it – except for the few. 

MCAS can explain a lot. 

Mast cells don’t typically act on their own. They are triggered by something. Triggers vary widely from one person to the next. 

Certain clinical scenarios make us think MCAS. Patients with hypermobility joint syndrome and POTS invariably also have MCAS. Lyme spirochetes may be a trigger as well as other infections. 

We look for clues: Recurring hives, unexplained itching, dermatographia and facial flushing. Patients may report sensitivity to scents and smells and to variation in temperature – hot or cold. A patient I saw today is sensitive to certain fabrics.  Chemicals may be a trigger. Foods and medicines are common triggers. It may be the inert ingredients in pills that triggers the response and some patients have all their meds compounded.  All of the above may be absent. 

Herxheimer reactions may have a MCAS component and may respond to appropriate therapy. 

Are there lab tests? Iffy. Labs tend to positive only in severe forms of the disease, not the syndromes we are discussing.  Occasionally serum tryptase or histamine may be elevated.  24-hour urine tests are sometimes abnormal. The diagnosis is usually clinical. 

MCAS is treatable -- frequently with remarkable results and commonly used meds are extremely safe. 

Diet may help.  Certain foods are known to be high in histamine or trigger histamine release. Reducing intake of certain foods can help.  Well-known examples include tomatoes, strawberries, avocado, nuts and deli meats. You may only have to cut down on certain foods, not eliminate them completely. Food reactions vary a lot amongst individuals. 

MCAS is not an allergic reaction. For example, an allergy to peanuts is something different, mediated by different pathways in the immune system. Still – there is some overlap. 

Meds. In most cases patients respond to simple, safe meds. But may have to take a lot of them.  The treatment has 2 parts:  Blocking the effects of inflammatory substances released from mast cells and stabilizing mast cells so they don’t activate in the first place.  There are 2 kinds of histamine receptors called H1 and H2.  H1 blockers are the familiar antihistamines. MCAS requires higher doses, and multiple antihistamines. The H2 blocker are thought of as ulcer/heartburn drugs, they block the production of stomach acid. The H2 receptors have other functions and blocking the receptors helps. Blocking leukotrienes (Singulair) is helpful.  Prostaglandin blockers, anti-inflammatories like aspirin may help. Stabilization is more problematic.  Cromolyn would be great but has poor bioavailabity but may still be effective. Ketotifen is mast cell stabilizer with antihistaminic properties.  It is available through compounding pharmacies. Effective mast cell stabilizers may include benzodiazepines and cannabinoids. More difficult cases may be treated with the asthma/hives injectable Xolair and an array of immunosuppressive drugs.