Lyme-Bartonella-B12-Folic acid and vitamin D

A 35 year old female was seen by my associate one month ago with complaint of fatigue, malaise joint pain and fatigue. The symptoms had been present for about 2 months. My associate ordered a Lyme Western Blot. Bingo. Three of three IgM bands were present: Lyme disease. Here are some additional result:B12 280, folic acid 5.8, C4a 3200, vitamin D 25-Hydroxy 26, vitamin D 1-25 dihydroxy 75. I saw her 3 weeks ago. Today was our second visit. The symptoms had really been present for the past 6 months or longer. She had experienced fever, swollen lymph nodes, muscle weakness--especially of the arms, profound fatigue, pain in knees-feet-shoulders, total body pain, brain fog and forgetfulness as well as episodes of confusion, depression, word salads, tingling and drenching sweats. The exam showed weakness of the arms and evidence of peripheral neuropathy.

Here is what I think I have learned and how I applied it for this patient. Lyme and Bartonella seem to be co-travellers. It is the combination that causes many of these symptoms, especially the cognitive ones. The swollen glands are a tip off-Bartonella. Soaking sweats do not always equate with Babesia. The low B12 and folic acid are a tip-off. These nutrients are essential for the manufacture of red blood cells. Depletion of these vitamins suggest a bacteria or parasite of red blood cells causing rapid turn over and depletion. Bartonella are present in large numbers whereas Babesia are present in relatively small numbers; these vitamin deficiencies would seem to be the calling card of Bartonellosis.

Vitamin D is a useful parameter. The conversion to active vitamin D in the kidneys occurs because the immune system is attempting to regain equilibrium. This push to the Th2 state away from Th1 occurs because the infection is causing excessive inflammation. As an aside, it doesn't matter if the patient is given supplemental D or not. More vitamin D might provide additional fuel to cool off the rambunctious Th1 response: it is OK to give and may help the patient feel better. Vitamin D toxicity is a non-issue. The only potential issue is hypercalcemia--excessively high levels of calcium in the blood. This is highly unlikely and can be monitored.
Forget the whole Marshall distraction.

I placed the patient on Doxycyline and low dose Cipro. Three weeks later she is doing fabulously.
The Herx was bad for 2 weeks. Now: the fog has lifted, her muscles are strong again and even the night sweats are gone.

The old Doxy plus Cipro was not treating Lyme by two different intracellular mechanisms; it was treating Lyme and Bartonella all along. That is why it has worked so well!

The low dose Cipro seems safe and effective. This patient has allergies to Penicillin and Sulfa.

It is all coming together.

The Untouchables

My critically ill patient is back in the office. She is literally disintegrating before my eyes, her encephalopathy worse. Confused, hallucinating and delusional-- she is unable to speak. A week ago she was somewhat mobile. Now she is confined to a wheel chair resembling many unfortunate patients I have cared for in nursing homes with end stage Alzheimer's disease: this patient is 47 years old. Another doctor had cared for her for 7 months. She has been under my care for only one month. She needs hospitalization. I have sent other patients to many hospitals over a period of years with poor outcomes. This different University Hospital is reputed to be a bit more friendly. We shall see.

I send her to the hospital with a stack of studies and a hand written summary. She is sero-positive for both Lyme and Ehrlichia--thank God! I have written down the name of a neurologist who is reputed to be "Lyme friendly."

The only way to be admitted to hospitals these days is through the ER, unless you are an "attending" with direct admitting privileges. And even this occurs rarely these days.

The intern is the first to call me: "We don't see anything acutely wrong with patient"--not wanting to admit her to his service.

She is very ill, please admit her.

I am called back by a supercilious second year resident, his boss. "The patient has been the same for a month--there is nothing acute here--we don't want to admit her. The neurologist whose name you wrote down won't be able to see her unless you call him. You should not have sent the patient to the ER: you have given her the erroneous impression that she will be admitted. I don't see any reason for an admission."

"Please admit this patient. She is getting worse. She has a severe progressive encephalitis. She absolutely must be admitted for a work up; she needs a a lumbar puncture. You cannot send this patient home"-- I implore.

"Humf, I will get neurology to see her." The neurologist you have requested will not see her unless you arrange it--here is his beeper number."

I page the doctor: no response.

The gatekeeper--the man who would keep my critically ill patient from admission to the esteemed University Hospital is a "sagacious" 26 year old doctor with a major "...tude."

The patient is crazy of course, the doctor a wack-job. Tick borne disease causing encephalopathy--"whatever". Reluctantly: "I'll see what neurology has to say."

The untouchables: cursed-- damned-- invisible.
At least that how it seems.

Why take the blue pill if the red one works just as well?

Something about chasing a white rabbit down a hole I think.

"I'm sorry-- which pill do we take?"

Bartonella re-visited

Bartonella is a facultative (difficult to culture), gram negative intracellular bacteria. New strains--known to cause human disease are being discovered on a regular basis. Standard serologic (antibody) tests ordered by physicians for Bartonella test only antibodies against B. henselae and B. quintana. A quick survey of medical literature shows a long list of Bartonella species with exotic sounding names: B. clarrideiae, B. koehlerae, B. vinsoni, B. berkhoffi, B. elizabethe, B. bovis, B. rochalimae, B. melophagi, B. facilliformis and others. The "species PCR Bartonella" test could miss other Bartonella species whose DNA is different. A CDC (Lyme-division) representative, recently said that new species of Bartonella in mice are being discovered on a regular basis. The CDC plans to publish a point-counterpoint piece regarding the significance of Bartonella in human disease.

Could the mystery bacteria seen in blood wet mounts and smears of many tick borne disease patients be yet unclassified forms of Bartonella? I think the answer is YES. These small bacteria stain gram negative and do not culture. Although Bartonella are intracellular organisms--live in cells, Bartonella species can exhibit prolonged bacteremia (bacteria in the blood).

Is the treatment of Bartonella different than that for Lyme? Both Lyme-Borrelia burdorferi and Bartonella are gram negative bacteria. The medical literature claims that both bacteria can for the most part be treated with the same antibiotics: Doxycyline, Biaxin, Zithromax, Rocephin, Levaquin and others. These drugs are bacteriostatic. Only two drugs are reputed to be bactericidal: Gentamycin and Rifampin. The standard medical literature also claims that Bartonella can be treated with short courses of antibiotics (similar to claims for Lyme). The literature indicates that Bartonella can cause brain infection but states that there is only one reported mortality. It is recommended that such cases should be treated more aggressively.

Back to the CDC. Most readers of this BLOG are familiar with the concept of tick borne disease. This concept is foreign to the CDC, despite a web-page which is misleading . The groups which study Lyme and co-infections are separated, even geographically(Colorado versus Georgia). Lyme is linked with spirochete diseases. Ehrlichia/Anaplasmosis are in a Rickettsia group. Babesia is in a parasite/protozoa group and Bartonella is in another group. The CDC admits it has never studied how multiple tick borne infections interact in a single host.

But I digress.

We don't really know what the germs (mystery bugs) are, what their role in disease is and how best to treat them.

A new patient, one who is extremely sick, was recently referred to my practice by one of my difficult patients--who is finally getting better--thanks.

This patient has a long history of chronic Lyme disease with pain and severe encephalopathy. She is only 45 years old but has moderate to severe dementia. Her previous physician, a well known Lyme treating doctor had prescribed a prolonged course of Rocephin--without benefit and essentially informed the patient and family that there was nothing else he could do.

I agreed to take the patient on to see if I could help. Based on experience I know that some patients respond to IV Zithromax even when IV Rocephin has failed. Perhaps this is a manifestation of the "Bartonella" syndrome.
There was a response. Within two weeks her pain was 50% better. Her encephalopathy worsened--a Baronella brain Herx?? At least it was something. These results are contemporaneous with this entry; adjustments in therapy are being made.

Clearly, there are patients who respond better to: Bactrim, IV Zithromax, Rifampin, Cipro, Levaquin and other drugs. LLMDS and their patients will attest to this.

Many patients are clinically diagnosed with the triad of: Lyme-Babesia-Bartonella--frequently on clinical grounds.

If there is a method to my madness I have found that patients respond best when the treatment strategy targets: Lyme then Babesia then Bartonella and then back to Lyme. Of course it may be desirable to use drugs which overlap in their ability to address the collection of infections. And so it goes.

Babesia questions

For convenience we can divide physicians into two camps: those who follow the IDSA and those who follow ILADS. This is an over-simplification. Many physicians fall in between. I am seeing more infectious disease physicians cross over into the chronic Lyme side of things. Many other physicians are becoming more interested in treating Lyme as a chronic disease and treating it as such. The paradigm has broadened for many of us; chronic Lyme has evolved into chronic tick borne disease. Many patients do not improve or recover, at least not fully, unless other co-infections are treated as well. The treatment of co-infections exposes Lyme aware physicians to increased criticisms by IDSA leaning physicians because the presence of these entities is frequently more difficult to demonstrate than Lyme--Borrelia burdorferi.

Readers must be reminded that in the main, laboratory evidence suggesting the presence of Babesia tells the physician only one thing: the patient has been exposed to Babesia. Here I am referring to serological antibody tests. Other, more convincing tests, for the non-believers, include a blood smear which shows the organisms or a FISH test offered by IgeneX. These tests are not particularly sensitive missing most cases. Serologically, we can test for two strains of Babesia through commercial labs: B. microti and B. duncani. There are numerous other strains of Babesia for which no simple test exists. Clongen lab can perform a Babesia "species" PCR test which is very specific but not all that sensitive. It screens for the presence of Babesia DNA for about 15 species of Babesia.

In routine lab panels described elsewhere, anybodies directed against B. microti and B. duncani or WA1 are routinely obtained. It is always nice to have one's clinical suspicions mirrored in a laboratory test. But like most things Lyme: the diagnosis of Babesiosis is a clinical one.

Many clinical signs and symptoms have been ascribed to Babesiosis. In my practice the primary symptom is sweating. Patients have night sweats, sweats after a hot shower, day sweats or chills and flu like symptoms which recur cyclically. A secondary feature is muscle pains in preference to joint pain.

Another helpful test is the evaluation of a wet mount slide. Many patients show a crescent shaped organism which resembles Toxoplasmosis. I do not believe this organism is Toxo: many patients with the organism have negative serology (antibodies) directed against Toxo. I will explain why I mention this finding in connection with Babesiosis in a moment.

The standard treatment for Babesiosis has been Mepron, usually combined with Zithromax.
Mepron is a yellow liquid which is unpleasant tasting and very expensive. It contains a single ingredient: Atovaquone. Malarone, on the other hand, contains two anti-parasite ingredients: Atovaquone and Proguanil. Malarone is a less expensive, convenient tablet.

Malarone seems to address this crescent shaped parasite whereas Mepron does not. It is my suspicion that this other, yet unknown parasite, is responsible for much muscle pain, including that associated with fibromyalgia syndromes.

Even though the dose of Atovaquone in Malarone is only 1/3 of that present in Mepron, I have found it is effective for Babesia symptoms. My experience has informed me that it is the length of therapy, not the dose of Atovaquone which helps ameliorate Babesia related symptoms and presumably infection. Anti-Babesia or parasite therapy can be augmented by adding the herbal medicine, Artemsin, usually 200mg twice daily.

So yes, there are more positive serologies for B. duncani than B. microti here on the east coast which contrasts with the views of local health officials, still, the diagnosis of this syndrome is made strictly on clinical grounds. There exists a subset of patients with antibodies to Babesia who never exhibit symptoms of this infection. Most of these patients improve even though this specific co-infection has not been treated. Presumably, in these cases, the infection was mild and eliminated by a well functioning immune system. Even so, the presence of these antibodies can be used to substantiate the diagnosis of chronic Lyme in patients who are Lyme seronegative: where there is smoke there is usually fire.

A basic rule of thumb which has served me well for over 25 years of medical practice still holds: treat the patient, not the labs.

Another comment: Zithromax is not very is not very effective against Lyme disease; its cousin macrolide Biaxin is. Biaxin is frequently avoided when antibiotics are combined because of its it "sloppy" tendency to cause adverse drug to drug interactions: it doesn't play well with others.

Biaxin may reduce blood levels of Atovaquone by 40%. Still, in patients where the treatment of Lyme is imperative along with the treatment of Babesia, this combination has still been effective in many patients.

Another, quite effective drug can be mixed with Malarone for Lyme disease: Cleocin. But this drug carries its own unique risks, especially C. diff colitis, the nemesis of physicians treating chronic Lyme and related disorders. As always the need for probiotics can not be stressed enough. I prefer the combination of Sacchromyces with an Acidophilus mix.

Ambien and a bump to the head with surprising consequences

A 42 year old female was in good health until she took an Ambien one night to help with some insomnia. Apparently she got up during sleep (sleep walking), went into the kitchen, and began to cook a meal. She then proceeded to fall down and bang her head. She presented to my office with a headache, some dizziness and severe pain and swelling in her lower extremities. Her calf muscles were extremely swollen and tender. I was concerned that she might have a subdural hematoma ( a clot in the skull) or rhabdomyolysis, a condition of muscle breakdown after injury which can lead to kidney failure. I sent her to the ER for a work up. The results were negative.

She came back in a day later. Her calf muscles were increasingly tight, swollen and painful. I was worried about a DVT (a blood clot). I sent her for a duplex (ultrasound) study to exclude this. It was negative. The pain was increasing in intensity. Narcotics, at a fairly high dose were needed to control the pain. The Percocet was not working; she returned with tears streaming down her face. She did not have myositis--inflammation of the muscles because the muscle enzyme CPK or CK was normal. Did she has some sort of myopathy? I ran some blood tests for an autoimmune disease. Oddly, her rheumatoid factor was elevated at 285. New symptoms appeared: there was now a tremor of her arms. I started a tapering dose of steroids. It was of no help.

A neurological exam was performed. Deep tendon reflexes were absent across the board. Pin prick sensation was decreased in a stocking/glove pattern affecting all limbs. Vibratory sensation was minimal in the feet. A tick borne disease panel was ordered.

The results: Lyme ELISA IgM 0.91--equivocal range, Lyme WB 41 IgM and IgG bands, Babesia WA1 antibody elevated 1:256, C6 peptide 0.2, CD57 63. Did she in fact have tick borne illness? Had trauma activated a latent tick borne infection leading to an autoimmune syndrome with progressive symptoms in a previously well individual? That was my thinking.

And her symptoms were progressive--rapidly. She developed uncontrolled rhythmic seizure like jerking of her arms. This was associated with uncontrolled vocalizations typical of Tourettes syndrome. The pain and muscle swelling continued to be severe and difficult to manage. She developed night sweats. None of these symptoms existed prior to her traumatic injury.

Treatment for Lyme and Babesia with typical antimicrobials over a 2 month period has been successful. The neuro symptoms--the seizures and Tourettes resolved. The pain and swelling has lessened. She is now returning to work half time, a feat which would have been unimaginable a few weeks ago.

This is the clinical vingette.

These are my thoughts--conjectures.

There are a large number of patients who harbor Lyme (Bb) and its associated co-infections without clinical illness. These parasitic entities are contained by the host and its immune system.
The healthy state can be quite tenuous. Many things can unleash the ticking bomb: intercurrent infection, stress or even physical trauma.

The percent of individuals in endemic areas who are assymptomatic carriers of TBD may be much higher than suspected, given my suspicion that the vast majority of infected individuals exhibit no symptoms of disease.

A positive Lyme ELISA test should not be discounted when the second tier--the Western Blot is negative. Any positive result for Lyme: ELISA, Western Blot or C6 peptide should be considered as potential evidence of the disease.

Positive tests for Babesia WA1 or Babesia duncani have become extremely common, much more so than B. microti. There has to date been no acknowledgement of this change in distribution of this parasite from the west coast to the east coast by health departments.

There are better sleeping medications than Ambien.