Wednesday, October 29, 2008

Evolving strategies

It is becoming clear to me that most patients have co-infections. The idea of combination therapy is morphing into combination therapy which transitions into co-infection therapy. Trying to treat "everything" at one times is counterproductive. Patients Herx too much. Let's take a typical mild/moderate case. We can start with Amoxil/Biaxin/Plaquenil. We have a cell wall agent, a protein synthesis blocker and a drug which is synergistic with Biaxin-reduces inflammation and may have some anti-cyst properties. If symptoms quiet down after some period of time we can transition into anti-Babesia therapy. Mepron and Artemesin can be added. To minimize the number of drugs Amoxil can be withdrawn. If "Lyme" symptoms recur, Amoxil can be reintroduced. I like Amoxil because of it's flexibility. The dose can be increased and Benemid can be added to increase serum levels if desired. Also, one can ease into Babesia therapy by introducing Artemesin before Mepron-or Malarone, to control secondary Herx responses. After Babesia symptoms clear the Mepron and Art are stopped. Bacteria in blood can be addressed(Bartonella, Mycoplasma and possibly Ehrlichia). Rifampin can be introduced. Plaquenil can be stopped. If needed, Levaquin or Cipro can be started. Amoxil would be stopped. Biaxin can be changed to Doxycycline to cover Mycoplasma and Ehrlicia better. We still have to address Cystic Lyme forms. If the patient is generally better, Lyme treatment can be resumed with Flagyl, Amoxil and Biaxin or Doxy. This can be continued until the patient has been asymptomatic for about two months. At that point, may be in remission. This can only be determined if the patient remains symptom free off therapy. The order of treatment can be modified based on a clinical sense of what is causing the mosts symptoms. Flagyl can be added early on for more agressive Lyme therapy or Bartonela/Mycoplasma can be treated first instead of Babesiosis. Bartonella and even Babesia do not always require therapy. They are opportunistic. Once Lyme has cleared the immune system may eliminate them.

All of these concepts are in a state of flux. The main idea is to overlap therapies which make transistions easier. It also important to attempt to reduce the total number of anti-microbials taken at any one time to minimize drug to drug interactions. One more comment: I find Biaxin to be more effective than Zithromax, but Zithro has less drug to drug interactions. Biaxin and Diflucan can cause prolongation of QT intervals and increase the likelyhood of heart block and even fatal arrythmias. EKG monitoring is advisable with these drugs.

The paradigm is complex and evolving.

Additional information: Clongen WBs are good. Clongen finds bacteria in blood smears and performs a variety of strains. A Bartonella PCR test is available for all strains. A PCR test for 15 strains of Babesia is under develpment.

Thursday, October 23, 2008

Case report validating the persistent of Borrelia burdorferi after extensive antibiotic treatment

There has been a longstanding debate between the IDSA and ILADS regarding Lyme symptoms which persist after standard doses of antibiotics as defined by the IDSA. They take the position that standard therapy eradicates the organism. Furthermore, they take the stance that symptoms which persist after standard therapy should be called "post Lyme," not chronic Lyme, because the cause relates to an autoimmune process. ILADS posits that persistent Lyme symptoms after IDSA recommended treatment are due to persistence of the organism. The following case should be written up and submitted to a peered reviewed journal for publication since it clearly sheds much light on this debate.

A 51 year old woman presented to my clinic on April 1, 2008. At that time she complained of multiple symptoms which she related to tick borne illness. She was in good health until August 2006. At that time she reported occupational exposure to Ixodes ticks and EM rash. She was evaluated by and infectious disease specialist in September 2006. This physician noted that symptoms started 3 to 4 days prior to the initiation of antibiotic therapy. She had received 6 weeks of doxycyline. The dose had ranged from 200mg to 400mg per day. This physician recommended two more weeks of doxycycline and follow up care. She subsequently went to another physician who had experience treating Lyme and tick born infections. He treated her with 5 weeks of Rocephin. The Rocephin was stopped due to an allergic reaction. She was treated with long term continuous oral antibiotics. These included: Zithromax, Mepron, Flagyl and Bactrim.

When I first saw her it was noted that an MRI of the brain was positive for WMD.
She complained of memory loss, headaches, fevers, swollen glands, muscle and joint pains, fatigue and numbness and tingling of the extremities. She had severe cognitive deficits and was fully disabled. Her neuro exam showed cognitive processing delay and evidence of peripheral neuropathy. It was noted that Lyme serology had been negative.

She was started on antimicrobial therapy including: Zithromax, Amoxil, Flagyl and Plaquenil. On May 7, 2008 the Flagyl was stopped and the other meds continued. On May 9, 2007 she was still on the same antibiotics. On May 16, 2008 the dose of Amoxil was increased. On May 21 she continued to have disabling symptoms. Intravenous antibiotic therapy was recommended. The results of a second Lyme serology Western Blot from IgeneX showed seroconversion. Her Bb IgM bands were positive in positions: 18,23,31,34,41,58 and 66. She was positive by both CDC and IgeneX criteria. Her IgG bands were positive by IgeneX internal criteria.

IV antibiotics were not covered by her insurance company. Therapeutic doses of oral antibiotic combinations were administered continuously through July 2008. She continued to have disabling muti-system symptoms and clinical neuroborreliosis. The IV antibiotics were finally approved in August 20008. While awaiting this approval she received a single dose of Bicillin 2.4 million units on August 1, 2008. On August 3, 2008 she was started on IV Primaxin, 500mg every 8 hours. This second line drug was picked because of a previous adverse reaction to Rocephin. The Primaxin was augmented with oral antibiotics including Zithromax and Flagyl. She also was re-treated for Babesia with Mepron. She symptomatically improved significantly for the first time. The intravenous therapy was only approved for 8 weeks. After this she was still symptomatic and oral antibiotics were continued.

On October 14, 2008, while still on oral antibiotics, she came into the office complaining of swelling and pain in both knees. An arthrocentesis was performed and the fluid was sent for analysis.

This patient's synovial fluid was PCR positive for Borrelia burdorferi.

Here is a very ill patient with chronic Lyme symptoms. After receiving standard therapy as defined by the IDSA, she was treated with very aggressive long term antibiotic therapy, both oral and intravenous, in accordance with ILADS' principals.

After more than two years of continuous antibiotic therapy this patient clearly demonstrates persistence of Borrelia burdorferi, the agent responsible for Lyme disease, presenting in synovial fluid. It should also be noted that prolonged therapy in this patient was associated with marked clinical improvement over time.

These findings refute the hypothesis that persistent symptoms are due to an autoimmune process. In fact they demonstrate the ability of the organism to persist in the face of massive anti-microbial therapy.

These findings provide evidence based support for ILADS based protocols for the management of chronic Lyme disease.

Tuesday, October 21, 2008

Lyme Lab 101

Unfortunately, practicing physicians are poorly trained regarding laboratory medicine. I have to admit that I am not well versed in the intricacies of IFA, PCR, gene sequencing and other cutting edge lab tests. But I did learn a little something more years ago than I want to admit. Once upon a time I worked in the trenches of the old D.C. General Hospital/Georgetown division. Patients were regularly admitted producing copious sputum. At 3am the rag tattered interns performed gram stains for bacteria and AFB stains for TB. We even spun down blood samples carefully pipetting off the white blood cells, the buffy coat, and gram stained this, looking for bacteria in the blood. If we saw gram positive bacteria in chains we suspected Streptococcal infection (Strep pneumo). If we saw weakly staining gram negative rods we suspected H. flu. We used this preliminary data to guide or choice of antibiotics. We still didn't know for sure which germ the patient had until the culture came back. Fry labs makes a diagnosis based on a blood smear. They don't even have a gram stain. Sorry. You can't distinguish Mycoplasma from Bartonella from Ehrlichia with these stains. You can't get a culture. But now there is a high tech answer. The DNA from the spotted bacteria can be extracted. All bacteria have a segment of DNA called 16S. This segment can be sequenced with technology that would have been unimaginable to the interns at D.C General working at those ungodly hours. The sequencing can be compared to a compendium of the sequencing of all known bacteria. It is like a fingerprint. The bacteria can be definitely identified. No guessing. (Clongen)

Lyme tests: All Western Blots are not equal. State of the Art technology can give results which are extremely accurate.
PCR: I got my first + result from synovial fluid: Supersensitive PCR assay.
I might have to take back things I said about Lyme and PCR in the past.
PCR: New test for Bartonella: 20 strains.
PCR: New test for Babesia, expected soon: 15 strains!
PCR: Mycoplasma: Many positives. First give anti-Mycoplasma antibiotics to chase bacteria from intracellular hiding space.
Ehrilchia: PCRs good: Serology OK and much cheaper.

I am putting together new panels with Clongen which should be very helpful for LLMDS. Clongen has a full service, high tech lab with a huge test menu. I am afraid Tick borne infection profiles will swamp this small lab soon.

ILADS Meeting

I am sorry. I don't have time to review all the responses on my blog. I am glad it has been so active. I wanted to give my impressions from the 9th annual ILADS meeting. I am going to go out on a limb and open myself to storm of criticism. But as a med school professor once told me: "You got to call 'em like you see 'em."
In fairness, I have not yet given my feedback to ILADS. It took me a while to "digest" the meeting. I was disappointed. This was my second ILADS annual meeting. I go to many CME activities. This conference was not up to the standard that I would expect.
None of the lecturing physician faculty hold academic appointments at Medical Schools. This was not true last year when Sam Donta and Dr. Fallon presented lectures. There may be very few medical school faculty/ practitioners who would or could present at the meeting; but there are many faculty members who could present basic science data. There is much work in this arena. Much of it is done in other countries. These sorts of presentations would have increased ILADS' credibility as an "international" organization. Perhaps these lectures would be boring to the average attendee; nevertheless these are an essential ingredient of high caliber CME activities.
Dr. Phillip's review of Chronic Lyme-An Evidence-Based Review, was the highlight of the meeting. This was a detailed presentation replete with scientific data and a thorough review of the literature. Other lectures were interesting, but lacked an evidenced based edge.
The latest break through for chronic Lyme, the Fallon study was not discussed or critiqued at the meeting. What I heard from faculty was: "You know, the Fallon study was limited; they had to work within narrow parameters."
Most of the lectures were not science based. There were based on theory, suppositions, anecdotal information and stuff that "everyone knows."
There was a lot of information related to alternative medicines and herbal therapies.
My opinion: ILADS needs to stay focused on the science of Lyme medicine. The Fallon study is important. Dr. Cameron, the president of ILADS published a study on the effectiveness of amoxicillin for chronic Lyme syptoms. This work was not presented. In fact, I asked one of the countries best know Lyme docs about amoxicillin. He told me that it doesn't work. He uses Omnicef. Based on what data?
There is a paucity of hard scientific data regarding the management of chronic Lyme disease. This is a problem. Meetings such as these need to focus on that data.
The meeting should at least be divided in some way. 1) Evidenced based science 2) Alternative and complementary medicine 3) Theortical issues, food for thought. The emphasis should have been on category 1.
The heavy hitters in the Lyme field all disagree with one another. Should Rocephin be used as a pulse therapy based on "kill kinetics." Where are the studies. Is Amoxil bad? Why don't you need to use Plaquenil any more with Biaxin? Oh, I am sorry, it depends on which luminary you pose the question to. Where is the evidence that chelation therapy or any of the herbal concoctions works? This list could go on ad nauseum. You get the idea.
Lyme docs are subject to an incredible witch hunt. We need to have the highest caliber national meetings.
Let's present the evidence-the data. There is more than readily meets the eye.
There is data regarding the use of Amoxil. There is data regarding the use of Rocephin. There is data regarding the use of Biaxin with Plaquenil. There is limited data regarding the use of Flagyl.
If there is no data regarding the use of combination therapy then carefully explain the rationale for this approach. You can't afford to make this stuff up when so much is at stake.
For one presenter every patient recieves thousands of dollars of lab work at the get-go. For another it is assumed that everyone has Babesia and Bartonella so no testing is needed. A highly regarded LLMD shoots off that Lyme is sexually transmitted: based on what evidence?
There should have been a critical appraisal of laboratory testing. What is the value of PCR testing? etc.
It was clear that the best Lyme experts in the land agree on very little.
I regularly attend meetings at places like Harvard. These guys are over the top evidence based.
Still, it is not unheard of for "experts" to vehemently disagree with each other. These folks can get away with it. They are not dealing with highly charged and divisive diseases and they have the curriculum vitae to back them up.

Put that all aside. The ILADS physicians are a wonderful group of dedicated caring physicians. They are on the cutting edge of changing everything that doctors thought they knew about medicine. There were many thought provoking lectures. ILADS doctors are the future of medicine!

I would have preferred for Dr. Steven Phillip's lecture to have set the tone of the meeting.
It is good to be open to many points of view. But perhaps it is better to entertain such things after the IDSA creates new Lyme guidelines which are reasonable. Or (I am being selfish) until such a time that Lyme docs come out of shadows and feel free to treat this epidemic without fearing the wrath of state medical boards who seem anxious to take them down.

I Love Lyme docs!

Tuesday, October 14, 2008

Quick post- promised a patient.

I had a hellacious day. Lyme patients out the wazoo. I apologized to a patient who had been waiting for over an hour. I told him the previous patient was "famous."
He said: "Hey, don't I rate?" I thought about it for a minute and told him I would write about his interesting case.

This 66 year old gentleman came to me first on September 5, 2008. He had just come back from New Jersey. He complained of an acute flu like syndrome with muscle pain, headache, neck pain,weakness, fever, chills and drenching sweats. The symptoms were occurring in 3 day cycles. His physical exam showed no obvious focus of infection. Of course I thought "ah ha" Babesia.
I started him right on Mepron and Biaxin. He saw me again on September 23. The sweats and chills were 100% gone. Now he had red cutaneous nodules and heel pain. "Ah ha." Bartonella.
I switched him to Cipro and Doxycyline.

Today I saw him again. The heel pain and nodules were gone. Now he felt tired and achy. "Now," I thought: "Typical Lyme." I looked at his labs. Standard co-infection panel negative. Lyme WB by IgeneX: IgM IND 41 band only, IgG 41 band ++, 31,34 and 39 bands-all IND.

"Looks like old Lyme." I scratched my head. Many patients have new infections which seem to activate old disease. In this case I suspect he had a fresh Ixodes bite injecting him with new Lyme and new co-infections. Now he was experiencing symptoms of typical chronic Lyme. The expression "let sleeping dogs lay" csmr to mind. It looks like the new exposure had kicked him into chronic Lyme mode. I prescribed Amoxil, Biaxin and Plaquenil and asked him to return in one month. This is an interesting presentation.

Every case is different.

Yes: it is Lyme disease. Not :Lymes disease. Many make this mistake. So what?
From high school lit: "A rose by any other name would smell as sweet."

Friday, October 10, 2008

41Kd band, again: (39 Kd band?)

I was about to shut of my computer. Then I remembered something else Dr. Kilani said. (You have to read the blog before this one first). "Everyone has a 41 band." "Its due to a dental spirochete." It is interesting, because he said he can also find a 39 band on most samples. There is much agreement that the 39 band is highly specific for Bb infection. He doesn't present interpretive results like IgeneX; he leaves this up to each physician, based on the model they employ. Can we settle this point? Can the dental spirochete(s) be isolated and injected into an animal model or human blood? Will the antibodies produced by such an infection produce a cross reacting Lyme 41 band? Or maybe there is a better way to do this research. He is the scientist. I am just a country doctor. If the results fall the way I suspect it would have a chilling affect on Lyme WB testing. If his assay for the 39Kd band is more sensitive.....
He told me about an individual whose Lyme WB bands all light up, and is in perfect health.
Perhaps everything will ultimately boil down to clinical diagnosis with less and less of a role for laboratory corroboration. (If most people have been exposed, egads). A radical idea. I know.

Clongen Labs: Where have I been?

I just had an exciting conversation with Dr. Kilani. He is the director of Clongen Labs. It turns out that Clongen is on my street, literally a 5 minute walk from my office. Dr. Kilani is a well trained clinical pathologist/molecular biologist. He has some international acclaim. His specialty is PCR testing. He developed the first PCR test for Blastocytis, a controversial GI parasite. He has done extensive research on Morgellons disease including and analysis of its genome (looks like lettuce?). His current thinking is that it is a small worm pathogen from the botanical world which has acquired genes which allow it to infect some humans. This follows the current theory of Dr. Stricker, the leading Morgellons doc in the country. It does highly correlate with Lyme infection.(Luckily I only have one Morgellons patient in my practice). He performs a Lyme Western Blot which has more bands than the IgeneX test. He reports that in a few patients not only do WB bands appear, but the whole strip turns black! He postulates an autoimmune reaction. He offers a PCR test for Mycoplasma fermentans, a Lyme co-infection. Up to now I have not been testing for this. He has a PCR test for Bartonella which is based on non-specific areas of the genome and covers 20 different species. (I think that's what he said; our conversation covered a lot of topics). He has ultra sensitive PCR assays and tells me that he gets a fair number of positive results for Lyme. He is well trained in microbiology and parasitology. We talked about the Babesia problem. He thought that Babesia patients were all critically ill. I corrected this misconception. We discussed the PCR problem here: if you don't know the DNA of the species you are looking for the test will not get you the answer you seek.(There is no broad spectrum PCR test available here). He is willing to do blood smears with a variety of stains, (trichrome may the best), to look for blood parasites. He does offer a variety of super sensitive PCR tests for other co-infections as well. This testing is expensive and I will have to evaluate which tests are cost effective. He is working closely with Dr. Jones and other LLMDs, performing various assays. He told me that Lyme IS sexually transmitted. Apparently he has done PCR on semen and vaginal secretions which were positive. I think we can settle part of this issue. He also has a sensitive culture medium for Borrelia. I will try to find a WB positive Lyme patient, who will be willing to donate such samples. (This may take a while to find). This should be done before any antibiotics are given. If the PCR is positive, he will attempt to culture the specimen for Bb. This would be a step closer to proving the sexual transmission hypothesis. He is also doing research on developing a new Lyme vaccine. We agreed that the previous Lymerix vaccine was doomed from the start. It was based on OspA which is down regulated in early Lyme and only shows up with advanced disease. He thought this might have been the cause of the autoimmune reactions associated with the vaccine. Clongen's vaccine, under early development, will be based on OpsC, which is present in early Lyme. I had an extended conversation with Dr. Kilani about many facets of laboratory medicine as it applies to tick borne infections. He will be at the ILADS meeting next week. He agrees that Lyme is a burgeoning plague of untold proportions. He has an extensive menu of PCR tests, covering the extended spectrum of infectious agents around the world. I'm afraid he is about to fall into the black hole of Lyme. Brilliant guy! Great for us.

Monday, October 6, 2008

31 band

Sometimes you only get a 31 band, like a patient I saw today. She has an IND 41 band with a +31 band. This is on the IgM side. Her IgG showed +++41, IND 31,34,39. IgeneX calls it negative. Her previous Labcorp WB showed no reactive bands. After antibiotics she had a typical Herx and was getting better. She still wanted more proof that she has LD. I spent 40 minutes explaining the nuances. She didn't get it. It is difficult to treat patients when the concepts seem so foreign. (This is not to disparage the patient since I would get the same response from mainstream doctors in the community). I could not get through even though I drew diagrams and did my best to simplify the issues. She, like many patients told me that she would no longer read things on the Internet. She would not see "Under Our Skin." She would not read this blog or books on Lyme disease. She is already incredibly anxious and the thought of doing more research throws her into panic mode.
So I ordered the $100.00 31 band confirmation test through IgeneX. This test uses an additional antigen which confirms exposure to Bb with 98% specificity. I still couldn't explain that a positive result would only confirm exposure to Bb. It does not mean you have Lyme disease. I am starting to understand why LLMDs charge $1000.00 per visit. It screens out patients who cannot grasp the concepts. By the time patients are willing to cough up that kind of money they know more about tick borne illness than their physicians.

It is frustrating when second opinions from ID specialists present only the IDSA point of view. There is no acknowledgment that another perspective exists at all.

I hope that other physicians in the community can become versed in the issues.
This will be a long and difficult process.

Paralyzed diaphram: Case report

Here is a male patient in his mid 40s. He has been a regular patient in my Family Practice office since 2001. He was initially seen for depression, anxiety, panic disorder and obesity. In April 2002 he presented with a paralysis of the left diaphram. This was associated with a great deal of shortness of breath. He was seen by pulmonary specialists and neurologists who confirmed the diagnosis but were unable to offer a cause or treatment. At that time I was not a LLMD. At that time I elicited a history of tick bite with rash in 2000. I started him on Docycyline 100mg twice daily. I noted other symptoms of headache, fatigue and joint pains. The paralyzed diaphram was due to dysfunction of the phrenic nerve. I ordered standard Lyme serology which consisted of an ELISA with a reflex WB. The test was negative. I referred him to an ID specialist who felt he did not have Lyme disease. In May 2002, after a month of Doxy he noted that his anxiety was better but that his depression was worse. He continued to have shortness of breath and also complained of some numbness in his hands at night. After 30 days the Doxy was stopped and he was referred to a psychiatrist. He was on numerous psychotropic drugs for depression and anxiety. He also was seen by a rheumatologist. He was diagnosed with fibromyalgia which was treated with Neurontin. I saw the patient in October 2oo7. My note indicated Lyme disease?
Again, I was not Lyme literate and I followed the recommendations of the "experts" of whom he had seen many. Moving ahead, in early 2003 he saw an ILADS, LLMD rheumatologists based on self referral. This physician wrote a detailed note which suggested a chronic infectious cause of his ongoing issues. She found biliary dyskinesia and recommended cholecytectomy before beginning long term antibiotics. I was not Lyme literate but found the detailed consultation "interesting." Salmonella was found in his stool and this was reported to be a contributing factor. Because of fatigue I recommended a sleep study. He had no gallbladder symptoms so the organ was not removed. By November 2003 the sleep study confirmed severe sleep apnea and C-PAP was initiated, but not until May 2004. He was seen frequently in our office was a multitude of multisystem complaints. The primary issues continued to be severe depression and anxiety.
In 2005 he reported seeing worms in his stool. An ova and parasite stool exam was negative. He was treated empirically with Flagyl and then Abendazole with resolution of this complaint. The C-PAP significally improved his fatigue but not his shortness of breath. He continued treatment for depression and fibromyalgia without much relief. He was a "frequent flyer" in my office. In January 2006 he reported a brief episode of left facial drooping which occurred in FLA while visiting his father. He was evaluated for a possible TIA; the work up was negative. By February 2007 I was in the early stage of Lyme literacy. At that time I combined symptoms into a complex. He had a history of tick bite with ECM. He had joint pains and fibromyalgia. He had an episode of facial droop (Bell's palsy?) and he had multiple psychiatric symptoms including memory loss. Lab studies at that time showed: Negative Lyme WBs, a Lyme C6 peptide aby index of 0.31, folic acid of 4.8, B12 of 313, vit D OH 25 of less than 7 and a CD57 count of 66. Screening for co-infections by Quest was negative. He was started on Ceftin and Biaxin. In March 2007 Plaquenil was added. Within a month he reported some cognitive improvements. Antibiotics were continued for several additional months. In June 2007 his C6 index had increased to .73. I felt that this was evidence of "seroconversion" of Lyme. Various antibiotic combinations were continued. These included Flagyl, Rifampin, quinolones and others. He complained of increased joint pain and ongoing fatigue and depression which did not improve. In March 2008 he reported stopping antibiotics with a prompt increase in cognitive deficits as well as joint and muscle pain. Antibiotics were restarted but were no longer as effective. Dizziness, Brain fog, joint pain, mood swings and fatigue continued. He developed new symptoms including a loss of bladder control. He became very discouraged. Supportive therapy with Welchol and Wobenzym-N were not helpful. In July 2008 and Igenex serology for Lyme was obtained. His IgM bands were positive only at the 58 and 66 positions. His IgG bands showed 41+++, 31,39,93 Ind. Shortness of breath due to the paralyzed diaphragm remained a significant symptom. I tried Diamox to stimulate respiration. It was somewhat helpful. On September 4, 2008 I reviewed his long record and realized he had never been tried on empiric anti-Babesia therapy. Month after month I had seen this patient for chronic Lyme disease. He had bouts of improvement followed by set backs. He barely functioned and had considered full disability and even suicide at times. I said lets treat Babesia to see if this helps. He was started on Mepron, Biaxin and Artemesia. When I saw him on October 2, 2008 I was expecting the usual. Still feeling lousy.
Instead I was greeted with: " No doc, its good news this time." He had Herxed terribly for about 5 days. He had considered stopping therapy. But then something miraculous occur ed. He felt great. It was the best he had felt in years! His fatigue was better. He had new found energy. His shortness of breath was better. His brain fog was lifting. His anxiety and depression were better.
Neck pain, which I had not focused on, was better. It was dramatic. After 18 months of treatment (not always consistent) he was better and optimistic. Why had I been holding out and not prescribing this miraculous treatment? This is a question I have to ask myself. Did he respond to anti-Babesia therapy because the Lyme had been thoroughly trounced? Or did I let this one slip through. I am still learning. I won't make this mistake again.
There is a notion amongst ILADS docs that 58 and 66 bands suggest Babesia. I have become suspicious that low folate and B12 suggest chronic RBC infection. Babesia is the most likely culprit. Ehrlicia and Bartonella probably don't persist that long if standard Bb therapy is used.
He is not the only Lyme patient I have seen with a paralyzed diaphram.
I have to be on the lookout. It is not just new patients who have Lyme. It is also old patients who have been in the practice for years with "mystery" illnesses.

Wednesday, October 1, 2008

Lupus patient

I have a stack of interesting cases which I plan to write blogs about sitting on my desk. Since I am at home, I will mention the story of one patient I saw last week. This patient had "lupus" or systemic lupus erythematosis for more than a decade. She had the classic butterfly rash. She had arthritis, fatigue and frequent episodes of pleurisy. Her rheumatologist had treated her with corticosteroids and Plaquenil. Her symptoms were poorly controlled. About 18 months ago I told her about the Lyme hypothesis. She agreed to be tested. Her results were equivocal. We decided to try antibiotic. Results: No rash, no fatigue, no arthritis and no pleurisy. She ran out of Plaquenil and the symptoms did not recur. This had not happened in a decade. I asked her if she felt comfortable with the new paradigm. Her answer: A resounding yes. We are continuing antibiotics which work better than standard fare. She avoids her Harvard trained rheumatologist now. She is tired of hearing that her experiences are impossible and that her physician does not know what he is doing. It's all a placebo effect. Placebos don't work for an extended period. Find another explanation if you think mine is incorrect. More complex case summaries will follow.