Lyme 2010-2

Lyme Articles- 2

29 June 2010

Rhode Island Red, but not from E.M.

An interesting prediction about the burden of Lyme disease in Rhode Island this summer. It's in contrast to statements from other states (NY, VA, NH, MA, for example) predicting an increased number of cases of tick-borne Lyme disease.

URI scientist says expect fewer ticks, Lyme disease this summer

Tuesday, June 29, 2010

By Richard Salit

With mosquitoes thriving and allergies raging, there’s one less thing to be ticked off about this summer — deer tick populations are down.

Counts of the tiny ticks are about 30 percent lower than last year, a strong indicator that Lyme disease will be less prevalent this year, according to Thomas Mather, director of the University of Rhode Island’s Center for Vector-Borne Disease.

“It will result in 20 percent to 25 percent fewer cases this year,” Mather estimated. But he still emphasized the need to prevent tick bites by wearing protective clothing and being aware of tick habitats.

Mather, Sen. Jack Reed and infectious-disease specialists gathered at Hasbro Children’s Hospital on Monday to discuss the latest efforts to battle Lyme disease.

“We have some of the world’s and the nation’s best experts here in Rhode Island,” said Reed, who praised the work of Mather’s department.

Last summer, URI received a share of $13 million in National Institute of Health funding to develop vaccines for Lyme disease, hepatitis and stomach cancer. Mather said he is working with guinea pigs to create a vaccine that would stimulate the immune system to attack tick saliva. It could be delivered by a skin patch, he said, envisioning a partnership with Isis Biopolymer, the Jewelry District developer of a transdermal drug-delivery patch.

Reed said he has also secured more than $1.3 million in federal funds for URI to develop Lyme disease prevention programs. Mather’s department has created a Web site to raise awareness of how to avoid tick bites. The site gets 300 to 400 hits a day, from as far away as Canada and Poland.

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Labels: Lyme disease

26 June 2010

Lyme Disease Awareness Month

Last month was Lyme disease Awareness Month. If you did not know about it certainly many Lyme disease activist groups were made aware after April’s shower of cold reality.In 2006, Lyme activists persuaded the Connecticut Attorney General Richard Blumenthal to threaten the Infectious Diseases Society of America with a “restraint of trade” lawsuit over their voluntary recommendations for the treatment of Lyme infections. (Activists think the guidelines somehow interfere with patient treatment.) The suit had no legal or scientific merit, but the Society wanted to avoid a costly legal battle and agreed to have their recommendation reviewed by a second panel of infectious disease experts. On April 22, 2010, the panel declared the recommendations “medically and scientifically justified.” Undeterred by this second opinion, activists launched a petition urging Blumenthal to investigate the second panel for alleged voting irregularities.On April 29, the Institute of Medicine in Washington organized an expert panel to assess the state of the science concerning Lyme and other tick-borne infections. The IOM panel will not look at treatment (Blumenthal’s review answered those questions, thank you very much), but will likely recommend more research on the ecology and epidemiology of tick-borne diseases in the U.S. and maybe additional research on diagnostics. Immediately after the meeting, Lyme activists denounced the IOM panel for its membership, its procedures and reviewers, and even the timing of the meeting.

Is there a disconnect between activists and infectious disease experts? Yes. It’s a problem of perspective.

Much of Lyme activism takes place on the Internet where conspiracy theories, allegations of financial conflicts, and quack treatments are readily endorsed and exchanged. This activism has spawned a kind of “parallel universe” with its own self-described Lyme experts, meetings, publications, and even a patient-funded research center. It is a place where Lyme infections are described as incurable but requiring long-term antibiotics, transmitted from mother-to-child and husband-to-wife, capable of producing any symptom, and causing MS, ALS, Alzheimer’s, autism, and other illnesses. It is a place where alternative forms of microbiology, immunology and pharmacology exist independent of the sciences I know.

Offline and in the everyday world, Lyme disease remains a common bacterial infection—transmitted by ticks—that is treated and eradicated by common antibiotics, but which can lead to permanent joint or nerve damage if left untreated. In that regard, it is like most other bacterial infections. Clinical research continues to show long-term use of antibiotics does not help people with lingering symptoms resulting from prior infections.

These two perspectives cannot be reconciled.

How did it come to this? Space does not allow for a full history. Suffice to say that Lyme activism is an outgrowth of a larger anti-science phenomenon that encompasses anti-vaccination, HIV denialism, climate-change doubters, autism activists, and many other conspiracy-minded groups. None of them recognize objective scientific evidence as such. All of them trade in accusations and denunciations, regularly accusing mainstream scientists and physicians of being in the pay of “Big Pharma,” “Big Business,” or “Big Brother.” Sometime threats are made.

Infectious disease experts who have run afoul of various Lyme disease groups have been stalked, picketed at meetings, threatened with lawsuits, and had anonymous phone calls made to their deans, editors and employers. Nowadays, being on the wrong side of an obscure scientific issue can be dangerous.

Case in point. A few days ago, I got a phone call from a detective with the local FBI terrorism task force. According to the detective, a Lyme activist had reported me as a potential terrorist threat. Why me? Maybe someone didn’t like what I wrote. Who knows. In the 1950’s, you could get rid of a nosy neighbor or a pushy boss by denouncing them as communists and traitors to Hoover’s FBI. Today, you can accuse someone of being a terrorist.

The detective had done some research on Lyme disease and activists and so had a good sense of what was really going on with these accusations. After a few jokes, we hung up, both perhaps thinking that maybe accusers should be as carefully examined as the accused.

The world is seldom what we want it to be. Medicine often fails to heal and science is always turning up some inconvenient fact that may alter the course of business, behavior and belief. It’s not a conspiracy; it’s just the way the world works.

May was also Martini Month, Better Hearing and Speech Month, National Bike Month, and American Wetlands Month. I’m guessing no one involved in those activities was accused of being a terrorist.

Posted by Relative Risk at 10:15 0 comments Links to this post

Labels: IOM, Lyme disease, Politics

22 June 2010

Unwanted Advice

The IOM listening tour is really getting an earful. And probably a headache. Below are the often repeated charges of Kris Newby, self-described writer, producer, and expert on Lyme disease. I wonder how she’d like it if a bunch of I.D. docs and scientists showed up one day and started telling her how to make a documentary film or write a script. No doubt she’d be outraged at the assumptions of amateurs.

With that in mind, let’s take a look at what she told the IOM.

My name is Kris Newby, and I’m the Senior Producer of the award-winning documentary on Lyme disease, UNDER OUR SKIN.

[snip]

In my three-minute slot, I’ll suggest some science areas for the committee to pursue as it sets the course for research.

But first, I’d like to start off with a quote from Dr. Willy Burgdorfer, the NIH Scientist Emeritus who discovered the organism behind Lyme disease. While we were filming at his home in Hamilton, Montana, he told our film crew: “The controversy in the Lyme disease research is a shameful affair, and I say that because the whole thing is politically tainted. Money goes to people who have for the past 30 years produced the same thing -- nothing.”

I think there’s good reason to suspect Willy never said this. Though he is getting on in years, and it should be remembered that Willy himself was very well funded over the decades to do….. What? After identifying spirochetes in ticks in the early 80’s he did what exactly?

I believe the top priority of this committee should be to enlist a greater diversity of researchers and Lyme-treating clinicians to help set research priorities. Lyme disease serves as an excellent case study on how cronyism and conflicts of interest can lead to stagnation in medical research.

Note: this accusation (cronyism and conflicts) is one of the elements of standardconspiracy theory.

This research has been tightly controlled by the same lead IDSA Lyme guidelines authors for the last two decades. Collectively, their university labs have received over $130 million dollars in government grants since 1990. Over half of these grants have gone to only two universities, New York Medical College and Yale, and a disproportionate amount of the grants have been used to support these researchers’ personal interests in tick-borne disease vaccines and tests. For example, New York Medical College researchers alone have founded 5 test/vaccine companies in the last few years.

Anyone can log onto RePorter and look up data on Lyme related grants. I did. I found 1,026 research grants funded between 2010 and 1986. Yale was listed as having 99 grants; NYMC had 49. Other well funded universities included UConn (23), Tulane (24), the University of California system (68), the University of Texas schools (67), and other NY schools (104). Is it really surprising that an Ivy League research university and a high quality medical school in two highly endemic states might attract a good deal of Lyme research funding? As for patents listed in the same search—there were 37 (based on individual patent numbers). Most of those patents exist only as paper filings, and many are related to things other than Lyme disease, including leptospirosis, ehrichliosis, babesia and rickettsia. I don’t think anyone is getting rich of off patents and companies for non-existent Lyme vaccines.

Looking at the state of Lyme disease today, 20 years later, we still have no reliable testing and no effective treatments for the large percentage of Lyme patients who fail the IDSA protocols.

Newby must have an interesting definition of “reliable.” The FDA has approved the use of some 70 serologic assays for Lyme disease in recent years. I doubt the agency would have spent time and money approving unreliable assays. I doubt clinical labs would buy unreliable assays. I doubt physicians would pay to use unreliable assays. And as for “effective treatments,” let’s remember that Lyme is a common bacterial infection that is highly responsive to common antibiotics. It isn’t MDR-TB.

So, for your workshop on Lyme science, I say you urgently need to bring new ideas to the table, by enlisting the following researchers:

Dr. John Aucott of Johns Hopkins, who is identifying early Lyme disease serum markers to help develop tests that will work during the first month of infection.

He went to Hopkins as a student. Now he’s in private practice in Maryland. Still, there’s nothing preventing him from applying to NIH for research funds. They’re not going to knocking on his door and beg him to take their money.

Dr. Ben Luft of Stony Brook, who is working to identify which Lyme strains are the most virulent in different geographic regions, because our current FDA-approved Lyme tests only look for one of 120 known strains.

Ben is well funded by NIH and has been for years. The variable virulence in strains is interesting work, but that doesn’t mean one needs 120 different assays to diagnosis Lyme disease. So far, there’s little clinical evidence to suggest strain variation is having any impact on diagnosis or treatment.

Dr. Eva Sapi of the University of New Haven, who is investigating the role of biofilms in allowing Borrelia to create persistent illness.

Sapi isn’t serious. Hell, she publishes her work in the Townsend Letter.

Dr. Karen Newell of Texas A&M, who is working on a novel genomic strategy for overriding Lyme’s ability to disrupt the immune system.

I guess this is M. Karen Newell, formerly of UC, Colorado Springs, and Viral Genetics, Inc. Again, there’s nothing to prevent her from applying for Lyme funds.

Dr. Brian Fallon of Columbia University, who is developing new criteria for diagnosing late Lyme.

No, I think he’s back working on hypochondria and OCD. Unless, there’s a connection there with chronic Lyme disease?

Dr. Cheryl Koopman of Stanford University, who is working to define symptom clusters to aid in the diagnosis of Lyme disease.

Previously discussed here.

And finally, I feel it’s important to get input from the many community-based Lyme clinicians who are on the bleeding edge of treating the chronic manifestations of the disease.

The bleeding edge? If there’s any bleeding going on it’s probably from the many walletectomies performed by the LLMDs Newby thinks so highly of.

So ends a painful three minutes of unwanted advice.

Posted by Relative Risk at 17:47 0 comments Links to this post

Labels: IOM, Lyme disease

17 June 2010

Small Numbers, Big Consequences

One of the comments collected from the IOM’s recent emoting sessions with Lyme patient/activists was this:

Lyme Times Associate Editor Pam Cocks, the mother of two adult children with Lyme, points out that all of the controlled trials cited by the IDSA guidelines involved a mere 221 patients.

But in the end, a mere 221 patients have been involved in ALL THE CONTROLLED TRIALS completed and cited in the Lyme literature. Faced with such scientific uncertainty, more latitude should be given doctors to use their clinical discretion.

I’m not sure where she got the 221 number. Looking through the 2006 guidelines, one quickly finds numerous references to treatment trials. For example:

“Three randomized, prospective studies on the use of antibiotic chemoprophylaxis were reported through 1993.”

“In a larger and more recent chemoprophylaxis trial…of 247 subjects who received placebo….”

“There have been at least 9 randomized, prospective trials addressing the treatment of early Lyme disease in the United States.”

“The first randomized clinical trial on the treatment of erythema migrans compared erythromycin, tetracycline, and penicillin….in 112 adult patients.”

Two of the largest studies of the treatment of erythema migrans in adults compared cefuroxime axetil with doxycycline. The first was a multicenter study in which 123 patients with erythema migrans were randomized….”

“Duration of antibiotic therapy for erythema migrans was addressed in a prospective, randomized, double‐blind, placebo‐controlled clinical trial of 180 patients.”

The guidelines reviewed the merits and limitations of a number treatment trials. The word “trial” appears 62 times in the guidelines. “Placebo” appears 32 times. Mrs. Cocks doesn’t specify which trials she was referring to, so let’s guess they are the often cited trials by Krupp, Klempner and Kaplan (KKK?).

Neurology 2003;60:1923-1930

Study and treatment of post Lyme disease (STOP-LD). A randomized double masked clinical trial. L. B. Krupp, et al.

55 patients.

N Engl J Med. 2001 Jul 12;345(2):85-92.

Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. Klempner MS, et al.

78 and 51 patients.

Neurology. 2003 Jun 24;60(12):1916-22.

Cognitive function in post-treatment Lyme disease: do additional antibiotics help?

Kaplan RF, et al.

129 patients.

The total number of Lyme patients in those 3 trials is 313. If you throw in Brian Fallon’s 2008 trial—and ignore his 20 control subjects—that brings the total to 350. The only way I get 221 is to ignore the Klempner study entirely and add Fallon’s 37 Lyme patients, Krupp’s 55 patients, and Kaplan’s 129 for a total of 221.

Neurology. 2008 Mar 25;70(13):992-1003. Epub 2007 Oct 10.

A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy.

Fallon BA, et al.

37 patients, 20 controls.

I suppose what Mrs. Cocks was trying to suggest in her conversation with theIOM study group on Lyme and tick-borne infections is that big conclusions have been drawn from small numbers. True. Good trials with few, but well-defined patients can tell you a lot. More to the point, the small number of well-defined patients further suggests the rarity of patients with potentially persistent Borrelia infections who might be expected to benefit from longer-term use of antibiotics. Fallon’s study was nearly undermined by a lack of such well-defined patients.

So thanks, Mrs. Cocks, for pointing out the scarcity of “chronic” Lyme patients and the ability of good clinical treatment trials to drawn broad conclusions.

By the way, I counted 41 Lyme-related trials between 1988 and 2008. Some are good; others are very bad. Some are placebo-controlled. Some are comparative. Some are prospective or pilot studies. Some are preventive or behavioral in nature. Patient numbers in these studies range between 5 patients with evident Lyme disease and 482 persons reporting a tick bite.

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Posted by Relative Risk at 13:18 0 comments Links to this post

Labels: IOM, Lyme disease

27 May 2010

Proof That Chronic Lyme Disease Exists

Interdisciplinary Perspectives on Infectious Diseases

Volume 2010, Article ID 876450, 4 pages

Proof That Chronic Lyme Disease Exists

Daniel J. Cameron

Wow, proof at last. It’s too bad this amazing news could only be broadcast through the pages of an open access journal published from the Nasr neighborhood of Cairo, Egypt. (Though it could have been worse; could have been from the Imbaba part of town.)

Anyway, this four-page “research article” contains no research, but plenty of shop-worn assertions from ILADS and the Lymee activists. (Cameron is the immediate past president of that online gang of private practitioners who dabble in quackery and wackery. Quackery being the medical use of worthless potions and procedures, and wackery being the belief in and dissemination of wacky ideas.)

Cameron provides no definition of what exactly “chronic Lyme disease” is, but it’s safe to assume he is referring to a persistent infection by B. burgdorferi. Why else would one want to prescribe long-term antibiotics? He writes in the paper, “there is no objective way to rule out an active infection.” So apparently, unable to proof a negative, he suggests we all just assume the persistence of complains (objective and subjective) is the work of a B. burgdorferi infection and not something completely different.

I don’t know what compelled him to write this silly proclamation, but I think it’s just further proof that he should not write anything at all. Even from Cairo.

Posted by Relative Risk at 23:12 0 comments Links to this post

Labels: Cameron, Lyme disease

20 May 2010

The Letters Keep on Coming

Well, the dynamic duo is back. Back in the pages of Clinical Infectious Diseases2010; 50(12):1683-85 to be exact. I understand why Stricker busies himself with these inflammatory letters to the editor. It’s a cheap way to puff up ones resume, it allows a person to cite himself in future letters, and often the letters can be mistaken (or misrepresented) as original research articles instead of what they are: argumentative griping about other peoples’ original research. As for Johnson, I can’t imagine how she could contribute to a piece of writing that tries to address issues of clinical trials, statistics, and patient outcomes. She’s a lawyer! Maybe she too has a resume in need of some filler.

In any case, they were bitching about the February report of Kowalski, et al. on “Antibiotic Treatment Duration and Long‐Term Outcomes of Patients with Early Lyme Disease from a Lyme Disease–Hyperendemic Area.” (Clinical Infectious Diseases 2010;50:512–520.) They didn’t like the not too surprising conclusion that more antibiotics don’t help. So without bothering anyone with the Stricker-Johnson analysis, lets just jump to the reply of Kowalski and colleagues about their findings and conclusions. Here’s most of their reply:

We…disagree with their conclusions on statistical and scientific grounds. They suggest performing intention-to-treat statistical analysis on our cohort and counting those who did not return surveys as having experienced treatment failure. This is neither a plausible nor appropriate analytic strategy. First, our definition of treatment failure was based on clinical data obtained from a review of medical records over an average follow-up period of 2.9 years. The survey had no effect on the determination of treatment failure, making their point irrelevant. Second, intention-to-treat analysis is to be applied to prospective, randomized clinical trials seeking pragmatic treatment- effectiveness end points. To apply intention-to-treat methodology to a retrospective cohort study is nonsensical.

We wish to reaffirm our study findings: the 2-year treatment failure–free rate for all patients was 98.9%–99.2%, using predetermined definitions of treatment failure.

Stricker and Johnson also claim that treatment failure was defined too stringently. We counter that nonspecific subjective complaints such as fatigue, musculoskeletal complaints, and insomnia are ubiquitous; of themselves, they cannot possibly be used to discern whether someone is suffering from Borrelia burgdorferi infection or countless other acute and chronic physical, emotional, and psychological maladies that manifest identically.

For a cohort study to maintain scientific integrity, it is necessary to use clear, objective, unambiguous, and measurable outcome criteria that are defined in advance, so as to avoid uninterpretable results.

Stricker and Johnson’s emphasis on the persistence of subjective complaints in our population does emphasize the key take home point of our study: longer antibiotic courses did not decrease symptoms better than shorter courses in patients with early Lyme disease. Objective clinical failure, subjective complaints, and the objective functional status of patients (measured by the SF-36 health-assessment survey) were similar among patients regardless of the duration of antibiotic treatment.

The conclusion is clear. When it comes to antibiotic treatment duration for early Lyme disease, longer is not better. As physicians, we should recall one of our first oaths before prescribing prolonged or repeated courses of antibiotics for early Lyme disease: primum non nocere [First, do no harm].

Anyone know the Latin for “Write no more letters”?

Posted by Relative Risk at 22:12 0 comments Links to this post

Labels: Lyme disease

14 May 2010

Some Notes on Predicting Diagnostic Utility

The positive predictive value of Borrelia burgdorferi serology in the light of symptoms of patients sent to an outpatient service for tick-borne diseases.

Andra´s Lakos, Jen}o Reiczigel, Norbert Solymosi

Inflammation Research, May 2010-05-14

Borrelia burgdorferi infection is often suspected to be the cause of many different complaints and symptoms and, even when the symptoms are not typical for Lb, antibody testing is ordered by general practitioners as well as specialists.

Abundant use of serology tests is supported by recent numbers reported by Binnicker et al. that Borrelia serology was performed at the Mayo Clinic more than 75,000 times in 1 year, and about 2.5 million times per year in the USA. Already more than a decade ago, Tugwell et al. warned against testing patients with nonspecific signs and symptoms (headache, fatigue, myalgia, arthralgia, etc.) when the pretest probability is <0.20 or >0.80 (i.e., in cases with reasonable suspicion of EM). They described testing patients with low pre-test probability may result in more false than true positives.

The present study consists of two parts. First we present the data of some relevant publications dealing with the incidence of Lb and sensitivity/specificity of the best Borrelia burgdorferi antibody tests.

In the second part, we analyze the composition of symptoms of patients visiting our outpatient service specializing in Lb diagnostics to check what proportion of Lyme serology tests are ordered in case of non-specific symptoms and how this influences its predictive values.

The maximal incidence of Lb in the United States is 100 reported cases per 100,000 people per year. Except for the southern region of Europe (Greece, Italy, Spain, Portugal) and Great Britain, the published incidence of Lb is >10/100,000 per year throughout Europe.

The typical initial sign of Lb, EM, appears in 60–80% of infected people. The sensitivity of the test depends on many inherent components, but the most important factor is the number of early infections (EM patients) among those examined. If these patients visit the medical service shortly after the appearance of EM, the antibody response is still undetectable. Therefore, the maximal sensitivity is likely to be [less than or equal to] 90%. In these cases, if the infection is not generalized, most patients have no detectable antibody response shortly after presenting this early clinical sign. The intensity of the immune response depends mainly on the time elapsed between the onset of clinical symptoms and serological testing/antibiotic treatment.

Detection of the Borrelia antibody may be related to a past or convalescent infection, therefore seropositivity does not imply that a current clinical symptom is actually due to Lb. This is the most important reason (beside cross reactivity) why no serological test for actual Lb can have a specificity of 100% in an endemic region.

A positive Borrelia antibody test has been reported in >5% of the healthy population in many seroprevalence studies. According to the package insert of the C6 ELISA kit, the prevalence of a positive antibody reaction among healthy blood donors was 3% in an endemic region.

Assume that we have a high standard serology test with 90% sensitivity and 99% specificity. As noted above, these limits are the most optimistic ones at present. The average incidence of Lb is expected to be about 1/1,000 per year in the endemic region of the World (probably for Hungary, too). Under these assumptions, considering a 1-year period 10 Lb cases are expected among 10,000 people examined. The 90% sensitivity implies that nine of these patients will be test positive. Based on the 99% specificity, there will be about 100 false positives (0.01 X 9,990 = 99.9), so altogether 109 positive results will be registered. Therefore, the probability that a positive result reflects to an actual Borrelia burgdorferi infection is only 9/109 = 8.3%. Even with a sensitivity of 100%, the positive predictive value turns out to be as low as 9.1%.

We considered 21,614 complaints/symptoms of 19,659 patients with non-specific symptoms thought to be suggestive for Lb and 7,696 typical Lb symptoms of 7,293 patients, as well as 242 patients with TIBOLA, which is a newly recognized Rickettsia slovaca infection with characteristic clinical symptoms.

The proportion of patients having positive Lyme serological result in the above mentioned groups was <2%, similarly to the general population.

Huge numbers of serology tests performed in low-risk groups imply masses of false positives. Aguero-Rosenfeld et al., calculating with about 2.7 million tests done per year in the United States, concluded that each 1% reduction in test specificity would produce approximately 27,000 false positive results per year, while the incidence of disease is about 20,000 cases/year. In particular, a decrease of specificity from 99 to 98% doubles the number of false positives. It should be stressed that a specificity of 98% for a Borrelia antibody test is still very good; none of the seven commercial ELISA kits and two immunoblot tests we examined fulfilled this. In a European multicentre Lyme immunoblot study, in which the most acknowledged six laboratories participated, only one reached the 99% specificity at the expense of very low sensitivity (56%). Targeted Lyme serological testing of EM patients is unnecessary because if a patient has typical EM that fulfills the case definition, treatment for Lb should be started immediately, without waiting for the serological result. Moreover, many of the EM patients are still serologically negative.

In the interpretation of a test result, the clinician should use the available epidemiological and clinical data.

Most clinicians find it unbelievable that a high standard diagnostic test may result in predictive values as low as these.

Our study suggests that consuming Lyme serological tests in the recent practice results in more harm than benefit. A false-positive Borrelia antibody test results in repeated and unnecessary antibiotic treatments, and additionally, in delayed recognition of the correct diagnosis. Moreover, subsequent complaints will suggest the possibility of Lb ‘‘relapse.’’ Most patients with falsely diagnosed Lb do not heal after repeated courses of antibiotic treatments, or their symptoms will relapse, which augments the false belief of chronic and incurable Lb.

One can ask whether we should discard B. burgdorferi antibody testing in the light of the above results. Surely not. The solution could be sample pair examinations. When the clinical symptoms are not suggestive for Lb and the serology shows reaction above the cut-off, instead of antibiotic treatment a second sample drawn a few weeks or months later should be tested in parallel with the previous one. If a serological progression is seen, an actual B. burgdorferi infection is proven, otherwise the diagnosis can be ruled out. We are working on defining the rules and characteristics of the serological progression in untreated Lb.

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Posted by Relative Risk at 16:51 0 comments Links to this post

Labels: diagnostics, Lyme disease

05 May 2010

This article may be a bit dated, but it still offers some well-written comments on the social phenomenon of Lyme disease advocacy and the need for scientists to develop and deploy better communication tools.

The Ongoing 30-Year Lyme Disease War: Case Study of a Failure to Communicate

By Leslie P. King, MD, MPH | November 25, 2008

The Yale Forum on Climate Change & The Media

Lyme disease, dubbed one of the “deadly dozen” by a recent Wildlife Conservation Society report, could skyrocket as global shifts in temperature and precipitation transform ecosystems.

From a public policy standpoint, the situation is compounded by the communications issues complicating it, bringing to mind the well-known quote from the late actor Strother Martin in the 1967 film “Cool Hand Luke” — What we’ve got is failure to communicate.

Concluding paragraph...

Lyme disease is indeed a cautionary tale. It teaches that scientists must modify their practice of publishing solely for scholarly journals and must also communicate their findings to a larger audience. Their scientific expertise can help in contesting advocacy interests and policy makers unfamiliar with the full scientific picture. In the absence of that fuller understanding, potential climate-driven ecological changes could lead to increased incidences of widespread infection, and the toxic scientific environment surrounding Lyme disease could become a perfect storm that fuels a significant epidemic.

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Posted by Relative Risk at 16:37 0 comments Links to this post

Labels: Lyme disease, Politics

02 May 2010

There's a Tick on my iPhone

The application includes information on the abundance of infected ticks at the location of the user (within the US) as determined by GPS. If ticks are determined to be present, the user is given a list of precautions to avoid tick-bites. A tick identification chart is provided with life-size photos of black-legged ticks (also called deer ticks) so that each life stage can be determined, since some stages cannot transmit Lyme disease. If bitten by a tick, instructions on how to properly remove a tick are provided along with a narrated video. The application also provides life-sized photos of ticks at various stages of blood engorgement and advises patients to seek medical attention if a removed tick is determined to have been attached for 48 hours or longer. Lyme disease can be transmitted after 48 hours of feeding by an infected tick and most physicians will treat such patients with a short course of antibiotics to prevent Lyme disease. A panel of skin rash photos characteristic of Lyme disease, along with other symptoms, prompts users to seek immediate medical attention if they are infected. A physician locater finds doctors nearest to the user, again using GPS location, and provides the phone number and directions to each physician’s office.

Content for the application was provided by Lyme disease researchers at Yale in cooperation with the US Centers for Disease Control, the American Lyme Disease Foundation, and Intuwin, an applications development company based in New York City. It is available through the Apple iTunes Store for $1.99. Proceeds will be used for support the research and education mission of the American Lyme Disease Foundation, of Lyme CT.

Check it out at....

By the American Lyme Disease Foundation, Inc.

Posted by Relative Risk at 08:49 0 comments Links to this post

Labels: Lyme disease

27 April 2010

“Why don’t he write?”

[A line from the movie, “Dances with Wolves”.]

Just when I was beginning to wonder why Stricker (and his lawyer sidekick) haven’t fired off another letter to the editor...he does.

Letter to the Editor: Anti-Neural Antibody Reactivity in Patients with Post-Treatment Lyme Disease. Raphael B. Stricker, Lorraine Johnson

DOI: 10.1016/j.bbi.2010.04.011

Brain, Behavior, and Immunity, April 2010-04-27

It’s the usual stuff: criticism of others’ work, misleading statements, and references to his prior (critical, but data-free) letters to editors.

This time around, the letter of complaint is about the recent finding of anti-neural antibodies in patients with persistent, post-Lyme symptoms. He (or they) write: "This study demonstrating ‘objective immunologic abnormalities’ (yes) underscores the pathophysiologic nature of post-treatment Lyme disease (yes) and discredits the sychosomatic theory advanced by some (no) as the cause of persisting symptoms.” Not bad, two out of three.

The psychosomatic dig is in reference to the paper of Hassett et al. about psychiatric co-morbidity in patients with ‘chronic Lyme disease.’ Hassett et al. wrote:

Our data supported previous observations that the chronic symptoms of most patients presenting to academic Lyme disease referral centers cannot be attributed to ongoing infection with B. burgdoferi. While some of our patients had another medical condition that explained the complaints attributed to Lyme disease, the physical, cognitive, and emotional symptoms of most patients were more consistent with Chronic Multi-symptom Illness or psychiatric disorders. Almost 49% of patients in our Chronic Multisymptom Illness group had clinical disorders like Major Depressive Disorder or Generalized Anxiety Disorder, in contrast to the comparison group with a rate of 21.1%, which is closer to the rate observed in the general population, 26.2%. In conclusion, psychiatric comorbidity and other psychological factors are prominent in the presentation and outcome of some patients who inaccurately ascribe longstanding symptoms to “chronic Lyme disease.” Less than 20% of patients presenting to our Lyme disease specialty center had a current infection with B. burgdorferi. Most patients had other medical conditions or Chronic Multisymptom Illness, but were being treated with antibiotics for Lyme disease.

The word “psychosomatic” never appears in the Hassett paper.

Next, Stricker suggests there is “a growing list of animal and human studies supports persistent infection in post-treatment Lyme patients” and demonstrates this by citing two of his letters to the editor and one actual piece of research involving infected mice and one type antibiotic. It’s not much of a “growing list” and, with few exceptions, men are not mice.

Then he claims “current models of autoimmunity in other diseases suggest that persistent infection is required for the production of autoantibodies…” and cites another one of his letters, and coxsackie virus as a model. Coxsackie virus? The self-limiting agent of Hand-Foot-Mouth Syndrome in children? Couldn’t he come up with some better examples? Maybe LCMV or EBV or H. pylori or B19?

The whole point of this letter is to argue that “it is likely that persistent infection with the Lyme spirochete Borrelia burgdorferi may be driving production of these antibodies.”

Well, that would be a convincing argument if someone could actually find persisting B. burgdorferi in patients with persisting evidence of disease. Show us. Stop writing letters and do some actual research. As creative writing teachers are fond of saying, “Show. Don’t tell.”

There are some additional digs at the authors of the anti-neural antibodies paper. Antibody assays are described (twice) as a “home brew” methodology. Hardly. It’s all standard materials and standard techniques from reputable companies.

ELISA kit (ICL), 96-well polystyrene plates (BD Biosciences), B. burgdorferi B31 antigen (Meridian).

Antibodies to brain proteins were detected by immunoblotting.

Mini-PROTEAN II Multiscreen apparatus (Bio-Rad), HRP-conjugated sheep anti-human IgG (Amersham), Detection of bound antibodies was by the ECL system (Millipore) and BioMax MR film (Kodak), stripping buffer (Pierce), reblotted with HRP-conjugated rabbit anti-β tubulin antibody (Novus), Conversion of immunoblots to line graph by the Unscan-It program (Silk Scientific).

Maybe he thinks they should have used Igenex, the preferred diagnostic company of LLMDs and chronic Lyme patients.

Finally, even the serum samples used in the study are criticized: “Patient samples were selected based on the time from diagnosis rather than the presence of specific neurologic symptoms....” Well, again, no. The original serum samples are described below.

So that’s it. Thanks for writing.

Serum samples from 83 individuals with a history of Lyme borreliosis and persistent symptoms, recruited as part of a previous clinical trial (Klempner et al., 2001), were used in this study (37 female, 46 male; mean age 55.6 ± 12.0 y (SD); mean elapsed time since the original diagnosis of Lyme disease 5.0 ± 2.9 y (SD)). Selection of these specific specimens from the original cohort was based on limiting the elapsed time between diagnosis of acute Lyme disease and serum specimen collection to between 1 and 12 years. Patients had at least one of the following: a history of erythema migrans (EM) skin lesion, early neurologic or cardiac symptoms attributed to Lyme disease, radiculoneuropathy, or Lyme arthritis. Documentation by a physician of previous treatment of acute Lyme disease with a recommended antibiotic regimen was also required. Patients had one or more of the following symptoms at the time of enrollment: widespread musculoskeletal pain, cognitive impairment, radicular pain, paresthesias, or dysesthesias. Fatigue often accompanied one or more of these symptoms. The chronic symptoms had to have begun within 6 months after the infection with B. burgdorferi. Control subjects included 27 individuals who had been treated for early localized or disseminated Lyme disease associated with single (n = 18) or multiple (n = 9) EM, but had no post-Lyme symptoms after at least 2 years of follow-up (12 female, 15 male; mean age 54.4 ± 14.7 y (SD); mean elapsed time since the original diagnosis of Lyme disease 5.4 ± 3.8 y (SD)). The diagnosis of acute Lyme disease in control subjects was confirmed by recovery of B. burgdorferi in cultures of skin and/or blood sample. The elapsed time between diagnosis of acute Lyme disease and serum specimen collection was limited to between 1 and 12 years for post-Lyme healthy subjects. In addition to the above, serum samples from 15 patients with systemic lupus erythematosus (SLE) and 20 healthy individuals were analyzed in the study. All SLE patients met four or more of the American College of Rheumatology classification criteria for diagnosis (Tan et al., 1982). Serum specimens were stored at −80 °C prior to use. This study was approved by the Institutional Review Board of the Weill Medical College of Cornell University.

Posted by Relative Risk at 11:56 0 comments Links to this post

Labels: Lyme disease

24 April 2010

Mixed Messages from the Mixed Nuts of LymeLand

Well, Stricker’s paper on i.v. treatments for Lyme disease isn’t much more enlightening than the earlier abstract.As a reminder, the authors of this trial are 1) people who believe in long-term antibiotic use for the persistent symptoms of presumptive Lyme disease, 2) people who are members of an organization (ILADS) dedicated to the use of long-term antibiotics for presumptive Lyme disease, 3) people from a home infusion company who market themselves as a “Lyme literate” pharmacy*, and 4) people who are members of a patient advocacy group dedicated to the belief in chronic antibiotic usage for chronic Lyme disease. Therefore, expect some serious bias.

So Stricker et al. gathered up some data on 200 patients (in 18 states) who had been diagnosed and treated for Lyme disease.

According to the authors, “all patients had significant neuropsychiatric symptoms,” which the authors and the treating physicians apparently attributed solely to Lyme disease. No inclusion criteria for patient selection are provided in the text. There’s no case definition for persistent neurologic Lyme disease. There is only a reference to Fallon’s 2008 clinical trial in which he famously had so much trouble finding well-defined chronic Lyme patients. (After screening 3,368 potential patients, he found 37 with some convincing evidence of Lyme disease. They got treated with 10 weeks of iv ceftriaxone after which Fallon concluded: “10 weeks of iv ceftriaxone…is not an effective strategy.” I wonder why he’s not on this particular study?)

All of the patients also tested positive for B. burgdorferi, but again, they don’t say how they were tested or where. (I’m guessing the various treating physicians in the unnamed 18 states had Igenex do some serology.)

The patients were largely middle-aged (mean 41 years) women (141 women vs. 59 men), plugged into some manner of i.v. device for an average of 118 days. (Interesting sex ratio. According to the CDC surveillance data, men and women contract Lyme in about equal numbers. Then why so many women with “significant neuropsychiatric symptoms”?)

The i.v. devices include PICC lines, peripheral catheters, s.c. ports, c.v. catheters, and midline catheters. The particular device was selected by the various treating physicians, along with the particular antibiotic and dosage. Table 1 in the paper lists 13 different antibiotics used among 200 patients.

So we have 200 people who may or may not have an active borreliosis, enrolled based on vague criteria from an unknown number of primary care physicians using five different i.v. devices and 13 different kinds of antibiotics over a period of time that ranged from 7 to 750 days.

What a mess of variables and unknowns. The stats software must have imploded trying to make sense of this trial. But then some of the virtues of InStat software are 1) that it “does not assume that you are a statistics whiz,” 2) “you don’t have to know the name of the test you need," and 3) “all prompts to the user are in plain English and simple to follow.” Stats for Dummies.

Conclusions?

Table 2 lists complications from the i.v. devices and the medication. There were 24 patients with complications. So that’s 12% of the study population who experienced an adverse event. Is that considered safe? Stricker says so.

Is it effective? Stricker writes, “It remains to be seen whether this length of treatment was able to reduce or eliminate an underlying infection.” (Assuming one ever existed.) Apparently we have to wait for the sequel in the form of another bad paper in an obscure foreign journal. He writes, “The present study…makes no comment about the efficacy of this treatment.”

Was this really ethical? Lining up a bunch of people (with significant neuropsychiatric symptoms) to see if procedure X is not therapeutic but merely safe? Sounds like something you’d do with guinea pigs.

*"The QMedRx Clinical Staff and Medical Advisory Committee have prepared a web based patient outcome questionnaire. Our goal is to help your physician maximize your response to treatment, make data easier for you to document and easier for your physician to retrieve. Some benefits may include the collection and publishing of data to document the positive outcome of IV antibiotic treatment."

Posted by Relative Risk at 22:41 0 comments Links to this post

Labels: ILADS, Lyme disease, Stricker

22 March 2010

The Law of the Lyme

If I'm reading this legalese correctly, it doesn't sound like things went to well for the Lyme patient wannabe. I wonder who the New York expert neurologist could have been?

RYAN v. SANTANA

2010 NY Slip Op 02364

DAVID RYAN, ET AL., PLAINTIFFS, AND JESSICA RYAN, PLAINTIFF-RESPONDENT,

v.

HECTOR B. SANTANA, M.D., JAMES B. TURCHIK, M.D., DEFENDANTS-APPELLANTS, ET AL., DEFENDANTS.

CA 09-00369.

Appellate Division of the Supreme Court of New York, Fourth Department.

Decided March 19, 2010.

SMITH, SOVIK, KENDRICK & SUGNET, P.C., SYRACUSE (LAURENCE F. SOVIK OF COUNSEL), FOR DEFENDANT-APPELLANT HECTOR B. SANTANA, M.D.

SUGARMAN LAW FIRM, LLP, SYRACUSE (JENNA W. KLUCSIK OF COUNSEL), FOR DEFENDANT-APPELLANT JAMES B. TURCHIK, M.D.

IRWIN BIRNBAUM, SYRACUSE, FOR PLAINTIFF-RESPONDENT.

PRESENT: CENTRA, J.P., PERADOTTO, CARNI, PINE, AND GORSKI, JJ.

It is hereby ORDERED that the order so appealed from is affirmed without costs.

Memorandum: Plaintiffs commenced this action seeking damages for, inter alia, the medical malpractice of Hector B. Santana, M.D. and James B. Turchik, M.D. (defendants), which included their failure to diagnosis and treat the alleged case of Lyme disease sustained by Jessica Ryan (plaintiff). Defendants appeal from an order denying those parts of their respective motions seeking summary judgment dismissing the complaint against them with respect to plaintiff. We affirm, inasmuch as we agree with Supreme Court that plaintiffs raised a triable issue of fact with respect to those parts of defendants' motions (see generally Alvarez v Prospect Hosp., 68 NY2d 320, 324-325).

In opposition plaintiffs submitted the affirmation of a neurological expert stating that, because defendants' differential diagnoses for plaintiff included Lyme disease, defendants' reliance on negative test results of Lyme disease tests in the absence of a confirmed alternative diagnosis deviated from the accepted standard of medical care. According to that expert, the immediate commencement of antibiotic therapy was required because early intervention offered a patient the best chance of recovery. The expert further stated that discharging plaintiff without a confirmed diagnosis and without consideration of antibiotic or antibacterial treatment in the absence of a confirmed diagnosis was also a significant departure from the accepted standard of medical care, particularly in light of the warning given on plaintiff's discharge that plaintiff might become comatose (see Wahila v Kerr, 204 AD2d 935, 937). Additionally, plaintiffs submitted the letter affirmation of an expert in infectious diseases who stated that the initial negative result on the Lyme disease test could have resulted from medication taken by plaintiff prior to her examination by defendants. The infectious diseases expert similarly concluded that defendants' failure to confirm an alternative diagnosis or to begin plaintiff on an appropriate antibiotic therapy was a deviation from the accepted standard of medical care (see id.).

We cannot agree with the dissent that the record is devoid of evidence that plaintiff in fact suffered from Lyme disease (cf. Kane v City of New York, 137 AD2d 658, 660). The record establishes that, when they examined plaintiff, defendants observed that she exhibited symptoms that could be attributed to Lyme disease, and plaintiffs' neurologist stated that those symptoms, including target lesions, were in fact indicative of Lyme disease (cf. Czeisler v Williams, 259 AD2d 278, 279). Further, the conclusions of plaintiffs' experts were also based in part on the medical records of a physician who examined plaintiff subsequent to defendants' examination of her. Although those medical records are unsworn, they nevertheless are in admissible form inasmuch as they were submitted in support of the motion of defendants A.L. Lee Memorial Hospital and Jasmdiner Luthra, M.D. for summary judgment dismissing the complaint against them and are included in the record on appeal (see Kearse v New York City Tr. Auth., 16 AD3d 45, 47 n 1). Thus, plaintiffs are entitled to rely on those records in opposing defendants' respective motions (see generally Feggins v Fagard, 52 AD3d 1221, 1223).

The physician noted therein that there was "reasonable serologic evidence of Lyme disease," that plaintiff's symptoms were similar to two of his patients with Lyme disease, and that plaintiff's test results supported a diagnosis of central nervous system Lyme disease. The physician also indicated that he had seen improvement in plaintiff with the application of antibiotics with respect to her cerebellar syndrome and the evidence of Lyme disease. We thus conclude that plaintiffs raised triable issues of fact concerning the alleged malpractice of defendants (see generally Alvarez, 68 NY2d at 324-325).

All concur except Peradotto and Pine, JJ., who dissent and vote to reverse the order insofar as appealed from in accordance with the following Memorandum:

We respectfully dissent. In our view, Hector B. Santana, M.D. and James B. Turchik, M.D. (defendants) met their burdens on those parts of their respective motions for summary judgment seeking dismissal of the complaint against them with respect to Jessica Ryan (plaintiff) by establishing that they did not deviate from accepted medical practice in treating plaintiff, and plaintiffs failed to raise a triable issue of fact with respect to the alleged malpractice of either defendant (see generally Alvarez v Prospect Hosp., 68 NY2d 320, 324-325).

Significantly, although plaintiffs' allegations of malpractice are premised upon the failure of defendants to diagnose and treat plaintiff for Lyme disease, plaintiffs failed to submit evidentiary proof in admissible form establishing that plaintiff in fact had Lyme disease. In the spring of 2000, the time period of the alleged malpractice, plaintiff presented to defendants with neurological symptoms, including slurred speech and an abnormal gait. Plaintiff also exhibited four lesions on her skin. The three physicians who observed plaintiff's lesions, including defendants, all determined that the lesions were not typical of Lyme disease and were instead indicative of a fungal infection. As noted by the majority, plaintiffs' expert neurologist stated in an affirmation that "target lesions" are indicative of Lyme disease. However, the expert neurologist did not observe plaintiff's lesions, and failed to address the deposition testimony of defendants and the emergency room physician who treated plaintiff in the spring of 2000 that plaintiff's lesions were not characteristic of Lyme disease. Moreover, during plaintiff's hospital stay in May 2000, defendants ordered a Lyme titer test to screen for the presence of Lyme disease antibodies in plaintiff's blood and cerebrospinal fluid, the results of which were negative. Following plaintiff's discharge from the hospital and at the request of plaintiff mother, Dr. Santana repeated the Lyme titer test on two different occasions and, again, the results were negative. After plaintiff left the care of Dr. Santana in June 2000, she saw numerous physicians, including at least four neurologists, none of whom diagnosed plaintiff as having Lyme disease. Plaintiff also underwent additional tests for Lyme disease, which were negative.

The majority relies on the unsworn medical records of a physician who first examined plaintiff in September 2001, more than a year after the alleged malpractice.

Even assuming, arguendo, that the records were in admissible form (see Gonzalez v Sisters Hosp., 309 AD2d 1277; cf. Feggins v Fagard, 52 AD3d 1221, 1223), we note that the physician acknowledged that plaintiff had no history of tick attachments or "any rashes definitely pathognomic for Lyme disease," and further stated that plaintiff did not exhibit "many extra-neurologic features that commonly may be seen in Lyme disease." After his first examination of plaintiff, the physician concluded that she suffered from a "cerebellar syndrome," which possibly was caused by Lyme disease. That hypothesis was based upon a Western Blot test administered in April 2001 that detected the presence of Lyme disease antibodies in plaintiff's blood. The Centers for Disease Control and Prevention (CDC) does not recommend Western Blot testing unless a patient first tests positive by standard testing because "[d]oing so increases the potential for false positives" and, in any event, the Western Blot test results did not meet CDC criteria for a positive finding of Lyme disease. The physician ordered numerous follow-up tests, all of which were negative or, at best, inconclusive. Notably, plaintiffs did not submit an affirmation or any other sworn statement from that physician diagnosing plaintiff with Lyme disease. In the absence of a diagnosis or other conclusive evidence that plaintiff suffered from Lyme disease, we conclude that plaintiffs failed to raise a triable issue of fact sufficient to defeat defendants' motions (see Czeisler v Williams, 259 AD2d 278, 279; Kane v City of New York, 137 AD2d 658, 660).

Even assuming, arguendo, that plaintiff was subsequently diagnosed with Lyme disease, we conclude that the expert affidavits submitted by plaintiffs are insufficient to raise a triable issue of fact (see generally Alvarez, 68 NY2d at 324-325). It is well established that "[g]eneral allegations of medical malpractice, merely conclusory and unsupported by competent evidence tending to establish the essential elements of medical malpractice, are insufficient to defeat defendant physician[s'] summary judgment motion[s]" (id. at 325; see Mendez v City of New York, 295 AD2d 487). Plaintiffs submitted the affirmation of an expert neurologist who stated that defendants deviated from the accepted standard of medical care by relying on negative test results of Lyme disease to exclude their differential diagnosis of Lyme disease. The expert neurologist also faulted defendants for failing to prescribe antibiotics, stating that, "[i]n a circumstance in which there is a differential or presumptive diagnosis of Lyme disease without a specific confirmed or well-supported alternative diagnosis, antibiotic therapy should be instituted immediately."

In our view, the conclusions of plaintiffs' expert neurologist are not supported by the record and are thus insufficient to raise a triable issue of fact (see Selmensberger v Kaleida Health, 45 AD3d 1435, 1436). As an initial matter, we note that plaintiff's hospital records do not support the proposition that Lyme disease was a "presumed" or even a differential diagnosis. The consultation report of Dr. Turchik that was provided to Dr. Santana does not mention Lyme disease as a possible diagnosis and states that the most "tantalizing diagnosis" is a demyelinating disease, such as multiple sclerosis. Dr. Santana's diagnoses were viral cerebellitis or a demyelinating disease, and both defendants believed that the lesions were caused by a fungal infection, i.e., ringworm. Moreover, contrary to the assertion of plaintiffs' expert neurologist, defendants did not exclude Lyme disease on the basis of negative test results; rather, both defendants reached their respective diagnoses on the basis of plaintiff's clinical presentation before they received the negative test results. Thus, inasmuch as the assertions of plaintiffs' expert neurologist are "unsupported by any evidentiary foundation . . ., the [expert's] opinion should be given no probative force and is insufficient to withstand summary judgment" (Diaz v New York Downtown Hosp., 99 NY2d 542, 544).

With respect to the assertion of plaintiffs' expert neurologist that defendants departed from the accepted standard of medical care by discharging plaintiff from the hospital without a confirmed diagnosis, we note that, according to the documentation in the record on appeal, plaintiff still does not have a confirmed diagnosis of Lyme disease or, indeed, any other disease. Plaintiff was discharged as neurologically stable after defendants conducted numerous tests and procedures, and plaintiffs' expert neurologist failed to identify what else defendants should have done before releasing plaintiff from the hospital. In any event, the expert's affidavit contains no allegation, let alone any evidence, that plaintiff's discharge from the hospital in May 2000 caused or contributed to plaintiff's injuries (see Lebron v St. Vincent's Hosp. & Med. Ctr., 261 AD2d 246).

Plaintiffs also submitted the letter affirmation of an expert in infectious disease who stated that defendants deviated from the accepted standard of medical care in failing to treat plaintiff with antibiotics in a timely manner. That opinion is based upon two assumptions that are unsupported by the record, however, and the letter affirmation thus is insufficient to raise a triable issue of fact (see Shahid v New York City Health & Hosps. Corp., 47 AD3d 800, 802; Selmensberger, 45 AD3d at 1436). The first assumption is that plaintiff was "eventually diagnosed and treated" for Lyme disease. As discussed above, that was not established by the submission of evidence in admissible form (see Gonzalez, 309 AD2d at 1277) or, for that matter, by any evidence in the record. The second assumption, that plaintiff's neurological symptoms cleared while plaintiff was taking an antibiotic for a sinus infection and recurred when she ceased taking the antibiotic, is an incorrect statement of the facts (see Micciola v Sacchi, 36 AD3d 869, 871). Indeed, the record reflects that plaintiff first exhibited neurological symptoms while she was taking the antibiotic, which led the emergency room physician who treated plaintiff in May 2000 to conclude that she was experiencing an adverse reaction to the medication.

In light of the foregoing, we conclude that defendants established their entitlement to judgment as a matter of law, and plaintiffs failed to raise any triable issues of fact with respect to the alleged malpractice of either defendant concerning plaintiff (see generally Darling v Scott, 46 AD3d 1363). We therefore would reverse the order insofar as appealed from, grant in their entirety the respective motions of defendants for summary judgment, and dismiss the complaint against them.

This copy provided by Leagle, Inc.

Posted by Relative Risk at 17:25 0 comments Links to this post

Labels: Lyme disease