posted
This is important because Dr. Shapiro is on the panel for the hearing that will decide on Dr. Jones case.
My intention was to paste in some of the abstracts from the National Library of Medicine database. But most of Shapiro's don't have abstracts (the paragraph summarizing content of article)!!! It is unusual for so many of one author's articles to include no abstract in these listings. So, I will post the full text of one article (thanks S.) and say that Shapiro is a pediatrician at Yale and one of the co-authors of the Lyme treatment guidelines of the Infectious Diseases Society of America (IDSA). These guidelines are being used by insurance companies and state medical boards against patients and doctors. Can read guidelines here: http://tinyurl.com/7cdv6
Here is his article, full text, from Pediatric Annals journal in 2002. It is very long, if not up to reading the whole thing, check out the sections in red. The big problems with him come from his position on diagnosis and treatment, and also from his dismissal of the risks of infection. Basically what these errors lead to is missed cases and undertreatment.
Lyme Disease: Fact Versus Fiction
Eugene D. Shapiro, MD; and Michael A. Gerber, MD
In part because of inordinate publicity in the lay press, misconceptions about Lyme disease abound in the medical community and among the general public. Although there still is much to learn about Lyme disease, many aspects are well understood. Conventional treatment with antimicrobials is usually effective, and the long-term prognosis for children with Lyme disease is excellent.
ETIOLOGY AND EPIDEMIOLOGY Lyme disease is caused by the spirochete Borrelia burgdorferi sensu lato, a fastidious, microaerophilic bacterium that replicates slowly and requires special media to grow in the laboratory.l Based on studies of its DNA, the organism has been subclassified into several genospecies: B. burgdorferi sensu stricto, Borrelia garinii, and Borrelia afzelii. In the United States, only B. burgdorferi sensu stricto has been isolated from humans. In contrast, there is substantial antigenic variability among isolates of B. burgdorferi from humans in Europe.
Lyme disease occurs throughout the world. In Europe, most cases occur in Scandinavia and central Europe (especially Germany, Austria, and Switzerland), although cases have been reported from throughout the region. Most cases of Lyme disease in the United States occur in southern New England, southeastern New York, New Jersey, eastern Pennsylvania, eastern Maryland, Delaware, and parts of Minnesota and Wisconsin. There were 16,273 cases of Lyme disease reported to the Centers for Disease Control and Prevention (CDC) in 1999.2 More than threequarters of these cases occurred in fewer than 70 counties, an indication of how geographically circumspect disease occurrence is.
The incidence of Lyme disease varies substantially from region to region and even within local areas. Information about true incidence is complicated by reliance on passive reporting and by the high frequency of misdiagnosis. The incidence is highest among children 5 to 10 years old, nearly twice as high as the incidence among adults. Connecticut has the highest reported incidence in the United States: 98 cases per l00,000 persons in the year 1999.2
B. burgdorferi is transmitted by ixodid ticks in the United States, primarily by Ixodes scapularis, the deer tick.l Ixodid ticks have a 2-year, threestage life cycle. Larvae hatch in early summer and are usually not infected with B. burgdorferi.
Ticks may become infected at any stage of their life cycle by feeding on a host that is a natural reservoir for B. burgdorferi, usually a small mammal such as the white-footed mouse. Larvae then lie dormant during the winter and emerge the following spring in the nymphal stage, which is the stage most likely to transmit the infection. Nymphs molt to adults in the fall. Adult females, which often spend the winter attached to deer (hence the name " deer tick" ), lay their eggs the following spring before they die, and the 2-year life cycle begins again. Several factors are associated with the risk of transmission of B. burgdorferi from ticks to humans. First, the tick must be infected. The proportion of infected ticks varies greatly by both geographic area and the stage of the life cyclc. Lyme disease is uncommon in Pacific states because few I. pacificus ticks (the western blacklegged tick) are infected with B. burgdorferi. In endemic areas, rates of infection of I. scapularis are approximately 2 % for larvae, 15% to 30% for nymphs, and 30% to 50% for adults.
Studies with experimental animals indicate that an infected tick must feed for 48 to 72 hours or longer to transmit B. burgdorferi. These experimental findings were recently confirmed in a study in which the risk of transmission from ticks (for which the duration of feeding could be assessed) to humans was 25% for nymphal ticks that fed for 72 hours or more and O% for those that fed for fewer than 72 hours.
This can be explained by the fact that the bacteria live in the midgut of the tick, which needs to become engorged with blood before the bacteria can migrate to the salivary glands and the saliva, from which the organism is injected into the host. Individuals with increased occupational, recreational, or residential exposure to tick-infested woodlands in endemic areas are at increased risk of Lyme disease.
CLINICAL MANIFESTATIONS The clinical manifestations of Lyme disease depend on the stage of disease~early localized, early disseminated, or late.14 Erythema migrans, the manifestation of early localized disease, appears at the site of the tick bite 7 to 10 days (range, 3 to 30 days) after the bite. Erythema migrans is found in approximately 90% of patients with objective evidence of infection with B. burgdorferi.
It begins as a red macule or papule and expands for days to weeks to form a large, annular, erythematous lesion that is at least 5 cm and as much as 70 cm in diameter (median, 15 cm), This lesion may be uniformly erythematous or it may look like a target with variable degrees of central clearing (Figure). It can vary greatly in shape, and, occasionally, may have vesicular or necrotic areas in the center.
Erythema migrans is usually asymptomatic but may be pruritic or painful, and it may be accompanied by systemic findings such as fever, malaise, headache, regional lymphadenopathy, stiff neck, myalgia, or arthralgia. The most common manifestation of early disseminated Lyme disease is multiple erythema migrans. Secondary skin lesions, which usually appear from 3 to 5 weeks after the tick bite, consist of multiple, annular, erythematous lesions similar to, but usually smaller than, the primary lesion.
Other common manifestations of early disseminated disease are cranial nerve palsies, especially involving the facial nerve, and meningitis. Systemic symptoms such as fever, myalgia, arthralgia, headache, and fatigue are common in this stage. Carditis, which usually manifests as various degrees of heart block, is rare. The most common manifestation of late Lyme disease, which occurs weeks to months after the initial infection, is arthritis. This is usually monoarticular or oligoarticular and affects the large joints, particularly the knees. Although the affected joint is typically swollen and tender, the intense pain associated with septic arthritis usually is not present. Encephalitis, encephalopathy, and polyneuropathy are also manifestations of late disease, but they are rare in children.
Clinical manifestations of Lyme disease may depend on the species of B. burgdorferi causing the infection. The differences in species found in Europe and North America may account for differences in the frequencies of certain clinical manifestations of Lyme disease in those areas. For example, neurologic manifestations of Lyme disease are more common in Europe, whereas rheumatologic manifestations are more common in North America.
In addition, certain manifestations of Lyme disease in the skin and soft tissues (eg, acrodermatitis chronica atrophicans and lymphocytomas) occur in Europe, but are extremely rare in the united States. Ixodid ticks may transmit other pathogens in addition to B. burgdorferi, including babesia, ehrlichia, other Borrelia species, and viruses. These agents may be transmitted either separately from or simultaneously with B. burgdorferi. However, the frequency with which coinfection occurs is unknown and its impact on both clinical presentation and response to the treatment of Lyme disease is not well established.
DIAGNOSIS The diagnosis of Lyme disease, especially when the characteristic rash is absent, may be difficult, because other clinical manifestations of Lyme disease are not specific. Recognition of erythema migrans may even be difficult because, in its early stage, the rash can be confused with nummular eczema, granuloma annulare, insect and spider bites, ringworm, or cellulitis. The relatively rapid expansion of erythema migrans helps to distinguish it from these other conditions.
The sensitivity of culture for B. burgdorjeri is only fair and special media are required; moreover, patients must undergo biopsy or other invasive procedures to obtain appropriate material for culture. Consequently, culture is indicated only in rare circumstances. Likewise, diagnostic tests that are based on the identification of antigens or genetic sequences of B. burgdorferi, including polymerase chain reaction, have not been shown to be sufficiently accurate to be used outside of study conditions. Preliminary studies in research laboratories suggest that polymerase chain reaction is promising. By contrast, the Lyme urine antigen test is inaccurate.7 Consequently, laboratory confirmation of Lyme disease usually rests on the demonstration of antibodies to B. burgdorferi in the patient's serum. It is well documented that the sensitivity and specificity of antibody tests for Lyme disease vary substantially. The accuracy and reproducibility of prepackaged commercial kits are much poorer than those of tests performed by "reference" laboratories that maintain tight quality control and regularly prepare materials that are used in the tests.
Official recommendations from the Second National Conference on Serologic Diagnosis of Lyme Disease and the CDC are that physicians use a two-step procedure when ordering antibody tests. First, a sensitive screening test, such as enzyme-linked immunosorbent assay (ELISA), should be performed. If the result is positive or equivocal, a Western immunoblot should be performed to confirm the result.8 If the result of the ELISA is negative, an immunoblot is not necessary.
The ELISA provides a quantitative estimate of the concentration of antibodies against B. burgdorferi. The immunoblot provides information about the specificity of the antibodies; positive "bands" mean that antibodies against specific protein antigens of the spirochete are present. Most authorities require the presence of antibodies against at least 2 (for IgM) or 5 (for IgG) specific proteins of B. burgdorferi for the results of the immunoblot to be considered positive. Antibody tests are not useful for the diagnosis of early localized Lyme disease, because only a few patients with a single erythema migrans will have detectable antibodies at the time they present.
It is critically important to understand that the predictive value of antibody tests, even accurate tests, is highly dependent on the prevalence of the infection among the patients who are tested. Antibody tests for Lyme disease should not be used as screening tests.
Unfortunately, because many lay persons have the erroneous belief that chronic, nonspecific symptoms alone (eg, fatigue or arthralgia) may be manifestations of Lyme disease, parents of children with these symptoms frequently demand that their child be tested for Lyme disease. In truth, Lyme disease is the cause of nonspecific symptoms in few such children, if any. However, because the specificity of even the best antibody tests for Lyme disease rarely exceeds 90% to 95%, some test results for children with nonspecific signs or symptoms are positive; most of these are false positive results.Unfortunately, an erroneous diagnosis of Lyme disease is often made based on the results of these tests, and such children are often treated unnecessarily with antimicrobials. Physicians should realize that although a symptomatic patient has a positive serologic test result for B. burgdorferi, it is possible that Lyme disease may not be the cause of that patient's symptoms. In addition to the possibility that the test result is falsely positive (a common occurrence ), the patient may have been infected with B. burgdorferi previously, and the patient's symptoms may be related to a new disease process.
Once serum antibodies to B. burgdorferi develop, they may persist for many years despite adequate treatment and clinical cure of the illness.11 In addition, because some individuals who become infected with B. burgdorferi never have symptoms, there is a background rate of seropositivity among patients in endemic areas who have never had clinically apparent disease.
Physicians should not routinely order antibody tests for Lyme disease for patients who have not been to endemic areas or for patients who have only nonspecific symptoms.
TREATMENT (TABLE) Early Localized Disease Doxycycline is the drug of choice for children 8 years and older with early localized Lyme disease. Exposure to the sun should be avoided because of photosensitivity, which develops in sun-exposed areas of 20% to 30% of individuals taking the drug. The use of sunscreen may decrease this risk.
Amoxicillin is recommended for children younger than 8 years and those who cannot tolerate doxycycline. For patients allergic to penicillin, alternative drugs are cefuroxime axetil, erythromycin, or azithromycin, but the latter two may be less effective than other agents. Most experts recommend a 21-day course of therapy for early localized Lyme disease, although many believe that 10 to 14 days is adequate for uncomplicated cases. There is usually a prompt clinical response to therapy, with resolution of the erythema migrans within several days.
Occasionally, a Jarisch-Herxheimer reaction, consisting of elevated temperature and worsening myalgia, develops shortly after antimicrobial treatment is initiated. These reactions typically last 1 to 2 days, are not an indication to discontinue antimicrobial therapy, and respond to nonsteroidal antiinflammatory agents. Appropriate therapy for erythema migrans almost always prevents development of the later stages of Lyme disease.
Early Disseminated and Late Disease Multiple erythema migrans and initial episodes of arthritis should be treated with oral antibiotics. If peripheral facial nerve palsy is the only neurologic manifestation of Lyme disease, the patient can also be treated with oral antibiotics. If facial nerve palsy is accompanied by clinical evidence of central nervous system involvement (eg, severe headache or nuchal rigidity), a lumbar puncture should be performed. If pleocytosis is present, parenteral antibiotics should be prescribed. Meningitis and recurrent or persistent arthritis should also be treated parenterally. However, some experts prescribe a second course of oral antibiotics for recurrent or persistent arthritis before initiating intravenous therapy. Although mild carditis is usually treated orally with doxycycline or amoxicillin, most experts recommend parenterally administered therapy for severe carditis. Other neurologic manifestations of late Lyme disease (eg, encephalitis, encephalopathy, and polyneuropathy) should be treated with parenteral antibiotics. The optimal duration of therapy for the various stages of Lyme disease is not well established, but there is no evidence that children with any manifestation of Lyme disease benefit from either prolonged (greater than 4 weeks) or repeated courses of oral or parenteral antibiotics. Similar to other infections, Lyme disease may trigger a fibromyalgia syndrome that does not respond to additional courses of antimicrobials but may improve with symptomatic therapy.
OUTCOMES The long-term prognosis for children who are treated appropriately for Lyme disease, regardless of stage, is excellent. The most common reason for a lack of response to appropriate antimicrobial therapy is misdiagnosis (ie, the patient actually does not have Lyme disease). Approximately 10% of adults and fewer than 5% of children with Lyme arthritis have inflammatory joint disease that typically affects one knee for months to years and does not respond to antimicrobial therapy. There is an increased frequency of certain HLA-DR4 alleles in these patients and recent findings suggest that an autoimmune process is involved.
Nonspecific symptoms such as fatigue, arthralgia, or myalgia may persist for several weeks, even in patients with early Lyme disease that was successfully treated. The presence of these symptoms should not be regarded as an indication for additional treatment with antimicrobials, but nonsteroidal anti-inflammatory agents usually help. Within 6 months of patients' completing the initial course of antibiotics, these vague, nonspecific symptoms usually have resolved without additional antimicrobial therapy. For those unusual patients who have persistent symptoms beyond that time, an attempt should be made to determine whether these symptoms are the result of a postinfectious phenomenon or another illness.
Klempner et al. recently reported the results of two controlled trials of antibiotic treatment for adults with chronic musculoskeletal pain, neurocognitive symptoms, or both that persisted after antibiotic treatment for well-documented Lyme disease.13 One study included patients who were seropositive for IgG antibodies to B. burgdorferi at the time of enrollment; the other included patients who were seronegative.
In both studies, patients were randomly assigned to receive either intravenous ceftriaxone for 30 days followed by oral doxycycline for 60 days or matching regimens with intravenous and oral placebos. There were no significant differences in the outcomes of patients treated with antibiotics compared with those treated with placebo among either seropositive or seronegative patients. These findings support earlier recommendations that such patients are best treated symptomatically rather than with prolonged courses of antibiotics, which can be associated with serious side effects.
CONGENITAL LYME DISEASE Much of the initial information about the potential for transplacental infection with Lyme disease was alarming. However, this information came from a small number of case reports, most of which involved women with unrecognized and untreated Lyme disease during their pregnancies.]5 There has been a considerable amount of skepticism about these cases because there was no evidence of inflammation and no consistent pattern of disease. In addition, although spirochetes compatible with B. burgdorferi were seen in pathologic specimens, B. burgdorferi was never isolated in culture from any of these cases. Several subsequent studies found no consistent pattern of disease and no clearly documented B. burgdorferi infections of either fetuses or infants. In addition, obstetric outcomes were similar among women who had documented Lyme disease during their pregnancies and those who did not. Moreover, in a survey of 162 neurologists practicing in areas endemic for Lyme disease, investigators were unable to identify any well-documented cases of prenatally acquired neuroborreliosis.14 Although there have been instances in which a temporal relationship between Lyme disease during pregnancy and an adverse outcome was reported, a causal relationship was not established. There is no evidence of increased risk of abnormal outcomes with Lyme disease during pregnancy.15 Transmission of Lyme disease via breastfeeding has not been documented.
PREVENTION Reducing the risk of tick bites is one obvious strategy to prevent Lyme disease. In endemic areas, clearing brush and trees, removing leaf litter and woodpiles, and keeping grass mowed may reduce tick exposure. Application of pesticides to residential properties is effective in suppressing tick populations, but this may be harmful to other wildlife and to humans. Erecting fences to exclude deer from residential yards and maintaining tickfree pets may also reduce exposure.
Tick and insect repellents that contain n, n-diethylmetatoluamide (DEET) applied to the skin provide additional protection but require reapplication every 1 to 2 hours for maximum effectiveness. Serious neurologic complications in children from either frequent or excessive application of repellents containing DEET have been reported, but these are rare and the risk is low when these products are used according to their labeling.l The use of products with concentrations of DEET greater than 30% is not necessary and increases the risk of adverse effects. DEET should be applied sparingly only to exposed skin, but not to a child's face or hands or skin that is irritated or abraded. After the child returns indoors, skin that was treated should be washed with soap and water.
Permethrin, a synthetic pyrethroid, is available as a spray for application to clothing only and is particularly effective because it kills ticks on contact. Because most individuals (approximately 75%) who recognize that they were bitten by a tick remove the tick within 48 hours, the risk of Lyme disease from recognized deer tick bites is low, approximately 1% to 3% in areas with a high incidence of Lyme disease.1 Indeed, the risk of Lyme disease is higher for unrecognized bites, because these ticks feed for a longer time. Parents should be taught to inspect themselves and their children's bodies and clothing daily after possible exposure to ixodid ticks. An attached tick should be grasped with medium-tipped tweezers as close to the skin as possible and removed by gently pulling it straight out. If some of the mouth parts remain embedded in the skin, they should be left alone, because they usually are eventually extruded. Additional attempts to remove these parts often result in unnecessary damage to tissue and may increase the risk of local bacterial infection.
Analysis of ticks to determine whether they are infected is not indicated because the predictive value of such tests for the development of disease in humans is unknown. A recent study of antimicrobial prophylaxis for tick bites among adults found that a single 200-mg dose of doxycycline was 87% effective in preventing Lyme disease, although the 95% confidence interval around this estimate of efficacy was wide.
In this study, the only individuals who had Lyme disease had been bitten by ticks in the nymphal stage that were at least partially engorged. The risk of Lyme disease in this group was 9.9% (among recipients of placebo ), whereas it was 0% for bites by all larval and adult deer ticks. Unfortunately, the expertise to identify the species, stage, and degree of engorgement, and thereby assess the degree of risk, is rarely available to individuals who are bitten. Consequently, routine use of antimicrobial agents to prevent Lyme disease in individuals who are bitten by a deer tick, even in highly endemic areas, is not generally recommended because the overall risk of disease is low (1% to 3% ); only doxycycline, which is not routinely recommended for children younger than 8 years, has been shown to be effective; and treatment for disease, if it does develop, is effective.16
Serologic testing for Lyme disease after a recognized tick bite also is not recommended. Antibodies to B. burgdorferi detected at the time of the bite reflect a false-positive test result or an earlier infection with B. burgdorferi. Likewise, in this setting, the predictive value of a positive result of a follow-up test is low.
VACCINES A vaccine for Lyme disease that uses recombinant outer surface protein A (rOspA) as the immunogen is approved for individuals 15 to 70 years old.17.18 The vaccine contains 30 .ug of purified rOspA lipidated protein combined with 0.5 mg of aluminum adjuvant. The efficacy of the vaccine in preventing clinically apparent disease after two doses was 49% (95% confidence interval, 15% to 69% ) in the first year.18 After a third dose, the efficacy was 76% (95% confidence interval, 58% to 86% ). Three doses of the vacci11e are required for optimal protection in adults; the second dose is given 1 month after the first dose and the third dose is given 12 months after the first dose. Preliminary data suggest that other immunization schedules (eg, 0, 1, and 6 months or 0, 1, and 2 months) are safe and induce antibody responses similar to the 0-, 1-, and 12-month schedule. However, only the 0-, 1-, and 12-month schedule is currently approved by the Food and Drug Administration. The rOspA vaccine has a unique mode of action. OspA is expressed by B. burgdorferi that reside in the midgut of the tick; expression of OspA is later downregulated in response to a blood meal. Because ticks must become engorged with blood before they transmit B. burgdorferi, the human host who becomes infected with B. burgdorferi has little exposure to the OspA protein (at least in the early stages of infection). When an immunized host is bitten by an infected tick, the host's vaccine-induced antibodies against OspA are ingested during the tick's blood meal. Antibody-dependent killing of B. burgdorferi occurs within the tick, thereby preventing transmission to the host. However, because the host is not directly exposed to the OspA antigen, boosting of the immune response to OspA through natural exposure does not occur. Consequently, it is likely that additional booster doses of the rOspA vaccine will be needed to maintain immunity. The most frequently reported adverse side effects of the vaccine are pain, redness, and swelling at the site of the injection. These are usually mild and self-limited.In prelicensure studies, there was no evidence that the vaccine exacerbated prior Lyme arthritis, caused neurologic disease, or caused arthritis in subjects, including those with a history of Lyme disease. Currently, the rOspA vaccine is not approved for children younger than 15 years, but the Food and Drug Administration is considering an application for approval in this age group. The decision to recommend the Lyme disease vaccine should be based on a determination of the individual's risk of Lyme disease, which depends on the likelihood of being bitten by ticks infected with B. burgdorferi.
For most individuals, even those who live in endemic areas, the overall risk is relatively low. The potential benefits of the vaccine ( compared with other protective measures, including early diagnosis and treatment of Lyme disease) should be considered, as should the costs and adverse side effects of the vaccine. The Lyme disease vaccine does not protect all recipients from infection with B. burgdorferi and provides no protection against other tick-bome diseases. Therefore, vaccinated individuals should continue to practice personal protective measures against tick bites.
LYME HYSTERIA A panel of experts who developed clinical guidelines for treating patients with Lyme disease for the Infectious Diseases Society of America concluded that there is no such diagnostic entity as "chronic Lyme disease."12 This contention is supported by clinical trials that found that long-term treatment with antimicrobials was not effective for patients who believed that they had chronic Lyme disease.13 In some of the original reports of Lyme disease, the proportions of patients who also had nonspecific symptoms such as arthralgia, myalgia, headache, or fatigue were substantial. Of course, all of the patients in those reports also had specific objective signs (eg, erythema migrans, facial nerve palsy, or arthritis) that are associated with Lyme disease. Nevertheless, some have erroneously inferred that nonspecific symptoms can often be the sole manifestation of Lyme disease. The nonspecific symptoms sometimes attributed to Lyme disease are highly prevalent in the general population and can be caused by common ailments such as viral infection, anxiety, or depression. Nevertheless, the idea that Lyme disease might be the cause of nonspecific symptoms alone, without any objective signs of the illness, has been publicized by patient-advocate groups and augmented by misinformation in the lay press and on the Internet. In some instances, anxious (often misinformed) parents are driven by the fear that their child's nonspecific complaints may be a manifestation of Lyme disease, which, if not detected and treated, could lead to serious, chronic disability. As mentioned previously, there is a large body of evidence that Lyme disease rarely causes long-term problems.19 Although long-term problems have been documented, they are extremely rare and have occurred almost exclusively among adults with objective evidence of Lyme disease, most of whom either were not treated with antimicrobials or received treatment only many years after the onset of Lyme disease.
Nevertheless, physicians in referral centers who specialize in Lyme disease continue to be inundated with patients who are thought to have, or who believe they have, chronic Lyme disease. Reports from such centers indicate that in most instances the patients either do not have Lyme disease or the symptoms that led to the referral are not due to Lyme disease.2� The challenge for physicians who are faced with such patients or their parents is to be able to address their concerns without dismissing them. Sometimes, a parent's anxiety about a child's behavior can be allayed by reassurance. In other instances, a parent may insist that the child is ill, although objective signs of organic illness are not present. Helping such patients obtain the type of assistance they need without alienating them may be difficult. Sometimes this can best be accomplished by explaining that you simultaneously want to assess the possibilities of both organic and behavioral causes of the problem.
REFERENCES 1. Shapiro ED, Gerber MA. Lyme disease. Clin Infect Dis 2000;31.533-542. 2. Centers for Disease Control and Prevention. Lyme disease-United States, 1999. MMWR. 2001;50.181-185. 3. Nadelman RB, Nowakowski J, Fish D, et al. Prophylaxis with single-dose doxycycline for the (rest of the refs not available)
[ 29. November 2005, 08:41 AM: Message edited by: lou ]
Posts: 8430 | From Not available | Registered: Oct 2000
| IP: Logged |
Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
Sickening, maddening drivel.
Thanks for posting, Lou.
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
| IP: Logged |
posted
So infuriating to read this....especially when you know the guy has made megabucks from insurance companies.
I thank the good Lord that my grandson ended up with Dr. Jones and not this self-serving nitwit! His treatment started at age 5....he is now 12, and has been off antibiotics for one year and is doing fine!
Wonder how many kids' lives have been saved by this bird.
-------------------- nan Posts: 2135 | From Tick Country | Registered: Oct 2000
| IP: Logged |
NP40
Frequent Contributor (1K+ posts)
Member # 6711
posted
Anybody send this drivel to Doc J's lawyer ? How can it not be a conflict of interest to have him sit in judgement of Doc J. ?
Posts: 1632 | From Northern Wisconsin | Registered: Jan 2005
| IP: Logged |
WildCondor
Unregistered
posted
What a jackass. I love how he makes up these percentages, and statistics. Just try to picture him out in his biohazard suit actually studying ticks...probably cry like a little baby, make some Lyme infected breast milk would help soothe his pathetic ego. VOMIT!
IP: Logged |
posted
Yes, I could vomit now.....except I'm too damned angry
.......there is no evidence that children with any manifestation of Lyme disease benefit from either prolonged (greater than 4 weeks) or repeated courses or oral or parenteral antibiotics......
It is quite obvious he's not visited with Dr. Jones!!!!!!!!!!!!!.....he's severely lacking in his lyme literacy
The medical literature is out there if one searches for it.....quite obvious he does not want to know about it.
Gail
-------------------- Strength does not come from physical capacity. It comes from an indomitable will ~ Gandhi Posts: 562 | From Wellsville, PA, USA | Registered: Jan 2004
| IP: Logged |
posted
either in the pre-ssri-era, or pre-1972 psychiatric/psychoanalytic nosology of the expression, "character structure," statistically, the "schizoid character" structure was found to be SIGNIFICANTLY represented by those holding Ph.D.s (note 1).
obtaining a Ph.D. necessarily requires the highest level of intellectual functioning. in many cases,early on in life, the schizoid escaped to, and developed the realm of the intellect, thereby escaping from(avoiding) the emotional-social and physical-instinctual spheres of life.
because it almost exclusively engages intellectual functioning to the exclusion of the emotional-social and physical-instinctual spheres of life,research is one area ideally suited to the schizoid character structure.
what happens to the research subject is of little, if any, concern to the researcher. the research is more important to the researcher than the subject of the research.
the schizoid character structure has a better degree of felcitous 'integration' of the thinking-spiritual, emotional-social, and instinctual-physical realms of existance, than the schizophrenic, wherein the latter, there is a complete split-off of these realms of existence from one another; however, given particular kinds of stressor(s), and the intensity, and duration of these stressors, the schizoid can become schizophrenic.
when it comes to medical research on people, in particular babies, AND, given the past, current and apparent promise of more of the same treatment/lackthereof, by shapiro, et.al. whose data is at such an extreme variance with the overwhelming pubmed studies, studies published in peer-review literature, and the realities of tick(insect-borne illness(-es) as to be insubstantive, perhaps someone other than his patients and their parents, and frontline doctors needs to be examined----psychiatrically.
1) it is NOT the case that all who hold a Ph.D. are schizoid character types.
Posts: 2708 | Registered: Feb 2005
| IP: Logged |
posted
Here's another one on Shapiro doing grand rounds.
Phylis Mervine found this one...am printing it here...and to think he is teaching doctors about this disease! Sorry for the length, but it is very telling about this weasel. I would guess this one is definitely in the hands of Jones' lawyer.
Lucille Packard Children's Hospital Stanford Medical School
Grand Rounds Presentation Transcript
September 24, 2004
About 50-60 pediatricians, residents, and other MDs were in attendance. It was open to the public.
Lyme Disease: The Truth About Ticks
Eugene Shapiro, MD
Prof. Pediatrics, Epidemiology and Investigative Medicine
Yale University School of Medicine
This is a picture of the tick that transmits Lyme disease giant photo of a tick under an electron microscopic. This is another picture of the same tick photo of very small tick on a blade of grass. And the difference between this one and this one is simply perspective.
And one of the problems about Lyme disease is that many people have really lost perspective about this illness. And hopefully today we can bring a little perspective to it.
Today I'm going to talk a little about the etiology of it. You'll probably learn more than you'll ever want to know about ticks. About the clinical features of Lyme disease. Quite a bit about diagnosis, which is one of the one big bugaboos. And I may or may not get to much about prevention.
So Lyme disease is caused by a spirochetal bacteria, called Borrelia burgdorferi. Bb. In the Northeast and upper Midwest, where most Lyme disease occurs, the vector is always Ixodes scapularis, the black-legged tick. It's also called the deer tick, for reasons I'll explain later. On the Pacific Coast, Ixodes pacificus tick, which looks the same, called the Western Black-legged tick, is the vector for Lyme disease. You can sometimes find the spirochete in a few other ticks, but those ticks cannot transmit it to humans.
But the natural reservoir for Bb is really small mammals, like the white-footed mouse in the Northeast and Upper Midwest. And other small mammals may serve as reservoirs. Birds may contribute to spread to new areas when the ticks attach to them and the birds migrate. Deer are not competent hosts for the bacteria. So bacteria don't live in the deer. But the deer are important for the lifecycle of the tick, at least in the East. Less so, probably in the West.
On the Pacific Coast, lizards are the main hosts for Ixodes pacificus, and lizards not only have a low rate of infection, but - I was reading about this in preparation for this talk - but as I'll show you, they actually seem to kill the bacteria in the ticks that feed on the lizards. The wood and kangaroo rats, which are present here in California, as well as white-footed mice, do serve as a reservoir for Bb on the West Coast.
Slide of 4 stages of tick development
So here is a picture of the different stages of the life cycle of the tick. The larvae -- and the larvae are born uninfected, as you'll see - the nymph, which is the stage that is most likely to transmit it. You'll notice it has 8 legs. These are actually arachnids, related to spiders. The adult male and adult female, if you forget, I do have the life cycle on my tie. And you can see the red color of the tick of the adult female is actually the adult female color before they've fed. But here's the real culprit - this is a little mouse - and you can see the ticks that are attached to the mice.
Picture of a mouse with dozens of nymph ticks on its ear.
And the mice serve as reservoirs, and the ticks become infected by feeding on these mice. And it doesn't have to be a mouse that's limping across the field. These mice can be spirochetemic for long periods of time, and at the same time asymptomatic. In fact, there's evidence that there's a chemo-attractant between the mouth parts of the tick and the bacteria in the bloodstream of the mice.
Picture of Bb lifecycle: mouse-tick-deer circle
So this is a picture of the lifecycle of the Western Black-Legged tick. It's a two-year lifecycle. The female tick lays its eggs, and the larvae are born uninfected. And they feed once at each stage of their cycle. And they "quest" - they get on blades of grass and they have little sense organs under their legs and they glomp onto a host when it comes by. And it takes hours for the mouth parts to implant. It's not like the bite of a mosquito or something. They also elaborate enzymes that break down mediators of inflammation like Bradykininases. So the bites are painless. You don't feel them. So the larvae will feed. And it might feed on a mouse. And it might become infected. Or it could feed on a lizard, and the lizards aren't infected, so that it might not become infected. So then it molts, and emerges.
The larvae are usually born in the late summer or mid summer. After they feed, they spend the winter somewhere in the ground and they emerge in early spring as nymphal stage ticks. And the nymphs, again, may feed on any of these hosts or they feed on a human, and if it became infected at an early stage of its lifecycle, it might transmit it to humans. They drop off and molt and become adults usually in the fall and winter. And again in the winter they feed on any of these hosts. They particularly like deer. They like large deer hosts, and that's why it's called the deer tick in the East. Hunters back in the East find lots of these attached. And again they may feed on humans. Then they die and the two year life cycle begins again.
LYME DISEASE: Proportion of Ticks Infected with B. burgdorferi
Tick Nymphs Adults
Ixodes scapularis 20-25% 40-50%
Ixodes pacificus 3-8% 1-2%
But what's important to realize, is that there's a huge difference in infection rates from the East and Midwest and the West Coast. So with scapularis on the East Coast, about 20-25% of the nymphal ticks are infected, whereas with Ixodes pacificus, it's 3%, maybe 8% infected. You might find in some areas 10% or 12%, but many areas it's fewer than that. And the adult ticks in the East they can become infected in each stage of the life cycle, so of course the adults have a higher rate of infection.
It turns out, interestingly enough, on the West coast, the Ixodes pacificus adults have a lower rate of infection, and the reason for that is that when they feed on these Western Fence lizards and other lizards, it seems to kill the bacteria in the gut. So very few of the adult ticks are infected because they actually feed on lizards that seems to kill those that are infected at an earlier stage of development.
Picture of an engorged I. dammini nymph tick, a little bigger in diameter than a head of a pin.
This gives you an idea of the size of these things. This is an engorged Ixodes pacificus next to the head of a pin. So these are nymphal stage ticks. So these nymphs are quite small, as you can see, and difficult to detect.
Picture of engorged and engorged female adult ticks.
Now this is an adult female tick, engorged and unengorged. So they can become quite large and actually feed. And they can become as large as adult ticks.
But you can notice this little scutum hard plate on back of tick's neck that doesn't change in size. You can actually estimate how long the tick has fed based on the weight and the scutum index, which is the ratio of the length of the entire tick to the distance to the scutum.
CDC US Map of Lyme distribution
So here's a map of reported cases of Lyme disease by county in the U.S. This happens to be for the year 2000, but it would be virtually identical for any year. And you can see the darker colors have the higher rates. Most ld occurs in Southern NE and the Eastern Midatlantic states. And there's a little pocket in Wisconsin and Minnesota. A little bit in Michigan.
Pointing to Death Valley on the CDC Lyme surveillance map
California. This is ridiculous. This is the desert here. But if some nut reports a case of Lyme disease, it gets included. But most of the disease in California is up in this area Mendocino County on the West Coast. But there really isn't much.
Notice, here's Colorado. I don't think there were any cases reported this year.
O.K. What are the clinical manifestations of Lyme disease? They can be divided into 3 categories:
1.. Early localized disease 2.. Early disseminated disease 3.. Late disease
In early localized disease, it's simply erythema migrans EM, which by the way may be completely asymptomatic. It may be associated with headache or fever. It may itch and occasionally it may be painful, rarely.
Picture of erythema migrans rash
And what you hear . This is someone's back. It's actually called erythema migrans. It actually starts out as a macule at the site of the tick bite. Then it enlarges or migrates. And without treatment it will continue to enlarge for a week. And people talk about central clearing and the bull's-eye clearance, and this is an example of this on somebody's back. But really more commonly it's really uniformly erythemytis. So don't think that since it's not cleared in the center that it can't be Lyme disease. It can be.
The other thing I point out is that it's not perfectly round. It's often somewhat eccentric in its shape. But this again is someone's back.
Picture of submarine-shaped rash, 1/2 way around a midriff, solid red.
Here's another one. This is one on a child's abdomen. You can see if a kid comes in with a fever, you might think it's cellulitis very easily.
Erythema migrans rash with rough edges and necropathy in center
And this is actually on the leg of a teenager. I happened to be attending in the ER the night this kid showed up some years ago. Chief complaint was fever, headache, and by the way I have a rash.
Pointing to dark center of erythema migrans rash
These are vesicles, and they thought the kid had shingles. And indeed if you just saw these vesicles you'd think that. But look at this large area of erythema around it. That would never happen with shingles. What this is vesicular erythema migrans and occasionally you may have vesicles or some small necrotic area in the center of the rash where the center of the rash, where presumably where the bacteria are injected by the tick. This child subsequently developed Bell's palsy and seroconverted, actually.
DIFFERENTIAL DX of ERYTHEMA MIGRANS
1.. Eczema (nummular) 2.. Ringworm 3.. Cellulitis 4.. Granuloma annulare 5.. Spider bites or other bites 6.. Erythema multiforme
So the differential diagnosis of erythema migrans. The main things that it gets confused with is eczema nummular and ringworm. Ringworm tends to be scaly and raised on the edge, which erythema migrans is not.
Cellulitis. Granuloma annulare. Spider bites and other bites. And if you have multiple erythema migrans, it can be confused as erythema multiforme.
So if you have someone who you think might have erythema migrans, but you're not certain, there's no harm in waiting and watching for a couple days. If it's erythema migrans and untreated, it's going to be there for awhile. If it's gone in a day or two, it isn't erythema migrans.
This is a picture of multiple erythema migrans. Sometimes the primary lesion will be larger than others and then you'll see smaller ones. Here's another one with the child with multiple erythema migrans. Again, you'll notice that they're not perfectly round. And what this represents is a spirochetemic spread of the bacteria to multiple sites in the skin. If you biopsy and culture these, you might grow bacteria, and you might even grow bacteria in some of the apparently uninfected skin. And typically when you have multiple erythema migrans, these kids are mostly going to have fever, and flu-like symptoms and be ill. And this is the common manifestation of disseminated Lyme disease in the U.S., and I'll show you the percentages later on.
Now can a flu-like illness alone be caused by the manifestation of Lyme disease? Yes, it probably can, but in my opinion, that's not a diagnosable condition. Because, if you send Lyme titers for every person with a flu-like illness, for everyone that you accurately diagnose, there are going to be thousands that you're going to call Lyme disease that don't really have it. So, I never try to diagnose Lyme disease with a flu-like illness, because there are too many false positive tests. And we'll talk about that in a moment.
But I think it's quite uncommon, and if you don't treat them either, they'll spontaneously get better or they'll develop arthritis or some later manifestation. And you'll treat them then, and they'll be fine. Other manifestations of early disseminated Lyme are aseptic meningitis, neuritis, and particularly the 7th nerve palsy, and carditis, which is quite rare. And that usually manifests itself as some degree of heart block.
Just a word about meningitis. It's quite uncommon. Clinically it presents like meningitis, but it tends to be of much longer duration. So in the summer in the Northeast, enteralviral (sp?) meningitis is far more common than Lyme disease. So I don't start looking for Lyme disease on every kid who comes in with aseptic meningitis, but when it's lasted for a week or 10 days, or longer, without any improvement, then you start thinking about Lyme Disease. Or if they happen to have the erythema migrans or come in covered with ticks.
LYME DISEASE: Early Disseminated Disease
1.. Meningitis 1.. uncommon 2.. clinically presents like aseptic meningitis but of long duration 3.. Papillodema common
The other thing that is rather common, for reasons that aren't clear with Lyme is papillodema. Nearly 20-30% of children with meningitis will have papillodema. Then I'd start thinking about Lyme.
LYME DISEASE: Early Disseminated Disease
2.. Seventh-nerve palsy 1.. Relatively uncommon 2.. Unaffected by treatment 3.. Do not use corticosteroids 4.. Complete resolution is the usual outcome
7th nerve palsy is relatively common. It's unaffected by treatment. So we don't treat children with palsy due to Lyme disease to make the palsy get better faster or more completely. The reason we treat it is to treat late Lyme disease. Do not use corticosteroids. It certainly doesn't help, and there are some early studies, mostly in adults, that 3 or 4 adults who didn't do as well happened to get corticosteroids.
Clearly it's not beneficial. Complete resolution is the usual outcome with seventh-nerve palsy due to Lyme disease. Once in awhile there might be some residual and very, very rarely some residual. And usually it gets better with or without treatment.
LATE LYME DISEASE
1.. Arthritis 1.. The knee is affected >90% of the time 2.. Mono- or pauci-articular 3.. Duration of arthritis is variable 4.. Usually resolves completely with treatment, though it may recur 5.. Chronic/recurrent arthritis is associated with HLA-DR4 (and DR2) allotypes.
Late Lyme disease. I used to have late neurological Lyme on this slide, but I took it off because I've never seen a child with late neurological Lyme. It has been described in adults, mostly in more elderly adults who had objective evidence of Lyme disease but were not treated for many, many years. And those people - it's extremely, extremely rare. It does respond to treatment but, it's not something we see in kids, so I took it off the slide.
But we certainly do see arthritis. In Lyme arthritis, the knee is affected more than 90% of the time. Why that is, I don't think anybody knows. It's a mono or pauci-articular arthritis, the duration is variable. It may come and go away without treatment. I saw one kid who had a swollen knee for six months before he came to the doctor.
So it's usually sub acute, and often they'll think, "Oh, he fell off his bicycle or a treat branch whacked his knee while we were out walking. And that's the cause of it. But it can be very sub acute. Occasionally it can present like an acute bacterial arthritis. But, in any case, the arthritis usually resolves completely with treatment of orally administered antibiotic, thought occasionally it may reoccur. There is a chronic recurrent arthritis that seems to be an autoimmune phenomenon triggered by an infection that isn't treated promptly, and it occurs only with patients with certain DR4 and DR2 allotypes. It's very rare in kids. We've seen it in adults, but very clearly it's rare. But that recurrence of arthritis seems to be an autoimmune phenomenon. It's not that the antibiotics could not adequately eradicate the bacteria.
Timeline of Lyme disease
Week 1-2: Flu
Week 2: Cardiac, secondary skin, early neurological
Week 3-12: Arthritis, late neurological
This is a time course of Lyme disease. So erythema migrans flu-like symptoms usually occur in the first month, typically 7 to 14 days after the bite. It could be up to a month afterwards. Early disseminated disease occurs anywhere from 3 weeks to 2, 2 and a half months afterwards. And late Lyme disease - I should've crossed out the "late neurological" - can go from anywhere 6 to 8 weeks. So we'll see kids in March who were obviously infected sometime in the previous summer or fall.
Newspaper ad
Recurring Symptoms Getting Worse?
Muscle or joint pain
Chronic fatigue
Upset stomach
Disturbed sleep
Dizziness
Fevers, chills sweats
Sever headache
Stiff neck
Memory loss
Mood swings
You may have Lyme disease, a debilitating but treatable bacterial infection transmitted by the deer tick. You can pick up a tick in a wooded area and shore areas, even from your cat or dog. Lyme disease symptoms mimic lifestyle problems and other illnesses, which complicate diagnosis. Our center is a complete Lyme disease resource. Skilled registered nurses will provide you with information or direct you to a physician in your area specializing in Lyme Disease and a support group. You can be helped. Call now.
The Lyme Care Center
1-800-TICK-BITE
End of newspaper ad
So here's an ad that appeared one day in the New Haven Register. It occurred on the obituary page, by the way. laughter It says, symptoms getting worse, muscles or joint pains, chronic fatigue, mood swings. You may have Lyme disease, a debilitating but treatable bacterial infection. Lyme disease symptoms mimic lifestyle problems. You can be helped, call now.
And you can call and they list Madison, CT as the location, which is a suburb of New Haven. But it turns out if you call this number you get connected to someone that is sitting in an office in NJ that's supported by a home IV infusion company, and no matter what your symptoms, they'll refer you to the local doctor that happens to be Dr. Jones in the New Haven area, who . Dr. Jones by the way once diagnosed a teenage who attacked a cat with an ax, diagnosed this as chronic Lyme disease over the telephone. I kid you not. I was involved with the court case. And they will refer you to the operator who will undoubtedly tell you that you need treatment. Probably long term treatment, and they'll help arrange for the IV therapy.
Here's another ad: "Do you have unexplained symptoms. Have you had the following? -and they list every symptom known to man. laughter
Wait a second. Look at this: a Lyme disease support group in Colorado. Remember how many Lyme cases we had in Colorado every year? It's probably one case a year, and they probably vacationed on the Cape.
You know, so what's going on? The amount of anxiety and angst over this is incredible. Just let me tell you. You can't believe the stuff I get in my emails. Here's an email that I got one day. You'll notice that it's from RedNeck5. I can't wait to hear from RedNecks one through four. laughter
Redneck Email
I heard your public comments and they make me mad. You could not handle the pain, because your Yale pansy *** could not handle it.
If there is no such thing as Chronic Lyme, why don't you inject Lyme into your body and see if you're right? And please respond.
Redneck Email end
And I can tell you this anxiety gets to not only the patients.But let me show you a picture of me before I got involved with Lyme. [Has a bushy head of hair and beard. He's bald now.
So, what is it about these non-specific symptoms of Lyme?
LYME DISEASE: Nonspecific Chronic Symptoms
1.. Nonspecific symptoms associated with Lyme disease 1.. Fatigue 2.. Arthralgia 3.. Myalgia 4.. Headache Never the ONLY manifestation of Lyme disease.
Nonspecific subjective symptoms accompany OBJECTIVE signs of Lyme disease
Has anyone in this room had these symptoms in the last three months? How about the last three minutes? Sure. Do people with Lyme disease get these? Sure they do, but it's never the only manifestation of Lyme disease. These non-specifics symptoms accompany OBJECTIVE signs of Lyme disease. So, sure you may have a swollen knee and feel tired, but you may have a headache and erythema migrans. If all you had is a headache or aches and pains, it ain't Lyme disease. And we'll come back to that.
"CHRONIC" Lyme Disease
Clinical Trial of Treatment
1.. Randomized double-blind trial of "long-term" treatment with antibiotics 1.. Sponsored by the NIH 2.. Enrolled patients with a "history" of Lyme disease and subsequent chronic symptoms 3.. Stratified into those seropositive or seronegative at time of enrollment 4.. Received either ceftriaxone IV for 4 weeks then 8 weeks of doxycycline PO or placebo IV for 4 weeks then 8 weeks of placebo PO
The NIH. Some of these Lyme disease support groups really put a lot of pressure on us. And the NIH is really under pressure by lawmakers to do something to study this problem. So there was this problem trial looking at treatment of chronic Lyme disease sponsored by the NIH. It's a double-blind trial of long term treatment of antibiotics. Patients were enrolled with a history of chronic symptoms. Most of these patients had already been treated for an average of something ridiculous, like 4 months. And they were enrolled and stratified into those who were seropositive or seronegative at time of enrollment. And the patients in each of these trials received either ceftriaxone IV for 4 weeks then 8 weeks of doxycycline orally, or placebo IV for 4 weeks, then 8 weeks of placebo PO in a double-blind manner.
"CHRONIC" Lyme Disease
Clinical Trial of Treatment
2.. Independent data safety and monitoring board 1.. Stopped the clinical trial early before full enrollment had been competed. 2.. Virtually no difference in proportions of treatment and of placebo groups that improved, worsened or were unchanged reported symptoms were rather labile - about 1/3 improved and 1/3 worsened. 3.. Concluded that the chance of finding an effect of treatment, even with full enrollment, was virtually nil.
Now there was an independent data-safety monitoring board that stopped the trial early, before full enrollment had been completed. And the reason was that there was virtually no difference in the proportions of treatment and placebo groups that improved, worsened or unchanged. It's not that the symptoms didn't change. They were actually rather labile. About a third changed, a third worsened, and a third stayed the same. It's just that it didn't matter if you got an antibiotic or a placebo. And they concluded even if they reached full enrollment, the chance of finding an effective treatment was virtually nil, it was something like 3%.
So clearly, these patients were sick. They had problems. It's just that antibiotic deficiency was not one of them. laughter.
New Yorker-style cartoon of patient in the hospital with a lime over his head. I don't know if you can read this, but, "It's one of the hardest ailments to detect, but I think you have Lyme disease."
LYME DISEASE: Diagnosis
1.. Clinical Diagnosis 2.. 2. CDC Criteria 1.. Physician-diagnosed erythema migrans >/= 5 cm 2.. One or more clinical manifestations of early disseminated or of late Lyme disease plus positive serology.
And that's really the big bugaboo with Lyme disease - diagnosis. Now, people will tell you it's a clinical diagnosis. It is. But the CDC have criteria for epidemiological purposes, and it turns out that those criteria are pretty good to use clinically. And those criteria are physician-diagnosed erythema migrans of at least 5 cm. Or One or more clinical manifestations of early disseminated or of late Lyme disease plus a positive serology
Clinical manifestations mean objective findings. And one of the things that people get confused about is that arthralgia is not an objective manifestation. Swollen knee joint - objective evidence of inflammation of the joint - is. But arthralgia is not, and is very common.
Now these are the objective manifestations. And if someone told me that they got bitten, right here, and a week later they developed this rash, and it looks like a erythema migrans rash, but it's only 4cm, I wouldn't say, "Oh, no. It's not Lyme disease." But in general, these are pretty good criteria.
LYME DISEASE: Tests for Antibody
1.. Immunofluorescent antibody IFA 2.. Enzyme-linked immunosorbent assay ELISA 3.. Western immunoblot
The problem is that if they don't have the rash, we end up having to use the antibody test to make the diagnosis. And tests for antibodies include IFAs assay, which nobody does anymore except for Stanford.
Someone in the audience, objects
"Oh, is it an ELISA? Because I thought I saw IFA on the report I just read."
Clarification from transcriber: Stanford still uses the IFA.
But most places do an ELISA, which is a quantitative test, followed up with a Western Blot, which is a qualitative test.
PROBLEMS WITH ANTIBODY TESTS
1.. Enzyme-linked immunosorbent assay ELISA
And the ELISA measures a crude mixture of antigens. Basically you grind up the tick and you put it a plate. It sticks to the wells, you pour in the serum, and if people have the antibody, it sticks to the antigens of the bacteria. Then you use a marker system to measure the quantity of antibody that's present. The problem is that it's poorly standardized, especially commercial kits. Reactivity to cross antibodies are quite common.
PROBLEMS WITH ANTIBODY TESTS
2.. Western Immunoblot 1.. Measures antibodies against specific protein antigens 2.. Cross-reactive antibodies 3.. Controversy about minimal criteria for positivity 4.. Reports of results often confusing and frequently misinterpreted
The Western immunoblot, on the other hand, measures antibodies to specific antigens. So you take the same crude preparation. You put it on a gel and you put a charge across it. And the proteins move different distances depending on their molecular weight, then pour the patients serum on, and if they have antibodies, they stick, and you use a marker system. And it makes a band if at that site, if the patient has antibody against that specific protein. The problem is the controversy for minimum criteria for positive reactivity. So clearly if you have ten reactions against 10 antibodies, yes, that's a positive test. But what if it's 4 or 5? Generally people say that for IgG, you need 5 positive bands, and ideally some of the more low specific molecular weight.
The criteria for IgM positivity I think is extremely liberal. You need only 2 of any 3 bands. And false IgM tests are extremely, extremely common, including Western Blots. And people say that you should never make a diagnosis on Lyme disease based solely on IgM. Especially when someone has had symptoms for more than a month.
And the other problem with this is that the reports of results are often confusing and misinterpreted. So people will look at it and say, "Oh yes. It's a positive band at 41 so and 29 positive bands, so it's positive, but actually it's negative, because you need 5 to be positive. And it's only 2. So it's frequently misinterpreted.
LYME DISEASE: Serologic Tests
1.. Antibodies may be bound in immune complexes early in the course of the illness 2.. Early treatment with antimicrobials may ablate the antibody response 3.. Once antibodies develop, they may remain positive indefinitely.
There are other problems. Antibodies may be bound in immune complexes early in the course of the illness, so that . Remember I showed you that usually you see the rash 7 to 14 days after the bite? Well, the antibodies usually aren't detectable for 3 to 4 weeks afterwards. So if you get an antibody test from someone with a erythema migrans, and it's negative, that's normal. And most people with a erythema migrans will not have a positive antibody test, so you shouldn't send a test in on someone with a erythema migrans. Furthermore, early treatment with antimicrobials will further ablate the response. So if you treat somebody for erythema migrans, don't get another test in a month to see if they really had Lyme disease, because even if it truly was Lyme disease, it really could be negative.
Once a person's been treated for Lyme disease, it'll remain positive indefinitely.
Now this seems like a simple concept. But people have this misconception that the antibodies are a sign of disease activity.
If you had a headache, nobody would walk into an office and say, "Ah, ha! Your measles antibody is positive. You've got measles." But God forbid you should have a positive antibody for Lyme disease. You know, you walk across the street and say, it's Lyme disease. People are ready to attribute anything to Lyme disease.
LYME DISEASE: Serologic Tests
4.. IgM Antibodies to B. burgdorferi 1.. False-positive tests common 2.. True-positive test may persist even after treatment and cure of the disease 5.. Western immunoblot does not = "truth" 1.. Generally should not be used instead of ELISA 2.. False-positive tests not uncommon
So the way you. and I often get calls, "Well, I had this child with Lyme arthritis, and I repeated the antibody test, and it's higher than it was. What do I do?"
Well, how's the knee?
"It's all better."
Well, that's how you tell if it's all better. Not by the Lyme titer. And these titers, by the way, are not all that reproducible. I would not ever look at a titer from time A and compare it to time B, and say it's high on time B, so therefore .. Because unless it's run in the same batch, there is a lot of variability from batch to batch. So you never want to do that.
IgM antibodies for Bb, as I said, false positive tests are common. True positive tests may persist even after treatment and cure of disease. That's important to realize. People think that IgM has got to be there early in the disease if it's positive. That isn't true.
First of all, there are lots of false positives. Second, there are well documented cases of people with Lyme arthritis who've had positive IgMs who've been treated and cured. IgM can persist for years.
Western immunoblot does not equal "truth". Sometimes we see people only ordering a Western immunoblot, without giving a qualitative test. It should not be used in place of an ELISA. And false positives, even for Western Blots, are not uncommon.
Really, what's recommend is a two step process. First a quantitative test like an ELISA, then if the test is positive or equivocal, then confirm the specificity of the test with the Western immunoblot.
EVALUATION OF SEROLOGIC TESTS FOR LYME DISEASE
1.. Association of State and Territorial Public Health Laboratory Directors and the Centers for Disease Control. 2.. Seven commercial kits with the best concordance with the CDC's own ELISA test. 3.. Four state public health laboratories and the CDC blindly tested 158 reference serum specimens positives and negatives with the seven kits.
And just to show you some of the problems, the State and Territorial Public Health Laboratory Directors and the Centers for Disease Control did a study - and this was some time ago - where they took seven commercial kits with the best concordance with the CDC's own ELISA test, and then they had 4 state health departments and the CDC itself blindly tested 158 reference serum specimens, known positives and negatives, with the seven kits, and what they found, was the mean agreement between laboratories using Kappa - Kappa is a statistical test of agreement.
EVALUATION OF SEROLOGIC TESTS FOR LYME DISEASE
1.. Mean agreement between laboratories Kappa ranged from 0.35 to 0.61 (fair). 2.. Mean agreement between kits (Kappa) ranged from 0.16 to 0.690 (poor to fair). 3.. Mean sensitivity: 26-57% 4.. Mean specificity: 12-60%
That takes into account ?, it goes from 0 to 1. So zero is no agreement, one is perfect agreement. And the mean agreement between laboratories, for the same serum sample, the same kit, but different laboratories ranged from 0.35 to 0.61, only fair.
The main agreement between kits, that is, now we're talking about the same laboratory, same serum sample, different kits, ranged from 0.16 to 0.690 poor to fair. The mean sensitivity was from 26 to 57% . The Mean specificity was 12-60%.
Well, let's give it the benefit of the doubt and say it's 50% sensitive and 50% specific. I have a quarter here in my pocket that we can flip laughter.
And the conclusion - not my conclusion, but their conclusion, too - that the currently available tests to test for antibodies for Bb are very inaccurate. And the use of these tests will result in a high rate of misdiagnosis.
This was done quite a number of years ago. I think the tests have improved somewhat, but there was a paper. they tried to replicate this in Wisconsin, a few years ago, and they found the same thing.
TEST FOR ANTIBODIES AGAINST B. BURGDORFERI
1.. Sensitivity: 95% 2.. Specificity: 90% 3.. Prevalence of Lyme disease in the population pre-test probability
But here's. And what I'm going to say now is the most important thing. if you remember one thing from this talk, besides my tick tie, is remember this. Let's suppose you have a good test. Let's suppose we have a VERY good test for antibody. Let's suppose the sensitivity 95% and the specificity is 90%. Not a bad test. There aren't too many tests that we do that are better than that. But let's suppose that the prevalence of the disease in the population that we're testing is 1%. The pretest probability, OK?
And I can tell you if you test on people with aches and pains and headaches and fatigue, the percentage of those people in California. or even in Connecticut, too, that have those symptoms due to Lyme disease is going to be way less than 1%. But just for the sake of argument, let's take a population of 10,000 people with 1% prevalence of disease.
TEST FOR ANTIBODIES AGAINST B. BURGDORFERI
Test Lyme Disease No Disease Total
Positive 95% 990 1,085
Negative 5% 8,910 8,915
Total 100% 9,900 10,000
So there are 10,000 people. 1% of them, or 100 of them have Lyme disease. The test is 95% sensitive. So 95 will have a positive test, 5 will have a negative test. That leaves 9,900 without Lyme disease. 90% specificity. So there are 990 positive tests. So there is a total of 1,085 positive tests, of which 990 or 91% are false positives. That's if it's 1% prevalence. If it's .001%, which is more likely, this is going to be 99% of your tests are going to be false positives.
This is simply Bayes Theorem. This is not specific to Lyme disease. This is for any diagnostic test. But it is something that patients don't understand, and most physicians don't understand.
LYME DISEASE: Clinical Situation
1.. Patient with non-specific, vague symptoms not likely to be Lyme disease 1.. Antibody to B. burgdorferi: Negative diagnosis: Not Lyme disease 2.. Antibody to B. Burgdorferi: Positive diagnosis: Not Lyme disease 2. Moral: Don't order Lyme titers
So, if you have a clinical situation, where a patient has vague symptoms, not likely to be Lyme disease. Antibody for Bb is negative, not likely to be Lyme disease. Antibody for Bb positive, diagnosis: Not Lyme disease.
The moral of the story is don't order Lyme titers on these patients. I can't tell you how many calls I get every week, where the docs have done this, and they're in this situation.
And I know it's hard because, you know sometimes you have a parent come in who wants the test, because they've been on the Internet. You know that if you don't do it, there're just going to go to someone else. It gets complicated, but .
Photo: Tick Crossing Sign
OK. There are some areas of the country where ticks are a problem.
Photo: Christy Brinkley with pet Guinea Hens
Do you know who this is? Right, Christy Brinkley. Now Christy Brinkley was deathly afraid, and she lived in a big estate on Long Island. She was deathly afraid of getting Lyme disease. So she employed these guinea hens. Lots of these guinea hens that eat ticks supposedly. They spread out on her property to try and eat the ticks. Supposedly she got Lyme disease anyway, the poor thing. laughter
LYME DISEASE: Tick Bites
How should person bitten by a tick be managed?
So, how should a person bitten by a tick be managed?
LYME DISEASE: Tick Bites
1.. Transmission of B. burgdorferi 1.. Proportion of infected ticks 2.. Duration of attachment 3.. Risk substantial i. Infected nymphs: >36-48 hours
ii. Infected adult females: >48-72 hrs
Well, there are a few things. Transmission of Bb is going to depend on the proportion of infected ticks. So, if you're somewhere in California, where 1 or 2 or 3 % of the ticks are infected, the chance of getting infected by this disease is extremely low. But the other thing that's important is duration of attachment. It turns out that there is a lot of evidence that the risk doesn't become substantial with an infected nymphal stage tick until at least 48 hours or more. Adult ticks, 72hrs or more.
LYME DISEASE: Clinical Trial of Treatment for Ticks Bites
1.. Randomized trial in Westchester County, NY 1.. Persons >11 years of age who had removed I. scapularis tick within previous 72 hrs. 2.. Ticks identified by a medial entomologist 3.. Received either 200 mg of doxycycline a single dose or placebo.
And there was a randomized trial done in Westchester County, NY, which has one of the highest risk of Lyme disease in the world. Much, much, much higher than in California.
What they did is enroll people 11 years of age who had removed an I. scapularis tick within 72hrs. Now the ticks were identified by a medical entomologist. Most of you probably don't have medical entomologists in your office, which is a problem we'll talk about in a minute. There are actually studies of ticks submitted by doctors for identification. About a third of them aren't ticks. laughter They're dirt, head lice.
And what they did was treat them with a single dose of doxycycline, 200mg of doxycycline, which is a high dose, double the normal dose. Or placebo in a double-blind manner.
LYME DISEASE: Clinical Trial of Treatment for Ticks Bites
New Infection with B. burgdorferi
Treatment Proportion
Doxycycline 1/235 (0.4%)
Placebo 8/247 (3.2%)
Protective efficacy=87% P<0.05
95% CL: 25-98% lower limit may be 1%
And what they out was that 1 in 235, or 4% of the patients developed erythema migrans that got doxycycline and 8 of 235, or 3.2% of the placebo group got a erythema migrans.
Now, the protective efficacy of doxycycline was 87%. And it was statistically significant. But the confidence level around that was very wide. It was not very robust. Because of the small numbers. It could be consistent with 25% or 1, depending on how you calculate the 95% confidence level, even 1% effectiveness.
But there are some interesting things we can learn from this. One thing is that in the placebo group.actually the doxycycline group, too. The only people who got Lyme disease were bitten by nymphal stage ticks. So overall, there was a little over 5% bitten by nymphal ticks got Lyme disease. If they were at all engorged, it was almost 10%. That means 90% bitten by an engorged tick didn't get Lyme disease. And none of 59 who had flat, unfed ticks got it. Among persons who were bitten by adult ticks, none of 97 and none of 8 who were bitten by larvae got infected.
Furthermore, remember I told you you can estimate how long the ticks have fed by the scutum index? Among the ticks where they could actually estimate how long they've fed, if a nymph fed more than 72 hours, 25% 3 of 12 developed Lyme disease. Whereas, none of 48 developed Lyme disease if the nymph fed for less than 72 hours.
It turns out from studies that most people who recognize that they've been bitten, actually pull the tick off in less than 48 hours. At least 75% who recognize that they've been bitten pull it off in less time.
LYME DISEASE: Clinical Trial of Treatment for Ticks Bites
1.. High risk of minor adverse side effects 1.. A. Nausea/vomiting 2.. B. Doxycycline not given with food 2.. All infected patients developed erythema migrans no asymptomatic seroconverters 3.. Nearly 20% of subjects had another tick bite during the 6 weeks of follow up 4.. Cannot extrapolate to amoxicillin for younger children.
But there were some problems. There were some high risks of minor adverse side effects. Nausea and vomiting was common, and people were driving off the road and puking. This was in part because they didn't give it with food, so if you ever, for any reason, decide to give it, give it with food.
All infected patients developed EM. There were no asymptomatic seroconverters. So all we're doing is talking about preventing a little rash. This isn't AIDS that we're talking about or preventing, folks.
It's not a big deal if you get Lyme disease. It's easy to treat and cure.
Nearly 20% of subjects had another tick bite during the six weeks of follow up. So if you're going to give prophylactic antibiotics, you're going to be giving a lot of antibiotics to these people. You can not extrapolate that a single dose of amoxicillin would work for younger children, though probably doxycycline in one dose isn't going to stain the teeth of younger children, anyway.
As I said, although one dose is effective, the results were not very statistically robust and it could have a much lower than 50% ? specificity. As I said the ticks were identified by a medical entomologist. Most people don't have those. And anyway, here California, the risk of Lyme disease was low. It's only 3%.
The risk is really greater from the tick bite that is not recognized. Where the tick can feed to completion. So if you recognize a tick bite, most people clear it off before it could transmit the disease, even if it is an infected tick.
So watching and waiting is the most reasonable approach.
SUMMARY AND CONCLUSIONS
1.. The risk of developing Lyme disease after a deer tick bite is very low. Even lower in California than in the Northeast. 2.. Routine prophylactic antimicrobial treatment for deer tick bites is not indicated certainly not in California
3.. In summary, the risk of developing Lyme disease after a deer tick bite is very low. And it's certainly even much lower in California than in the Northeast. Routine prophylactic antimicrobial treatment for tick bites of any sort is not indicated and certainly not in California.
What about analyzing ticks? Little is known about the accuracy of testing for Bb in ticks, either the sensitivity, the specificity, or reproducibility of the assays. And anyway, what we're really interested in is what's the risk in the person that's bitten, not whether the tick is infected, per se. It may be, you know, people do PCR tests on these ticks, and conceivably could detect as little as one spirochete in the tick, and maybe you need 100,000 per cc in tick juice before the risk becomes substantial. So, we don't recommend getting assays to see if the tick is infected.
Photo: Tweezers grabbing embedded tick by head.
How do you remove a tick? And you can see there was a letter in the Lancet several years ago, where they said in the Southern hemisphere you should turn it this way, and the Northern hemisphere, turn it that way.laughter All you do is grab tick as close to the mouthparts, the skin, as you can and pull it out. Actually a friend of my at Yale who is a acarologist, people who study ticks, let some lab ticks feed on him, then I pulled it out and videotaped it, and made a CD-ROM for the AAP. So if you want to watch somebody doing it, if some of the mouthparts remain in the arm, do not amputate. laughter
You know you see some kids come in who are hacked up. It's not going to change your risk of getting Lyme disease. It's just a little foreign body. If there's a little mouthpart in there, it'll get extruded. Don't worry about it.
LYME DISEASE: Congenital Disease
1.. Infection of fetus had been documented but congenital DISEASE has not. 2.. No pattern of congenital malformations associated with infection of the mother Prevalence of congenital malformations among offspring of seropositive and seronegative women is similar
What about congenital Lyme disease? Actually infection of the fetus has been documented but congenital Lyme has not. There is no pattern of congenital malformations related to infection of the mother. And the prevalence of congenital malformations among offspring of seropositive and seronegative women is similar.
Mike Erber did a survey of all pediatric neurologists in endemic areas, and none of them had ever seen a credible case. So I think it either doesn't exist, or it's so rare as to not be a problem.
LYME DISEASE
Transmission of Lyme disease via breast milk has not been documented.
INITIAL CLINICAL MANIFESTATIONS OF LYME DISEASE
N=201
Single erythema migrans 66%
Multiple erythema migrans 23%
Arthritis 6%
Facial nerve palsy 3%
Aseptic meningitis 2%
Carditis 0.5%
This just shows you - this is a study we did of 201 consecutive cases of Lyme disease in Southeastern Connecticut. And it just shows you. And you can see that in 66% of children had a single erythema migrans, and only 23% had multiple erythema migrans. So about 90% of children who developed Lyme disease had erythema migrans. 6% had Arthritis. 3% had Facial nerve palsy. 2% meningitis and one child, 0.5% had carditis.
LYME DISEASE IN CHILDREN: Outcomes
1. By 4 weeks after initiation of treatment:
a. All symptoms resolved in 97%
b. Non-specific symptoms arthralgia, fatigue, neck pain present in 3% 7/201
c. By 5 months all symptoms had resolved
d. At follow up a median of 2.5 years later NONE had either chronic or recurrent symptoms
By 4 weeks after initiation of treatment, all symptoms resolved in 97%. So, non-specific symptoms, like arthralgia, fatigue, neck pain, were still present in 3%. By six months, all symptoms had resolved, and at follow up, in a meeting 2.5 years later, none had current or chronic symptoms.
LYME DISEASE: Long-term outcomes
1.. A number of studies have found that long-term outcomes of person treated for Lyme disease are excellent. 2.. When asked about symptoms of problems with normal activities 5-10 years later, 5-40% reported worsening. 3.. Most problems attributed to aging or co morbid illnesses 4.. Frequency of complaints similar among age-matched controls.
A number of studies have found that long-term outcomes of person treated for Lyme disease are excellent. When asked about symptoms of problems with normal activities 5-10 years later, depending on what question you asked, 5-40% reported worsening. Most problems attributed to aging or comorbid illnesses. If you ask me if my memory today is as good as it was 10 years ago, it ain't, but I don't have Lyme disease.
But it turns out that the frequency of complaints are similar among age-matched controls. So there isn't any evidence that Lyme disease is really related to any long term outcome.
LYME DISEASE Coninfections
1.. Ehrlichiosis 1.. HGE Human granulocytic ehrlichiosis i. Anaplasmic phagocytophilia
2.. Babesiosis 1.. Babesia microti
One word about coinfections. Human ehrlichiosis, which is now known to be caused by Anaplasmic phagocytophilia. I think it's changed its name again to phagocytophilim.
And Babesia microti, both of these are transmitted by the same tick, Ixodes scapularis, and there is some in California.
There is no chronic form of HGE. Those kids. it's indistinguishable from a flu or a viral-like infection. Occasionally you'll see someone who's really sick. Those kids typically have leucopenia, thrombocytopenia, and they look pretty ill. And the treatment is doxycycline.
Babesia is rarely a problem unless you're immunocompromised or don't have a spleen. There is some evidence that it can cause some minor symptoms. But we usually don't make a diagnosis of these in Connecticut. We don't see it at all. Except EXTREMELY rarely. So it's even less of a problem in California.
I think I'm going to stop right there and entertain some questions. Couldn't hear all the questions.
Q: The distribution of Lyme disease in the U.S. - it's been stable all these years?
A: Yes, it has.
Q: How reliable is the testing for Ehrlichiosis and Babesiosis?
A: It depends on which tests you're doing. You can detect these in blood smears if you see them, or a PCR from a reliable laboratory would be pretty good. Most of what's done are antibody tests, which I think are not very good. And again, I frequently see people diagnosed with chronic ehrlichiosis, of which, there is no such thing to start with. But they'll have a positive IgG in their blood, for Ehrlichia. And I don't know what that means, but it certainly isn't a cause of any symptom, and most likely it is a false positive test. Or they were truly infected in the past and they cleared it.
Q: Dogs frequently pick up ticks. Do they get Lyme Disease?
A: Yes, they do get Lyme disease, but as with humans, I think it's grossly overdiagnosed. But they do get it and the vets in our area find Lyme disease to be a lucrative disease.
Q:Inaudible
A: There are many physicians, throughout the country. You can go to New Mexico and get IV therapy for Lyme disease, even though we know there is no Lyme disease there. So there are these groups of physicians who will treat for prolonged periods - and I've read the records of these patients, and it's pretty sad, really. And there are a number of kids who've had their gallbladders out because of complications of long term ceftriaxone, and so on.
Q: The question is what is the mechanism for prolonged IgM activity?
A: I don't know what the mechanism is, but it's clearly documented. Not that everyone does it, it's just occasionally people have it. It occurs.
Q: How do you convince people who are committed to the diagnosis of Lyme disease, that Lyme disease is not the cause of their non-specific symptoms, especially after they have the support of their own physician, confirming this diagnosis.
A: I have a whip! laughter And this is a very difficult problem, as you right say. I get many, many calls about this. And it varies. There are many people that you can convince, and some that you cannot. What I try to talk about is what we know about Lyme disease. What the cause is. I think some people One of the stories you often get is that they've been on antibiotics for six months, and the day they stopped, all the symptoms came back. Now, how is that possible? Let's think about how the inflammation caused by bacteria. That just can't be. It really varies, but you see the whole spectrum and some of this is Munchausen's by Proxy. I have had situation where I've had a call into the department of family services to get involved. There are varying degrees, and you just do what you can.
One thing I say, and I didn't get to my slide, but how to prevent it. The best thing to do is order serological tests appropriately to avoid misdiagnosis, because most of Lyme disease is overdiagnosed because of inappropriate ordering of serologic tests. Occassionally if you're backed into a situation where you have to test, then I'd say, do we'll do it but there are lots of false positve tests, and if it's positive, we're going to send it to this other lab, a reference lab at Yale - which I have no relationship with the Yale Lab, or the Univ. of Conn. Or some reference lab. And it's just like any psychological problem -- sometimes you need to get people to talk about what their fears are. And sometimes you can shake it, and sometimes you can't.
Moderator: As a case in point, Gene has agreed to see a patient of ours, a teenage boy. He's reviewed the records. ?required blood cell It's really an unusual thing. And we don't have an explanation for it. And the patient is seeing another doctor in California, and has been given the diagnosis of Lyme disease. And he's been seen by our ID people, and they have not confirmed that. So we don't have an explanation for it, but it's probably not Lyme disease.
Q: The question is Lyme vaccine, and do I recommend it for anybody?
A; Well, it wouldn't matter whether I recommend it for anybody, because it was taken off the market, not because of any problem with the vaccine, but because it was not profitable. Actually the mechanism by which the vaccine worked was interesting. It was a single protein vaccine and that protein is not expressed in early disease. And by the spirochete, but it is by the tick. So what happens was is that you immunize people, but the tick has to feed awhile before it's transmitted. Because the bacteria live in the gut of the tick and they have to migrate up to the so the tick is feeding on the immunized person. It ingests antibody, and antibody dependent killing took place in the tick. But as a consequence of that, people the vaccine, would never get a boost to immunity. So it turns out it was recommended that three doses be given. It was recommend that 3 doses be given, anyway. Back when it was available, the only situation where I'd recommend it was when someone was working out in the fields or utility lines in Lyme, CT. Then it might be reasonable. For most people it wasn't easy for people to get.
Q: If there are so many false positive tests, when can you have confidence that the test is accurate?
A: Again, I think the key point is the point I tried to make about Bayes Theorem. So it doesn't matter what the test result is in someone who walks in with aches and pains and fatigue for six months. That ain't Lyme disease, whether the test is positive or negative. On the other hand if you have a subacute knee joint - at least in Connecticut - the probability that that's Lyme disease is pretty high. We published a paper using that same algebra that I showed you. If you have 50% prior predictability then the positive predictability is terrific, it's pretty good.
So the key thing is you have objective findings of Lyme disease and you have a positive test, then it's likely to be Lyme disease. If you have a positive test with some non-specific tests that everybody has, or somebody's nose falls off and somebody got a Lyme titer that is positive, probably Lyme disease is not the cause of that problem.
-------------------- nan Posts: 2135 | From Tick Country | Registered: Oct 2000
| IP: Logged |
posted
I've had it with regular doctors and their "no documented proof" bull****. How on earth could there be positive documentation when THEY DON'T TEST!!!
I wonder if these guys still believe the earth is flat, or if they finally got the news.
Posts: 856 | From Texas | Registered: Jan 2005
| IP: Logged |
posted
Eugene shapiro is the worst of the worst, really, he and henry feder...if I'm dr. jones, I might WANT shapiro on the board...because much of what he spews is demonstrably wrong. that could be the focus of an appeal, demonstrating that shapiro is in fact incompetent.
shapiro is consumed with hatred for lyme disease patients, who have failed to conform to his greedy disgusting schemes. BTW, shapiro is very stupid and pigheaded, he has never published anything beyond an undergraduate level of comprehension. He is one of those IDSA "power whores" who in actuality have contributed NOTHING to our understanding of lyme disease - at the clinical or biological level.
he's a propagandist.
Posts: 523 | From Stillwater,OK,USA | Registered: Sep 2004
| IP: Logged |
The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:
The
Lyme Disease Network of New Jersey 907 Pebble Creek Court,
Pennington,
NJ08534USA http://www.lymenet.org/
UBBFriend: Email this page to someone!
![[Mad]](mad.gif)
![[puke]](graemlins/puke.gif)
![[rant]](graemlins/rant.gif)
![[loco]](graemlins/loco.gif)
![[confused]](graemlins/confused.gif)
Printer-friendly view of this topic