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The Lancet - Infectious Diseases
Volume 4, Number 10 01 October 2004
http://infection.thelancet.com/journal/vol4/iss10/abs/laid.4.10.reflection_and_reaction.30768.1
Lyme borreliosis: perspective of a scientist–patient
Ron Hamlen
In their review of Lyme borreliosis, Ulrich Hengge and colleagues[1]
declare, "Extensive and often inaccurate publicity about the risk and
outcomes of Lyme borreliosis has produced considerable anxiety about the
disease. One result of this reaction is the inappropriate use of
serological testing for Lyme borreliosis to identify the cause of widely
prevalent, non-specific symptoms, such as pain and fatigue. This
practice, in turn, has led to a virtual epidemic of over-diagnosis and
over-treatment of patients with Lyme borreliosis". This is one side of
the intense debate over Lyme borreliosis. There is a division among
physicians; because of their fiercely held positions, communication
among adversaries has not been productive, and issues of diagnosis and
treatment remain unresolved. [2 and 3] This deplorable situation has
damaged the quality of patient care and makes Lyme borreliosis a
public-health threat. As a Lyme borreliosis patient who has worked in
biological science in academia and industry for over 30 years, I am
compelled to address the conflict between physicians, insurance
companies, and government agencies, as well as the confusion over
patient management.
According to the US Centers for Disease Control and Prevention (CDC),
Lyme borreliosis is the fastest growing zoonotic disease; from 2001–2002
there was a 40% increase in cases surveyed, to 23763 cases.[4] The CDC
acknowledges under-reporting. Reliable estimates are at least ten times
those reported, or about 250000 new cases per year [4]—more than five
times the annual number of new AIDS cases in the USA. [5] According to
these statistics, there are more than 2 million people with chronic Lyme
borreliosis in the USA.
Lyme borreliosis is a multisystem, protean infection from multiple
strains[6] and morphological forms [7] of Borrelia burgdorferi. Even
when treated with antibiotics, this spirochete can cause persistent
infection and lead to debilitating chronic illness in some people.[2 and
8] Symptoms during infection vary among patients and can include
erythema migrans, flu-like illness (fever and chills), rheumatological
(musculoskeletal pain), neurological (headache, fatigue, vertigo,
confusion, and impairments of cognition, sleep, hearing, memory, and
vision), and cardiac manifestations, and psychiatric illness. [2 and 9]
Given the incidence of Lyme borreliosis in the USA, it is perplexing
that people living in endemic areas are ill for months or years before
they are diagnosed and treated. In the literature, this problem is
attributed to non-specific and fluctuating symptoms, re-infection,
relapse, latent and asymptomatic infection, and the inadequacy of
serological tests.[1, 2, 3, 9 and 10] However, the best explanation is
the confusion generated by the medical and sociopolitical controversy
over the incidence and seriousness of Lyme borreliosis and the existence
of persistent infection. [1, 2, 3, 9 and 11]
Physician diagnosis of early B burgdorferi infections is made from
assessment of clinical symptoms. After testing for co-occurring
infections—such as babesia, ehrlichia, bartonella, and anaplasma[2 and
3]—aggressive antimicrobial treatments are prescribed at therapeutic
dosages and duration. [2] Because society is mobile, physicians in areas
that are non-endemic for Lyme borreliosis can encounter patients with
early to chronic Lyme borreliosis. Misdiagnosis or ineffective treatment
of early Lyme borreliosis can result in neurological illness and lead to
expensive, long-term, intravenous antibiotic therapy—a cost that is
difficult for patients and insurance companies to support.
Although there is not a commonly agreed to effective treatment for Lyme
borreliosis,[2] the widely held medical and political view (illustrated
in the Hengge review) is that it is a minor illness, easily treated, and
reliably cured with 14–21 days of oral antibiotic therapy, [1 and 11]
even though there is no objective test to confirm cure. [2] This
conservative position argues that most Lyme borreliosis cases meet the
CDC restrictive surveillance criteria: [12] erythema migrans, positive
ELISA, and IgM/IgG western blot results. [1 and 11] However, when
erythema migrans is absent, [3 and 13] serology is negative, [1, 2 and
14] or acute, non-specific symptoms are inconsistent with the
physician's understanding of Lyme borreliosis, the diagnosis may be
overlooked in up to 90% of cases. [2] When diagnosis is delayed and
serology remains negative, physicians tend to dismiss B burgdorferi
infection. The probability of a false-negative result[2 and 14] is
rarely considered even though the CDC warn that surveillance criteria
alone should not determine diagnosis and treatment. [4] Furthermore,
physicians rarely seek the assistance of laboratories and practitioners
who specialise in tick-borne infections and use western blots with
multiple B burgdorferi strains (assessing dissimilarity in reactivity
patterns that are dependent on the strain used as the antigen
source),[14] PCR [2 and 9] and CD57 [15] assays, or functional brain
imaging (such as single photon emission computed tomography). [16]
In the absence of objective evidence it is not unusual for physicians
who are confronted with fluctuating and non-specific symptoms to tell
their patients: "You don't have Lyme disease, but I don't know what's
wrong with you". If a short-course of empirical antimicrobial therapy is
prescribed, it is reasonable to ask how many patients remained ill, did
not return to that physician, but did seek help from a practitioner
experienced with tick-borne infections. The literature discusses the
harmful effects and expense of over-prescribing antibiotics; however,
the discussion rarely encompasses the long-term individual and societal
consequences of untreated Lyme borreliosis.
Hengge and colleagues state: "Since Lyme borreliosis is a popular
explanation for many poorly understood symptoms, such as arthralgias or
chronic fatigue syndrome, proper instruction to physicians is key to
prevent misdiagnosis or overdiagnosis". Conversely, the fact that
symptoms of persistent B burgdorferi infection overlap those of chronic
fatigue syndrome, fibromyalgia, multiple sclerosis, and motor neuron
disease contributes to the misdiagnosis and inadequate treatment of this
spirochetal illness.[2, 17, 18 and 19]
As numerous specialists are consulted, the patient may feel unheard and
trivialised, and become overwrought in dealing with multiple diagnoses,
each aligned with a physician's specialty yet not contributing to
improved health. The suggestion that unresolved emotional issues are
causing the patient's symptoms can be overwhelming for the patient and
lead to questions of factitious or psychoneurotic illness. Cognitive
impairment[2, 9 and 20] and chronic pain from neuropathy can activate
depressive illness. [2 and 9] Neuropsychiatric manifestations of Lyme
borreliosis in school-age children are often misdiagnosed as learning,
behavioural, or attention deficit disorders. [9 and 20]
Lyme disease is a complex and extremely serious illness that affects
patients and the entire medical community. I hope my comments will
broaden the perspective on Lyme borreliosis presented in Hengge and
colleagues’ review.
References
1. UR Hengge, A Tannapfel, SK Tyring, R Erbel, G Arendt and T. Ruzicka,
Lyme borreliosis. Lancet Infect Dis 3 (2003), pp. 489–500. SummaryPlus |
Full Text + Links | PDF (3939 K)
2. ILADS Working Group. Evidence-based guidelines for the management of
Lyme disease. Expert Rev Anti-infect Ther 2004; 2 (suppl 1): 1–13.
3. RB Stricker and A. Lautin, The Lyme wars: time to listen. Expert Opin
Investig Drugs 12 (2003), pp. 1609–1614. Abstract-MEDLINE | Full
Textvia CrossRef
4. CDC, Lyme disease—United States, 2001–02. MMWR Morb Mortal Wkly Rep
53 (2004), pp. 365–369.
5. CDC, Notice to readers: final 2002 reports of notifiable diseases.
MMWR Morb Mortal Wkly Rep 52 (2003), pp. 741–750.
6. DA Mathiesen, JH Oliver, Jr, CP Kolbert et al., Genetic heterogeneity
of Borrelia burgdorferi in the United States. J Infect Dis 175 (1997),
pp. 98–107. Abstract-MEDLINE
7. I Gruntar, T Malovrh, R Murgia and M. Cinco, Conversion of Borrelia
garinii cystic forms to motile spirochetes in vivo. APMIS 109 (2001),
pp. 383–388. Abstract-Elsevier BIOBASE | Abstract-EMBASE |
Abstract-MEDLINE | Full Textvia CrossRef
8. V Preac-Mursic, K Weber, HW Pfister et al., Survival of Borrelia
burgdorferi in antibiotically treated patients with Lyme borreliosis.
Infection 17 (1989), pp. 355–359. Abstract-EMBASE | Abstract-MEDLINE
9. BA Fallon, JM Kochevar, A Gaito and JA. Nields, The underdiagnosis of
neuropsychiatric Lyme Disease in children and adults. Psychiatr Clin
North Am 21 (1998), pp. 693–703. Abstract-PsycINFO | Abstract-EMBASE
10. AC Steere, VK Sikand, RT Schoen and J. Nowakowski, Asymptomatic
infection with Borrelia burgdorferi. Clin Infect Dis 37 (2003), pp.
528–532. Abstract-MEDLINE | Abstract-Elsevier BIOBASE | Abstract-EMBASE
| Full Textvia CrossRef
11. GP Wormser, RB Nadelman, RJ Dattwyler et al., Practical guidelines
for the treatment of Lyme disease. Clin Infect Dis 31 suppl 1 (2000),
pp. 1–14. Abstract-MEDLINE | Full Textvia CrossRef
12. CDC, CDC recommendations for test performance and interpretation
from the second national conference on serologic diagnosis of Lyme
disease. MMWR Morb Mortal Wkly Rep 44 (1995), pp. 590–591.
13. AC Steere, A Dhar, J Hernandez et al., Systemic symptoms without
erythema migrans as the presenting picture of early Lyme disease. Am J
Med 114 (2003), pp. 58–62. SummaryPlus | Full Text + Links | PDF (76 K)
14. R. Kaiser, False-negative serology in patients with neuroborreliosis
and the value of employing of different borrelial strains in serological
assays. J Med Microbiol 49 (2000), pp. 911–915. Abstract-EMBASE |
Abstract-Elsevier BIOBASE | Abstract-MEDLINE
15. RB Stricker, JJ Burrascano and EE. Winger, Longterm decrease in the
CD57 lymphocyte subset in a patient with chronic Lyme disease. Ann Agric
Environ Med 9 (2002), pp. 111–113. Abstract-EMBASE | Abstract-MEDLINE
16. BA Fallon, J Keilp, I Prohovnik, R Van Heertum and JJ. Mann,
Regional cerebral blood flow and cognitive deficits in chronic Lyme
disease. J Neuropsychiatry Clin Neurosci 15 (2003), pp. 326–332.
Abstract-EMBASE | Abstract-MEDLINE | Abstract-PsycINFO | Full Textvia
CrossRef
17. D Buchwald and D. Garrity, Comparison of patients with chronic
fatigue syndrome, fibromyalgia, and multiple chemical sensitivities.
Arch Intern Med 154 (1994), pp. 2049–2053. Abstract-EMBASE |
Abstract-MEDLINE
18. E. Schmutzhard, Multiple sclerosis and Lyme borreliosis. Wein Klin
Wochenschr 114 (2002), pp. 539–543. Abstract-EMBASE | Abstract-MEDLINE
19. Dangond F. Amyotrophic lateral sclerosis.
http://www.emedicine.com/neuro/topic14.htm (accessed Sept 2, 2004)
20. F Tager, B Fallon, J Keilp, M Rissenberg, C Jones and M. Liebowitz,
A controlled study of cognitive deficits in children with chronic Lyme
disease. J Neuropsychiatry Clin Neurosci 13 (2001), pp. 500–507.
Abstract-MEDLINE | Abstract-EMBASE | Abstract-PsycINFO | Full Textvia
CrossRef
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