Lyme disease overview: Difference between revisions
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The disease presentation varies widely, and may include a rash and [[flu]]-like symptoms in its initial stage, then [[musculoskeletal]], [[arthritic]], [[neurologic]], [[psychiatric]] and [[cardiac]] manifestations. In a majority of cases, symptoms can be eliminated with [[antibiotics]], especially if treatment begins early in the course of illness. Late or inadequate treatment often leads to "late stage" Lyme disease that is disabling and difficult to treat. [[Lyme disease controversy|Controversy]] over diagnosis, testing and treatment has led to two different standards of care.<ref name="Johnson-a">{{cite web | author = Johnson L | title = Lyme disease: two standards of care | publisher = International Lyme and Associated Diseases Society | date = 2005-02 | url = http://www.ilads.org/insurance.html | accessdate = 2007-08-21}}</ref><ref name="Johnson-b">{{cite journal | author = Johnson L, Stricker R | title = Treatment of Lyme disease: a medicolegal assessment. | journal = Expert Rev Anti Infect Ther | volume = 2 | issue = 4 | pages = 533-57 | year = 2004 | pmid = 15482219}}</ref> | The disease presentation varies widely, and may include a rash and [[flu]]-like symptoms in its initial stage, then [[musculoskeletal]], [[arthritic]], [[neurologic]], [[psychiatric]] and [[cardiac]] manifestations. In a majority of cases, symptoms can be eliminated with [[antibiotics]], especially if treatment begins early in the course of illness. Late or inadequate treatment often leads to "late stage" Lyme disease that is disabling and difficult to treat. [[Lyme disease controversy|Controversy]] over diagnosis, testing and treatment has led to two different standards of care.<ref name="Johnson-a">{{cite web | author = Johnson L | title = Lyme disease: two standards of care | publisher = International Lyme and Associated Diseases Society | date = 2005-02 | url = http://www.ilads.org/insurance.html | accessdate = 2007-08-21}}</ref><ref name="Johnson-b">{{cite journal | author = Johnson L, Stricker R | title = Treatment of Lyme disease: a medicolegal assessment. | journal = Expert Rev Anti Infect Ther | volume = 2 | issue = 4 | pages = 533-57 | year = 2004 | pmid = 15482219}}</ref> | ||
==Causes== | |||
Lyme disease is caused by [[Gram-negative]] [[spirochetal]] [[bacteria]] from the [[genus]] ''[[Borrelia]]''. At least 37 ''Borrelia'' species have been described, 12 of which are Lyme related. The ''Borrelia'' [[species]] known to cause Lyme disease are collectively known as ''Borrelia burgdorferi'' sensu lato, and have been found to have greater [[genetic diversity|strain diversity]] than previously estimated.<ref name="Bunikis-a">{{cite journal | author=Bunikis J, Garpmo U, Tsao J, Berglund J, Fish D, Barbour AG | title=Sequence typing reveals extensive strain diversity of the Lyme borreliosis agents ''Borrelia burgdorferi'' in North America and ''Borrelia afzelii'' in Europe | journal=Microbiology | year=2004 | pages=1741-55 | volume=150 | issue=Pt 6 | pmid= 15184561 | url=http://mic.sgmjournals.org/cgi/reprint/150/6/1741.pdf | format=PDF}}</ref> | |||
Until recently it was thought that only three genospecies caused Lyme disease: ''B. burgdorferi'' sensu stricto (predominant in North America, but also in Europe), ''B. afzelii'', and ''B. garinii'' (both predominant in Eurasia). However, newly discovered genospecies have also been found to cause disease in humans. | |||
==Diagnosis== | ==Diagnosis== | ||
Due to the difficulty in [[Microbiological culture|culturing]] ''Borrelia'' bacteria in the laboratory, diagnosis of Lyme disease is typically based on the clinical exam findings and a history of exposure to [[endemic (epidemiology)|endemic]] Lyme areas.<ref name=Sherris /> The [[Erythema migrans|EM rash]], which does not occur in all cases, is considered sufficient to establish a diagnosis of Lyme disease even when serologies are negative.<ref name="Brown">{{cite journal | author=Brown SL, Hansen SL, Langone JJ | title=Role of serology in the diagnosis of Lyme disease | journal=JAMA | year=1999 | pages=62-6 | volume=282 | issue=1 | pmid= 10404913}}</ref><ref name="Hofmann">{{cite journal | author=Hofmann H | title=Lyme borreliosis--problems of serological diagnosis | journal=Infection | year=1996 | pages=470-2 | volume=24 | issue=6 | pmid= 9007597}}</ref> [[serology|Serological]] testing can be useful, but is not diagnostic.<ref name=Sherris /> | Due to the difficulty in [[Microbiological culture|culturing]] ''Borrelia'' bacteria in the laboratory, diagnosis of Lyme disease is typically based on the clinical exam findings and a history of exposure to [[endemic (epidemiology)|endemic]] Lyme areas.<ref name=Sherris /> The [[Erythema migrans|EM rash]], which does not occur in all cases, is considered sufficient to establish a diagnosis of Lyme disease even when serologies are negative.<ref name="Brown">{{cite journal | author=Brown SL, Hansen SL, Langone JJ | title=Role of serology in the diagnosis of Lyme disease | journal=JAMA | year=1999 | pages=62-6 | volume=282 | issue=1 | pmid= 10404913}}</ref><ref name="Hofmann">{{cite journal | author=Hofmann H | title=Lyme borreliosis--problems of serological diagnosis | journal=Infection | year=1996 | pages=470-2 | volume=24 | issue=6 | pmid= 9007597}}</ref> [[serology|Serological]] testing can be useful, but is not diagnostic.<ref name=Sherris /> | ||
Revision as of 23:52, 3 February 2013
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Lyme disease overview On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Lyme disease is an emerging infectious disease caused by spirochete bacteria from the genus Borrelia.[1] The vector of infection is typically the bite of an infected black-legged or deer tick, but other carriers (including other ticks in the genus Ixodes) have been implicated.[2] Borrelia burgdorferi is the predominant cause of Lyme disease in the US and Borrelia afzelii and Borrelia garinii are in Europe.
The disease presentation varies widely, and may include a rash and flu-like symptoms in its initial stage, then musculoskeletal, arthritic, neurologic, psychiatric and cardiac manifestations. In a majority of cases, symptoms can be eliminated with antibiotics, especially if treatment begins early in the course of illness. Late or inadequate treatment often leads to "late stage" Lyme disease that is disabling and difficult to treat. Controversy over diagnosis, testing and treatment has led to two different standards of care.[3][4]
Causes
Lyme disease is caused by Gram-negative spirochetal bacteria from the genus Borrelia. At least 37 Borrelia species have been described, 12 of which are Lyme related. The Borrelia species known to cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato, and have been found to have greater strain diversity than previously estimated.[5]
Until recently it was thought that only three genospecies caused Lyme disease: B. burgdorferi sensu stricto (predominant in North America, but also in Europe), B. afzelii, and B. garinii (both predominant in Eurasia). However, newly discovered genospecies have also been found to cause disease in humans.
Diagnosis
Due to the difficulty in culturing Borrelia bacteria in the laboratory, diagnosis of Lyme disease is typically based on the clinical exam findings and a history of exposure to endemic Lyme areas.[1] The EM rash, which does not occur in all cases, is considered sufficient to establish a diagnosis of Lyme disease even when serologies are negative.[6][7] Serological testing can be useful, but is not diagnostic.[1]
Clinicians who diagnose strictly based on the U.S. Centers for Disease Control (CDC) Case Definition for Lyme are in error, as the CDC explicitly states that this definition is intended for surveillance purposes only, and is "not intended to be used in clinical diagnosis."[8][9]
Importantly, virtually no controlled studies of late lyme encephalopathy have been performed, and the CDC diagnostic criteria were not formulated for use on this entity. Once lyme disease is well established in the brain, it can occur as a very disabling diffuse encephalopathy which however is difficult to diagnose using standard serological or intrathecal testing for reasons outlined below. Lyme is a deep tissue infection and by the time encephalopathy is established, few if any CFS antibodies can be detetected, and PCR is unreliable. Seronegative disease can occur for the same reason that this phenomenon occurs in neurosyphilis, with incomplete or intercurrent antibiotic treatment abrogating the serum antibody response, but not eliminating the infection.
It is in this context that advanced imaging studies like SPECT or PET can provide objective evidence of global brain dysfunction. Resort is often made to neuropsychological testing, but a normal result does not rule out the illness, which can be very subtle and manifest as a disabling mood disorder accompanied by massive and debilitating fatigue, with few objective signs.
Diagnosis of late-stage Lyme disease it is often difficult due to the multi-faceted appearance which can mimic symptoms of many other diseases. For this reason Lyme has often been called the new "great imitator".[10] Lyme disease may be misdiagnosed as Multiple sclerosis, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome (CFS), or other autoimmune and neurodegenerative diseases.
References
- ↑ 1.0 1.1 1.2 Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. 434&ndash, 7. ISBN 0838585299.
- ↑ Johnson RC (1996). "Borrelia". Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. ISBN 0-9631172-1-1.
- ↑ Johnson L (2005-02). "Lyme disease: two standards of care". International Lyme and Associated Diseases Society. Retrieved 2007-08-21. Check date values in:
|date=(help) - ↑ Johnson L, Stricker R (2004). "Treatment of Lyme disease: a medicolegal assessment". Expert Rev Anti Infect Ther. 2 (4): 533–57. PMID 15482219.
- ↑ Bunikis J, Garpmo U, Tsao J, Berglund J, Fish D, Barbour AG (2004). "Sequence typing reveals extensive strain diversity of the Lyme borreliosis agents Borrelia burgdorferi in North America and Borrelia afzelii in Europe" (PDF). Microbiology. 150 (Pt 6): 1741–55. PMID 15184561.
- ↑ Brown SL, Hansen SL, Langone JJ (1999). "Role of serology in the diagnosis of Lyme disease". JAMA. 282 (1): 62–6. PMID 10404913.
- ↑ Hofmann H (1996). "Lyme borreliosis--problems of serological diagnosis". Infection. 24 (6): 470–2. PMID 9007597.
- ↑ "Lyme Disease (Borrelia burgdorferi): 1996 Case Definition". CDC Case Definitions for Infectious Conditions under Public Health Surveillance. 1996. Retrieved 2007-08-23.
- ↑ "CDC Testimony before the Connecticut Department of Health and Attorney General's Office". CDC's Lyme Prevention and Control Activities. 2004-01-24. Retrieved 2007-08-23.
- ↑ Pachner AR (1989). "Neurologic manifestations of Lyme disease, the new "great imitator"". Rev. Infect. Dis. 11 Suppl 6: S1482–6. PMID 2682960.