Lyme disease overview
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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]
Historical Perspective
Lyme disease was first described in 1983 by Alfred Buchwald. Later Arvid Afzelius proposed that it was spread by Ixodes tick. The full syndrome now known as Lyme disease was recognized when uster of cases originally thought to be juvenile rheumatoid arthritis was identified in three towns in southeastern Connecticut in 1975, including the towns Lyme and Old Lyme, which gave the disease its popular name.[5]
Classification
Lyme disease is classified into three stages. They are localized Lyme disease, disseminated Lyme disease and late disseminated Lyme disease. DUring stage 1, the patient can develop erythema migrans rash. Ten to twenty percent of the patients who has Lyme disease can develop post treatment Lyme disease syndrome.
Pathophysiology
Lyme disease is caused by Borrelia burgdorferi and is transmitted by tick named Ixodes scapularis. Ticks can attach to any part of the human body but are often found in hard-to-see areas such as the groin, armpits, and scalp. In most cases, the tick must be attached for 36 to 48 hours or more before the Lyme disease bacterium can be transmitted.
Epidemiology and Demographics
Lyme disease is the most common tick borne disease in North America and the the ratio of Lyme disease infection is 7.9 cases for every 100,000 persons. The number of people diagnosed with Lyme disease each year in the United States is around 300,000. This disease is concentrated heavily in the northeast and upper Midwest.
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.[6]
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.
Differentiating Lyme from other Disease
The differential diagnosis of Lyme's disease include babesiosis, leptospirosis, mononucleosis, viral meningitis and chronic diseases such a SLE, fibromyalgia and Chronic fatigue syndrome.
Risk Factors
Natural History, Complications and Prognosis
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.[7][8] 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."[9][10]
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".[11] Lyme disease may be misdiagnosed as Multiple sclerosis, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome (CFS), or other autoimmune and neurodegenerative diseases.
History and Symptoms
Physical Examination
Laboratory Findings
Other Imaging Findings
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
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.
- ↑ Steere AC (2006). "Lyme borreliosis in 2005, 30 years after initial observations in Lyme Connecticut". Wien. Klin. Wochenschr. 118 (21–22): 625–33. doi:10.1007/s00508-006-0687-x. PMID 17160599.
- ↑ 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.