Lyme disease overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anmol Pitliya, M.B.B.S. M.D.[2]
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 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
In 1883, Alfred Buchwald was the first to describe a condition associated with Lyme disease which is now known as acrodermatitis chronica atrophicans. Arvid Afzelius first observed ring-like lesions, now known as Erythema migrans, and associated the rash with tick bites. In the United States, Lyme disease was not recognized until 1975, when a cluster of cases was identified in three towns in Southeastern Connecticut (including towns Lyme and Old Lyme), which gave Lyme disease its popular name. In 1981, the infectious agent (a spirochete) was isolated by Willy Burgdorfer, a researcher at the National Institutes of Health, from the midgut of Ixodes ticks. The spirochete was named Borrelia burgdorferi in honor of Willy Burgdorfer.
Classification
Lyme disease can be classified into three stages. The first stage is localized Lyme disease, the second is disseminated Lyme disease, and the third is late disseminated Lyme disease. During stage 1, the patient can develop erythema migrans rash. Ten to twenty percent of the patients who have Lyme disease can develop post treatment Lyme disease syndrome. There are various genospecies of Borrelia burgdorferi sensu lato complex that can cause Lyme disease. A novel spirochete, Borrelia mayonii, has been recently discovered to be responsible for Lyme disease.
Pathophysiology
Lyme disease is caused by Borrelia burgdorferi and is transmitted primarily by tick species 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 spirochetes can be transmitted. Very few people affected with Lyme disease recall a tick bite. B. burgdorferi have two morphological forms, a spiral form and a spheroplast form. Survival strategies of B. burgdorferi include: antigenic variation, physical sequestration, intracellular invasion, and immune system supression.
Epidemiology and Demographics
Lyme disease is the most commonly reported vector-borne illness in the United States. In 2015, it was the sixth most common nationally notifiable disease. The number of people diagnosed with Lyme disease each year in the United States is around 30,000. This disease is concentrated heavily in the Northeast and upper Midwest. Lyme disease has a seasonal variation and incidence increases during months of May to August.
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.
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
Because Lyme disease is a tick-borne disease, an individual is at a heightened risk of contracting it when traveling or residing within endemic regions. Risk within endemic regions is higher during the spring and summer months, with peaks in June and July. Other factors that may increase the risk of contracting Lyme disease include owning a domesticated animal such as a dog or cat, as both of these pets may be potential hosts for a blacklegged tick. In summary, individuals who spend much of their time outdoors and/or have pets that go outdoors and who live in endemic regions, are at a higher risk of contracting tick-borne diseases.[6]
Screening
There is insufficient evidence to recommend routine screening for Lyme disease.
Natural History, Complications and Prognosis
Lyme disease may present as a red, expanding rash called erythema migrans (EM) along with flu-like symptoms such as fatigue, arthralgia, myalgias, headache, fever and/or chills, stiff neck, anorexia, and regional lymphadenopathy. EM resolves in approximately 28 days in untreated patients.Lyme disease is effectively managed by prompt treatment.
Untreated infection may spread from the site of the bite to other parts of the body, producing a range of symptoms including neurological, cardiac and dermatological manifestations. Many of these symptoms will resolve over a period of weeks to months, even without treatment. However, lack of treatment can result in additional complications. Lyme arthritis is the most frequently presented symptom in late disseminated Lyme disease.
Prognosis is mainly affected by a failure to treat in a timely manner as well as simultaneous infections with other tick-borne diseases. Sometimes, patients with Lyme disease have symptoms that last months to years after treatment with antibiotics. These symptoms includes muscle and joint pains, cognitive defects, sleep disturbance, or fatigue. The condition is referred to as post-treatment Lyme disease syndrome (PTLDS).
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 CSF 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. Resolve 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
Lyme disease is divided into 3 stages and symptoms are stage specific. Initial symptoms include bullseye rash with accompanying flu-like symptoms. Lyme disease can progress to cardiovascular or neurological complications.
Physical Examination
The physical examination of Lyme disease is necessary for diagnosis. Erythema migrans and fever are commonly seen on physical examination in early disease.[12] Disseminated disease is characterized by multiple erythema migrans, neurological, musculoskeletal, and cardiac symptoms.[13]
Laboratory Findings
Laboratory blood tests are helpful if used correctly and performed with validated methods. Laboratory tests are not recommended for patients who do not have symptoms typical of Lyme disease. The Centers for Disease Control recommends a two-tier testing protocol for Lyme disease. Polymerase chain reaction (PCR) tests for Lyme disease have also been developed to detect the genetic material (DNA) of the Lyme disease spirochete. Currently, PCR is the only means to detect the presence of organism. Identification and testing of the individual tick after removal is generally not useful.
Electrocardiogram
There are no ECG findings associated with Lyme disease. However, an ECG may be helpful in the diagnosis of complications of Lyme disease, which include Lyme carditis. Most of the time, Lyme cariditis symptoms are related to fluctuating degrees of atrioventricular block (first-degree block to complete heart block) including lightheadedness, palpitations, shortness of breath, chest pain, and syncope.[14]
X-ray
There are no X-ray findings associated with Lyme disease. However, an X-ray may be helpful in the diagnosis of complications of chronic Lyme arthritis.
CT Scan
There are no CT scan findings associated with Lyme disease.
MRI
MRI is not helpful in diagnosis of Lyme disease. However, an MRI may be helpful in diagnosing neurologic manifestations of early and late disseminated Lyme disease. MRI scan in patients with neurological Lyme disease may demonstrate increased intensity in white matter at multiple foci on T2-weighted images, suggesting demyelination or inflammatory changes. After antibiotic therapy, spontaneous resolution of MRI white matter hyper-intensities has been observed in Lyme disease.
Ultrasound
There are no ultrasound findings associated with Lyme disease.
Other Imaging Findings
Single photon emission computed tomography is one of the major other imaging modalities of Lyme disease. In Lyme patients cerebral hypoperfusion of frontal subcortical and cortical structures has been reported.
Other Diagnostic Studies
There are no additional diagnostic findings associated with Lyme disease.
Treatment
Medical Therapy
The mainstay of therapy for Lyme disease is antimicrobial therapy. Antimicrobial therapy may include either doxycycline, amoxicillin, cephalosporins, or macrolides. The choice of antimicrobial therapy depends on the stage of Lyme disease. Individuals who remove attached ticks should be monitored closely for signs and symptoms of tick-borne diseases for up to 30 days.
Surgery
Surgical intervention is not recommended for Lyme disease.
Primary Prevention
Primary prevention of Lyme disease involves reducing exposure to ticks. Scientists have been developing all-natural chemical compounds made from plants that can repel or kill ticks. A Lyme disease vaccine is no longer available.
Secondary Prevention
The secondary prevention of Lyme disease is similar to its primary 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.
- ↑ 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.
- ↑ General Information (2015). http://www.cdc.gov/ticks/index.html Accessed on December 30, 2015
- ↑ 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.
- ↑ Steere AC, Bartenhagen NH, Craft JE, Hutchinson GJ, Newman JH, Rahn DW; et al. (1983). "The early clinical manifestations of Lyme disease". Ann Intern Med. 99 (1): 76–82. PMID 6859726.
- ↑ Steere, Allen C. (1989). "Lyme Disease". New England Journal of Medicine. 321 (9): 586–596. doi:10.1056/NEJM198908313210906. ISSN 0028-4793.
- ↑ Hu LT (2012). "In the clinic. Lyme disease". Ann Intern Med. 157 (3): ITC2-2–ITC2-16. doi:10.7326/0003-4819-157-3-20120807-01002. PMID 22868858.