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Lyme disease or Lyme borreliosis is the most common tick-borne disease in the United States and Europe, and one of the fastest growing infectious diseases in the United States. It was first described in the United States in the town of Old Lyme, Connecticut in 1975, but has now been reported in most parts of the United States. Lyme disease is caused by a bacterial infection with a spirochete from the species complex Borrelia burgdorferi sensu lato, and is most often acquired from the bite of an infected Ixodes tick. Borrelia burgdorferi was first identified in 1982 by Willy Burgdorfer, a tick-borne disease expert at Rocky Mountain Labs in Hamilton, Montana. While Borrelia burgdorferi sensu stricto is the predominant cause in the U.S., Lyme disease in Europe is more often caused by Borrelia afzelii or Borrelia garinii. The disease varies widely in its presentation, which may include a rash, flu-like symptoms, neurologic, arthritic and/or cardiac manifestations. Early detection and prompt antibiotic treatment usually result in an excellent prognosis, though some patients remain symptomatic. Delayed or inadequate treatment may lead to a chronic illness that is disabling and difficult to treat. Amid great controversy over diagnosis, testing and treatment, two different standards of care for Lyme disease have emerged. Symptoms Lyme disease has many signs and symptoms, but skin signs, arthritis and/or various neurological symptoms are often present. Like syphilis, the symptoms frequently seem to resolve, yet the disease progresses. Conventional therapy is with antibiotics. People who suspect they have been exposed to Lyme disease should consult a doctor with knowledge of the disease immediately. Acute (early) symptoms that may occur Erythema migrans rash (EM) - Contrary to popular belief, the characteristic "bull's-eye" rash with central clearing is not the most common form. Rashes that are homogeneously red are seen more frequently.•• Multiple painless EM rashes may occur, indicating disseminated infection. The true incidence of the rash is disputed, with estimates ranging from less than 50%•• to over 80% of those infected. The symptoms of Lyme disease are fever, malaise, fatigue, headache, muscle and joint aches in large joints, sore throat, sinus infection Other consequences, include facial paralysis - usually associated with Lyme meningitis or Rocky Mountain spotted fever, palpitations, kidney and intestinal pains. The incubation period from infection to the onset of symptoms is usually 1–2 weeks, but can be much shorter (a couple of days), or even as long as one month. Chronic (late) symptoms The late symptoms of Lyme disease can appear months after infection. Lyme disease may be misdiagnosed as multiple sclerosis, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome (CFS), or other (mainly autoimmune and neurological) diseases, which leaves the infection untreated and allows it to further penetrate the organism. Some of these conditions may be misdiagnosed as Lyme disease, although this is thought to be a rare occurrence. False positive Lyme diagnosis is most commonly due to false positive serology in a subset of patients who may suffer from syphillis, rheumatologic diseases, or infectious mononucleosis. More confounding is that patients may present with Lyme Disease and a related disease such as MS. This makes diagnosis exceptionally difficult. It should be noted that this kind of misdiagnosis is the exception rather than the rule as it is widely held that Lyme Disease is underdiagnosed and underreported ranging from factors of 10 to upwards of 40. It is important to remember that chronic fatigue syndrome (CFS) is by definition a diagnosis of exclusion, meaning it would be inaccurate to say that a patient does not have Lyme because he or she has CFS. The substantial overlap in symptomatology between Lyme and CFS makes this a crucial point. Transmission by ticks Hard-bodied (Ixodes) ticks are the primary Lyme disease vectors. In Europe, Ixodes ricinus, known commonly as the sheep tick, castor bean tick, or European castor bean tick is the transmitter. In North America, Ixodes scapularis (black-legged tick or deer tick) has been identified as the key to the disease's spread on the east coast, while on the west coast the primary vector is Ixodes pacificus (Western black-legged tick). Another possible vector is Amblyomma americanum (Lone Star tick),• which is found throughout the southeastern U.S. as far west as Texas, and increasingly in northeastern states as well. The longer the duration of tick attachment, the greater the risk of disease transmission, but, typically, for the spirochete to be transferred, the tick must be attached for a minimum of 12 hours, although, only the first part of this statement can be said to be strictly correct. (see Proper Removal of Ticks). Unfortunately only 20% of persons infected with Lyme by the deer tick are aware of any tick bite,• making early detection difficult in the absence of a rash. Tick bites usually go unnoticed due to the small size of the tick in its nymphal stage, as well as tick secretions that prevent the host from feeling any itch or pain from the bite. New research suggests that transmission can occur within a few hours of tick attachment, and that the rate of transmission by infected ticks may be much higher than previously assumed. Congenital Lyme disease Lyme disease can be transmitted from an infected mother to fetus through the placenta during pregnancy, possibly resulting in stillbirth.•• The risk of transmission is minimized if the mother receives prompt antibiotic treatment, though physicians disagree as to the duration of treatment required. Other modes of transmission There is at least one case report of transmission by a biting fly.• Lyme spirochetes have been found in biting flies as well as mosquitos.• Some researchers believe biting insects do not feed long enough to transmit the infection, while others including Borrelia burgdorferi discoverer Willy Burgdorfer believe more research is needed.• There is also some anecdotal, largely unconfirmed evidence of sexual transmission. Lyme spirochetes have been found in semen• and breast milk,• though transmission by these routes has yet to be proven. Strains Lyme disease is caused by spirochetal bacteria from the genus Borrelia, which has well over three hundred known genomic strains. 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.• 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: B. lusitaniae• in Europe (especially Portugal), North Africa and Asia, B. bissettii•• in the U.S. and Europe, and B. spielmanii•• in Europe. Additional B. burgdorferi sensu lato genospecies suspected of causing illness, but not confirmed by culture, include B. valaisiana (Eurasia, especially England, Switzerland and the Netherlands); B. japonica, B. tanukii and B. turdae (Japan); B. sinica (China); and B. andersonii (U.S.). Some of these species are carried by ticks not currently recognized as carriers of Lyme disease. Note: At present, diagnostic tests are based only on B. burgdorferi sensu stricto (the only species used in the U.S.), B. afzelii and B. garinii. Apart from this group of closely related genospecies, additional Borrelia species of interest include B. lonestari, a spirochete recently detected in the Amblyomma americanum tick (Lone Star tick) in the U.S.• B. lonestari is suspected of causing STARI (Southern Tick-Associated Rash Illness), also known as Masters disease in honor of its discoverer. The illness follows a Lone Star tick bite and clinically resembles Lyme disease, but sufferers usually test negative for Lyme.• There is currently no diagnostic test available for STARI/Masters, and no official treatment protocol, though antibiotics are generally prescribed. The B. miyamotoi spirochete, related to the relapsing fever group of spirochetes, is also suspected of causing illness in Japan. Spirochetes similar to B. miyamotoi have recently been found in both I. ricinus ticks in Sweden and I. scapularis ticks in the U.S.•• Genomic characteristics One of the most striking features of B. burgdorferi as compared with other eubacteria is its unusual genome, which is far more complex than that of its spirochetal cousin Treponema pallidum, the agent of syphilis.• The genome of B. burgdorferi includes a linear chromosome approximately one megabase in size, with 21 plasmids (12 linear and 9 circular) - by far the largest number of plasmids found in any known bacterium.• Genetic exchange, including plasmid transfers, contributes to the pathogenicity of the organism.• Long-term culture of B. burgdorferi results in a loss of some plasmids and changes in expressed protein profiles. Associated with the loss of plasmids is a loss in the ability of the organism to infect laboratory animals, suggesting that the plasmids encode key genes involved in virulence. Structure and growth B. burgdorferi is a highly specialized, motile, two-membrane, spiral-shaped spirochete ranging from about 9 to 32 micrometers in length. It is often described as gram-negative and has an outer membrane with LPS, though it stains only weakly in the Gram stain. B. burgdorferi is a microaerophilic organism, requiring little oxygen to survive. It lives primarily as an extracellular pathogen, although it can also hide intracellularly (see Mechanisms of persistence section). Like other spirochetes such as T. pallidum (the agent of syphilis), B. burgdorferi has an axial filament composed of flagella which run lengthways between its cell wall and outer membrane. This structure allows the spirochete to move efficiently in corkscrew fashion through viscous media, such as connective tissue. As a result, B. burgdorferi can disseminate throughout the body within days to weeks of infection, penetrating deeply into tissue where the immune system and antibiotics may not be able to eradicate the infection. B. burgdorferi is very slow growing, with a doubling time of 12-24 hours (in contrast to pathogens such as Streptococcus and Staphylococcus, which have a doubling time of 20-30 minutes). Since most antibiotics kill bacteria only when they are dividing, this longer doubling time necessitates the use of relatively longer treatment courses for Lyme disease. Antibiotics are most effective during the growth phase, which for B. burgdorferi occurs in four-week cycles. Some clinicians have observed that chronic Lyme patients commonly experience a worsening of symptoms every four weeks; these periodic flare-ups are thought to correspond to the growth phase of B. burgdorferi.• Mechanisms of persistence While B. burgdorferi is susceptible to a number of antibiotics in vitro, there are contradictory reports as to the efficacy of antibiotics in vivo. B. burgdorferi may persist in humans and animals for months or years despite a robust immune response and standard antibiotic treatment, particularly when treatment is delayed and dissemination widespread. Numerous studies have demonstrated persistence of infection despite antibiotic therapy. Various survival strategies of B. burgdorferi have been posited to explain this phenomenon, including the following: Diagnosis The most reliable method of diagnosing Lyme disease is a clinical exam by an experienced practitioner, taking into account symptoms, history, and possible exposure to ticks in an endemic area. 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."•• and herpes simplex type virus 2.••••• Polymerase chain reaction (PCR) tests for Lyme disease may also be available to the patient. A PCR test attempts to detect the genetic material (DNA) of the Lyme disease spirochete, whereas the Western blot and ELISA tests look for antibodies to the organism. PCR tests are rarely susceptible to false-positive results but can often show false-negative results. Given the testing difficulties described above, some patients are employing a vitamin D metabolites test as an alternative indicator. A finding of a low 25-hydroxyvitamin D level coupled with a high 1,25-dihydroxyvitamin D level can be associated with an infection by B. burgdorferi or other spirochetal bacteria. • Since such abnormal vitamin D levels can also be caused by other disease processes, further evaluation is warranted to rule those out before initiating treatment. Prognosis For early cases, prompt treatment is usually curative. However, the severity and treatment of Lyme disease may be complicated due to late diagnosis, failure of antibiotic treatment, simultaneous infection with other tick-borne diseases including ehrlichiosis, babesiosis, and bartonella, and immune suppression in the patient (sometimes resulting from inappropriate treatment with steroids). A meta-analysis published in 2005 found that some patients with Lyme disease have fatigue, joint and/or muscle pain, and neurocognitive symptoms persisting for years despite antibiotic treatment.• Patients with chronic Lyme disease have been shown to experience a level of physical disability equivalent to that seen in congestive heart failure.• The disease is rarely fatal in and of itself, although deaths have been reported.••••• Treatment Persons who remove attached ticks should be monitored closely for signs and symptoms of tick-borne diseases for up to 30 days. Single-dose doxycycline therapy may be considered for deer tick bites when the tick has been on the person for at least 36 hours. Traditional treatment of acute Lyme disease usually consists of a minimum two-week to one-month course of antibiotics. In later stages, the bacteria disseminate throughout the body and may cross the blood-brain barrier, making the infection more difficult to treat. Chronic or late diagnosed Lyme is treated with oral or IV antibiotics, frequently ceftriaxone, for a minimum of four weeks. With little research conducted specifically on chronic Lyme disease, treatment remains controversial. Currently there are two sets of peer-reviewed published guidelines; the International Lyme and Associated Diseases Society (ILADS) advocates extended courses of antibiotics for chronic Lyme patients, while the Infectious Diseases Society of America does not recognize chronic infection and recommends no treatment for persistent symptoms following infection (see The Lyme controversy--Two standards of care). Double-blind, placebo-controlled trials of long-term antibiotics for chronic Lyme have produced mixed results (see The Lyme controversy--Long-term antibiotic therapy). Many alternative (or supplemental) therapies have been suggested. For example, melittin, a peptide from bee venom, has been shown to exert "profound inhibitory effects" on lyme bacteria. Despite its demonstrated potency, apparently no further research has been conducted on melittin as a possible lyme treatment. Clinical trials of large doses of IV sodium ascorbate (vitamin C) have been shown to kill cancer cells and possibly parasites in the body. Largely due to this, there are many chronic lyme disease sufferers turning to natural therapies. The Lyme controversy Although there is no doubt that Lyme disease exists, and most clinicians agree on the treatment of early Lyme disease,• there is considerable controversy as to the prevalence of the disease, the proper procedure for diagnosis and treatment of later stages, and the likelihood of a chronic, antibiotic-resistant Lyme infection. On one side are those who believe that Lyme disease is relatively rare, easily diagnosed with available blood tests, and easily treated with two to four weeks of antibiotics.• On the other side are those who believe that Lyme disease is under-diagnosed, that available blood tests are unreliable, and that extended antibiotic treatment is often necessary.•••• The majority of public health agencies such as the U.S. Centers for Disease Control maintain the former position, and recommend adherence to the IDSA guidelines. While this narrower position is sometimes described as the "mainstream" view of Lyme disease, published studies involving non-randomized surveys of physicians in endemic areas found physicians evenly split in their views, with the majority recognizing seronegative Lyme disease, and roughly half prescribing extended courses of antibiotics for chronic Lyme disease.•• In Europe, the earliest known cases of Lyme disease date back about 30 years. However, the disease was not thoroughly recognized before 1998. Patients entering doctor's offices with vague symptoms such as chronic exhaustion and joint pains where often wrongly diagnosed. Fortunately, more knowledge of the disease and its treatment is available now, and many patients are treated with antibiotics on time to prevent serious infection. However, many people in countries such as The Netherlands and France were diagnosed too late and still suffer from the disease in spite of regular antibiotics treatment. In some cases alternative therapy including homeopatic medication may help, but it is not indicated how exactly this would work upon the mechanism of Lyme. Two standards of care The CDC case definition Confusion about the significance of the U.S. Centers for Disease Control Case Definition for Lyme disease lies at the heart of the controversy over diagnosis. The CDC has explicitly stated that the following definition is meant to be used for surveillance purposes, not diagnostic purposes. CDC Case Definition for Lyme disease: A number of well-documented signs of chronic Lyme disease including encephalopathy (manifested by memory loss, mood changes and sleep disturbance) are not part of the CDC case definition. Therefore clinicians using the CDC criteria for diagnostic purposes will misdiagnose patients who have the disease. Additionally, reliance on the CDC case definition for clinical purposes would result in the misdiagnosis of those with false-negative test results, a widely reported phenomenon (see Diagnosis). Testing The debate over Lyme disease testing remains a heated one, with concern over both false-positives and false-negatives (see Diagnosis). Tests currently rely on indirect methods of detection (i.e. the body's immune system response), because it is very difficult to culture the bacteria directly from patients. Specific issues with regard to the testing controversy include the following: Long-term antibiotic therapy There is little concrete evidence either for or against the use of antibiotics for chronic Lyme disease, because only three such double-blind, placebo-controlled clinical trials have been funded to date by the U.S. National Institutes of Health, with conflicting results. Evidence from controlled studies 1) Klempner et al (2001). One month of intravenous ceftriaxone followed by two months of low-dose oral doxycycline or placebo given to chronic Lyme patients with one or more of the following symptoms: musculoskeletal pain, cognitive impairment, radicular pain, paresthesias or dysesthesias. 2) Krupp et al (2003). Four weeks of intravenous ceftriaxone or placebo given to chronic Lyme patients with "persistent severe fatigue". 3) Fallon et al (not yet published). Results presented on October 22, 2004 at the Columbia University/Lyme Disease Association Conference in Rye, NY Intensive treatment helps people with Lyme disease (Press release). Ten weeks of intravenous ceftriaxone or placebo given to chronic Lyme patients with ongoing memory impairment. It is important to note that Fallon et al's study is the only biological examination of chronic Lyme Disease to date. In the two other studies, results were interpreted using questionnaires, often administered over the phone. Fallon's study had several blinds. This level of methodology has never before been attempted in a study of chronic Lyme Disease. One of the reasons that many levels of blind were used in Fallon's study has to do with the controversy surrounding Lyme Disease. The aim of this study was to include people for whom there was little disagreement in terms of a correct Lyme Disease diagnosis. Secondly, the strict methodology, though tedious, was required because scientific rigor of a very high degree was necessary given the political nature of Lyme Disease. In this study, patients with chronic Lyme Disease were given SPECT scans before and after treatment. A SPECT scan of the brain qualitatively or quantitatively (depending on the sophistication of the equipment) measures metabolic and blood flow activity within the brain. This is a physical marker that can scientifically examine cause and effect as opposed to questionnaires which are open to the opinions of the participant and influence of the examiner. Patients were also administered purely quantitative examinations aimed at assessing disability, ie: neuropsychological testing. Lastly, as in other studies, patients were asked how they felt after treatment. All of these tests included several degrees of blind, ie: radiologist blind to diagnosis, neuropsychiatrists blind to diagnosis, patient blind to treatment, etc.. Evidence from uncontrolled studies While the results of placebo-controlled studies are mixed, several uncontrolled studies suggest that longer durations of antibiotic treatment may be beneficial for chronic Lyme disease. Implications for treatment The widely publicized results of the Klempner study have led some to proclaim that long-term antibiotics are unhelpful for patients with chronic Lyme disease, warning patients and clinicians that the evidence does not support their use. Others see this as an abuse of the concept of evidence-based medicine. They argue that treatment failure in one questionably designed clinical trial does not justify such warnings in light of other evidence, and that withholding antibiotic treatment is unethical in the face of patient suffering. Since the optimal choice of antibiotic(s) and treatment duration is unknown and may vary by strain, many believe additional research on chronic Lyme disease is needed before strict treatment recommendations can be issued. Prevention The best prevention involves avoiding areas in which ticks are found and can reduce the probability of contracting Lyme disease. Other good prevention practices include wearing clothing that covers the entire body when in a wooded area; using mosquito/tick repellent; after exposure to wooded areas, check all parts of the body (including hair) for ticks. A method of protecting your whole property - Damminix - is also cited. It consists of biodegradable cardboard tubes stuffed with permethrin-treated cotton and works in the following way: Mice collect the cotton for lining their nests. The pesticide on the cotton kills any immature ticks that are feeding on the mice. It is important to put the tubes where mice will find them, such as in dense, dark brush or at the base of a log; mice are unlikely to gather the cotton from an open lawn. Best results are obtained with regular applications early in the spring and again in late summer. The more neighbors who also use Damminix, the better. Damminix appears to help control tick populations, particularly in the year following initial use. Note that it is not effective on the West Coast. A potential alternative to Damminix, the Maxforce Tick Management system, is based on plastic baitboxes that attract rodents. Rodents entering these baitboxes would then be painted with fipronil. This product requires professional installation. As of June 2006, this product is no longer available. The reason appears to have been that in 2005, there were selective reports of grey squirrels "chewing" into some Maxforce TMS boxes in areas of the northeastern United States, compromising the child resistant box. Due to this problem, the Federal Environmental Protection Agency (EPA) has asked that all similarly designed TMS boxes applied in 2006 be covered with a protective shroud capable of preventing squirrel damage. An unusual, organic approach to control of ticks and prevention of Lyme disease involves the use of domesticated guineafowl. Guinea Fowl are voracious consumers of insects and have a particular fondness for ticks. They may reduce dependence on chemical pest-control methods.•. Many victims of ticks and others with concern often turn to the Guinea Fowl Breeders Association found at Guinea Fowl Breeders Association for advice on this topic. A vaccine against a North American strain of the spirochetal bacteria was available between 1998 and 2002. When taking it off the market, the manufacturer cited poor sales, though some people believe that the actual reason was that the vaccine was not safe or effective at all. The advice of the UK's Hospital for Tropical Diseases is that significant exposure (an attached mite for more than twelve hours) should be managed, as in America & Germany, with Doxycycline 100 mg twice a day for three days. Patients should be advised to report any Erythema migrans over the subsequent two to six weeks. If there should be suspicion of disease, then a course of Doxycycline should be immediately given for ten days; without awaiting serology tests which only yield positive results after an interval of one to two months. Proper Removal of Ticks There are many urban legends about the proper and effective method to remove a tick. One legend states that something hot (cigarette; burnt match) should be applied to the back of the tick, which causes the tick to remove its head from the victim. It further states that ticks "screw" their heads into their victims; therefore, one must "unscrew" the head. These legends are incorrect and potentially dangerous. Proper removal of a tick: use a pair of tweezers, grab the head of the tick near the mouth, and pull it out. The area should then be disinfected with rubbing alcohol or hydrogen peroxide. If the head is not completely removed, local infection of the person/animal bitten may result, and a doctor should be consulted (or a veterinarian if the tick was removed from a pet). Ecology Urbanization and other anthropogenic factors can be implicated in the spread of the Lyme disease into the human population. In many areas, expansion of suburban neighborhoods has led to the gradual deforestation of surrounding wooded areas and increasing "border" contact between humans and tick-dense areas. Human expansion has also resulted in a gradual reduction of the predators that normally hunt deer as well as mice, chipmunks and other small rodents--the primary reservoirs for Lyme disease. As a consequence of increased human contact with host and vector, the likelihood of transmission to Lyme residents has greatly increased.•• Researchers are also investigating possible links between global warming and the spread of vector-borne diseases including Lyme disease.• The deer tick (Ixodes scapularis, the primary vector in the northeastern U.S.) has a two-year life cycle, first progressing from larva to nymph, and then from nymph to adult. The tick feeds only once at each stage. In the fall, large acorn forests attract deer as well as mice, chipmunks and other small rodents infected with B. burgdorferi. During the following spring, the ticks lay their eggs. The rodent population then "booms." Tick eggs hatch into larvae, which feed on the rodents; thus the larvae acquire infection from the rodents. (Note: At this stage, it is proposed that tick infestation may be controlled using acaricides (miticide). A commercial method is to provide nesting material soaked in permethrin (Damminix).) The infected larvae molt into nymphs. These infected nymphs transmit the majority of Lyme infection to humans, feeding on humans and small animals from spring through summer. The nymphs then molt into adults, which feed on larger animals such as deer in the fall and early spring. Adult ticks may also transmit disease to humans. After feeding, female adult ticks lay their eggs on the ground, and the cycle is complete. Note: on the west coast, Lyme disease is spread by the western black-legged tick (Ixodes pacificus), which has a different life cycle. The risk of acquiring Lyme disease does not necessarily depend on the existence of a local deer population, as is commonly assumed. New research suggests that eliminating deer from smaller areas (less than 2.5 ha or 6.2 acres) may in fact lead to an increase in tick density and the rise of "tick-borne disease hotspots".• Epidemiology The number of reported cases of the disease have been increasing, as are endemic regions in North America. For example, it had previously been accepted that Borrelia burgdorferri couldn't be maintained in an enzootic cycle in the Southern United States because it was assumed the large lizard population would dilute the prevalence of Borrelia burgdorferri in local tick poplations. The reason this assumption was made was based upon a study which found that lizard blood from certain species was lethal to Borrelia burgdorferri. Secondly, in areas where lizards are abundant, they are often used as blood meals by sequestering ticks. However, when this theory has been examined it has failed to be as promising in the real world as it had been in previous lab experiments. This suggests that the enzootic cycle in areas of the country other than New England are highly complex and the study needed to identify risk factors will be a difficult epidemiological task. For example, in recent studies from Clark, results have shown that the prevalence of Borrelia burgdorferri has been very high, even among lizards. The author speculated that the enzootic cycle in nature for Borrelia burgdorferri in the South was quite different from that found in New England. For instance, in repeated studies from Clark, a high prevalence of Borrelia burgdorferri sensu lato was found in her study of Southern enzootic cycles of Borrelia burgdorferri, whereas in New England, enzootic cycles are almost entirely Borrelia burgdorferri sensu stricto. Lyme disease is reported in nearly every state in the U.S., but there are concentrated areas in the north-east, mid-Atlantic states, Wisconsin, Minnesota, and northern California. Lyme disease is also endemic to Europe and Asia. History Lyme disease is named after a cluster of cases that occurred in and around Old Lyme and Lyme, Connecticut in 1975. Before 1975, elements of Borrelia infection were also known as Tickborne meningopolyneuritis, Garin-Bujadoux syndrome, Bannwarth syndrome or sheep tick fever. The disease was first documented as a skin rash in Europe in 1883. Over the years, researchers there identified additional features of the disease, including an unidentified pathogen, its response to penicillin, the role of the Ixodes tick (black legged tick) as its vector, and other symptoms including those affecting the central nervous system. In the U.S., Borrelia burgdorferi has been isolated in the skin of white-footed mice in museum specimens that date back to the 1870s in Massachusetts, but researchers were unaware of the organism's existence until the 1970s. Interest in tick-borne infections in the U.S. began with the first report of tick-borne relapsing fever in 1905, and the discovery of the wood tick's role as a vector of Rocky Mountain spotted fever the following year. However, the full syndrome now known as Lyme disease was not recognized until a cluster of cases originally thought to be juvenile rheumatoid arthritis was identified in three towns in southeastern Connecticut in 1977. Two of these towns, Lyme and Old Lyme, gave the disease its popular name. In 1982 a novel spirochete was isolated and cultured from the midgut of Ixodes ticks, and subsequently from patients with Lyme disease. The infecting agent was first identified by Jorge Benach, and soon after isolated by Willy Burgdorfer, a scientist at the National Institutes of Health, who specialized in the study of spirochete microorganisms. The spirochete was named Borrelia burgdorferi in his honor. Burgdorfer was the partner in the successful effort to culture the spirochete, along with Alan Barbour. | |||||||
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