Jump to content

Lyme disease

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Rmky87 (talk | contribs) at 20:33, 20 March 2007 (alphabetized cats). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Lyme disease
SpecialtyInfectious diseases, dermatology, neurology, cardiology Edit this on Wikidata

Lyme disease or Lyme borreliosis is the most common tick-borne disease in North America and Europe, and the fastest-growing infectious disease in the United States.[citation needed] It is named after the town of Lyme, Connecticut where a cluster of cases was identified in 1977, although clinical features of the disease had been described in Europe as early as 1909.[1] Although Lyme disease has now been reported in 49 of 50 states in the U.S, about 99% of all reported cases are confined to just five geographic areas (New England, Mid-Atlantic, East-North Central, South Atlantic, and West North-Central). The cause of Lyme disease is a bacterial infection with a spirochete from the species complex Borrelia burgdorferi sensu lato, which 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 the U.S. National Institute of Allergy and Infectious Diseases' Rocky Mountain Laboratories 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 and flu-like symptoms in its initial stage, followed by musculoskeletal, arthritic, neurologic, psychiatric and/or cardiac manifestations. Early detection and prompt antibiotic treatment most often result in an excellent prognosis. However early detection is difficult when the characteristic rash is not present, and even those who are diagnosed and treated early may remain symptomatic.[2]

Delayed or inadequate treatment may often lead to late stage Lyme 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. One is advocated by the International Lyme and Associated Diseases Society (ILADS);[3][4] the other has been developed by the Infectious Diseases Society of America (IDSA).[5]

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.

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 were 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.

Microbiology

Main article: Lyme disease microbiology
File:Borrelia image.jpg
Borrelia burgdorferi the causative agent of lyme disease. Magnified 400 times.

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.[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: B. lusitaniae[7] in Europe (especially Portugal), North Africa and Asia, B. bissettii[8][9] in the U.S. and Europe, and B. spielmanii[10][11] in Europe. B. valaisiana was detected by PCR in human spinal fluid in Greece,[12] and is present in (Eurasia, especially England, Switzerland and the Netherlands); Additional B. burgdorferi sensu lato genospecies suspected of causing illness, but not confirmed by culture, include 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.[13] 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.[14] 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.[15][16]

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),[17] 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;[citation needed] typically, for the spirochaete 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,[18] 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.[citation needed]

Congenital

Lyme disease can be transmitted from an infected mother to fetus through the placenta during pregnancy, possibly resulting in stillbirth.[19][20] The risk of transmission is minimized if the mother receives prompt antibiotic treatment,[citation needed] though physicians disagree as to the duration of treatment required.[citation needed]

Other

There is at least one case report of transmission by a biting fly.[21] Lyme spirochetes have been found in biting flies as well as mosquitos.[22] 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.[23] There is also some anecdotal, largely unconfirmed evidence of sexual transmission.[citation needed] Lyme spirochetes have been found in semen[24] and breast milk,[25] though transmission by these routes has yet to be proven.

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.[26][27] Researchers are also investigating possible links between global warming and the spread of vector-borne diseases including Lyme disease.[28]

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".[29]

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 burgdorferi couldn't be maintained in an enzootic cycle in California because it was assumed the large lizard population would dilute the prevalence of Borrelia burgdorferi in local tick poplations. The reason this assumption was made was based upon a study which found blood from the Western Fence Lizard was lethal to Borrelia burgdorferi, wihch is pertinent because in areas where lizards are abundant, they are often used as blood meals by nymphal stage ticks. For years it was believed that ticks in California had Minimum Infection Rates of only 2% or 3% because of the Western Fence Lizard and its role in the ecosystem. However, a landmark study in 2003 by the San Jose State Entomology Department published in the Journal of Medical Entomology found 17.8% Minimum Infection Rates in adult ticks. This suggests that the enzootic cycle in areas of the country other than New England are highly complex. For example, in recent studies from Clark, results have shown that the prevalence of Borrelia burgdorferi has been very high, even among lizards. The author speculated that the enzootic cycle in nature for Borrelia burgdorferi in the South was quite different from that found in New England. For instance, in repeated studies from Clark, a high prevalence of Borrelia burgdorferi sensu lato was found in her study of Southern enzootic cycles of Borrelia burgdorferi, whereas in New England, enzootic cycles are almost entirely Borrelia burgdorferi 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.

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.

For clothing, you should wear long sleeve shirts and pants that are tucked into socks or boots. One should also wear light colored clothing so that you can see the tick on you before it attaches itself.

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. [30]

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.[31] 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 neither safe nor effective.[32]

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.[33] 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.

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 because if a tick is disturbed it may regurgitate its stomach contents into the host including the agents of tick borne disease if the tick is infected. Proper removal of a tick: use a pair of tweezers, grab the head of the tick near the mouth, and pull it straight out, no turning or twisting. 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). It is important not to handle the tick with bare hands or let it crawl on you because simply touching a tick that has RMSF (Rocky Mountain Spotted Fever) may transmit that infection.

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

Bull's-eye-like rash caused by Lyme disease.

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.[34][35] Multiple painless EM rashes may occur, indicating disseminated infection. The true incidence of the rash is disputed, with estimates ranging from less than 50%[36][37] to over 80%[citation needed] of those infected.

Other early symptoms of Lyme disease are usually nonspecific and include fever, malaise, fatigue, headache, muscle and joint aches. Heart palpitations, kidney and intestinal pain may also occur. Early objective manifestations which may be present include meningitis, facial paralysis such as Bells palsy, and/or heart block.

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 months to years. Asymptomatic infection exists, but the incidence of this is unknown.[citation needed]

Late stage 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 disperse and invade various organs and tissue. 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.[citation needed] 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. 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.[36]

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."[38][39]

The EM rash, which does not occur in all cases, is considered sufficient to make a diagnosis of Lyme disease and prompt treatment without further testing. In fact because of the undisputed high rate of false negatives during the early stage of the disease (before a sufficient antibody response has been established), it is recommended that tests not be performed when a patient has an EM rash.[35][40][41]

The serological laboratory tests available are the Western blot and ELISA. In the two-tiered protocol recommended by the CDC according to their case definition, the ELISA is performed first, and if it is positive or equivocal, a Western blot is then performed to support the diagnosis. The reliability of testing in diagnosis remains controversial (see Lyme disease controversy#Testing).

False-positive results for the Western blot IgM are described with varicella-zoster virus,[42][43] Epstein-Barr virus,[44][45] cytomegalovirus.[44] and herpes simplex type virus 2.[46] However studies show the Western blot IgM has a specificity of 94-96% for patients with symptoms suggestive of Lyme disease.[47][48]

False-negative test results have been widely reported in both early and late disease.[49][50][51][52][53]

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. [54] 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.

Also, a rash around the bitten area might be a sign for the disease too. Unfortunately, though, only about three-fourths of the people who are infected with the disease get a rash.

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. 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 so called chronic Lyme disease, treatment remains controversial. Currently there are two sets of peer-reviewed published guidelines; the International Lyme and Associated Diseases Society (ILADS)[55] advocates extended courses of antibiotics for chronic Lyme patients in light of evidence of persistent infection, while the Infectious Diseases Society of America[56] does not recognize chronic infection and recommends no treatment for persistent symptoms (see Lyme disease controversy#Two standards of care). Double-blind, placebo-controlled trials of long-term antibiotics for chronic Lyme have produced mixed results (see Lyme disease controversy#Long-term antibiotic therapy).

A number of alternative therapies have been suggested, though clinical trials have not been conducted. For example, the use of hyperbaric oxygen therapy (which is used conventionally to treat a number of other conditions), as an adjunct to antibiotics for Lyme has been discussed.[57] Though there is no published data from clinical trials to support its use, preliminary results using a murine model suggest its effectiveness against Borrelia burgdorferi both in vitro and in vivo.[58] Alternative medicine approaches include bee venom because it contains the peptide melittin, which has been shown to exert profound inhibitory effects on lyme bacteria in vitro.[59] The herb andrographis, though not specifically studied for Borrelia species, has been found to have both antimalarial and antibacterial properties against a wide range of organisms in vitro and in vivo, leading some herbalists to recommend it for Lyme.[60] Other alternative practitioners recommend large doses of salt combined with vitamin C, based on the theory that this protocol kills bacteria by enhancing the activity of elastase and possibly by other mechanisms,[61] though the safety and efficacy of this approach remains unproven.

A pilot study has shown potential for the drug diflucan in the treatment of Lyme.[62]

Prognosis

For early cases, prompt treatment is usually curative.[2] 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.[63] Patients with Late Stage Lyme disease have been shown to experience a level of physical disability equivalent to that seen in congestive heart failure.[64] The disease can be fatal in and of itself; deaths have been reported.[65][66][67][68][69] The first CDC recognized death from Lyme disease was Amanda Schmidt, 11.[70]

Controversy

Main article: Lyme disease controversy

There is no doubt that Lyme disease exists, and most clinicians agree on the treatment of early Lyme disease,[71] 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.[72] 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.[73][74][75][76]

The majority of public health agencies such as the U.S. Centers for Disease Control maintain the former position. 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.[77][78]

Since October 2006, the Lyme controversy has heated up dramatically beginning with the release of updated diagnosis and treatment guidelines from the Infectious Diseases Society of America (IDSA).[79] The new IDSA recommendations are even more restrictive than before, requiring either an EM rash or positive laboratory tests for diagnosis. Seronegative Lyme disease is no longer acknowledged, except in early Lyme. The authors of the guidelines maintain that chronic Lyme disease does not result from persistent infection, and therefore treatment beyond 2-4 weeks is not recommended by the IDSA, even in late stage cases.

References

  1. ^ Sternbach G, Dibble C (1996). "Willy Burgdorfer: Lyme disease". J Emerg Med. 14 (5): 631–4. PMID 8933327.
  2. ^ a b Nowakowski J, Nadelman R, Sell R, McKenna D, Cavaliere L, Holmgren D, Gaidici A, Wormser G (2003). "Long-term follow-up of patients with culture-confirmed Lyme disease". Am J Med. 115 (2): 91–6. PMID 12893393.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Johnson, Lorraine (2005-02). "Lyme disease: two standards of care". International Lyme and Associated Diseases Society. Retrieved 2006-11-17. {{cite web}}: Check date values in: |date= (help)
  4. ^ Johnson L, Stricker R (2004). "Treatment of Lyme disease: a medicolegal assessment". Expert Rev Anti Infect Ther. 2 (4): 533–57. PMID 15482219.
  5. ^ Wormser, Gary (2006). "The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America". Clin Infect Dis. 43: 1089–1134. {{cite journal}}: Unknown parameter |author link= ignored (|author-link= suggested) (help)
  6. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Collares-Pereira M, Couceiro S, Franca I, Kurtenbach K, Schafer SM, Vitorino L, Goncalves L, Baptista S, Vieira ML, Cunha C (2004). "First isolation of Borrelia lusitaniae from a human patient" (PDF). J Clin Microbiol. 42 (3): 1316–8. PMID 15004107.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Postic D, Ras NM, Lane RS, Hendson M, Baranton G (1998). "Expanded diversity among Californian borrelia isolates and description of Borrelia bissettii sp. nov. (formerly Borrelia group DN127)" (PDF). J Clin Microbiol. 36 (12): 3497–504. PMID 9817861.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Maraspin V, Cimperman J, Lotric-Furlan S, Ruzic-Sabljic E, Jurca T, Picken RN, Strle F (2002). "Solitary borrelial lymphocytoma in adult patients". Wien Klin Wochenschr. 114 (13–14): 515–23. PMID 12422593.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Richter D, Postic D, Sertour N, Livey I, Matuschka FR, Baranton G (2006). "Delineation of Borrelia burgdorferi sensu lato species by multilocus sequence analysis and confirmation of the delineation of Borrelia spielmanii sp. nov". Int J Syst Evol Microbiol. 56 (Pt 4): 873–81. PMID 16585709.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Foldvari G, Farkas R, Lakos A (2005). "Borrelia spielmanii erythema migrans, Hungary". Emerg Infect Dis. 11 (11): 1794–5. PMID 16422006.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Diza E, Papa A, Vezyri E, Tsounis S, Milonas I, Antioniadis A. (2004). "Borrelia valaisiana in cerebrospinal fluid [letter]". Emerg Infect Dis. 10 (9): 1692–3. PMID 15503409.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Varela AS, Luttrell MP, Howerth EW, Moore VA, Davidson WR, Stallknecht DE, Little SE (2004). "First culture isolation of Borrelia lonestari, putative agent of southern tick-associated rash illness" (PDF). J Clin Microbiol. 42 (3): 1163–9. PMID 15004069.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ Masters E, Granter S, Duray P, Cordes P (1998). "Physician-diagnosed erythema migrans and erythema migrans-like rashes following Lone Star tick bites". Arch Dermatol. 134 (8): 955–60. PMID 9722725.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Scoles GA, Papero M, Beati L, Fish D (2001). "A relapsing fever group spirochete transmitted by Ixodes scapularis ticks". Vector Borne Zoonotic Dis. 1 (1): 21–34. PMID 12653133.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Bunikis J, Tsao J, Garpmo U, Berglund J, Fish D, Barbour AG (2004). "Typing of Borrelia relapsing fever group strains". Emerg Infect Dis. 10 (9): 1661–4. PMID 15498172.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  17. ^ Clark K (2004). "Borrelia species in host-seeking ticks and small mammals in northern Florida" (PDF). J Clin Microbiol. 42 (11): 5076–86. PMID 15528699.
  18. ^ Wormser G, Masters E, Nowakowski J, McKenna D, Holmgren D, Ma K, Ihde L, Cavaliere L, Nadelman R (2005). "Prospective clinical evaluation of patients from missouri and New York with erythema migrans-like skin lesions". Clin Infect Dis. 41 (7): 958–65. PMID 16142659.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ MacDonald AB (1989). "Gestational Lyme borreliosis. Implications for the fetus" (PDF). Rheum Dis Clin North Am. 15 (4): 657–77. PMID 2685924.
  20. ^ Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT (1985). "Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi". Ann Intern Med. 103 (1): 67–8. PMID 4003991.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Luger S (1990). "Lyme disease transmitted by a biting fly" (html). N Engl J Med. 322 (24): 1752. PMID 2342543.
  22. ^ Magnarelli L, Anderson J (1988). "Ticks and biting insects infected with the etiologic agent of Lyme disease, Borrelia burgdorferi" (PDF). J Clin Microbiol. 26 (8): 1482–6. PMID 3170711.
  23. ^ Burgdorfer W (1998). "Increased evidence of mosquito/spirochete associations." (html). 11th International Scientific Conference on Lyme Disease, 1998. {{cite conference}}: Unknown parameter |booktitle= ignored (|book-title= suggested) (help)
  24. ^ Bach G (2001). "Recovery of Lyme spirochetes by PCR in semen samples of previously diagnosed Lyme disease patients." (html). 14th International Scientific Conference on Lyme Disease, 2001. {{cite conference}}: Unknown parameter |booktitle= ignored (|book-title= suggested) (help)
  25. ^ Schmidt B, Aberer E, Stockenhuber C, Klade H, Breier F, Luger A (1995). "Detection of Borrelia burgdorferi DNA by polymerase chain reaction in the urine and breast milk of patients with Lyme borreliosis". Diagn Microbiol Infect Dis. 21 (3): 121–8. PMID 7648832.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. ^ LoGiudice K, Ostfeld R, Schmidt K, Keesing F (2003). "The ecology of infectious disease: effects of host diversity and community composition on Lyme disease risk". Proc Natl Acad Sci U S A. 100 (2): 567–71. PMID 12525705.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ^ Patz J, Daszak P, Tabor G, Aguirre A, Pearl M, Epstein J, Wolfe N, Kilpatrick A, Foufopoulos J, Molyneux D, Bradley D (2004). "Unhealthy landscapes: Policy recommendations on land use change and infectious disease emergence". Environ Health Perspect. 112 (10): 1092–8. PMID 15238283.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Khasnis A, Nettleman M. "Global warming and infectious disease". Arch Med Res. 36 (6): 689–96. PMID 16216650.
  29. ^ Perkins S, Cattadori I, Tagliapietra V, Rizzoli A, Hudson P (2006). "Localized deer absence leads to tick amplification". Ecology. 87 (8): 1981–6. PMID 16937637.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. ^ Protecting Property from Tick Infestation: Damminix [1] University of Maryland Medical Center
  31. ^ Duffy, DC (June 1992). "The effectiveness of Helmeted Guineafowl in the control of the deer tick, the vector of Lyme disease" (PDF). The Wilson Bulletin. 104 (2): 342–45. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  32. ^ Safety/Efficacy concerns re: Lyme vaccine: LYMErix Controversy LymeInfo.net
  33. ^ Antibiotic Prophylaxis After Tick Bite For Prevention Of Lyme Disease An Annotated Bibliography
  34. ^ Smith RP, Schoen RT, Rahn DW, Sikand VK, Nowakowski J, Parenti DL, Holman MS, Persing DH, Steere AC (2002). "Clinical characteristics and treatment outcome of early Lyme disease in patients with microbiologically confirmed erythema migrans" (PDF). Ann Intern Med. 136 (6): 421–8. PMID 11900494.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ a b Edlow JA (2002). "Erythema migrans". Med Clin North Am. 86 (2): 239–60. PMID 11982300.
  36. ^ a b Donta ST (2002). "Late and chronic Lyme disease". Med Clin North Am. 86 (2): 341–9, vii. PMID 11982305.
  37. ^ Cameron D, Gaito A, Narris N, Bach G, Bellovin S, Bock K, Bock S, Burrascano J, Dickey C, Horowitz R, Phillips S, Meer-Scherrer L, Raxlen B, Sherr V, Smith H, Smith P, Stricker R; ILADS Working Group (2004). "Evidence-based guidelines for the management of Lyme disease" (PDF). Expert Rev Anti Infect Ther. 2 ((1 Suppl)): S1-13. PMID 15581390.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ "Lyme Disease (Borrelia burgdorferi): 1996 Case Definition". CDC Case Definitions for Infectious Conditions under Public Health Surveillance. Retrieved 2006-03-15.
  39. ^ "CDC Testimony before the Connecticut Department of Health and Attorney General's Office". CDC's Lyme Prevention and Control Activities. Retrieved 2006-03-15.
  40. ^ Brown SL, Hansen SL, Langone JJ (1999). "Role of serology in the diagnosis of Lyme disease". JAMA. 282 (1): 62–6. PMID 10404913.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  41. ^ Hofmann H (1996). "Lyme borreliosis--problems of serological diagnosis". Infection. 24 (6): 470–2. PMID 9007597.
  42. ^ Feder HM Jr, Gerber MA, Luger SW, Ryan RW (1991). "False positive serologic tests for Lyme disease after varicella infection". N Engl J Med. 325 (26): 1886–7. PMID 1961232.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  43. ^ Woelfle J, Wilske B, Haverkamp F, Bialek R (1998). "False-positive serological tests for Lyme disease in facial palsy and varicella zoster meningo-encephalitis". Eur J Pediatr. 157 (11): 953–4. PMID 9835449.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  44. ^ a b Goossens HA, Nohlmans MK, van den Bogaard AE (1999). "Epstein-Barr virus and cytomegalovirus infections cause false-positive results in IgM two-test protocol for early Lyme borreliosis". Infection. 27 (3): 231. PMID 10378140.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  45. ^ Berardi VP, Weeks KE, Steere AC (1988). "Serodiagnosis of early Lyme disease: analysis of IgM and IgG antibody responses by using an antibody-capture enzyme immunoassay". J Infect Dis. 158 (4): 754–60. PMID 3049839.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  46. ^ Strasfeld L, Romanzi L, Seder RH, Berardi VP (2005). "False-positive serological test results for Lyme disease in a patient with acute herpes simplex virus type 2 infection". Clin Infect Dis. 41 (12): 1826–7. PMID 16288417.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  47. ^ Engstrom SM, Shoop E, Johnson RC (1995). "Immunoblot interpretation criteria for serodiagnosis of early Lyme disease" (PDF). J Clin Microbiol. 33 (2): 419–27. PMID 7714202.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  48. ^ Sivak SL, Aguero-Rosenfeld ME, Nowakowski J, Nadelman RB, Wormser GP (1996). "Accuracy of IgM immunoblotting to confirm the clinical diagnosis of early Lyme disease". Arch Intern Med. 156 (18): 2105–9. PMID 8862103.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  49. ^ Cite error: The named reference Lawrence was invoked but never defined (see the help page).
  50. ^ Coyle PK, Schutzer SE, Deng Z, Krupp LB, Belman AL, Benach JL, Luft BJ (1995). "Detection of Borrelia burgdorferi-specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease". Neurology. 45 (11): 2010–5. PMID 7501150.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  51. ^ Paul A (2001). "[Arthritis, headache, facial paralysis. Despite negative laboratory tests Borrelia can still be the cause]". MMW Mortschr Med. 143 (6): 17. PMID 11247357.
  52. ^ Pikelj F, Strle F, Mozina M (1989). "Seronegative Lyme disease and transitory atrioventricular block". Ann Intern Med. 111 (1): 90. PMID 11247357.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  53. ^ Oksi J, Uksila J, Marjamaki M, Nikoskelainen J, Viljanen MK (1995). "Antibodies against whole sonicated Borrelia burgdorferi spirochetes, 41-kilodalton flagellin, and P39 protein in patients with PCR- or culture-proven late Lyme borreliosis" (PDF). J Clin Microbiol. 33 (9): 2260–4. PMID 7494012.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  54. ^ Marshall TG, Marshall FE (2004). "Sarcoidosis succumbs to antibiotics--implications for autoimmune disease". Autoimmun Rev. 3 (4): 295–300. PMID 15246025.
  55. ^ International Lyme and Associated Diseases Society (ILADS)
  56. ^ Infectious Diseases Society of America
  57. ^ Taylor R, Simpson I (2005). "Review of treatment options for lyme borreliosis". J Chemother. 17 Suppl 2: 3–16. PMID 16315580.
  58. ^ Pavia C (2003). "Current and novel therapies for Lyme disease". Expert Opin Investig Drugs. 12 (6): 1003–16. PMID 12783604.
  59. ^ Lubke LL, & Garon CF. "The antimicrobial agent melittin exhibits powerful in vitro inhibitory effects on the Lyme disease spirochete." Clin Infect Dis 1997 Jul;25 Suppl 1:S48-51. PMID 9233664.
  60. ^ Buhner, SH (2005). Healing Lyme. Randolph, VT: Raven Press. ISBN 0-9708696-3-0.
  61. ^ Bradford RW and Allen HW. "Lyme Disease, Potential Plague of the 21st Century." Townsend Letter 2005 Jan. [2]
  62. ^ [3]
  63. ^ Cairns V, Godwin J (2005). "Post-Lyme borreliosis syndrome: a meta-analysis of reported symptoms". Int J Epidemiol. 34 (6): 1340–5. PMID 16040645.
  64. ^ Klempner MS, Hu LT, Evans J, Schmid CH, Johnson GM, Trevino RP, Norton D, Levy L, Wall D, McCall J, Kosinski M, Weinstein A (2001). "Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease". N Engl J Med. 345 (2): 85–92. PMID 11450676.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  65. ^ Kirsch M, Ruben FL, Steere AC, Duray PH, Norden CW, Winkelstein A (1988). "Fatal adult respiratory distress syndrome in a patient with Lyme disease". JAMA. 259 (18): 2737–9. PMID 3357244.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  66. ^ Oksi J, Kalimo H, Marttila RJ, Marjamaki M, Sonninen P, Nikoskelainen J, Viljanen MK (1996). "Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature". Brain. 119 (Pt 6): 2143–54. PMID 9010017.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  67. ^ Waniek C, Prohovnik I, Kaufman MA, Dwork AJ (1995). "Rapidly progressive frontal-type dementia associated with Lyme disease". J Neuropsychiatry Clin Neurosci. 7 (3): 345–7. PMID 7580195.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  68. ^ Cary NR, Fox B, Wright DJ, Cutler SJ, Shapiro LM, Grace AA (1990). "Fatal Lyme carditis and endodermal heterotopia of the atrioventricular node". Postgrad Med J. 66 (772): 134–6. PMID 2349186.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  69. ^ Reimers CD, de Koning J, Neubert U, Preac-Mursic V, Koster JG, Muller-Felber W, Pongratz DE, Duray PH (1993). "Borrelia burgdorferi myositis: report of eight patients". J Neurol. 240 (5): 278–83. PMID 8326331.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  70. ^ [4]
  71. ^ Murray T, Feder H (2001). "Management of tick bites and early Lyme disease: a survey of Connecticut physicians". Pediatrics. 108 (6): 1367–70. PMID 11731662.
  72. ^ Wormser G (2006). "Clinical practice. Early Lyme disease". N Engl J Med. 354 (26): 2794–801. PMID 16807416.
  73. ^ Stricker RB, Lautin A, Burrascano JJ (2006). "Lyme Disease: The Quest for Magic Bullets". Chemotherapy. 52 (2): 53–59. PMID 16498239.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  74. ^ Phillips SE, Harris NS, Horowitz R, Johnson L, Stricker RB (2005). "Lyme disease: scratching the surface". Lancet. 366 (9499): 1771. PMID 16298211.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  75. ^ Phillips S, Bransfield R, Sherr V, Brand S, Smith H, Dickson K, and Stricker R (2003). "Evaluation of antibiotic treatment in patients with persistent symptoms of Lyme disease: an ILADS position paper" (PDF). International Lyme and Associated Diseases Society. Retrieved 2006-03-15.{{cite web}}: CS1 maint: multiple names: authors list (link)
  76. ^ Harvey WT, Salvato P (2003). "'Lyme disease': ancient engine of an unrecognized borreliosis pandemic?" (PDF). Med Hypotheses. 60 (5): 742–59. PMID 12710914.
  77. ^ Ziska MH, Donta ST, Demarest FC (1996). "Physician preferences in the diagnosis and treatment of Lyme disease in the United States". Infection. 24 (2): 182–6. PMID 8740119.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  78. ^ Eppes SC, Klein JD, Caputo GM, Rose CD (1994). "Physician beliefs, attitudes, and approaches toward Lyme disease in an endemic area". Clin Pediatr (Phila). 33 (3): 130–4. PMID 8194286.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  79. ^ "New Lyme Disease Guidelines Spark Showdown". U.S. Department of Health and Human Services. 2006-11-09. Retrieved 2006-11-17.
Wikispecies has information related to Borrelia.

Government and university resources

Professional societies, disease foundations and advocacy resources

Other resources, memorials etc.

Template:FA link

Template:Link FA

Retrieved from "https://en.wikipedia.org/w/index.php?title=Lyme_disease&oldid=116611592"