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Results for “Lyme Disease”

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At least 19 recordsLinked to original sources
PubMed1986

[Disease (Lyme disease) in pediatric patients in Switzerland caused by spirochetes (Borrelia burgdorferi) of Ixodes ricinus].

Lyme disease in children is studied in the light of questionnaires sent out twice to departments and divisions of pediatrics in Switzerland. Thirty-six serologically proven cases were collected. The 48 clinical signs attributed to Lyme disease involved the skin in 40%, the nervous system in 40%, and the joints in 20%. They were erythema chronicum migrans (13), lymphocytoma (4), acrodermatitis chronica atrophicans (2), peripheral facial palsy (14), sensomotor radiculoneuritis (2), meningoencephalitis (3) and arthritis (10, 7 of which were monoarthritic). Only half the patients had a history of tick-bite. Antibiotic therapy, usually with penicillin, reduced both the duration of symptoms and frequency of secondary disease. Cardiac involvement and chronic stages with residua were not observed in this series.

Adolescent↗
PubMed1990

The enlarging clinical spectrum of Lyme disease: Lyme cerebral vasculitis, a new disease entity.

The case of a patient with cerebral vasculitis with a right thalamic infarct associated with cerebral spinal fluid Lyme disease is presented. This entity has not been described in the United States, and only one similar case in the world literature could be found. The patient presented with a progressive headache and subsequent development of grand mal seizure activity. Lyme disease has been associated with cranial nerve palsies, peripheral and cranial radiculopathies, aseptic meningitis, encephalitic symptoms, chorea, and demyelinating polyneuropathy presenting like Guillain-Barré syndrome. These syndromes can occur separately or in combination. Stroke and strokelike syndromes have been attributed to Lyme disease. The literature concerning the neurologic manifestations of Lyme disease is reviewed.

Adult↗
PubMed2003

Lyme disease (Lyme borreliosis).

Lyme borreliosis (Lyme disease) is a systemic infectious disease with a wide spectrum of symptoms affecting the skin, the heart, and the nervous and musculoskeletal systems. Lyme borreliosis is caused by the spirochaete Borrelia burgdorferi and transmitted by ticks. The disease occurs in endemic pockets with an incidence of from 50 to more than 100 cases per 100,000 inhabitants. Despite increasing knowledge about the virulence factors of the spirochaetes and the immune response of the host, many aspects of the pathogenesis, for example of chronic treatment-resistant disease, are still a matter of debate. The diagnosis is based on clinical findings and confirmed by serology. Diagnostic problems arise from patients with non-specific symptoms and a positive IgG serology. In about 80% of the patients, the disease can be cured by adequate antibiotic therapy. Evidence-based guidelines for treatment have been recently published. The only vaccine to prevent Lyme disease, licensed in the USA, has been discontinued due to disappointing sales despite good efficacy and tolerability.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Neural manifestations in Lyme disease (Lyme borreliosis of the nervous system)].

The involvement of the nervous system is common during Lyme's disease, and the term neuroborreliosis has been established. All structures of the nervous system, from meninges to periferial nerves, can be involved. Neurological manifestations are most common in the second stage (dissemination). The article deals with the most important neurological manifestations, as well as with the contemporary pathogenetic considerations and therapy. Eleven patients with neuroborreliosis who were treated at Dr. Kosta Todorovitsh Institute of Infectious and Tropical Diseases, are reviewed. Five of them had acute meningoencephalitis, of whom two had concurrent neuritis; one patient had Banawart's syndrome with arthralgias, arthritis and fatigue syndrome; two patients had neuritis; one had bilateral facial palsy; two had chronic fatigue syndrome.

Adult↗
PubMed1993

Lyme disease (Lyme borreliosis) in horses.

This article reviews epizootiology, public health considerations, antibody testing, and molecular biology of Lyme borreliosis. Correlation of clinical signs with titer response is discussed.

Animals↗
PubMed1995

Early disseminated Lyme disease: Lyme meningitis.

Lyme meningitis is the direct result of invasion of the nervous system by Borrelia burgdorferi. Occurring within the first few months of infection, it initially presents as a chronic basilar meningitis. Much about the pathogenesis of Lyme meningitis has been learned from animal models, the best being the adult Rhesus macaque. Injection of these animals with a highly infective strain of B. burgdorferi has led to a very predictable course of events: erythema migrans within the first few weeks after injection, development of anti-B. burgdorferi antibody, detection of spirochetemia in weeks 3 and 4, and central nervous system (CNS) invasion within 1 month with cerebrospinal fluid (CSF) pleocytosis. In humans, facial palsy is the earliest clinical indicator. Headache and meningismus are symptoms of inflammation of the subarachnoid space. Severe fatigue and arthralgia are common extra-CNS symptoms. Culture is not generally useful for detecting or confirming Lyme meningitis. False-positive serologic tests may occur in patients with other infections, inflammatory processes, or malignancies. Immunoblotting will differentiate true-from false-positive antibody reactivity. Lack of a consistently positive serum antibody titer should make the diagnosis of Lyme meningitis suspect. Positive CSF antibody is almost universal in patients with Lyme meningitis. Polymerase chain reaction is a direct test that is highly specific and sensitive. The antibiotic treatment of choice is intravenous (i.v.) cephalosporins or penicillin for 2-3 weeks. If the clinical picture is anything less than absolutely classic, a lumbar puncture and Western blot of serum should be obtained in a seropositive patient before initiating intravenous antibiotic therapy. There is no role at this time for long-term (> 1 month) intravenous antibiotics. Nonsteroidal antiinflammatory agents can also be of benefit.

Diagnosis, Differential↗
PubMed1987

Focal encephalitis in a young woman 6 years after the onset of Lyme disease: tertiary Lyme disease?

A 19-year-old woman had severe focal inflammatory encephalitis. Six years previously, she had had classic untreated Lyme disease characterized by erythema chronicum migrans, bilateral facial palsies, and lymphocytic meningitis. During her recent encephalitic illness, Lyme disease serologic tests were positive by indirect immunofluorescence microscopy, enzyme-linked immunosorbent assay, and western blot (immunoblot technique) testing. We hypothesize that the patient's focal inflammatory encephalitis was a result of a persistent spirochetal infection of the central nervous system.

Adolescent↗
PubMed1992

Prevention of Lyme disease.

Lyme disease and the use of tick repellents and physical protective measures to prevent the disease are discussed. Lyme disease is a multiple-organ-system, immune-mediated inflammatory disorder transmitted by the bites of ixodid ticks infected with Borrelia burgdorferi. An individual is at greatest risk for infection when a tick has been attached to the skin for more than 24 hours. Lyme disease occurs in three stages and may affect the skin, nervous system, cardiac system, and joints. Antimicrobials used in management consist primarily of penicillins, cephalosporins, tetracyclines, and erythromycin. Tick repellents are divided into those applied to the skin and those applied to clothing. Skin repellents include N,N-diethyl-meta-toluamide (DEET), 2-ethyl-1,3-hexanediol, and dimethyl phthalate. Permethrin is by far the most effective clothing repellent. DEET plus a permethrin-containing clothing repellent offers the best overall protection. The adverse effects of repellents are minimal, but cases of hypersensitivity have been reported, especially in children. Physical measures to prevent tick bites include avoiding tick-infested areas, wearing light-colored clothing for easy identification of crawling ticks, regularly checking the body and pets for ticks, wearing protective garments and closed-toed shoes, and removing attached ticks promptly by using tweezers or forceps to apply a steady upward pull. A vaccine for the active immunization of humans against Lyme disease remains to be developed. Although antimicrobial therapy is available for persons with Lyme disease, the best approach for those who may be exposed to infected ticks is to apply topical skin or clothing repellents and to practice common-sense measures of physical protection.

Animals↗
PubMed1997

Simultaneous expression of Borrelia OspA and OspC and IgM response in cerebrospinal fluid in early neurologic Lyme disease.

Lyme disease is the major tick-borne disease, caused by Borrelia burgdorferi (Bb). Neurological involvement is common in all stages. In vivo expression of Bb antigens (Ags) and the immune response to them has not been well investigated in the cerebrospinal fluid (CSF). Upregulation of outer surface protein (Osp) C and concomitant downregulation of OspA before tick inoculation of the spirochete has been reported in skin and blood in animals. CSF OspA Ag in early disease suggests otherwise in CSF. Early Ag expression and IgM response in human CSF was investigated here. Paired CSF and serum was collected from 16 early, predominantly erythema migrans Lyme disease patients with neurologic problems, 13 late Lyme disease patients, and 19 other neurologic disease (OND) controls. Samples were examined for IgM reactivity to recombinant Bb-specific Osps using ELISA and immunoblot. Of 12 early Lyme disease patients with neurologic involvement with both CSF and serum IgM against OspC, 7 (58%) had IgM to OspA (n = 5) or OspB (n = 2) that was restricted to the CSF, not serum. Overall, 12 of 16 (75%) of these early Lyme disease patients with neurologic involvement had CSF and serum IgM against OspC. Only 3 of 13 (23%) late Lyme disease patients and none of 19 OND controls had CSF IgM directed against OspC. In conclusion, in CSF, OspC and OspA can be coexpressed, and IgM response to them occurs in early Lyme disease patients with neurologic involvement. This biologic finding may also provide a discriminating marker for CNS infection in Lyme disease.

Adolescent↗
PubMed1997

Neuro-ophthalmic manifestations of Lyme disease.

Lyme disease is a multisystem disorder caused by infection with the Borrelia burgdorferi spirochete. The diagnosis of Lyme disease usually is based on several clinical criteria, with supportive data from laboratory testing. The presence of the bullseye skin lesion, erythema migrans, is the single pathognomonic criterion. In the 20 years since the initial description of Lyme disease in the United States, B. burgdorferi has been implicated as an etiologic agent in numerous ophthalmic and neuro-ophthalmic syndromes, involving most structures from the cornea to the cranial nerves. Neuro-ophthalmic and ocular manifestations of Lyme disease include meningitis with papilledema, cranial neuropathies, follicular conjunctivitis, nummular keratitis, and intraocular inflammation. Although an association with Lyme disease has been purported for numerous other syndromes, a definite causal relationship has not been proved in many cases. During a period of rapidly increasing awareness of Lyme disease, a high index of suspicion and poorly defined criteria for its presence have resulted in over-diagnosis of Lyme disease. In the authors' experience, the incorrect diagnosis of Lyme disease initially has been made in patients with allergic conjunctivitis, keratoconus, morning glory syndrome, craniopharyngioma, meningioma, CNS lymphoma, paraneoplastic syndrome, multiple sclerosis, sarcoid, syphilis, and functional illness. Nevertheless, this treatable infection must be an important consideration in the differential diagnosis of certain ocular or neurologic diseases.

Eye Diseases↗
PubMed1994

Orthopaedic manifestations of Lyme disease.

Lyme disease is caused by the spirochete Borrelia burgdorferi and is transmitted by the Ixodes tick. Early diagnosis is difficult because the tick bite may go unnoticed and the distinguishing rash, erythema chronicum migrans, often does not occur. Serologic tests are both sensitive and specific in the later stages of the disease but not in stage 1. Thus diagnosis of Lyme disease remains clinical. Knowledge of the orthopaedic manifestations of Lyme disease may aid in early diagnosis and help differentiate from possible cases of juvenile rheumatoid arthritis and septic arthritis. If septic arthritis is suspected, appropriate antibiotic therapy should be initiated while awaiting serology for Lyme disease. Recurrence of Lyme arthritis following antibiotic treatment is rare. Lyme disease should be considered in any patient with arthritis and a history of rash, fever, or neurologic or cardiac abnormality.

Adult↗
PubMed1998

[Lyme disease].

Lyme disease is a tick-borne disease, and recognized as a complex, multisystem disorder. An outbreak [correction of outback] of Lyme disease was first described in the United States in the 1970s. The presence of Borrelia burgdorferi, its causative agent, in the skin results in the development of characteristic expanding red skin lesions, erythema migrans (EM). EM may be associated with cardiac abnormalities, meningitis, and cranial peripheral neuropathies. Arthritis, neurologic and skin manifestations may persist for several years and become chronic in a small percentage of patients. Studies on the classification of B. burgdorferi resulted in the identification of three closely related genospecies, and different clinical manifestation of Lyme disease have been correlated with the infecting genospecies. The diagnosis of Lyme disease should be based primarily on the clinical presentation, epidemiological information and serological tests. Antimicrobials are effective in the treatment of Lyme disease in most patients. Lyme disease is a zoonosis and endemic in areas where suitable mammalian reservoirs for B. burgdorferi and appropriate hosts for the tick vector are present. According to changes in the natural environment, the distribution of infected ticks and reservoirs is anticipated to expand.

Animals↗