Thirty-two patients with the onset of erythema chronicum migrans, Lyme arthritis, or both in mid-1976 were studied prospectively. The skin lesion (24 patients) typically lasted about 3 weeks, beginning as a red macule or papule that expanded to form a large ring with central clearing. Associated symptoms ranged from none to malaise, fatigue, chills and fever, headache, stiff neck, backache, myalgias, nausea, vomiting, and sore throat. Three patients had been bitten by ticks at the site of the initial lesion 4 to 20 days before its onset. Nineteen patients suddenly developed a monoarticular or oligoarticular arthritis 4 days to 22 weeks (median, 4 weeks) after onset of the skin lesion; eight developed arthritis without a preceding skin lesion. Seven of these 27 experienced migratory joint pains. Arthritis attacks, most commonly in the knee, were typically short (median, 8 days) but sometimes persisted for months. Other manifestations included neurologic abnormalties, myocardial conduction abnormalities, serum cryoprecipitates, elevated serum IgM levels, and elevated erythrocyte sedimentation rates. The diagnostic marker is the skin lesion; without it, geographic clustering is the most important clue.

Erythema chronicum migrans and lyme arthritis. The enlarging clinical spectrum

. Lyme borreliosis is a tick-borne infection caused by the spirochete Borrelia burgdorferi, whose discovery in 1982 solved an aetiological mystery involving a variety of dcrmatological and neurological disorders and explained their association with Lyme disease. Lyme borreliosis occurs frequently and is readily treatable with antibiotics.



Along with its discovery, however, came the realization that it is difficult to diagnose accurately, especially antibody diagnosis. False-positive antibody results in particular led to gradual widening of the clinical spectrum, and differential diagnosis became increasingly difficult.



This prospective, multicentre study presents a systematic description of Lyme borreliosis in childhood, emphasizing epidemiological and clinical issues. Because, predominantly, inpatients were examined, Lyme neuroborreliosis was the focus of the study, with the chief concern being to minimize false-positive results. To this end, we chose to narrow the diagnostic criteria, using the presence of specific antibodies in the cerebrospinal fluid as the determining factor.



The epidemiological investigation was focused on the incidence of Lyme neuroborreliosis in childhood in southern Lower Saxony as well as on the prevalence of Lyme neuroborreliosis among acute-inflammatory neurological illnesses in children. The clinical part of the study aimed at establishing criteria for differential diagnosis in addition to the detection of specific antibodies. The detection of specific IgM antibodies using an IgM capture ELISA confirmed the presence of acute Lyme borreliosis.



The study examined 208 children with Lyme borreliosis, of whom 169 had Lyme neuroborreliosis, from mid-1986 until the end of 1989. The yearly incidence of Lyme neuroborreliosis in Lower Saxony was 5.8 cases/100,000 children aged 1 to 13. The manifestation index was 0.16, or one case of Lyme neuroborreliosis per 620 infected children, compared with the presence of specific antibodies against B. burgdorferi for children in the same age group and region. Both the seasonal distribution of Lyme borreliosis, which peaked in summer and autumn, as well as the information about when the tick bites took place point to an incubation period of a few weeks.



The most frequent manifestation of Lyme neuroborreliosis in childhood was acute peripheral facial palsy, found in 55% of all cases (n = 93). Lyme borreliosis proved to be the most frequently verifiable cause of acute peripheral facial palsy in children, causing every second case of this disorder in summer and autumn. Bilateral facial palsy was, without exception, found to be caused by Lyme borreliosis; thus it can be considered a specific neurological sign of this infection.



The second most common manifestation of Lyme neuroborreliosis in childhood was aseptic meningitis (27.2%, n = 46). Lyme borreliosis was the third most common cause of aseptic meningitis in childhood (11.8%).



Meningoradiculoneuritis with peripheral nerve involvement (Bannwarth syndrome) was diagnosed in only 3.6% of the children (n = 6), although this is the most common symptom of Lyme neuroborreliosis in adult patients.



The head and neck region proved to be the predominant site of tick bites in children; adults experience most bites on their extremities. The difference in the site of the infection, as well as the short duration of the illness in children and the early treatment, may partially explain the profound differences in the clinical spectrum of Lyme neuroborreliosis in children and adults.



Nearly all cases with a positive history of tick bite and/or erythema migrans in the head and neck region showed ipsilateral facial palsy suggesting a direct invasion via the affected nerve by B. burgdorferi.



Inflammatory changes in the cerebrospinal fluid along with the presence of specific antibodies are the conditio sine qua non for a diagnosis of Lyme neuroborreliosis. The presence of IgM antibodies in the cerebrospinal fluid has proved to be the most reliable diagnostic criterion, and is responsible for the early diagnosis of acute Lyme neuroborreliosis in children. The IgM capture ELISA facilitated the simple and reliable detection of intrathecal antibody synthesis which could be successfully demonstrated in three-quarters of the cases with Lyme neuroborreliosis. Specific IgG testing was negative in most cases because of the relatively short duration of the illness in children, and is therefore of less importance here than in the diagnosis of cases of Lyme neuroborreliosis in adults.



Acute Epstein-Barr and varicella-zoster viral infections both caused false-positive findings in the IgM capture ELISA.



High dose intravenous penicillin G proved to be highly effective in paediatric cases of Lyme neuroborreliosis. Although the rate of spontaneous remission may be very high, it is not possible to predict on a patient-by patient basis just when this will occur. Thus consistent antibiotic therapy is indicated.

Epidemiology and clinical manifestations of lyme borreliosis in childhood : a prospective multicentre study with special regard to neuroborreliosis

The parallels between syphilis and Ixodes-borne borreliosis (erythema migrans borreliosis, Lyme borreliosis) are striking. Sir William Osler’s description of syphilis as the great imitator of other diseases’ is also true for the current borreliosis. Dermatologic as well as neurologic manifestations may present in a multiplicity of fashions. Both spirochetoses are infections with a potentially long-lasting course. Isolation of spirochetes from the skin of a patient with acrodermatitis chronica atrophicans with a disease duration of greater than 10 years shows the possibility of long-term survival of borreliae in humans.’ There are both historical and traditional reasons for the somewhat confusing nomenclature and the multiplicity of terms that are applied to this borreliosis and its different manifestations. In contrast to syphilis, where much of the course of the disease and its different stages (characterized by Philippe Ricord by 1838) was known long before the discovery of Treponema pallidum in 1905, the course of Ixodes-borne borreliosis was only fully realized and understood when the infecting agent, Borrelia burgdorferi, was revealed. In Europe different manifestations such as erythema migrans (EM), lymphadenosis benigna cutis (LABC), acrodermatitis chronica atrophicans (ACA), and the lymphocytic meningoradiculitis later named Bannwarth’s syndrome have been recognized since the first decades of this century. These various clinical syndromes, which were at least partly defined long before the causative borreliae were discovered, had previously been described as separate entities. The arthritis was first recognized in the 1970s in the United States by Allen Steere as a new form of inflammatory arthritis, initially named Lyme arthritis, and the credit for delineating Lyme disease belongs to him.-’-’ The differences in the current clinical descriptions of Ixodes-borne borreliosis may also appear somewhat confusing. Owing to the wide clinical spectrum, clinicians from many specialties encounter these patients. Different selections of patients may thus result in some dissimilarities in the clinical descriptions. Universal heterogeneity among the spirochetes involved may also explain some of the dissimilarities, however. Syphilis is divided into early (“infectious”) and late infection, the former comprising the primary and secondary stages. Syphilis of more than 2 years’ duration, including latent syphilis of more than 2 years’ duration, is classified as late infection.6 In Ixodes-borne borreliosis somewhat varying classifications have hitherto been used.

Early and late cutaneous manifestations in Ixodes-borne borreliosis (erythema migrans borreliosis, Lyme borreliosis).

Lyme borreliosis is caused by certain genospecies of the Borrelia burgdorferi sensu lato complex, which are transmitted by hard ticks of the genus Ixodes. The most common clinical manifestation is erythema migrans, an expanding skin redness that usually develops at the site of a tick bite and eventually resolves even without antibiotic treatment. The infecting pathogens can spread to other tissues and organs, resulting in manifestations that can involve the nervous system, joints, heart and skin. Fatal outcome is extremely rare and is due to severe heart involvement; fetal involvement is not reliably ascertained. Laboratory support-mainly by serology-is essential for diagnosis, except in the case of typical erythema migrans. Treatment is usually with antibiotics for 2 to 4 weeks; most patients recover uneventfully. There is no convincing evidence for antibiotic treatment longer than 4 weeks and there is no reliable evidence for survival of borreliae in adequately treated patients. European Lyme borreliosis is a frequent disease with increasing incidence. However, numerous scientifically questionable ideas on its clinical presentation, diagnosis and treatment may confuse physicians and lay people. Since diagnosis of Lyme borreliosis should be based on appropriate clinical signs, solid knowledge of clinical manifestations is essential.

Lyme borreliosis-from tick bite to diagnosis and treatment.

Lyme borrelosis is a multi-systemic disease caused byBorrelia burgdorferisensu lato. A complete presentation of the disease is an extremely unusual oberservation, in which a skin lesion follows a tick bite, the lesion itself is followed by heart and nervous system involvement, and later on by arthritis; late involvement of the eye, nervous system, joints and skin may also occur. Information on the relative frequency of individual clinical manifestations of Lyme borreliosis is limited; however, the skin is most frequently involved and skin manifestations frequently represent clues for the diagnosis. The only sign that enables a reliable clinical diagnoisis of Lyme borreliosis is a typical erythema migrans. Laboratory confirmation of a borrelial infection is needed for all manifestations of Lyme borreliosis, with the exception of typical skin lesions.

Clinical manifestations and diagnosis of lyme borreliosis.

Über eine seltene Erythemform (Erythema chronicum migrans)

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Über eine seltene Erythemform (Erythema chronicum migrans)