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PubMed2000

Lyme borreliosis.

Lyme borreliosis is a worldwide, multistage, and multi-system disease caused by borrelia spirochetes, which are transmitted by ixodes ticks. It is focally endemic in temperature climates of the northern hemisphere. Primary erythema migrans occurs at the site of inoculation. Secondary erythema migrans occurs at sites of hematogenous dissemination. Variations in genospecies account for variations in presentation, including borrelial lymphocytoma. Disseminated disease includes constitutional signs and symptoms, intermittent oligoarticular arthritis, meningitis, cranial neuritis, radiculoneuropathy, encephalopathy, atrioventricular block, and myopericarditis. Late persistent disease includes acrodermatitis chronica atrophicans, chronic arthritis, neurological impairment, and fatigue. There can be difficulties with both clinical and laboratory diagnosis. First-line oral therapies for early uncomplicated disease are doxycycline and amoxicillin. First-line intravenous therapy for complicated or resistant disease is ceftriaxone. Prevention includes avoiding tick habitats, dressing sensibly, judicious use of repellants, and early removal of imbedded ticks. Vaccination is indicated only for frequent or prolonged exposure to tick-infested habitat.

Anti-Bacterial Agents↗

PubMed1985

[Erythema migrans borreliosis in the Federal Republic of Germany. Epidemiology and clinical aspects].

A positive antibody titre against Ixodes-ricinus-Borrelia (burgdorferi), using indirect immunofluorescence or ELISA, could be detected in serum and (or) liquor of 935 (32%) out of a total of 2955 patients between January 1984 and July 1985. In 289 of these cases the typical clinical manifestations were lacking whereas a characteristic disease picture enabled a diagnosis to be made in 171 patients with negative or borderline antibody titres. The 1106 cases of infection observed covered all regions of the country. A typical clinical syndrome was seen in 817 (74%) of these. Most common were erythema chronicum migrans (n = 458) and meningopolyneuritis Garin-Bujadoux-Bannwarth (n = 404); in 42% of the cases meningopolyneuritis was preceded by an erythema. Arthritis (n = 63), acrodermatitis chronica atrophicans (n = 72), carditis (n = 13) and lymphadenosis benigna cutis (n = 5) were much less common. Chronic Borrelian encephalomyelitis (n = 45) appeared surprisingly often (n = 45). The fact that in 73% of cases the various syndromes appeared alone, were double in 24% and combined only in 3%, illustrates the polymorphic nature of this disease.

Adolescent↗

PubMed2003

Anetoderma: another facet of Lyme disease?

Lyme disease has been suspected to be one cause of secondary anetoderma. We present a 25-year-old male patient with multiple lesions of anetoderma with a diameter of up to 2 cm that developed within the last 4 weeks without subjective symptoms. The histopathologic pattern was similar to the inflammatory stage of acrodermatitis chronica atrophicans. Polymerase chain reaction analysis out of the paraffin-embedded tissue, confirmed by sequencing of the obtained nucleotide product, revealed a part of the 23 S ribosomal RNA gene of Borrelia burgdorferi sensu lato. Enzyme-linked immunosorbent assay showed an increased serum IgG titer against B burgdorferi corroborated by Western blot analysis. After a treatment with oral doxycycline (100 mg twice a day) for 30 days the anti-B burgdorferi titer decreased significantly and no new lesions appeared. Some cases of anetoderma might be caused by Borrelia and patients with anetoderma should be examined for borreliosis including serology and polymerase chain reaction of lesional skin. In cases of Borrelia-induced anetoderma, early antibiotic treatment could prevent further progression of the disfiguring skin lesions and the underlying disease.

Adult↗

PubMed2001

Avidity determination of Borrelia burgdorferi-specific IgG antibodies in Lyme disease.

The avidity indices of Borrelia burgdorferi-specific IgG antibodies were estimated using ELISA in sera from patients with different stages of Lyme disease. In addition, sera from healthy students with proof of borrelial-specific IgG antibodies from standard serology were tested. Low avidity indices were detected predominantly in sera from patients with early-stage Lyme disease [erythema migrans (EM); n = 25]. High avidity indices were found in healthy students (n = 72) and in most of the patients with neuroborreliosis (NB; n = 44) and chronic late-stage Lyme disease [acrodermatitis chronica atrophicans (ACA); n = 36]. In conclusion, early-stage Lyme disease (EM) could be differentiated from advanced and chronic stages (NB, ACA) and from "seropositive" healthy persons using avidity determination in the majority of patients in this study.

Antibody Affinity↗

PubMed2000

Antigenic conservation of an immunodominant invariable region of the VlsE lipoprotein among European pathogenic genospecies of Borrelia burgdorferi SL.

Lyme disease is caused by genetically divergent spirochetes, including 3 pathogenic genospecies: Borrelia burgdorferi sensu stricto, B. garinii, and B. afzelii. Serodiagnosis is complicated by this genetic diversity. A synthetic peptide (C(6)), based on the 26-mer invariable region (IR(6)) of the variable surface antigen of B. burgdorferi (VlsE), was used as ELISA antigen, to test serum samples collected from mice experimentally infected with the 3 genospecies and from European patients with Lyme disease. Regardless of the infecting strains, mice produced a strong antibody response to C(6), which indicates that IR(6) is antigenically conserved among the pathogenic genospecies. Twenty of 23 patients with culture-confirmed erythema migrans had a detectable antibody response to C(6). A sensitivity of 95.2% was achieved, with serum samples collected from patients with well-defined acrodermatitis chronica atrophicans. Fourteen of 20 patients with symptoms of late Lyme disease also had a positive anti-IR(6) ELISA. Thus, it is possible that C(6) may be used to serodiagnose Lyme disease universally.

Amino Acid Sequence↗

PubMedDate not supplied

Clinical pathologic correlations of Lyme disease.

The multisystem effects caused by Borrelia burgdorferi in Lyme disease are multiple, varied, and unpredictable. In some patients, the full extent of the infection consists of a stage I acute systemic viral-like illness. Stage II primarily involves the cardiovascular system (myocarditis) and/or the central nervous system (CNS) (meningoencephalitis, polyradiculitis). More inflammatory cells are found in the heart and nervous system structures during this intermediate stage than are found in any tissues involved during stage I. Stage III is characterized by peripheral neuropathy and CNS disorders such as dementia or transverse myelitis and arthritis and synovitis of large joints such as the knee. Chronic Lyme disease is also associated with multiple and seemingly unrelated cutaneous manifestations such as acrodermatitis chronica atrophicans, sclerodermoid-like reactions, lichen sclerosus et atrophicus, subcuticular fibrous nodules, eosinophilic fasciitis-like lesions of the extremities, and, possibly, granuloma annulare. With care, spirochetes can be recovered or demonstrated by silver staining in most of the above lesions. Spirochetes have yet to be seen in the tissues of autonomic ganglia or peripheral nerves.

Acute Disease↗

PubMed1990

Spirochetal forms in the dermal lesions of morphea and lichen sclerosus et atrophicus.

Morphea and lichen sclerosus et atrophicus are cutaneous diseases that are manifest by an early edematous stage, followed later by sclerosis and atrophy. They share features with acrodermatitis chronica atrophicans and erythema chronicum migrans, diseases that have been linked to infection by the spirochete Borrelia burgdorferi. A modified silver stain was used to identify the presence of spirochetes in skin biopsy specimens of patients with morphea and lichen sclerosus et atrophicus. Spirochetal forms were identified in the lesional skin of 10 of 25 patients with morphea and in 10 of 21 cases of lichen sclerosus et atrophicus. These spiral forms of bacteria had a significant tendency to occur in early and fully developed lesions of morphea and in early lesions of lichen sclerosus et atrophicus, whereas they tended to be absent in lesions demonstrating late pathological changes.

Atrophy↗

PubMed1987

The surgical pathology of human Lyme disease. An enlarging picture.

Lyme disease is a multisystems infectious disorder caused by the spirochete, Borrelia burgdorferi. Infection occurs by ticks feeding on mammalian hosts, including humans. The distribution of the tick and spirochete is world-wide and is especially prevalent where there are large deer populations. The disease is seen in three stages. Stage I is a cutaneous rash (erythema chronicum migrans) consisting of lymphoplasmacytic infiltrates around dermal vessels. Stage II is characterized by varying forms of meningopolyradiculitis, with or without Bell's palsy or cardiac involvement (complete or incomplete heart block) and with interstitial endomyocarditis of lymphocytes and plasma cells. Lymphoplasmacellular infiltration is seen in the meninges, ganglia, and peripheral nerves. Chronic and intermittent oligoarthritis is the hallmark of stage III disease, characterized by hypertrophic synovitis, often with fibrinaceous deposits and synovial vascular occlusion. Stage III chronic dermatologic syndromes (lymphadenosis benigna cutis, acrodermatitis chronicum atrophicans) consist of cutaneous lymphoid hyperplasia and vascular changes. Neurologic demyelination syndromes also occur in stage III. Plasma cells occur in all stages, but are more prominent in stages II and III. Spirochetes can be demonstrated by silver impregnation stains in some cases.

Arachnid Vectors↗

PubMed1994

Primary cutaneous immunocytoma. A B-cell lymphoma that can easily be mistaken for cutaneous lymphoid hyperplasia.

It has been estimated that immunocytomas comprise roughly 2% of all cutaneous lymphomas. We studied five patients with primary cutaneous immunocytomas who presented with cutaneous nodules or plaques. Many of the infiltrates were "top-heavy" and polymorphous with admixed eosinophils, macrophages, lymphoid follicles, and non-neoplastic lymphocytes. Other potentially confusing findings were one case each of spongiotic dermatitis and leukocytoclastic vasculitis. The neoplastic cells were often situated at the peripheries of nodules and ranged from those with nuclei that resembled small lymphocytes to others that resembled immunoblasts. Most had eccentrically placed nuclei and fan-shaped cytoplasm. Monotypic kappa-light chain was found in all five cases, accompanied by gamma-heavy chain in two cases, and mu-heavy chain in one. In situ hybridization detected only kappa-mRNA in the four cases that yielded technically satisfactory results. The neoplastic cells did not express the B-cell antigen CD20; T-cells formed the centers of many nodules. Inappropriate staining for CD43 was evident in the neoplastic cells of one case. Because of reports of immunocytomas complicating acrodermatitis chronica atrophicans, we stained sections with an antiserum to Borrelia burgdorferi, which did not detect that organism. In situ hybridization did not detect EBER-1 RNA of the Epstein-Barr virus, which can be present in immunocytomas in immunocompromised patients. One patient died of disease after failing chemotherapy; another is alive with disseminated disease, and three are in remission following excision of lesions alone in two patients and chemotherapy in one patient who had relapsed following both excision and radiation therapy.

Adult↗

PubMed1994

Successful amplification of DNA specific for Finnish Borrelia burgdorferi isolates in erythema chronicum migrans but not in circumscribed scleroderma lesions.

Early diagnosis of Borrelia burgdorferi infection, hampered by the absence of detectable antibodies in most patients with erythema chronicum migrans is important to prevent late-stage neurologic, rheumatologic, and skin disorders. Furthermore, B. burgdorferi has been claimed to be the causative agent in localized scleroderma (morphea). We used PCR amplification to search for B. burgdorferi outer surface protein OspA-specific sequences in DNA obtained from lesional skin biopsies on Finnish patients with clinically suspect erythema chronicum migrans, lymphocytoma, morphea, or with diverse skin manifestations and persistent high antibodies to B. burgdorferi flagellar antigen. Seronegative patients with other skin lesions served as controls. The amplicons obtained with primers specific for B. burgdorferi type strain B31 ospA sequence did not hybridize to the corresponding probes, and thus the DNA amplified from a Finnish B. burgdorferi erythema chronicum migrans skin isolate was sequenced. This 98-nucleotide sequence of ospA (332-429) showed 11% to 14% nucleotide divergence compared with the North American type strain (B31), several European strains, and an East Siberian tick strain. The sequence was almost identical (99%) to a Swedish isolate from acrodermatitis chronica atrophicans. Using oligonucleotides specific for the Finnish strain, a positive polymerase chain reaction-based hybridization was obtained in six of seven untreated erythema chronicum migrans patients infected in Finland or in Estonia, and in the lymphocytoma patient. Only two of the erythema chronicum migrans patients had IgG or IgM antibodies to flagellin. However, all seven morphea lesions as well as the other lesions were polymerase chain reaction negative. Polymerase chain reaction-based hybridization of B. burgdorferi OspA gene from skin-derived DNA thus provides a sensitive and specific diagnostic tool. In conditions not unequivocally known to be caused by B. burgdorferi, like in morphea, this assay was negative. We also demonstrate that peri-Baltic B. burgdorferi isolates show homology in their OspA genes but differ from geographically more distant isolates.

Antibodies, Bacterial↗

PubMed2004

Cutaneous inflammatory pseudotumor--a spectrum of various diseases?

BACKGROUND: Inflammatory pseudotumor (IPT) also known as inflammatory myofibroblastic tumor (IMT) or plasma cell granuloma (PCG) has been rarely reported in the skin. METHODS: We describe five patients with cutaneous IPT and present clinicopathologic features along with detailed immunohistochemical analysis including anaplastic lymphoma kinase (ALK)-1. RESULTS: The patients age ranged from 15 to 89 years with a median of 56 years. All patients presented with solitary, firm, papules and nodules. There was no evidence of constitutional symptoms, local recurrence, or lymph node involvement. Histopathological examination revealed two distinct patterns; one type (n = 3) displayed dense, lymphoplasmacytoid infiltrates containing lymphoplasmacytoid cells and plasma cells with occasional germinal centers and hyalinized collagen bundles but was devoid of a myofibroblastic component. It showed features of tumors previously described as cutaneous PCG. Although an infectious etiology, including Borrelia burgdorferi-specific DNA, could not be demonstrated, we observed many features that overlapped with those of fibrous nodules of acrodermatitis chronica atrophicans. The other pattern (n = 2) revealed spindled myofibroblasts focally arranged in a fascicular pattern, an admixed lymphoplasmacytoid infiltrate set in a background of thickened collagen bundles, findings akin to the conventional type of IMT. The cases with a myofibroblastic component (n = 2) did not show any evidence of ALK-1 reactivity. CONCLUSIONS: We believe that the term cutaneous IPT subsumes lesions of diverse etiology. Tumors with detectable myofibroblasts represent true cases of IMT. Cutaneous PCG is a discrete disorder biologically distinct from conventional IMT representing a reaction pattern that is also found in disorders, such as spirochete-induced fibroid nodules and localized chronic fibrosing vasculitis.

Activin Receptors, Type I↗

PubMed1991

Lyme borreliosis--a review and present situation in Japan.

The skin diseases Erythema (chronicum) migrans (ECM, EM), Lymphadenosis benigna cutis (LABC), and Acrodermatitis chronica atrophicans (ACA) have long been described in northern Europe, and dermatologists are very familiar with these manifestations, which have been successfully treated with penicillin for about 40 years without the causative agent being known. Certain neurologic symptoms could be linked to tickbites during the 1920's and later also to EM. In 1977, Steere et al. reported a new form of inflammatory arthritis, mainly in school children in the community of Lyme, Connecticut, U.S.A., which they could also associate with preceding erythema and tickbites. Five years later, Burgdorfer was able to isolate Borrelia spirochetes from Ixodes ticks, which are known to be vectors of Lyme disease as well as of EM and ACA. The following year, Borrelia spirochetes were also isolated from Ixodes ticks and from skin lesions of patients in Sweden and Germany. These findings resulted in a large number of reports of new discoveries related to this infection, which is now known under the names of tick-borne or Lyme borreliosis and, in the U.S., also as Lyme disease or Lyme arthritis. It has proven to be a great imitator disease, mainly through its involvement of the neurological system, and to be far more widespread than previously thought. The full course of the disease is not yet known, however it is clinically, like another spirochetosis, syphilis, divided into early and late stages. Manifestations involve mainly the skin, the joints, the nervous system (Neuroborreliosis), and the heart. Antibiotic treatment is effective, especially in the early stages. Like syphilis, the disease can be self-healing without treatment. People who are exposed to ticks should be aware of the risk of contracting this disease, also in Japan where Ixodes ticks have been shown to be carriers of Borrelia spirochetes. Cases, particularly of EM, but also with neurological symptoms, have already been diagnosed in Hokkaido, Honshu, Shikoku, and Kyushu. As Lyme borreliosis is now proven to exist in Japan, it is beneficial for dermatologists to know about the various presentations of this disease. This paper will briefly summarize the historical background, the clinical stages, the diagnosis, and the treatment of Lyme borreliosis, with a summary of the present situation in Japan.

Animals↗

PubMed1993

Cutaneous fibroses induced by Borrelia burgdorferi.

Three cases of chronic infection with Borrelia burgdorferi are described. The patients presented with nodular or discoid fibrosis, partly in conjunction with acrodermatitis chronica atrophicans (ACA). Juxta-articular fibrotic nodules may develop within a few months of the onset of ACA. Nodular, discoid morphoea-like, and widespread cutaneous fibroses in chronic Borrelia infection may be provoked by trauma, surgery or electromagnetic radiation. They respond well to antibiotic therapy. These lesions offer an in vivo model for studying the evolution of immunologically induced fibrosis.

Adult↗

PubMed1994

Juxta-articular fibrotic nodules in Borrelia infection--ultrastructural details of therapy-induced regression.

Juxta-articular fibrotic nodules in chronic Borrelia burgdorferi infection commonly regress rapidly under antibiotic therapy. They may therefore serve as a good in vivo model for studying the development and regression of cutaneous fibrotic processes. As shown in a typical case of acrodermatitis chronica atrophicans, this spirochete-induced fibrosis in the upper subcutis of the elbow region is histologically characterized by broad hyalinized collagen tracts interspersed with prominent perivascular lymphocytes and plasma cells. These immune cells vanish completely after 5 days of antibiotic treatment, while fibroblasts discharge matrix vesicles and form elastic fibres.

Elbow↗

PubMed2006

Chronic polyneuropathy and Lyme disease.

Infection of the peripheral nervous system with Borrelia burgdorferi can present as a cranial neuropathy or radiculopathy with cerebrospinal fluid (CSF) pleocytosis and intrathecal antibody production against B. burgdorferi, or as an asymmetric peripheral neuropathy with acrodermatitis chronica atrophicans (ACA) and normal CSF findings. According to North American studies, it can also present as a symmetric chronic polyneuropathy without ACA or other Lyme manifestations. Our purpose was to investigate the prevalence of B. burgdorferi antibodies in patients presenting with isolated chronic polyneuropathy (PN) in a European region with high incidence of Lyme disease. Sera from 209 PN patients and 247 healthy blood donors from Vest-Agder County, Norway, were examined. Borrelia burgdorferi antibodies were detected in 43 (21%) PN patients and in 45 (18%) healthy blood donors (P = 0.553). The prevalence of B. burgdorferi antibodies was similar (P = 0.311) in cryptogenic PN (24/102, 24%) and PNs of identified etiologies (19/107, 18%). PN patients with B. burgdorferi antibodies had normal spinal fluid white cell count and they did not differ clinically or electrophysiologically from PN patients without antibodies. None of 20 antibody-positive PN patients responded to antimicrobial treatment. The study shows that, in Europe, chronic distal PN without ACA or other Lyme manifestations is very rarely caused by a B. burgdorferi infection.

Anti-Infective Agents↗

PubMed1998

Interpretation of immunoblots for Lyme borreliosis using a semiquantitative approach.

OBJECTIVE: To test the performances of new Borrelia garinii immunoblots specific for Borrelia burgdorferi sensu lato with a selected panel of sera from patients with various clinical presentations of Lyme borreliosis. METHODS: In order to establish the sensitivity and the specificity of these immunoblots, we tested serum samples obtained from patients with early- and late-stage Lyme disease (erythema migrans n=35, neuroborreliosis n=61, acrodermatitis chronica atrophicans (ACA) n=27 and arthritis n=41), from patients with diagnoses and laboratory findings associated with serologic cross-reactivity to Lyme disease (syphilis n=12, Epstein-Barr infection n=9, autoimmune markers n=29) and from blood donors residing in regions of low and medium endemicity (n=80, n=100). RESULTS: The combined sensitivity (IgG and IgM) of the tests was 90% for patients with erythema migrans, 92% for neuroborreliosis, 96% for ACA and 100% for Lyme arthritis. The specificity of the IgG immunoblot was 94%, and that of the IgM immunoblot was 97%, taking into account the prevalence of borrelia antibodies in the overall population. Interpretation of these immunoblots is based on scores allocated to different specific borrelia antigens. CONCLUSIONS: The Western blot technology is extremely useful in dissecting the immune response to borrelia infections, which develops gradually over a period of weeks to years and which involves the appearance of IgM and IgG antibodies directed against a number of borrelia-associated proteins.

Journal Article↗

PubMed1996

Role of Borrelia burgdorferi in the pathogenesis of morphea/scleroderma and lichen sclerosus et atrophicus: a PCR study of thirty-five cases.

Morphea (localized scleroderma), and lichen sclerosus et atrophicus (LSA) share common features with acrodermatitis chronica atrophicans (ACA), a known chronic form of borreliosis. These include similar histologic findings such as diffuse dermal fibrosis. These observations have led several investigators to consider the possibility of Borrelia burgdorferi (Bb) as a common etiologic factor among all of these diseases. The aim of this study is to investigate the role of Bb in the pathogenesis of morphea and LSA, by assaying for its presence in lesional skin biopsies from patients with these diseases. We utilized the nested polymerase chain reaction (PCR) technique to selectively amplify a longer segment of a Bb-specific somatic gene, on DNA from paraffin-embedded, formalin-fixed tissues. The results revealed no Bb-specific DNA sequence in 28 specimens of morphea/scleroderma and 7 of LSA with varying stages of disease. Furthermore, confirmatory Southern blot of the PCR product, resulted in similar findings. These data seriously question the role played by this spirochete in the pathogenesis of morphea and LSA, at least in the southeastern part of the USA.

Adult↗

PubMed1991

Improved immunoglobulin M serodiagnosis in Lyme borreliosis by using a mu-capture enzyme-linked immunosorbent assay with biotinylated Borrelia burgdorferi flagella.

A mu-capture enzyme-linked immunosorbent assay (ELISA) for detection of serum immunoglobulin M (IgM) antibodies to Borrelia burgdorferi by using biotinylated purified B. burgdorferi flagella was developed. The diagnostic performance of the mu-capture ELISA was compared with that of a conventional indirect ELISA. Sera from untreated patients with erythema migrans (n = 50), neuroborreliosis (n = 100), and acrodermatitis chronica atrophicans (ACA; n = 48) were investigated. The cutoff of the ELISAs was adjusted to a diagnostic specificity of 98% on the basis of examination of 200 serum specimens from healthy controls. The mu-capture ELISA increased the diagnostic sensitivity in patients with erythema migrans from 32 to 48% (P less than 0.01) and in patients with neuroborreliosis from 37 to 57% (P less than 0.001). Because of an increased signal/noise ratio, the mu-capture ELISA yielded a significantly better quantitative discrimination of individual positive measurements from the cutoff (P less than 0.001). The increased signal/noise ratio was most likely a consequence of the elimination of IgG competition for the test antigen. This may also explain why 12% of patients with ACA showed significantly increased specific IgM levels only by the mu-capture ELISA. Of patients with ACA, 27% had IgM rheumatoid factor. The mu-capture principle with a directly labeled antigen showed no interference with IgM rheumatoid factor, in contrast to the indirect ELISA. The high diagnostic performance and ease of this three-step mu-capture ELISA make it suitable for routine anti-B. burgdorferi IgM serodiagnosis.

Adolescent↗