Literature DB >> 2847622

Clinical pathologic correlations of Lyme disease by stage.

P H Duray1, A C Steere.   

Abstract

Lyme disease is capable of producing a wide variety of clinical pathologic conditions and lesions having in common histologic features of collagen-vascular disease. The plasma cell is an omnipotent inflammatory responder in most tissues involved by Lyme disease, ranging from relatively acute to lesions that have gone on for years. Vascular thickening also seems to be prominent, and in the dermis is accompanied by scleroderma-like collagen expansion. The disease in some ways resembles the responses seen in lupus erythematosus such as mild cerebritis with lymphocytes and plasma cells in the leptomeninges. Lymphoplasmacytic panniculitis of Lyme disease resembles lupus profundus, both in the infiltrate and the plasma cell-blood vessel relationship. The onion skin thickened vessels of the synovia resemble the vessels of lupus spleens, while the scleradermoid thickening of the dermis and various skin lesions of stage III Lyme disease suggest a collagen-vascular disorder. Finally, the perivascular lymphoid infiltrate in clinical myositis does not differ from that seen in polymyositis or dermatomyositis. All of these histologic derangements suggest immunologic damage in response to persistence of the spirochete, however few in number.

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Year:  1988        PMID: 2847622     DOI: 10.1111/j.1749-6632.1988.tb31839.x

Source DB:  PubMed          Journal:  Ann N Y Acad Sci        ISSN: 0077-8923            Impact factor:   5.691


  51 in total

Review 1.  The emergence of Lyme disease.

Authors:  Allen C Steere; Jenifer Coburn; Lisa Glickstein
Journal:  J Clin Invest       Date:  2004-04       Impact factor: 14.808

2.  Pancytopenia in a patient with Lyme disease.

Authors:  V Babu; S Sukumarannair; Z Saul
Journal:  Infection       Date:  2010-04-01       Impact factor: 3.553

3.  Lyme borreliosis: host responses to Borrelia burgdorferi.

Authors:  A Szczepanski; J L Benach
Journal:  Microbiol Rev       Date:  1991-03

4.  CD14 signaling reciprocally controls collagen deposition and turnover to regulate the development of lyme arthritis.

Authors:  Bikash Sahay; Anju Singh; Arumugam Gnanamani; Rebeca L Patsey; J Edwin Blalock; Timothy J Sellati
Journal:  Am J Pathol       Date:  2011-02       Impact factor: 4.307

5.  Kinetics of Borrelia burgdorferi dissemination and evolution of disease after intradermal inoculation of mice.

Authors:  S W Barthold; D H Persing; A L Armstrong; R A Peeples
Journal:  Am J Pathol       Date:  1991-08       Impact factor: 4.307

6.  Robust interferon signature and suppressed tissue repair gene expression in synovial tissue from patients with postinfectious, Borrelia burgdorferi-induced Lyme arthritis.

Authors:  Robert B Lochhead; Sheila L Arvikar; John M Aversa; Ruslan I Sadreyev; Klemen Strle; Allen C Steere
Journal:  Cell Microbiol       Date:  2018-10-17       Impact factor: 3.715

7.  Subcellular localization and chaperone activities of Borrelia burgdorferi Hsp60 and Hsp70.

Authors:  A Scopio; P Johnson; A Laquerre; D R Nelson
Journal:  J Bacteriol       Date:  1994-11       Impact factor: 3.490

8.  The outer surface protein A of the spirochete Borrelia burgdorferi is a plasmin(ogen) receptor.

Authors:  H Fuchs; R Wallich; M M Simon; M D Kramer
Journal:  Proc Natl Acad Sci U S A       Date:  1994-12-20       Impact factor: 11.205

9.  Borrelia burgdorferi upregulates expression of adhesion molecules on endothelial cells and promotes transendothelial migration of neutrophils in vitro.

Authors:  T J Sellati; M J Burns; M A Ficazzola; M B Furie
Journal:  Infect Immun       Date:  1995-11       Impact factor: 3.441

10.  Long-term protection of mice from Lyme disease by vaccination with OspA.

Authors:  E Fikrig; S W Barthold; F S Kantor; R A Flavell
Journal:  Infect Immun       Date:  1992-03       Impact factor: 3.441

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