Demonstration of spirochaetes in patients with Lyme disease with a modified silver stain

Koning, J. de; Bosma, R. B.; Hoogkamp-Korstanje, J. A. A.

doi:10.1099/00222615-23-3-261

Cited by 107 publications

(41 citation statements)

References 6 publications

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“…Tissue sections were stained with the Bosma-Steiner silver stain as reported originally for detecting of spirochaetes in patients with Lyme disease (De Koning et al 1987), and used in a previous study for demonstration of T. paraluisleporis in hares .…”

Section: Methodsmentioning

confidence: 99%

Widespread treponemal infections of hare populations (Lepus europaeus) in the Netherlands

Lumeij

2010

Eur J Wildl Res

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Further to the first description of treponemal infection in hares (Lepus europaeus) in one province of the Netherlands (Flevoland), this report provides further evidence for the widespread occurrence of hare syphilis in this country. Hunter-bagged hares which had the typical lesions of the disease were serologically examined using the Treponema pallidum hemagglutination assay and the fluorescent treponemal antibody absorption test, and tissue samples were stained with the Bosma-Steiner modified silver stain. Nine out of 12 suspected hares from five different provinces from the Netherlands showed serological and histological evidence of syphilis. Hare populations from at least half of the provinces of the Netherlands are infected with this agent.

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Section: Methodsmentioning

confidence: 99%

Widespread treponemal infections of hare populations (Lepus europaeus) in the Netherlands

Lumeij

2010

Eur J Wildl Res

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“…When compared with the Warthin-Starry stain, this method has been reported to provide greater contrast between the spirochetes and the background tissues. Using this modified Steiner stain (Bosma-Steiner), de Koning et al reported 100% sensitivity in demonstrating spirochetes in skin biopsies of ECM patients and in synovial biopsies of Lyme arthritis patients (58). The spirochetelike structures were not seen in synovial biopsies from patients with rheumatoid arthritis or bursitis or in skin biopsies of patients with granuloma annulare, eczema, or lymphoma.…”

Section: Differential Diagnosismentioning

confidence: 99%

“…However, the Gram stain is not nearly as sensitive as Giemsa (39,40) and silver (31,58,61) stains for demonstrating the organisms. Acridine orange was used to detect spirochetes in phagocytic cells (29) and in the CSF of a patient with Bannwarth's syndrome (36).…”

Section: Differential Diagnosismentioning

confidence: 99%

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Laboratory aspects of Lyme borreliosis

Barbour

1988

Clin Microbiol Rev

129

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Lyme borreliosis (Lyme disease), a common tick-borne disorder of people and domestic animals in North America and Europe, is caused by the spirochete Borrelia burgdorferi. Following the discovery and initial propagation of this agent in 1981 came revelations that other tick-associated infectious disorders are but different forms of Lyme borreliosis. A challenge for the clinician and microbiology laboratory is confirmation that a skin rash, a chronic meningitis, an episode of myocarditis, or an arthritic joint is the consequence of B. burgdorferi infection. The diagnosis of Lyme borreliosis may be established by (i) directly observing the spirochete in host fluid or tissue, (ii) recovering the etiologic spirochete from the patient in culture medium or indirectly through inoculation of laboratory animals, or (iii) carrying out serologic tests with the patient's serum or cerebrospinal fluid. The last method, while lacking in discriminatory power, is the most efficacious diagnostic assay for most laboratories at present.

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“…In mammals, B. burgdorferi is frequently found associated with connective tissues (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13), and the bacterium is often detected in cartilaginous or collagen-rich tissues, such as skin and joints (6,7,9,(11)(12)(13)(14)(15)(16)(17)(18). Adhesins expressed by B. burgdorferi facilitate interactions with these tissues.…”

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confidence: 99%

Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease

et al. 2015

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The Lyme disease spirochete, Borrelia burgdorferi, expresses RevA and numerous outer surface lipoproteins during mammalian infection. As an adhesin that promotes bacterial interaction with fibronectin, RevA is poised to interact with the extracellular matrix of the host. To further define the role(s) of RevA during mammalian infection, we created a mutant that is unable to produce RevA. The mutant was still infectious to mice, although it was significantly less well able to infect cardiac tissues. Complementation of the mutant with a wild-type revA gene restored heart infectivity to wild-type levels. Additionally, revA mutants led to increased evidence of arthritis, with increased fibrotic collagen deposition in tibiotarsal joints. The mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, and this increase was abolished in the complemented strain. Therefore, while revA is not absolutely essential for infection, deletion of revA had distinct effects on dissemination, arthritis severity, and host response. Borrelia burgdorferi, the causative agent of Lyme disease, is a vector-borne pathogen that successfully colonizes both ticks and a variety of vertebrate hosts. In mammals, B. burgdorferi is frequently found associated with connective tissues (1-13), and the bacterium is often detected in cartilaginous or collagen-rich tissues, such as skin and joints (6,7,9,(11)(12)(13)(14)(15)(16)(17)(18). Adhesins expressed by B. burgdorferi facilitate interactions with these tissues. B. burgdorferi expresses a plethora of outer surface proteins that interact with numerous components of the extracellular matrix (ECM), such as fibronectin, decorin, and integrins (19-23). The attachment of B. burgdorferi to the host ECM is likely critical for pathogenesis and persistence in mammals. Indeed, for many of these adhesins, deletion mutants have significant defects in infectivity, fail to disseminate widely in the host, or have other effects on disease, such as alterations in the severity of arthritis (24-27).The interactions of B. burgdorferi with fibronectin are facilitated by several distinct bacterial surface proteins, including BBK32, RevA, BB0347, and CspA (BbCRASP-1) (28-31). The redundancy in adhesins makes it difficult to dissect the role of each B. burgdorferi fibronectin binding protein in the pathogenesis of Lyme disease. For example, real-time microscopic imaging in live mice revealed a significant role for BBK32 in interactions with host vasculature, yet bbk32 mutants are still able to infect mammals (32).RevA is a 19-kDa surface protein encoded on the circular plasmid 32 (cp32) family of plasmids (33). RevA expression is elevated during mammalian infection over its expression in the tick vector, suggesting a role in pathogenesis (30,(34)(35)(36). RevA binds to fibronectin, and anti-RevA antibodies block the binding of whole B. burgdorferi bacteria to fibronectin (30). RevA is antigenic, as evidenced by the fact that both mice and human Lyme disease patients produce antibodies...

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Demonstration of spirochaetes in patients with Lyme disease with a modified silver stain

Cited by 107 publications

References 6 publications

Widespread treponemal infections of hare populations (Lepus europaeus) in the Netherlands

Widespread treponemal infections of hare populations (Lepus europaeus) in the Netherlands

Laboratory aspects of Lyme borreliosis

Borrelia burgdorferi RevA Significantly Affects Pathogenicity and Host Response in the Mouse Model of Lyme Disease

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