Infection associated with medical devices

Tunney, M.M.; Gorman, S. P.; Patrick, Sheila

doi:10.1097/00013542-199610000-00002

Cited by 76 publications

(35 citation statements)

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“…Medical implants, such as catheters, prosthetic heart valves and joint replacements, can be colonised by micro-organisms that form an adherent biofilm on the surface of the device [1,2]. Biofilm cells are organised into structured communities enclosed within a matrix of extracellular material.…”

Section: Introductionmentioning

confidence: 99%

Mixed species biofilms of Candida albicans and Staphylococcus epidermidis

Adam

Baillie

Douglas

2002

Journal of Medical Microbiology

323

223

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A simple catheter disk model system was used to study the development in vitro of mixed species biofilms of Candida albicans and Staphylococcus epidermidis, two organisms commonly found in catheter-associated infections. Two strains of S. epidermidis were used: a slime-producing wild type (strain RP62A) and a slime-negative mutant (strain M7). In mixed fungal-bacterial biofilms, both staphylococcal strains showed extensive interactions with C. albicans. The susceptibility of 48-h biofilms to fluconazole, vancomycin and mixtures of the drugs was determined colorimetrically. The results indicated that the extracellular polymer produced by S. epidermidis RP62A could inhibit fluconazole penetration in mixed fungal-bacterial biofilms. Conversely, the presence of C. albicans in a biofilm appeared to protect the slime-negative staphylococcus against vancomycin. Overall, the findings suggest that fungal cells can modulate the action of antibiotics, and that bacteria can affect antifungal activity in mixed fungal-bacterial biofilms.

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Section: Introductionmentioning

confidence: 99%

Mixed species biofilms of Candida albicans and Staphylococcus epidermidis

Adam

Baillie

Douglas

2002

Journal of Medical Microbiology

323

223

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“…Biofilms consist of layers of microbial cells embedded within a matrix of extracellular polymeric material [ 1 -31. Release of micro-organisms from the biofilm can result in an acute disseminated infection which may be responsive to antimicrobial therapy. However, the biofilm itself is generally resistant, and will frequently persist as a reservoir of infection until the implant is removed [4,5]. Although the majority of implant infections are caused by bacteria -notably staphylococci -fungal infections are becoming increasingly common and Candida species are regarded as particularly important nosocomial pathogens [ …”

Section: Introductionmentioning

confidence: 99%

Role of dimorphism in the development of Candida albicans biofilms

Baillie¹,

Douglas²

1999

Journal of Medical Microbiology

264

193

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Two model biofilm systems, involving growth on disks of catheter material or on cylindrical cellulose filters, were used to investigate the structure of Candida albicans biofilms. To assess the importance of dimorphism in biofilm development, biofilms produced by two wild-type strains were compared with those formed by two morphological mutants, incapable of yeast and hyphal growth, respectively. Scanning electron microscopy and thin sections of biofilms examined by light microscopy revealed that biofilms of the wild-type strains formed on catheter disks consisted of two distinct layers: a thin, basal yeast layer and a thicker, but more open, hyphal layer. The hyphamutant produced only the basal layer, whereas the yeast-mutant formed a thicker, hyphal biofilm equivalent to the outer zone of the wild-type structures. Biofilms of the yeast-mutant were more easily detached from the catheter surface than the others, suggesting that the basal yeast layer has an important role in anchoring the biofilm to the surface. Biofilms formed on cylindrical cellulose filters were quite different in appearance. The hypha-mutant and both wild types produced exclusively yeast-form biofilms whereas the yeast-mutant generated a dense hyphal mat on the top of the filter. All these biofilms, irrespective of morphological form, were resistant to the antifungal agent, amphotericin B. Overall, these results indicate that the structure of a C. albicans biofilm depends on the nature of the contact surface, but that some surfaces produce biofilms with a layered architecture resembling to that described for bacterial systems.

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“…Once the biofilm mode of growth is established on prostheses such as heart valves and surgical implants (17,19), the sessile yeasts begin to display unique characteristics, including resistance to antifungal agents (6). This in turn leads to failure of antifungal therapy and chronic infection, remediated by surgery and/or removal of these devices (33). Factors thought to contribute to antimycotic resistance in Candida biofilms include the growth rate of the yeast (2) and the low diffusion gradient of the antimicrobial through the extracellular polymer matrix of the biofilm (2,3).…”

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confidence: 99%

In Vitro Method To Study Antifungal Perfusion in Candida Biofilms

Samaranayake

Yau

et al. 2005

J Clin Microbiol

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Antimycotic perfusion through Candida biofilms was demonstrated by a modification of a simple in vitro diffusion cell bioassay system. Using this model, the perfusion of three commonly used antifungal agents, amphotericin B, fluconazole, and flucytosine, was investigated in biofilms of three different Candida species (i.e., Candida albicans, Candida parapsilosis, and Candida krusei) that were developed on microporous filters. Scanning electron microscopy revealed that C. albicans formed a contiguous biofilm with tightly packed blastospores and occasional hyphae compared with C. parapsilosis and C. krusei, which developed confluent biofilms displaying structural heterogeneity and a lesser cell density, after 48 h of incubation on nutrient agar. Minor structural changes were also perceptible on the superficial layers of the biofilm after antifungal perfusion. The transport of antifungals to the distal biofilm-substratum interface was most impeded by C. albicans biofilms in comparison to C. parapsilosis and C. krusei. Fluconazole and flucytosine demonstrated similar levels of perfusion, while amphotericin B was the least penetrant through all three biofilms, although the latter appeared to cause the most structural damage to the superficial cells of the biofilm compared with the other antifungals. These results suggest that the antifungal perfusion through biofilm mode of growth in Candida is dependent both on the antimycotic and the Candida species in question, and in clinical terms, these phenomena could contribute to the failure of Candida biofilm-associated infections. Finally, the in vitro model we have described should serve as a useful system to investigate the complex interactions that appear to operate in vivo within the biofilm-antifungal interphase.

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Infection associated with medical devices

Cited by 76 publications

References 0 publications

Mixed species biofilms of Candida albicans and Staphylococcus epidermidis

Mixed species biofilms of Candida albicans and Staphylococcus epidermidis

Role of dimorphism in the development of Candida albicans biofilms

In Vitro Method To Study Antifungal Perfusion in Candida Biofilms

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