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Chapter 5 : Biomaterials: Factors Favoring Colonization and Infection

Authors: James M. Anderson1, Roger E. Marchant2
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Affiliations: 1: Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106; 2: Department of Biomedical Engineering, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-7207
Content Type: Monograph
Publication Year: 2000

Category: Clinical Microbiology

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Abstract:

For more than a decade, various aspects of medical device and biomaterial infections have been studied in an effort to develop a fundamental and applied basis for infection-resistant biomaterials. This chapter presents an approach and perspectives on factors favoring biomaterial colonization and infection. Infection is a potentially serious complication with implants and devices and a major impediment to the long-term clinical success of devices like vascular grafts, artificial heart valves, and ventricular assist devices. The microorganisms most frequently identified on infected polymer implants either are present in the host flora or are nosocomial in origin, most notably the coagulasenegative staphylococci, particularly . The virulence of the commensal is a result of the foreign-body implant, which acts to inhibit the normal host defense. Focal thrombosis is a common finding with cardiovascular devices such as prosthetic heart valves, vascular grafts, arteriovenous fistulas, and artificial hearts. Catastrophic failure with significant morbidity and possibly death may occur when infectious foci initiate thrombosis with subsequent septic embolization. Adhesion of bacteria to an implant surface through specific and nonspecific mechanisms is a critical initial step in the development of biomaterial-centered infection. The adhesion of directly on biomaterials appears to be governed by nonspecific interactions. The GRGDS pentapeptide sequence was selected as the inhibitor, since it binds to several platelet integrin receptors, including GPIIb/IIIa. The complement system and phagocytic leukocytes, which are the primary defense mechanisms against infection, are obvious targets for the down regulation of host defenses by the biomaterial.

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5

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Biomaterials: Factors Favoring Colonization and Infection
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Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
/content/10.1128/9781555818067.chap5.fig5-1
Figure 1

Interactions of with biomaterials. (A) Illustration of a multistage process, from mass transport to aggregation and biofilm formation. (B) Near-surface bacterial interaction leading to adhesion.

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Figure 1

Interactions of with biomaterials. (A) Illustration of a multistage process, from mass transport to aggregation and biofilm formation. (B) Near-surface bacterial interaction leading to adhesion.

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
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Figure 2

Role of surface topography in bacterial adhesion to Dacron. Scanning electron micrograph (×2,000) showing turbulent-flow-induced physical entrapment of in Dacron fiber interstices (A). The inclusion of plasma proteins in solution, which adsorb to the Dacron fiber, significantly decreases overall microbial adhesion (B). (Reproduced from the Journal of Biomedical Materials Research , with permission of John Wiley & Sons, Inc.)

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Image of Figure 2
Figure 2

Role of surface topography in bacterial adhesion to Dacron. Scanning electron micrograph (×2,000) showing turbulent-flow-induced physical entrapment of in Dacron fiber interstices (A). The inclusion of plasma proteins in solution, which adsorb to the Dacron fiber, significantly decreases overall microbial adhesion (B). (Reproduced from the Journal of Biomedical Materials Research , with permission of John Wiley & Sons, Inc.)

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
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Figure 3

(A) Relative surface concentration of RP62A bound to contact-activated platelets vs. PE with adsorbed plasma proteins. (B) Atomic force microscopy image of (RP62A) and human platelets on PE. (C) Fluorescence microscopy image of (RP62A) and human platelets stained by acridine orange on PE. Note the large number of bacteria on the platelet relative to surrounding (protein-coated) PE surface. Test medium is platelet-rich plasma.

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Image of Figure 3
Figure 3

(A) Relative surface concentration of RP62A bound to contact-activated platelets vs. PE with adsorbed plasma proteins. (B) Atomic force microscopy image of (RP62A) and human platelets on PE. (C) Fluorescence microscopy image of (RP62A) and human platelets stained by acridine orange on PE. Note the large number of bacteria on the platelet relative to surrounding (protein-coated) PE surface. Test medium is platelet-rich plasma.

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
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Figure 4

adhesion to platelets with replenished plasma and with the addition of platelet integrin inhibitor GRGDS. The inhibitor significantly decreases adhesion to platelets ( < 0.05).

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Image of Figure 4
Figure 4

adhesion to platelets with replenished plasma and with the addition of platelet integrin inhibitor GRGDS. The inhibitor significantly decreases adhesion to platelets ( < 0.05).

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
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Figure 5

Comparison of RP62A adhesion with shear stress to PE modified by poly(ethylene oxide) and dextran surfactant polymers. The dextran surfactant polymer contains a branch ratio of dextran: hexanoyl of 1:5. The dashed line represents the unmodified PE control ( ).

10.1128/9781555818067/fig5-5_thmb.gif
10.1128/9781555818067/fig5-5.gif
Image of Figure 5
Figure 5

Comparison of RP62A adhesion with shear stress to PE modified by poly(ethylene oxide) and dextran surfactant polymers. The dextran surfactant polymer contains a branch ratio of dextran: hexanoyl of 1:5. The dashed line represents the unmodified PE control ( ).

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
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Tables

Biomaterials: Factors Favoring Colonization and Infection
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Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
/content/10.1128/9781555818067.chap5.tab5-1
Table 1

Device-centered infections

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10.1128/9781555818067/tab5-1.gif
Generic image for table
Table 1

Device-centered infections

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
/content/10.1128/9781555818067.chap5.tab5-2
Table 2

Microbiology of implant infections

10.1128/9781555818067/tab5-2_thmb.gif
10.1128/9781555818067/tab5-2.gif
Generic image for table
Table 2

Microbiology of implant infections

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5
/content/10.1128/9781555818067.chap5.tab5-3
Table 3

SO release by fresh or pre-exposed PMNs on PEUU in response to different stimuli

10.1128/9781555818067/tab5-3_thmb.gif
10.1128/9781555818067/tab5-3.gif
Generic image for table
Table 3

SO release by fresh or pre-exposed PMNs on PEUU in response to different stimuli

Citation: Anderson J, Marchant R. 2000. Biomaterials: Factors Favoring Colonization and Infection, p 89-109. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch5

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