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Chapter 1 : Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections

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Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, Page 1 of 2

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Abstract:

A major argument in favor of local defects in the host defense against staphylococcal foreign-body infections was obtained by studies performed with experimentally infected animals. Effective protection from foreign-body infection was indeed obtained by injection of fresh neutrophils into tissue cages. In vitro studies aiming to describe mechanisms of bacterial attachment relevant to the colonization of indwelling devices are frequently performed in the absence of any hostrelevant factors. A section of this chapter emphasizes the critical role of host proteins, whether surface-bound or in the fluid phase, in modulating staphylococcal attachment to artificial implants. More recent studies using specific adhesin-defective mutants of confirmed the role of fibronectin in promoting bacterial attachment to subcutaneously implanted coverslips. The high susceptibility of patients with indwelling devices to microbial infections results from important defects in the cytokine and phagocytic-bactericidal responses. Experimental models have documented these defects in the vicinity of subcutaneously implanted tissue cages locally challenged with or . Such implanted tissue cages or coverslips were found to be progressively colonized by host-derived humoral and cellular elements. A number of approaches may be considered for reducing host susceptibility to foreign-body infections. An improved understanding of molecular and physiological mechanisms of phenotypic antibiotic tolerance of implant-associated organisms might bring new clues to more effective treatment strategies.

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1

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Complement System
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Bacterial Proteins
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Tumor Necrosis Factor
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Figures

Image of Figure 1.
Figure 1.

(A) View of a multiperforated tissue cage, with two inserted coverslips and two sealing caps. (B) Opsonic activity and total hemolytic complement levels in tissue-cage fluid at intervals after implantation and in pooled guinea pig serum. Data are means ± standard errors of the means (bars) of the reciprocal dilutions that gave either 50% killing of the bacteria in a phagocytic-bactericidal assay (K 50) or 50% hemolysis in a hemolytic system (CH 50). (Reprinted from reference 147 with permission.) (C) Bactericidal capacity of neutrophils obtained from sterile tissue-cage fluid (V) compared with peritoneal exudate neutrophils obtained after stimulation with glycogen (O). The phagocytic assay contained in a volume of 1 ml, 10 PMN, 10% pooled guinea pig serum, and either 2 × 10 cells of Wood 46 (solid line) or 2 × 10 cells of S. faecalis (dashed line). (Reprinted from reference 145 with permission.)

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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Image of Figure 2.
Figure 2.

Tumor necrosis factor (TNF) tissue-cage fluid concentrations (units/ml) and protection from infection in guinea pigs, measured 2 h and 1 day, respectively, after local injection of either saline, purified cell wall components, or purified peptidoglycan (PG). Infected and protected tissue cages are represented by closed and open symbols, respectively. Bars indicate median values. (Reprinted from reference with permission of University of Chicago Press.)

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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Image of Figure 3.
Figure 3.

(Left) Immunofluorescent staining of fibronectin recovered on PMMA coverslips excised from the guinea pigs after 4 weeks of subcutaneous implantation. (Reprinted from reference 128 with permission.) (Right) Adhesion of the parental strain 8325-4 of and its knockout mutant strain DU5883 defective in the production of both fibronectin-binding proteins. (Reprinted from reference with permission from Blackwell Science Ltd.)

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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Image of Figure 4.
Figure 4.

(Left) Radiographic appearance at 6 weeks after insertion onto the iliac bones of guinea pigs. (Right) Adhesion of the parental strain 879R4S of and its fibronectin adhesin-defective mutant strain 879R4S/1536 to titanium rniniplates or miniscrews explanted from the iliac bones of guinea pigs. (Reprinted from reference with permission.)

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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Image of Figure 5.
Figure 5.

Comparative attachment of 8325-4, its ClfA-defective mutant DU5880, or the parental strain overexpressing ClfA 8325-4(pCF4), by complementation with the clfA gene on a multicopy plasmid (see text for details), onto ex vivo polymer shunt tubing exposed for 5, 15, or 60 min to canine blood. (A) PVC. (B) Polyethylene. (Reprinted from reference with permission.)

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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Image of Figure 6.
Figure 6.

(A) Analysis of SDS-extracted proteins from inserted cannulas by SDS-PAGE. Protein extracts from four different cannulas (lanes 2 to 5) were electrophoresed in parallel with 100 ng of purified fibrinogen (lane 1) and 1000-fold diluted plasma (lane 6) in a 5 to 15% PAGE gradient and silver stained. (B) Identification of either fibrin(ogen) or plasmin(ogen) by immunoblots with specific antibodies. Two of these protein extracts were further probed by immunoblot with antifibrinogen antibodies (lanes 2 and 3) in parallel with purified fibrinogen (lane I). The first extract (lane 2) shows mainly beta-, but not alpha- and gamma-chains, whereas the second extract (lane 3) shows both alpha-and beta-chains. Immunoblots show one additional band of 95 kDa in both extracts, representing cross-linked dimers of gamma-chains, plus a major proteolytic fragment of 40 to 43 kDa in one extract (lane 2). Immunoblots with antiplasminogen antibodies also show the presence of plasminogen in one cannula protein extract (lane 5) run in parallel with purified plasminogen (lane 4). (P. Lerch, J. J. Morgenthaler, D. Pittet, and P. E. Vaudaux, unpublished data).

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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Image of Figure 7.
Figure 7.

In vitro compared with in vivo elimination (see text for details) of the methicillin-resistant strain MRGR3 of , by either teicoplanin (Teico), vancomycin (Vanco), daptomycin (Dapto), ciprofloxacin (Cipro), fleroxacin (Flero), sparfloxacin (Sparflo), or temafloxacin (Tema). These are pooled data from four reports ( ), except those on daptomycin which are unpublished. (Reprinted from reference with permission.)

Citation: Vaudaux P, François P, Lew D, Waldvogel F. 2000. Host Factors Predisposing to and Influencing Therapy of Foreign Body Infections, p 1-26. In Waldvogel F, Bisno A (ed), Infections Associated with Indwelling Medical Devices, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555818067.ch1
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