Chapter 15 : Infections

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This chapter discusses the spectrum of infections caused by . Hospital-acquired pneumonias, urinary tract infections, surgical-site infections, and bacteremias are among the nosocomial infections frequently caused by . The major cause of high morbidity and mortality in cystic fibrosis (CF) is chronic respiratory infection with . The lack of nitric oxide synthase (iNOS) production in CF may have two important repercussions. First, the reduced NO levels have been linked to the hyperabsorption of sodium in CF. Second, nitric oxide has also been directly implicated as a bactericidal and bacteristatic agent. The major causes of high morbidity and mortality presently associated with CF are chronic inflammation and the resulting respiratory tissue destruction. The first phase is an insidious infection, with intermittent isolation of from the lungs of the patient with CF. The mucoid phenotype of is rarely seen in infections other than CF, although mucoid strains can be isolated during chronic urinary tract infections, but all mucoid isolates produce chemically similar polymers based on the polyuronic acid exopolysaccharide alginate. The majority of the support for such a role of alginate in allowing to persist in the CF lung comes from in vitro studies that have previously been extensively reviewed. causes life-threatening infections in patients with compromised innate immune defenses, such as burn victims, neutropenic individuals undergoing chemotherapy, and persons with CF.

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15

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Tumor Necrosis Factor alpha
Type III Secretion System
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Inhalation exposure system adapted for use with aerosols. The system (Glas Col) is a whole-body exposure chamber for quantitative infection of animals by inhalation of airborne The system has a nebulizer-Venturi unit in which bacterial suspension is introduced. The suspension is atomized and mixed with filtered room air, and a bacterial cloud is introduced into the exposure chamber kept under negative pressure. A programmable control is used to preheat, nebulize, expose, and control bacterial decay. The exhaust air is filtered through a HEPA filter and passed through an incinerator in the back of the unit. Germicidal U V lamps are used for decontamination of the chamber. The five-compartment cage can accommodate up to 100 mice for simultaneous exposure. The initial deposition in the lungs is exceptionally uniform, and the variation from mouse to mouse is similar to sampling errors usually seen with bacterial plating. The system has been used for single-inhalation exposure to demonstrate reduced pulmonary clearance of mucoid ( ) and for the development of the repeated-respiratory-exposure inflammation model ( ).

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15
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Image of FIGURE 2

Eight-week-old (at t he inception of the experiment) C57BL/6J ( = 12) (open boxes) and IL-10T ( = 8) (shaded boxes) mice were exposed to once (−1) or 8 (−8) times. Pairwise comparison (Student-Newman-Keuls test) indicated that the histopathology indices relative to unexposed controls were significant ( < 0.005). Histopathology scores were as described in Y u et al. ( ). (Reproduced with permission from Yu et al. [ ].)

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15
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Image of FIGURE 3

Increased lung pathology in IL-10T mice after repeated exposure to Note perivascular, peribronchial, and intestinal inflammation and increased inflammatory changes in IL-10T (knockout) mice (B) relative to C57BL/6J mice (A). (C) Postmortem appearance of the lung from an IL-10T transgenic mouse (note numerous neutrophils) that succumbed after two exposures to . (Reproduced with modifications from Yu et al. [ ].)

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15
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Pseudomonas aeruginosa infections

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15
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Murine models in use for analysis of virulence

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15
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Decreased clearance of mucoid from the murine lung

Citation: Deretic V. 2000. Infections, p 305-326. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch15

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