Chapter 20 : Abscesses

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This chapter examines (i) the predisposing conditions that lead to abscess formation, (ii) the bacteria that predominate in various abscesses and their contribution to abscess formation, and (iii) the host response to the invading organisms and why that response is usually ineffective in eradicating the infection. The formation of intra-abdominal abscesses is used throughout the chapter as a model. Due to the prevalence of intra-abdominal abscesses, much research has been conducted to examine the molecular interactions between the invading microorganisms and the host that lead to abscess formation. The chapter discusses other examples of abscesses such as renal, brain, lung and skin. Intra-abdominal infection is caused by the leakage of gastrointestinal contents laden with bacteria. Following bacterial spillage, the majority of organisms are removed by the diaphragmatic lymphatics. The best-studied system for understanding the molecular interactions between host and microorganism that lead to abscess formation is the induction of intra-abdominal abscesses by the capsular polysaccharide complex (CPC) of . Studies in which the purified capsular polysaccharide from induced abscesses in the absence of viable organisms demonstrated the importance of this virulence factor in abscess formation. The authors propose that abscessogenic bacteria produce the structural components that induce the formation of abscesses because these structures serve an important function in the organisms' normal niche rather than serving solely as a mechanism to enhance their persistence as pathogens.

Citation: Comstock L, Tzianabos A. 2000. Abscesses, p 397-408. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch20

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Image of FIGURE 1

Proposed model for the initiation of intra-abdominal-abscess formation by CPC. The CPC binds to the peritoneal mesothelium, allowing bacterial attachment. The CPC also stimulates various immune cells to secrete IL-8 and tumor necrosis factor alpha. These factors have been shown to upregulate the expression of ICAM-1 on the mesothehal cells and recruit and activate PMNs. The upregulation of ICAM-1 allows for enhanced binding of PMNs to the mesothelium. This localization of bacteria and immune cells is necessary for the development of an abscess. PMΦ, peritoneal macrophage.

Citation: Comstock L, Tzianabos A. 2000. Abscesses, p 397-408. In Nataro J, Blaser M, Cunningham-Rundles S (ed), Persistent Bacterial Infections. ASM Press, Washington, DC. doi: 10.1128/9781555818104.ch20
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1. Ahrenholz, D. H.,, and R. L. Simmons. 1980. Fibrin in peritonitis. I. Beneficial and adverse effects of fibrin in experimental E. coli peritonitis. Surgery 88:4147.
2. Bornside, G. H.,, G. W. Cherry,, and M. B. Myers. 1973. Intracolonic oxygen tension and in vivo bactericidal effect of hyperbaric oxygen on rat colonic flora. Aerospace Med. 44:12821286.
3. Botta, G. A.,, C. Eftimiadi,, A. Costa,, M. Tonetti,, T. J. M. van Steenbergen,, and J. de Graaff. 1985. Influence of volatile fatty acids on human granulocyte chemotaxis. FEMS Microbiol. Lett. 27:6972.
4. Bryant, R. E., 1982. Effect of the suppurative environment on antibiotic activity, p. 313. In R. K. Root, and M. A. Sande (ed.), Contemporary Issues in Infectious Diseases, vol. 1. Churchill Livingstone, New York, N.Y.
5. Chalkiadakis, G.,, A. Kostakis,, P. E. Karayannacos,, H. Giamarellou,, I. Dontas,, I. Sakellariou,, and G. D. Skalkeas. 1983. The effect of heparin upon fibrinopurulent peritonitis in rats. Surg. Gynecol. Obstet. 157:257260.
6. Engler, H. D.,, and F. A. Kapral. 1992. The production of a bactericidal monoglyceride in staphylococcal abscesses. J. Med. Microbiol. 37:238244.
7. Foster, T. J.,, and M. Hook. 1998. Surface protein adhesins of Staphylococcus aureus. Trends Microbiol. 6:484488.
8. Gibson, F. C., III,, A. B. Onderdonk,, D. L. Kasper,, and A. O. Tzianabos. 1998. Cellular mechanism of intra-abdominal abscess formation by Bacteroides fragilis. J. Immunol. 160:50005006.
9. Gibson, F. C., III,, A. O. Tzianabos,, and A. B. Onderdonk. 1996. The capsular polysaccharide complex of Bacteroides fragilis induces cytokine production from human and murine phagocytic cells. Infect. Immun. 64:10651069.
10. Gregory, E. M. 1985. Characterization of the 02 -induced manganese-containing superoxide dismutase from Bacteroides fragilis. Arch. Biochem. Biophys. 238:8389.
11. Grigoryev, E. G.,, A. S. Kogan,, S. A. Kolmakov,, E. V. Nechaev,, S. A. Usov,, and T. V. Fadeeva. 1998. Immobihzed proteinases in the treatment of diffuse purulent peritonitis. Int. Surg. 83:245249.
12. Gupta, S.,, and P. K. Jain. 1985. Low-dose heparin in experimental peritonitis. Eur. Surg. Res. 17:167172.
13. Holdeman, L. V.,, I. J. Good,, and W. E. Moore. 1976. Human fecal flora: variation in bacterial composition within individuals and a possible effect of emotional stress. Appl. Environ. Microbiol. 31:359375.
14. Kapral, F. A.,, S. Smith,, and D. Lai. 1992. The esterification of fatty acids by Staphylococcus aureus fatty acid modifying enzyme (FAME) and its inhibition by glycerides. J. Med. Microbiol. 37: 235237.
15. Levison, M. A. 1992. Percutaneous versus open operative drainage of intra-abdominal abscesses. Infect. Dis. Clin. N. Am. 6:525544.
16. Lowe, A. M.,, D. T. Beattie,, and R. L. Deresiewicz. 1998. Identification of novel staphylococcal virulence genes by in vivo expression technology. Mol Microbiol 27:967976.
17. Meislin, H.W.,, S. A. Lerner,, M. H. Graves,, M. D. McGehee,, F. E. Kocka,, J. A. Morello,, and P. Rosen. 1977. Cutaneous abscesses: anaerobic and aerobic bacteriology and outpatient management. Ann. Intern. Med. 87:145149.
18. Nikolich, M. P.,, G. Hong,, N. B. Shoemaker,, and A. A. Salyers. 1994. Evidence for natural horizontal transfer of tetQ between bacteria that normally colonize humans and bacteria that normally colonize livestock. Appl Environ. Microbiol. 60:32553260.
19. Onderdonk, A. B.,, D. L. Kasper,, R. L. Cisneros,, and J. G. Bartlett. 1977. The capsular polysaccharide of Bacteroides fragilis as a virulence factor: comparison of the pathogenic potential of encapsulated and unencapsulated strains. J. Infect. Dis. 136:8289.
20. Onderdonk, A. B.,, R. B. Markham,, D. F. Zaleznik,, R. L. Cisneros,, and D. L. Kasper. 1982. Evidence for T cell-dependent immunity to Bacteroides fragilis in an intraabdominal abscess model. J. Clin. Investig. 69:916.
21. Pantosti, A.,, A. O. Tzianabos,, B. G. Reinap,, A. B. Onderdonk,, and D. L. Kasper. 1993. Bacteroidesfragilis strains express multiple capsular polysaccharides. J. Clin. Microbiol 31:18501855.
22. Pirlo, P.,, A. Arzese,, A. Cavallero,, and G. A. Botta,. 1988. Inhibitory effect of shortchain fatty acids produced by anaerobic bacteria on the phagocytosis of Staphylococcusaureus by human granulocytes, p. 223234. In J. M. Hardie, and S. P. Borriello (ed.), Anaerobes Today. John Wiley & Sons, Inc., New York, N.Y.
23. Rocha, E. R.,, T. Selby,, J. P. Coleman,, and C. J. Smith. 1996. The oxidative stress response in an anaerobe, Bacteroides fragilis. J. Bacteriol 178: 68956903.
24. Rocha, E. R.,, and C.J. Smith. 1995. Biochemical and genetic analysis of a catalase from the anaerobic bacterium Bacteroides fragilis. J. Bacteriol 177:31113119.
25. Rotstein, O. D.,, and J. Kao. 1988. Prevention of intra-abdominal abscesses by fibrinolysis using recombinant tissue plasminogen activator. J. Infect. Dis. 158:766772.
26. Rotstein, O. D.,, T. L. Pruett,, and V. D. Fiegel. 1985. Succinic acid, a metabolic byproduct of Bacteroides species, inhibits polymorphonuclear leukocyte functions. Infect. Immun. 48:402408.
27. Rotstein, O. D.,, T. Vittorini,, J. Kao,, M. I. McBurney,, P. E. Nasmith,, and S. Grinstein. 1989. A soluble Bacteroides by-product impairs phagocytic killing of Escherichia coli by neutrophils. Infect. Immun. 57:745753.
28. Salyers, A.A.,, and N. B. Shoemaker. 1996. Resistance genetransfer in anaerobes: new insights, new problems. Clin. Infect.Dis. 23(Suppl. 1):S36S43.
29. Sawyer, R. G.,, M. D. Spengler,, R. B. Adams,, and T. L. Pruett. 1991. The peritoneal environment during infection. The effect of monomicrobial and polymicrobial bacteria on p 02 and pH. Ann. Surg. 213:253260.
30. Seydoux, C.,, and P. Francioli. 1992. Bacterial brain abscesses: factors influencing mortality and sequelae. Clin. Infect. Dis. 15:394401.
31. Shapiro, M. E.,, D. L. Kasper,, D. F. Zaleznik,, S. Spriggs,, A. B. Onderdonk,, and R. W. Finberg. 1986. Cellular control of abscess formation: role of T cells in the regulation of abscesses formed in response to Bacteroides fragilis. J. Immunol. 137:341346.
32. Shoemaker, N. B.,, G. R. Wang,, and A. A. Salyers. 1992. Evidence for natural transfer of a tetracycline resistance gene between bacteria from the human colon and bacteria from the bovine rumen. Appl. Environ. Microbiol 58:13131320.
33. Shryock, T. R.,, and F. A. Kapral. 1992. The production of bactericidal fatty acids from glycerides in staphylococcal abscesses. J. Med. Microbiol 36:288292.
34. Sun, Y.,, C. H. Williams,, R. M. Hardaway,, and J. Shen. 1997. The effect of heparinization on intra-abdominal infection and acute pulmonary failure. Int. Surg. 82:367370.
35. Tzianabos, A. O.,, F. C. Gibson III,, R. L. Cisneros,, and D. L. Kasper. 1998. Protection against experimental intraabdominal sepsis by two polysaccharide immunomodulators. J. Infect. Dis. 178:200206.
36. Tzianabos, A. O.,, D. L. Kasper,, R. L. Cisneros,, R. S. Smith,, and A. B. Onderdonk. 1995. Polysaccharide-mediated protection against abscess formation in experimental intraabdominal sepsis. J. Clin. Investig. 96:27272731.
37. Tzianabos, A. O.,, A. B. Onderdonk,, B. Rosner,, R. L. Cisneros,, and D. L. Kasper. 1993. Structural features of polysaccharides that induce intra-abdominal abscesses. Science 262: 416419.
38. Tzianabos, A. O.,, A. B. Onderdonk,, D. F. Zaleznik,, R. S. Smith,, and D. L. Kasper. 1994. Structural characteristics of polysaccharides that induce protection against intra-abdominal abscess formation. Infect. Immun. 62:48814886.
39. Tzianabos, A.O.,, A. Pantosti,, H. Baumann,, J. R. Brisson,, H. J. Jennings,, and D. L. Kasper. 1992. The capsular polysaccharide of Bacteroides fragilis comprises two ionically linked polysaccharides. J. Biol. Chem. 267:182308235.
40. vanGoor, H.,, J. S. deGraaf,, J. Grond,, W. J. Sluiter,, J. van der Meer,, V. J. Bom,, and R. P. Bleichrodt. 1994. Fibrinolytic activity in the abdominal cavity of rats with faecal peritonitis. Br.J. Surg. 81:10461049.
41. van Goor, H.,, J. S. de Graaf,, K. Kooi,, W. J . Sluiter,, V. J. Bom,, J. vander Meer,, and R. P. Bleichrodt. 1994. Effect o f recombinant tissue plasminogen activator on intra-abdominal abscess formation in rats with generalized peritonitis. J. Am. Coll. Surg. 179:407411.

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