Peritonitis: Update on Pathophysiology, Clinical Manifestations, and Management

Johnson, Caroline C.; Baldessarre, James; Levison, Matthew E.

doi:10.1086/513658

Cited by 99 publications

(69 citation statements)

References 85 publications

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“…aeruginosa is a common pathogen found in peritonitides secondary to ruptured appendices in otherwise healthy children (1,35). It also accounts for up to 10% of cases associated with CAPD and is associated with high morbidity, CAPD failure, and late complications (12,13,18). Rodent models of P. aeruginosa peritonitis have been developed for the purpose of understanding the pathophysiology and evaluating various modes of intervention (2,21,33,34).…”

Section: Discussionmentioning

confidence: 99%

Antibacterial Efficacy of R-Type Pyocins towards Pseudomonas aeruginosa in a Murine Peritonitis Model

Scholl

Martin

2008

Antimicrob Agents Chemother

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R-type pyocins are high-molecular-weight bacteriocins carried within the chromosomes of some bacterial species, such as Pseudomonas aeruginosa, and almost certainly evolved from lysogenic bacteriophages of the Myoviridae family. They contain no head structures and no DNA and are used as defense systems, usually against other strains of the same bacterial species. They bind with their tail fibers to targeted bacterial surface molecules and then kill by inserting a core or needle that dissipates the bacterial membrane potential. Their mechanism of action, high bactericidal potency (one pyocin particle can kill one bacterium), and focused spectrum suggest that R-type pyocins could be developed as antibacterial agents. In a lethal mouse peritonitis model, submicrogram quantities of pyocin prevent death from 90% lethal dose inocula of a pyocin-sensitive, clinical isolate of P. aeruginosa. We show here the dose response curves, treatment windows, or periods of response after infection and the several-log-unit acute reduction of bacterial load in blood and spleen samples, suggesting that R-type pyocins have several characteristics that one would expect from an effective therapeutic.Many Pseudomonas species possess the genes for one or both of the two types of high-molecular-weight pyocins, the R type and the F type (17, 28). Both are carried in the bacterial genome. The R-type pyocin locus consists of 16 open reading frames including 10 structural genes plus regulatory and chaperone genes (24, 25). Morphologically and genetically, the Rtype pyocins resemble the tails of Myoviridae bacteriophages but have no head structure and thus no nucleic acid content (9,15,16,23). They are thought to have evolved from the tail structure of a P2 bacteriophage-related ancestor; but they are not simply defective phages. There are meaningful physical and chemical stability differences, such as differences in protease and acid resistance, between pyocins and phage tails as the former have been adapted for their role as defensive bactericidal agents (14,22). However, similar to bacteriophages, pyocins bind to specific "receptors" on target bacteria and penetrate their membranes with a "core," or needle-like structure (31). In contrast to bacteriophages, pyocins have no material to inject and their penetrating core remains patent. As an immediate consequence, the bacterium is killed by dissipation of its membrane potential, a bactericidal event that can result from the binding of a single pyocin particle (8,27,31). An R-type pyocin particle can act only once; once it kills a cell, it cannot go on to kill others. Bacteriophages and R-type pyocins share common ancestry, but in contrast to bacteriophages, pyocins kill without directly causing bacterial cell lysis, a feature likely desirable for treating systemic infections (7, 33).Francois Jacob discovered and first described pyocins as high-molecular-weight bacteriocins (11). Over subsequent decades, much effort has been expended studying Pseudomonas aeruginosa pyocin morphology, structure,...

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Section: Discussionmentioning

confidence: 99%

Antibacterial Efficacy of R-Type Pyocins towards Pseudomonas aeruginosa in a Murine Peritonitis Model

Scholl

Martin

2008

Antimicrob Agents Chemother

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“…In some instances of postoperative peritonitis, the anastomosis may be intact; however, the patient may remain sick because of residual peritonitis from diverse causes. Among them is the inadequate drainage of the initial septic focus, in which the surgeon failed to drain completely, or more commonly, the peritoneum does not have the sufficient defense capacity to control the problem [1,2,25].…”

Section: Postoperative Peritonitismentioning

confidence: 99%

Management of Peritonitis in the Critically Ill Patient

Ordóñez

Puyana

2006

Surgical Clinics of North America

111

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“…Peritonitis by P. aeruginosa is a serious threat also to the patients undergoing continuous ambulatory peritoneal dialysis (CAPD) (15), accounting for 10% of fatality cases associated with CAPD. The bacterial intoxication usually leads to high morbidity, CAPD failure, and late complications in those cases (14,15,17). Rodent models of P. aeruginosa peritonitis have been developed for understanding the pathophysiology implicated in peritonitis (32).…”

mentioning

confidence: 99%

Antibacterial Efficacy of Phages against Pseudomonas aeruginosa Infections in Mice and Drosophila melanogaster

Heo

Lee

Jung

et al. 2009

Antimicrob Agents Chemother

103

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Phage therapy against Pseudomonas aeruginosa infections has received renewed attention owing to the increasing prevalence of antibiotic resistance in this bacterium. Here, we isolated and characterized two new potentially lytic bacteriophages (MPK1 and MPK6), which produced large and clear plaques on P. aeruginosa strain PAO1. Based on their morphology, MPK1 belongs to the Myoviridae, while MPK6 belongs to the Podoviridae. The group B polysaccharide of lipopolysaccharide was required for infection, suggesting that their host spectra are associated with the serotypes of P. aeruginosa strains. Intramuscular and intraperitoneal administration of MPK1 and, to a lesser extent, MPK6 significantly protected mice from mortality caused by PAO1-induced peritonitis-sepsis (P < 0.01). Mice treated with either phage also had lower bacterial burdens in their livers, lungs, and spleens. The antibacterial efficacy of MPK1 and MPK6 was also evaluated based on Drosophila melanogaster systemic infection caused by P. aeruginosa, for which phages were administered by feeding. Both phages significantly delayed the PAO1-induced killing of D. melanogaster (P < 0.001), although MPK1 persisted longer than MPK6 in uninfected D. melanogaster tissue samples. These results suggest that a mini-scale experiment using D. melanogaster infection is valid for evaluating the antibacterial efficacy of phage therapy against P. aeruginosa infections.

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Peritonitis: Update on Pathophysiology, Clinical Manifestations, and Management

Cited by 99 publications

References 85 publications

Antibacterial Efficacy of R-Type Pyocins towards Pseudomonas aeruginosa in a Murine Peritonitis Model

Antibacterial Efficacy of R-Type Pyocins towards Pseudomonas aeruginosa in a Murine Peritonitis Model

Management of Peritonitis in the Critically Ill Patient

Antibacterial Efficacy of Phages against Pseudomonas aeruginosa Infections in Mice and Drosophila melanogaster

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