Experimental Escherichia coli endocarditis in rats: roles of serum bactericidal activity and duration of catheter placement

Abstract

Studies were undertaken to investigate the relationship of the sensitivity of Escherichia coli to the bactericidal properties of serum and the ability of different strains to induce and sustain endocardial infection in rats.Strains of E. coli demonstrated different degrees of serum sensitivity, as determined by a method which employed concentrations of serum from 10 to 95% and periods of incubation as long as 24 h. The greater the serunm sensitivity of the E. coli strain, the less able it was to initiate infection and the more rapidly it was spontaneously eliminated from established infections. Endocardial infection with E. coli was established by intravenous challenge in rats with polyethylene catheters passing through the aortic valve into the left ventricle. An E. coli strain of low serum sensitivity was used; the initiation of infection depended upon the length of time the catheter had been in place aind, in addition, whether the catheter was in place at the time of bacterial challenge. Removal of the catheter permitted spontaneous sterilization of the endocardial vegetations. The time necessary for sterilization was in direct proportion to the length of time the catheter remained in place following bacterial challenge. If the catheter was not removed, sterilization of the endocardial vegetations did not take place. These studies suggest that serum bactericidal activity is an important host defense mechanism, acting to prevent the initiation of endocarditis in the case of highly serum-sensitive E. coli and to sterilize experimentally induced endocarditis in the case of less-serum-sensitive bacteria. The catheter used to induce nonbacterial endocardial vegetations favored the colonization of vegetations by E. coli, and it delayed the spontaneous sterilization of infected vegetations which occurred in relation to the susceptibility of the strain to the bactericidal properties of the serum. This effect of the catheter was not attributable to bacteria remaining viable in its lumen, nor was it attributable to inhibition of the bactericidal capacity of the serum as measured in vitro. Whatever the mechanism responsible for the catheter effect, experimental studies of the evolution of infections established with this technique must take into consideration the duration of catheter placement and whether and for how long it was present before or after inoculation with test bacteria. * Corresponding author. t Deceased.

Effect of cefepime on hematological, immunological and oxidant/antioxidant parameters in rats experimentally infected with E. coli ATCC 25922

“…Lysozyme is an enzyme lytic the cell walls of certain bacteria, it is a protein in nature existing in the body fluids, cells and tissue of many living organisms where it appears to have a digestive and defense function [45]. The serum bactericidal activity is an important host defense mechanism, which plays a role in preventing the initiation of E. coli infection [46]. In our study, E.coli resulted in significantly increased the serum lysozyme activity, as the result of increased lysozyme gene transcription [47,48] or increased lysozyme release during infection from the lysosomal compartment because of phagocytosis-induced degranulation [49].…”

In vitro Assays of Staphylococcus epidermidis Characteristics and Outcome in an Endocarditis Model

“…Animal model: The University Animal Care and Use Committee approved the methods (4,16) used to produce endocarditis in 280 g S pragu e-Dawley rats (SASCO, Omaha, Nebraska). Th irty-two animals were used to test the adult staphylococcal is ola tes and 16 to test the pediatric isolates.…”

Guinea pig model for Staphylococcus aureus native valve endocarditis

“…The most widely used experimental models of IE are the rabbit (1,5,10) and rat (13) models, in which cardiac valve lesions are induced by a polyethylene catheter introduced into the left ventricle (10,13). Since the intracardiac catheter has a considerable influence on the ability of bacteria to colonize the endocardium (2,3,8,9,11,16), these models more closely mimic the pathogenesis of PVE. Also, the intracardiac catheter decreases the efficacy of the antibiotic therapy used for either therapeutic or prophylactic purposes (6,9,12,15).…”