Streptococcal infection of endocardial and other intravascular vegetations in rabbits: natural history and effect of dexamethasone

The dysgonic fermenter-2 bacterium is a newly recognized fastidious gram-negative bacillus that causes bacteremia and sometimes endocarditis in immunocompromised persons after they are bitten by dogs. To develop an experimental model of this infection, we placed polyethylene catheters across the aortic valves of New Zealand white rabbits, which were inoculated intravenously the next day with dysgonic fermenter-2 bacteria. After 1 week, the rabbits were killed and the endocardial vegetations were homogenized for quantitative culture. Large inocula (1.3 x 1010 to 2.1 x 1010 viable bacteria) were required to produce infected vegetations. All infected rabbits had negative blood cultures at the time of autopsy and most developed serum agglutinins against dysgonic fermenter-2 bacteria. Three daily injections of methylprednisolone (30 mg/kg), starting the day before inoculation, significantly increased the incidence of endocarditis and the number of bacteria per gram of infected vegetation (P < 0.05). Treatment with methylprednisolone prolonged the initial bacteremia and caused significant increases in the numbers of bacteria per gram of blood, spleen, and liver compared with those of untreated controls (P < 0.05). Rabbits that had previously undergone splenectomy showed prolongation of the initial bacteremia but no significant increase in the incidence of infected vegetations. These results showed that the dysgonic fermenter-2 bacterium is a pathogen that causes endocarditis in rabbits but that it requires a large inoculum and produces blood culture-negative infections. Treatment with methylprednisolone enhances infection by prolonging the initial bacteremia and probably by diminishing bactericidal activity in the vegetations.

Section: Discussionmentioning

confidence: 99%

Enhancement of experimental bacteremia and endocarditis caused by dysgonic fermenter (DF-2) bacterium after treatment with methylprednisolone and after splenectomy

Bütler¹,

Johnston²,

Gutierrez³

et al. 1985

“…Bacterial strain. A strain of S. intermedius originally isolated from the blood of a patient with infective endocarditis and previously used in other studies (12,15) was used. This bacterium is known to be resistant to the bactericidal effect of rabbit serum.…”

Section: Methodsmentioning

confidence: 99%

“…These microorganisms are resistant to complement-dependent serum bactericidal activity, and infection, once established, is thought not to be affected by nonspecific or antibody-mediated phagocytosis (20). Nevertheless, experiments with animals and gram-positive bacteria have repeatedly demonstrated that the spontaneous sterilization of infective endocarditis in the right side of the heart is a regular occurrence (12). The mechanisms responsible for the sterilization of these infections have not been identified.…”

mentioning

confidence: 99%

Effect of nitrogen mustard on natural history of right-sided streptococcal endocarditis in rabbits: role for cellular host defenses

Yersin¹,

Mp²,

Freedman³

1982

Self Cite

Cellular host defenses are considered to be ineffective in bacterial endocarditis; the microorganisms in infected vegetations are protected from phagocytic cells by dense layers of fibrin. To test this hypothesis, nitrogen mustard-induced agranulocytosis and leukopenia were produced in rabbits with right-sided streptococcal endocarditis. The spontaneous sterilization of tricuspid infection observed in the control animals was not present in the granulocytopenic, leukopenic animals. Since the bacterium Streptococcus intermedius is not sensitive to the complement-mediated bactericidal effect of serum and since the animals were not bacteremic during the time of agranulocytosis, an inhibitory effect of the drug on local cellular host defense mechanisms is postulated. We suggest that the spontaneous sterilization of infective endocarditis in the right side of the heart in rabbits is mediated by cellular host defenses.

“…It is already known that the catheter used to induce nonbacterial thrombotic vegetations in the experimental model of endocarditis plays a deleterious role in prophylaxis (10) and therapy of streptococcal infection (14). The effect of the catheter has been shown to depend upon the location of the streptococcal infection within the vascular tree (6). A deleterious role of the foreign body was also suggested in a model of experimental Serratia endocarditis (9).…”

Section: Discussionmentioning

confidence: 99%

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

Yersin

Guze

et al. 1988

Self Cite

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.