Influence of preformed antibody on the pathogenesis of experimental Candida albicans endocarditis

Abstract

The influence of preformed antibody on the induction of experimental Candida albicans endocarditis was investigated by both in vitro and in vivo techniques. Preincubation of C. albicans with immune serum (raised in rabbits by intravenous injection of Formalin-killed yeast cells) decreased adhesion to the constituents of nonbacterial thrombotic endocarditis, e.g., fibrin plus platelets, in vitro. Two different methods, with radiolabeled or viable yeast cells, were confirmatory and demonstrated decreased adhesion of immune serum-treated C. albicans cells to 0 to 7.8% of control values (P < 0.001). These results correlated with protection from the development of C. albicans endocarditis in the immunized rabbits. The mean (± standard deviation) infectious dose for 50% of the animals was 105.29 + 100.07 in 48 control animals versus 107.11 + 100.22 in 37 immunized rabbits (P < 0.001). These studies suggest that humoral antibody may protect against C. albicans endocarditis, perhaps through inhibition of adhesion, a crucial early step in the pathogenesis of endocarditis. Bacterial adhesion to fibrin and platelets, the forms were observed adherent to the traumaticonstitutents of nonbacterial thrombotic endo-cally induced aortic valve vegetations (comcarditis, is an important step in the pathogenesis posed of fibrin and platelets) within 30 min of of infective endocarditis. The relative frequency intravenous inoculation (2, 7). Various Candida of bacterial isolates in endocarditis cases correspecies differ in their ability to adhere to fibrinlates directly with the ability of these species to platelet surfaces in vitro; adherence correlates adhere to heart valves in vitro. Production of directly with the production of endocarditis in extracellular dextran by viridans streptococci experimental animals (34). These observations promotes adhesion to artificial fibrin-platelet suggest that differences in yeast adhesion to matrices (35) or damaged canine cardiac valve fibrin-platelet deposits may explain the relative tissue in vitro. In addition, anti-whole cell anti-frequency of isolation of Candida species in serum to Streptococcus sanguis decreases adhe-endocarditis cases. However, the role of antision to fibrin-platelet surfaces in vitro, which body in this interaction is unknown. Preliminary correlates directly with protection from endo-observations suggested that anti-yeast cell wall carditis development due to this organism in antibody decreases adhesion of C. albicans to preimmunized rabbits in vivo (36). fibrin-platelet surfaces (21, 22), similar to results Fungal endocarditis is increasing in frequency obtained with S. sanguis (36). These issues were and usually appears in three clinical settings: addressed further in the present experiments. after prosthetic valvular insertion, in intrave-The purpose of this study was to determine the nous drug abusers, and as a complication of influence of preformed anti-whole cell antibody prolonged intravenous antibiotic administration on yeast adhesion to the constitutents of nono...

Adherence of Staphylococcus epidermidis to fibrin-platelet clots in vitro mediated by lipoteichoic acid

“…Also, treatment of clots with free LTA blocked the adherence of the homologous and heterologous strains. These observations are similar to those reported earlier (10,21,22): decreased adherence of Candida albicans (O to 7.8% of control values; P < 0.001) and S. sanguis (40% of control values; P < 0.001) to the constituents of fibrin-platelet clots was reported when these organisms were preincubated with homologous rabbit immune sera. However, Adler et al (1) reported that rabbit antipneumococcal sera increased the in vitro adherence of pneumococci to fibrin-platelet surfaces (P < 0.001) and rabbit aortic valve cusps (P < 0.05).…”

Immunization with FimA protects against Streptococcus parasanguis endocarditis in rats

“…Previous studies have shown that immunization elicited antibodies that hampered microbial attachment (27,29). We performed in vitro adherence assays to determine if polyclonal FimA antibodies interfered with bacterial adherence to vegetations.…”

“…There have been several reports on the effect of vaccination on susceptibility to experimental endocarditis. Immunizations with killed whole cells of Streptococcus sanguis, Streptococcus mutans, Streptococcus pneumoniae, Pseudomonas aeruginosa, nutritionally variant streptococci, and Candida albicans were protective against the development of endocarditis or early septicemia in rabbits (1,2,7,27,36). In contrast, anti-whole cell antibody did not protect rabbits from Staphylococcus aureus endocarditis (10).…”

“…Vaccination studies in endocarditis models have provided insights into how immunoprophylaxis confers protection. Specific antibody conferred immunity by increasing bacterial clearance and by inhibiting bacterial attachment, a crucial early step in the pathogenesis of this disease (1,27,29,30,35).…”

Antibodies to capsular polysaccharides are not protective against experimental Staphylococcus aureus endocarditis

“…The pathogenesis of S. aureus endocarditis in animals is similar to that in humans (6), and the S. aureus inoculum needed to provoke endocarditis is relatively low (ϳ10 4 CFU per rat). In addition, antibody-mediated protection against the development of experimental infective endocarditis has been demonstrated for other microbial pathogens, including streptococci (1,11,43), Staphylococcus epidermidis (41), Pseudomonas aeruginosa (4), and Candida albicans (34). Two previous studies have examined the role of antibodies to staphylococcal surface antigens in protection against experimental endocarditis.…”