A rabbit model of right-sided Staphylococcus aureus endocarditis created with echocardiographic guidance
Tóm tắt
The most widely used experimental models of infective endocarditis (IE) are the rabbit and rat models, in which cardiac valve lesions are induced by a polyethylene catheter introduced into the left ventricle through the aortic valve. Our study was designed to create a rabbit model of IE right-sided with echocardiographic guidance. Thirty rabbits underwent both catheterization and inoculation (group A). These were divided into three subgroups of ten based on the time of catheter removal (immediately, after 24 h, and after death or moribundity for groups, A1, A2, and A3, respectively). Ten inoculated-only and ten catheterized-only rabbits served as controls. A catheter system consisted of a polyethylene catheter and a guide wire inside it. This system was passed through the rabbits’ tricuspid valves under echocardiographic guidance to damage them. The ratio of left ventricle to right ventricle (LV/RV) was measured in a four-chamber view before catheterization and at the time of death or moribundity. The peak velocity of tricuspid regurgitation (VTR) was measured in a four-chamber view at the time of catheterization and at the time of death or moribundity. Staphylococcus aureus (ATCC 29213) inoculation was performed 24 h after right heart catheterization to produce IE. IE was confirmed in 28 of 30 rabbits by macroscopic and histologic examination of tricuspid valves, blood cultures, and bacterial count in cardiac vegetations. Cardiac vegetations were confirmed in 25 of 28 IE rabbits by echocardiography. Enlargement of right ventricle dimension with a significantly decreased LV/RV ratio was confirmed in all IE rabbits at the time of death or moribundity than at the initial state (1.11 ± 0.35 vs. 1.95 ± 0.39, P < 0.01; 1.21 ± 0.34 vs. 1.98 ± 0.35, P < 0.01; 1.04 ± 0.31 vs. 2.00 ± 0.41, P < 0.01 for groups A1, A2, and A3, respectively). VTR was significantly higher in all the IE rabbits at the time of death or moribundity than at the time of catheterization (1.89 ± 0.46 vs 0.76 ± 0.45, P < 0.01; 2.04 ± 0.73 vs 0.68 ± 0.66, P < 0.01; 2.24 ± 0.51 vs 0.87 ± 0.55, P < 0.01 for group A1, A2 and A3, respectively). The models described herein closely reproduced the pathogenesis and pathophysiology of right heart catheter-induced endocarditis in humans. Echocardiographic guidance is helpful in the process of right heart catheterization. Some echocardiographic parameters, such as VTR and the LV/RV ratio could be used to assess the success or failure of the IE models.
Tài liệu tham khảo
Tornos P, Gonzalez-Alujas T, Thuny F, Habib G: Infective endocarditis: the European viewpoint. Curr Probl Cardiol. 2011, 36: 175-222. 10.1016/j.cpcardiol.2011.03.004
Highman B, Roshe J, Altland PD: Production of endocarditis with Staphylococcus aureus and Streptococcus mitis in dogs with aortic insufficiency. Circ Res. 1956, 4: 250-256. 10.1161/01.RES.4.3.250
Baddour LM, Christensen GD, Lowrance JH, Simpson WA: Pathogenesis of experimental endocarditis. Rev Infect Dis. 1989, 11: 452-463. 10.1093/clinids/11.3.452
Garrison PK, Freedman LR: Experimental endocarditis I. Staphylococcal endocarditis in rabbits resulting from placement of a polyethylene catheter in the right side of the heart. Yale J Biol Med. 1970, 42: 394-410.
Perlman BB, Freedman LR: Experimental endocarditis. II. Staphylococcal infection of the aortic valve following placement of a polyethylene catheter in the left side of the heart. Yale J Biol Med. 1971, 44: 206-213.
Santoro J, Levison ME: Rat model of experimental endocarditis. Infect Immun. 1978, 19: 915-918.
Durack DT, Beeson PB: Experimental bacterial endocarditis. I. Colonization of a sterile vegetation. B J Exp Pathol. 1972, 53: 44-49.
Baddour LM: Infective endocarditis: new concepts in pathogenesis. Curr Opin Infect Dis. 1999, 12: 201-204. 10.1097/00001432-199906000-00008
Maurin M, Lepidi H, La Scola B, Feuerstein M, Andre M, Pellissier JF, Raoult D: Guinea pig model for Staphylococcus aureus native valve endocarditis. Antimicrob Agents Chemother. 1997, 41: 1815-1817.
La Scola B, Lepidi H, Maurin M, Raoult D: A guinea pig model for Q fever endocarditis. J Infect Dis. 1998, 178: 278-281. 10.1086/517453
Pierce D, Calkins BC, Thornton K: Infectious endocarditis: diagnosis and treatment. Am Fam Physician. 2012, 85: 981-986.
Tsao MM, Katz D: Central venous catheter-induced endocarditis: human correlate of the animal experimental model of endocarditis. Rev Infect Dis. 1984, 6: 783-790. 10.1093/clinids/6.6.783
Carbon C: Animal models of endocarditis. Int J Biomed Comput. 1994, 36: 59-67. 10.1016/0020-7101(94)90095-7
Yersin B, Glauser MP, Guze PA, Guze LB, Freedman LR: Experimental Escherichia coli endocarditis in rats: roles of serum bactericidal activity and duration of catheter placement. Infect Immun. 1988, 56: 1273-1280.
Héraïef E, Glauser MP, Freedman LR: Natural history of aortic valve endocarditis in rats. Infect Immun. 1982, 37: 127-131.
Francioli PB, Freedman LR: Streptococcal infection of endocardial and other intravascular vegetations in rabbits: natural history and effect of dexamethasone. Infect Immun. 1979, 24: 483-491.
Pelletier LL, Petersdorf RG, Nielson K: Chemotherapy of experimental streptococcal endocarditis. V. Effect of duration of infection and retained intracardiac catheter on response to treatment. J Lab Clin Med. 1976, 87: 692-702.
Glauser MP, Francioli P: Relevance of animal models to the prophylaxis of infective endocarditis. J Antimicrob Chemother. 1987, 20 (Suppl A): 87-93. 10.1093/jac/20.suppl_A.87
Greenberg DP, Ward JI, Bayer AS: Influence of Staphylococcus aureus antibody on experimental endocarditis in rabbits. Infect Immun. 1987, 55: 3030-3034.
Gutschik E: The Enterococcus endocarditis model in experimental animals and its relevance to human infection. J Antimicrob Chemother. 1993, 31 (Suppl D): 87-95. 10.1093/jac/31.suppl_D.87
Silbiger JJ: The valvulopathy of non-bacterial thrombotic endocarditis. J Heart Valve Dis. 2009, 18: 159-166.