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EQUINE VETERINARY EDUCATION / AE / AUGUST 2006 251

Clinical Commentary Endocarditis in the horse E. J. M. M. VERDEGAAL* AND M. M. SLOET VAN OLDRUITENBORGH-OOSTERBAAN Department of Equine Sciences, Internal Medicine, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 12, 3584 CL Utrecht, The Netherlands.

Acute endocarditis is caused by certain pathogenic organisms, of is rarely determined, although the source has been such as and various streptococcal associated with jugular vein thrombophlebitis (Pipers et al. species, adhering to undamaged valvular tissue (Dedrick et al. 1979; Gardener et al. 1991; Maxson and Reef 1997). 1988; Karchmer 2001). During bacteraemia (in all species), bacterial organisms may In the pathogenesis of a subacute infectious endocarditis, invade the cardiac valves, sometimes through injured jet lesions on the endothelium are thought to be an important endothelial surfaces. Humoral and cell-mediated immune predisposing factor. They occur when high velocity streams systems are then activated, resulting in agglutination and and turbulent blood flows resulting from valve regurgitation complement-binding. Bacterial proliferation on the endothelium traumatise the endothelial surface (Dedrick et al. 1988; Ball stimulates and fibrin to form layered granulation tissue and Weldon 1992; Travers and Van Den Berg 1995). Because resulting in a . The bacterial organisms hidden in the pressure in the left is significantly higher than in the avascular vegetation are resistant to the immune system, and right, the atrial surface of the is more commonly valve destruction continues. Vegetations are most frequently affected (Else and Holmes 1972b; Pipers et al. 1979; Bonagura situated on the valvular leaflets, causing valvular insufficiency. and Pipers 1983; Buergelt et al. 1985; Hatfield et al. 1987; They are rarely found on the endocardial wall, and in this Dedrick et al. 1988; Weinstein 1989; Hillyer et al. 1990; location are less likely to cause problems (De Voogd van der Maxson and Reef 1997; Sage and Worth 1999). Straaten 1970; Dedrick et al. 1988; Weinstein 1989; A (histo)pathological post mortem study by Else and Holmes Korzeniowski and Kaye 1992; Travers and Van Den Berg 1995; (1972a,b) revealed that lesions of the mitral valve were twice De Groot et al. 1996; Church et al. 1998; Kittleson and Kienle as common as lesions of the (in a total of 1557 1998; Sage and Worth 1999; Karchmer 2001). cases, 70 and 35 cases, respectively). Although most horses with bacterial endocarditis are Infection of the heart valves is haematogenous and the younger than 3 years of age, there is no explanation for this result of a transient or persistent bacteraemia. In the horse, finding (Buergelt et al. 1985; Maxson and Reef 1997; Sage and spp. especially S. equi zooepidemicus, Worth 1999). There is also no explanation why stallions and Staphylococcus spp. and are most geldings are more frequently affected with bacterial endocarditis commonly found. Incidentally, Shigella spp., Mycobacterium than mares (Calvert 1982; Buergelt et al. 1985; Hines et al. tuberculosis, Pasteurella spp., Actinobacillus spp., Escherichia 1993; Maxson and Reef 1997; Sage and Worth 1999). coli, Rhodococcus equi, Klebsiella spp., Pseudomonas spp., Clinical signs of endocarditis usually occur within 2 weeks Erysipelothrix rhusiopathiae and other organisms such as after the bacteraemia and the most common sign is Candida spp have been previously described (Innes et al. 1950; with a severe cardiac murmur. Other more Buergelt et al. 1985; Hines et al. 1985; McCormick et al. 1985; nonspecific signs are low-grade , and Roby and Reef 1986; Dedrick et al. 1988; Hillyer et al. 1990; depression. Arterial and circulating immune Hines et al. 1993; Maxson and Reef 1997; Church et al. 1998; complexes may affect the coronary arteries and myocardium Ramzan 2000; Sponseller and Ware 2001). resulting in and cardiac , and also the In man, the primary source of infection is associated with kidney, spleen, brain, lung, eye and musculoskeletal system. surgical procedures, such as dental extraction, severe Increased work intolerance, shifting lameness, stiff gait and periodontal disease, lung and skin , and i.v. drug joint swelling are probably the result of septic emboli or abuse (Robins et al. 1986; Weinstein 1989; Korzeniowski and immune-complex mediated arthritis/synovitis (Brown 1985; Kaye 1992; Kittleson and Kienle 1998). In horses, the source Buergelt et al. 1985; Roby and Reef 1986; Hatfield et al. 1987; Dedrick et al. 1988; Nilsfors et al. 1991; Ball and Weldon 1992; Collatos 1992; Hines et al. 1993; Travers and Van Den *Author to whom correspondence should be addressed. Present address: Dahet Princess Haya, Royal Palaces, PO Box 2586, 11910 Berg 1995; Maxson and Reef 1997; Church et al. 1998; Sage Amman, Jordan. and Worth 1999; Ramzan 2000; Sponseller and Ware 2001). 252 EQUINE VETERINARY EDUCATION / AE / AUGUST 2006

Echocardiography, using 2-dimensional real time, M-mode combination, is recommended (Collatos 1992; and colour-flow Doppler, has been used successfully to Sponseller and Ware 2001). Although, the superior diagnose vegetations, and measure their size and location. penetrating ability of cephalosporins over gentamicin have Vegetations should be differentiated from ruptured chordae been demonstrated (Collatos 1992; Racklyeft and Love 2000), tendineae, flail valvular leaflets or nodular thickening. An slow metabolising bacteria are more resistant to antimicrobial indication of the prognosis is based on the degree of treatment particularly, the cell wall-active ones such as enlargement of the cardiac chambers, severity of regurgitation cephalosporins (Korzeniowski and Kaye 1992; Sponseller and and extent of myocardial dysfunction (Pipers et al. 1979; Ware 2001). Bonagura and Pipers 1983; Hatfield et al. 1987; Hillyer et al. With effective antimicrobial treatment, the pyrexia should 1990; Collatos 1992; Travers and Van Den Berg 1995; Maxson resolve in 5–7 days (Korzeniowski and Kaye 1992). Long-term and Reef 1997; Reef 1998; Sage and Worth 1999; Sponseller response to antimicrobial treatment can be assessed by the and Ware 2001; Verdegaal et al. 2002). use of serial measuring the size of the Haematology and blood biochemistry most commonly vegetations and the diameter of the cardiac chambers (Hillyer reveal anaemia, leucocytosis with mature neutrophilia, et al. 1990; Maxson and Reef 1997; Reef 1998; Sage and hyperproteinaemia as result of hypergammaglobulinaemia Worth 1999). Nonsteroidal anti-inflammatory agents are and azotaemia. Urinalysis may show proteinuria and considered by some authors to be useful in the therapy of haematuria (Hatfield et al. 1987; Dedrick et al. 1988; Hilyer et endocarditis to improve the ‘attitude’ of the horse (Collatos al. 1990; Sage and Worth 1999). 1992). In man, surgical replacement of the cardiac valve may A with antibiogram has to be performed to be the therapy of choice, but this has not been reported in the identify the bacterial organism and choose an appropriate horse (Weinstein 1989; Korzeniowski and Kaye 1992; antimicrobial therapy. However, a negative blood culture does Karchmer 2001). not rule out bacterial endocarditis. Because the bacteraemia is In the horse, the prognosis for endocarditis of the mitral usually intermittent, the best chance to obtain a positive blood and aortic valves is poor and, for tricuspid valve endocarditis is culture is to take 3 serial blood cultures of at least 10 ml, guarded (Dedrick et al. 1988; Kasari and Roussel 1989; Ball 1–2 h apart, preferably prior to antimicrobial therapy (Calvert and Weldon 1992; Collatos 1992; Sage and Worth 1999). This 1982; Buergelt et al. 1985; Hirsh et al. 1985; Hatfield et al. may be based on the fact that generally the diagnosis is only 1987; Kasari and Roussel 1989; Nilsfors et al. 1991; Hines et al. made in an advanced stage of the disease when already 1993; De Groot et al. 1996; Kittleson and Kienle 1998; Salonen significant valvular damage has occurred. Individual cases of et al. 1998; Sage and Worth 1999; Ramzan 2000; Karchmer successful treatment have been previously reported (Hillyer et 2001; Carmona et al. 2002). Sampling only during peak body al. 1990; De Groot et al. 1996; Maxson and Reef 1997; temperature has not previously shown to increase the isolation Sponseller and Ware 2001). Mortality in man is usually the of the bacterial organism (Hillyer et al. 1990; Korzeniowski and result of and major emboli which lead to Kaye 1992). The optimum time for obtaining a blood culture abscesses, haemorrhages and/or organ infarctions has been described as 2 h (Weinstein 1989) or 6 h before the (Korzeniowski and Kaye 1992). body temperature rises in cyclic pyrexia while bacteraemia precedes the onset of temperature elevation (Collatos 1992). References Treatment of bacterial endocarditis requires prolonged use of antimicrobials, preferably based on identification of the Anderson, M.J. and Janoff, E.N. (1998) Klebsiella endocarditis: report of two cases and review. Clin. Inf. Diseases 26, 468-474. bacteria and its sensitivity pattern and, if possible, this should Ball, M.A. and Weldon, A.D. (1992) Vegetative endocarditis in an be a bactericidal antimicrobial with good tissue penetration. appaloosa gelding. Cornell Vet. 82, 301-309. Early treatment is positively related to a positive outcome Bonagura, J.D. and Pipers, F.S. (1983) Echocardiographic features of (Calvert 1982; Brown 1985; Dedrick et al. 1988; Kasari and endocarditis in a dog, a cow, and a horse. J. Am. vet. Roussel 1989; Hillyer et al. 1990; Nilsfors et al. 1991; Collatos med. Ass. 182, 595-599. 1992; Travers and Van Den Berg 1995; De Groot et al. 1996; Brown, C.M. (1985) Acquired . Vet. Clin. N. Maxson and Reef 1997; Anderson and Janoff 1998; Salonen Am.: Equine Pract. 1, 371-382. et al. 1998). Therefore, treatment should start as soon as Buergelt, C.D., Cooley, A.J., Hines, S.A. and Pipers, F.S. (1985) possible and be continued over a long period (several months). Endocarditis in six horses. Vet. Pathol. 22, 333-337. Reaching a therapeutic level of the antimicrobial at the site Calvert, C.A. (1982) Valvular bacterial endocarditis in the dog. J. Am. of infection is often difficult because of the poor blood vet. med. Ass. 180, 1081-1084. penetration of the vegetations. 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