Fig. 3b ; . In four out of six cases, the valve leaflet most notably at the annulus and extending to the region of valve insertion overlying the ventricular septum ; was disrupted by small vessels and clefts Fig. 4 ; . By immunohistochemical analysis, the endothelium lining these spaces was reactive to fragmented, and individual or rafts of endothelial cells were often present within vascular lumen Fig. 4b ; . Scattered, individual, and clusters of histiocytes, T lymphocytes, and fewer B lymphocytes were present throughout the affected valve and rarely extended into the myocardial tissue at the base of the valve immunohistochemistry results with CD3, CD79a, and CD18 not shown ; . In two cases, scattered neutrophils were present in the affected valvular stroma. Histologic features of the 11 culturable bacteriaassociated endocarditis cases were consistent with acute bacterial infection and included thick, superficial, and intravalvular fibrin deposits, dense aggregates of viable and degenerate neutrophils, scattered valvular necrosis, and, infrequently, mineralization. Although small vessels were rarely present extending beyond the base of the valve, these were neither as reactive nor as prominent a feature as those associated with the Bartonella-infected valves. The characteristic histologic features of endocardiosis were similar to those described previously.9 Clinically, these cases were distinctly present in small breed dogs and affected the mitral valve. Histologically, marked fibroblast proliferation and myxomatous change were distinct features not consistently present in Bartonella-associated valves. Proliferation of vessels was present in all cases of endocardiosis; however, in general, the vessels in these cases were more organized, less reactive, and there was no detectable endothelial necrosis. Warthin-Starry and Steiner's silver stains were of limited value in interpreting the etiology of the valvular lesions because there was extensive background staining and because, when present, the size and shape of proteobacteria is variable. In dog No. 2, there were intracytoplasmic, intraendothelial 5- m-long bacteria that were confirmed by transmission electron microscopy. In the other five cases, the presence of Bartonella could not be confirmed confidently by silver or Gram's stains. Transmission electron microscopy of three Bartonella cases revealed regions of reactive valvular and annular endothelium with evidence of endothelial proliferation and necrosis. Evidence of endothelial cell damage included swelling and distortion of mitochondria, vacuolation, and chromatin clumping Fig. 5 ; . Bacillary organisms in this study were relatively rare compared with a previous report, 1 but similar to this report, bacilli were slightly curved, 0.20.4 m in diameter and 13 m in length Fig. 6 ; . Bacteria were present within endocardial endothelial cells, within small vessel lumen, and scattered within the valvular interstitium. Bartonella were associated with endocarditis in a significant proportion of the endocarditis cases in dogs presenting at the Veterinary Medical Teaching Hospital in Davis. Histologic alterations of Bartonella infection include chronic histiocytic and lymphocytic endocarditis, mineralization, and endothelial cell and vascular proliferation. None of these features, alone or in combination, are pathognomonic for infection with Bartonella. However, the histology is distinguished from both acute, non-Bartonella bacterial endocarditis and and adriamycin.

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