Bartonella vinsonii subsp. berkhoffii and related members of the alpha subdivision of the Proteobacteria in dogs with cardiac arrhythmias, endocarditis, or myocarditis

Abstract

Cardiac arrhythmias, endocarditis, or myocarditis was identified in 12 dogs, of which 11 were seroreactive to Bartonella vinsonii subspecies berkhoffii antigens. Historical abnormalities were highly variable but frequently included substantial weight loss, syncope, collapse, or sudden death. Fever was an infrequently detected abnormality. Cardiac disease was diagnosed following an illness of short duration in most dogs, but a protracted illness of at least 6 months' duration was reported for four dogs. Valvular endocarditis was diagnosed echocardiographically or histologically in eight dogs, two of which also had moderate to severe multifocal myocarditis. Four dogs lacking definitive evidence of endocarditis were included because of seroreactivity to B. vinsonii antigens and uncharacterized heart murmurs and/or arrhythmias. Alpha proteobacteria were not isolated from the blood by either conventional or lysis centrifugation blood culture techniques. Using PCR amplification and DNA sequencing of a portion of the 16S rRNA gene, B. vinsonii was identified in the blood or heart valves of three dogs. DNA sequence alignment of PCR amplicons derived from blood or tissue samples from seven dogs clustered among members of the alpha subdivision of the Proteobacteria and suggested the possibility of involvement of one or more alpha proteobacteria; however, because of the limited quantity of sequence, the genus could not be identified. Serologic or molecular evidence of coinfection with tick-transmitted pathogens, including Ehrlichia canis, Babesia canis, Babesia gibsonii, or spotted fever group rickettsiae, was obtained for seven dogs. We conclude that B. vinsonii subsp. berkhoffii and closely related species of alpha proteobacteria are an important, previously unrecognized cause of arrhythmias, endocarditis, myocarditis, syncope, and sudden death in dogs.

FIG. 1

Left auricle and base of mitral valve of dog 2, infected with B. vinsonii, distended by inflammatory exudate. Inflammation extends into the adjacent auricular myocardium on the left. Hematoxylin and eosin stain; bar = 268 μm.

FIG. 2

Coronary artery of dog 2, infected with B. vinsonii. Shown is the coronary artery with an adherent mass of inflammatory exudate bulging into the arterial lumen, with transmural inflammation of the arterial wall beneath the inflammatory exudate. Severe inflammation surrounding inflamed artery effaces the normal tissue architecture. Hematoxylin and eosin stain; bar = 107 μm.

FIG. 3

Comparative alignment of partial 16S rRNA gene sequences of Brucella canis, Rasbo bacterium, and amplicons derived from dogs 4 to 10. The sequence of the noncoding RNA strand is shown. The numbers correspond to the Escherichia coli numbering scheme. Unless noted in boldface type in the table, all intervening sequences between no. 45 and 207 for all isolates were identical. Dashes (a) indicate the lack of comparable sequence. aP, alpha proteobacterium.