At necropsy, thick tan-to-brown encrustations (dental calculus) adhered to the canine, premolar, and molar teeth. The maxillary
fourth premolars and molars exhibited gingival recession up to 7 mm and were easily moveable with gentle digital pressure.
Periodontal probing of the left maxillary first molar tooth indicated communication with the palatal root (measuring 8 mm
in depth). The loss of normal periodontal structures to the level of the apex—thus, allowing communication of oral flora and
the endodontic system of the tooth—is known as a class II perio-endo lesion.1 This tooth was easily extracted with digital pressure. The apex of the palatal root of this tooth was swabbed for culture.
1. The left atrium of the heart contained a raised, roughened, plaque-like lesion (white arrow) at the base of the atrioventricular
valve consistent with endocarditis and smooth nodular thickening (black arrows) along the free margins of the valve leaflets
indicative of chronic valvular disease (endocardiosis).
Within the left atrium of the heart, a rough, slightly raised, red-and-tan, plaque-like lesion measuring about 1 cm in diamet
you er was present on the endocardial surface of the left atrioventricular valve (Figure 1). The margins of the valve leaflets had smooth, nodular thickening consistent with endocardiosis. Multiple pinpoint-to-1-to-2-mm
dark red foci were present on the epicardium and endocardium, within the renal cortex (Figure 2), and on the leptomeningeal surface of the cerebrum.
2. On the cut section of the kidney, multiple dark red pinpoint-to-1-to-2-mm foci were distributed throughout the renal cortex.
The pulp cavity of the examined first molar contained granular necrotic debris, hemosiderin, nonstaining cholesterol clefts,
and numerous gram-negative bacterial rods with lesser numbers of gram-positive cocci. The tooth roots were irregularly scalloped
and heavily colonized by bacteria. The left atrioventricular valve had full-thickness infiltration and expansion by numerous
neutrophils, fibrin, hemorrhage, and blood vessels lined by plump (reactive) endothelial cells (Figure 3). Gram-negative bacterial rods colonized the surface of the inflamed valve (Figure 3 inset), which had nonuniform damage to the endothelium. Discrete, unencapsulated foci of neutrophilic inflammation with associated
hemorrhage, necrosis, and variable vascular fibrinoid necrosis were present in the myocardium, kidney (typically centered
on renal glomeruli [Figure 4]), small intestine, leptomeninges, cerebrum, and spinal cord. Within the central nervous system, foci of suppurative inflammation
were predominantly observed in grey matter. Gram-negative bacterial rods were rarely identified in affected glomeruli (Figure 4 inset) and were not observed in other affected tissues.
3. Histopathologic examination of the plaque on the atrioventricular valve revealed marked, full-thickness fibrinosuppurative
inflammation with colonization by bacteria (arrow) (hematoxylin-eosin stain). Inset: Bacteria were gram-negative (Brown &
Hopps stain; inset bar=25 microns).
Aerobic culture of the suspected tooth root abscess yielded abundant growth of normal respiratory flora as well as Pasteurella species, Acinetobacter lwoffii, and Enterobacter cloacae. Aerobic culture of the right kidney and heart also grew Pasteurella pneumotropica and Enterobacter cloacae. The right kidney and heart also grew Klebsiella pneumoniae, Cronobacter sakazakii, a gram-positive cocci that was not further characterized, and Clostridium perfringens.
4. Histopathologic examination of the kidney revealed intense fibrinosuppurative inflammation centered on glomeruli (arrow)
and extending into the surrounding renal interstitium (hematoxylin-eosin stain). Inset: Rare gram-negative bacterial colonies
were identified in renal glomeruli (arrowhead) (Brown & Hopps stain; inset bar=25 microns).
Given the similar morphology and gram staining of bacterial organisms identified in the pulp canal and heart valve in histologic
sections as well as the bacterial culture of two common bacteria from the apex of the palatal root of the left maxillary first
molar tooth and the pooled kidney and heart tissues, it is postulated that bacteremia secondary to periodontal disease was
the cause of endocarditis in this case. Endocarditis subsequently led to septic embolization with multiorgan involvement.