A challenging case: Endocarditis in a Boston terrier - Veterinary Medicine
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A challenging case: Endocarditis in a Boston terrier
Was this dog's tooth root abscess the cause of its severe, progressive systemic illness?



Periodontal disease

Periodontal disease is one of the most common health problems in pets and has been reported to affect more than 75% of dogs.2 A recent multihospital report, in which the facilities primarily see healthy pets, found that dental calculus was the top diagnosis affecting 78% of dogs older than 3 years.3 Inoffensive breath and white teeth are important to pet owners, but the numerous health benefits resulting from a thorough evaluation and appropriate periodontal disease treatment are often overlooked. Periodontal disease not only affects the health of the oral cavity but may also be associated with serious systemic illness.

Many studies in human literature have looked at the potential of periodontal disease to cause systemic illness. Periodontal disease has been associated with infective endocarditis, aspiration pneumonia, necrotizing fasciitis, diabetes, and atherosclerosis.4 But the potential association between periodontal disease and systemic illness has not been as well-researched in veterinary medicine. Postmortem evaluation of 45 dogs did show significance between the extent of periodontal disease and histopathologic changes in other organs, including the kidneys, myocardium, and liver.5 Another study found that increasing severity of periodontal disease in dogs was associated with increased C-reactive protein concentrations, a systemic inflammatory marker, and renal indices. The study also found a decrease in the C-reactive protein concentrations after appropriate treatment of periodontal disease, showing that there may be a systemic impact with periodontal disease.6


Compared with periodontal disease, endocarditis is rare in dogs, with prevalence ranging from 0.05% to 6.6%.7 The pathogenesis of bacterial endocarditis in dogs is complex, and our understanding of it is mostly extrapolated from human data. Many people with endocarditis have predisposing cardiac conditions. Since normal vascular endothelium is resistant to bacterial adhesion and colonization, underlying heart defects may cause damage to vascular endothelium secondary to turbulent or high-velocity blood flow.8

In dogs, as in people, damage to the vascular endothelium is an important step in bacterial colonization. Thus, it is interesting to note that, unlike in people, most underlying heart diseases do not appear to predispose dogs to infectious endocarditis.9 In this patient, the previously reported heart murmur was likely due to endocardiosis of the mitral valve. This assumption is made based on the patient's signalment and history and was confirmed by postmortem examination findings. The prevalence of endocarditis in dogs with endocardiosis is low.9 However, the prevalence of bacterial endocarditis is low in general. As endocardiosis progresses, the endothelium undergoes uneven damage, leading to areas of denuded valve and exposure of the basement membrane or collagen matrix.10,11 Endocardiosis and subsequent valvular endothelial damage could theoretically allow bacterial adhesion and colonization. Thus, the role of underlying endocardiosis in the development of bacterial endocarditis in this patient is uncertain.

Table 2: Criteria for Diagnosing Endocarditis*
A diagnosis of bacterial endocarditis can be difficult to make in antemortem patients. Endocarditis is definitively diagnosed based on pathology of the heart valve or when the patient meets two of the major criteria or one major and two minor criteria (Table 2).12 In one study, only 44% of dogs with endocarditis had temperatures > 103 F (39.4 C).13 A new or previously undiagnosed heart murmur often raises the suspicion of endocarditis; however, 59% of dogs with bacterial endocarditis do not have a new murmur on physical examination.14 Another study found that only 33% of cases of bacterial endocarditis had a new heart murmur or change in intensity of an existing heart murmur.13 CBC results that support a diagnosis of endocarditis include monocytosis, anemia, and thrombocytopenia, which are nonspecific findings.7 Echocardiography is the single most useful diagnostic test for endocarditis and is reported to have sensitivities as high as 90%.9,12 However, an echocardiogram alone is usually insufficient in diagnosing infective endocarditis in most cases.12

In this case, the patient did not have a temperature > 103 F (39.4 C) on presentation. This finding may have been influenced by the antibiotic treatment the patient was receiving for two weeks before presentation. The patient also did not have a new heart murmur, as its record indicated the presence of a heart murmur for at least a year. Although monocytosis is present in more than 90% of cases,7 neither monocytosis nor thrombocytopenia were present in this case. Thus, the only findings that supported the diagnosis of endocarditis in this patient were anemia and an increase in the intensity of the heart murmur, although the latter may reflect a difference in the practitioners evaluating the murmur or in the patient's systemic condition.

Patients with bacterial endocarditis frequently have many nonspecific clinical signs on presentation, which is true in this case as well. Many of these clinical signs are due to septic embolization to a variety of organ systems. It has been reported that 32% of dogs with endocarditis had septic emboli found on necropsy.13 The kidneys are the most common organ to suffer ischemic insult because of septic emboli. Immune-complex glomerulonephritis is also commonly found on necropsy.7 Neurologic signs also occur because of septic emboli. In the case reported here, bacterial colonies were still present in the kidney despite antibiotic therapy. Meningoencephalitis was also present, but no bacterial emboli were detected.

The patient's collapsing episode may be explained by cardiac arrhythmia. The degree of disease present in the myocardium, including neutrophilic inflammation and necrosis, may have led to significant arrhythmias and subsequent collapse. Neurally mediated syncope, also called vasovagal syncope, may have also occurred. Increased vagal tone—in this case vomiting—is associated with acute decreases in systemic blood pressure and heart rate. Because of the patient's severe neurologic signs, including dull mentation, other causes of collapse such as central nervous system bacterial thromboemboli cannot be ruled out.


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