Cardiobacterium hominis endocarditis: Two cases and a review of the literature.

Cardiobacterium hominis, a member of the HACEK group (Haemophilus parainfluenzae, Haemophilus aphrophilus, and Haemophilus paraphrophilus, Actinobacillus actinomycetemcomitans, C. hominis, Eikenella corrodens, and Kingella species), is a rare cause of endocarditis. There are 61 reported cases of C. hominis infective endocarditis in the English-language literature, 15 of which involved prosthetic valve endocarditis. There is one reported case of C. hominis after upper endoscopy and none reported after colonoscopy. Presented here are two cases of C. hominis prosthetic valve endocarditis following colonoscopy and a review of the microbiological and clinical features of C. hominis endocarditis. Patients with C. hominis infection have a long duration of symptoms preceding diagnosis (138+/-128 days). The most common symptoms were fever (74%), fatigue/malaise (53%), weight loss/anorexia (40%), night sweats (24%), and arthralgia/myalgia (21%). The most common risk factors were pre-existing cardiac disease (61%), the presence of a prosthetic valve (28%), and history of rheumatic fever (20%). Of the 61 cases reviewed here, the aortic valve was infected in 24 (39%) and the mitral valve in 19 (31%) patients. The average duration of blood culture incubation before growth was detected was 6.3 days (range, 2-21 days). Complications were congestive heart failure (40%), central nervous system (CNS) emboli (21%), arrhythmia (16%), and mycotic aneurysm (9%). C. hominis is almost always susceptible to beta-lactam antibiotics. Ceftriaxone is recommended by the recently published American Heart Association guidelines. The prognosis of C. hominis native valve and prosthetic valve endocarditis is favorable. The cure rate among 60 patients reviewed was 93% (56/60). For prosthetic valve endocarditis, the cure rate was 16/17 (94%). Valve replacement was required in 27 (45%) cases.

Neutrophils and reactive oxygen intermediates mediate glucan-induced pulmonary granuloma formation through the local induction of monocyte chemoattractant protein-1.

Monocyte chemoattractant protein-1 (MCP-1), which is required for full development of glucan-induced granulomas, in the rat, is expressed in the walls of blood vessels at sites of glucan embolization. Early (1 hour) vessel wall expression of MCP-1 is temporally and anatomically linked to the transient accumulation of neutrophils, even though these cells are not present within definitive lesions. To ascertain the potential pathophysiologic role of neutrophils in glucan-induced granuloma formation, rats were neutrophil-depleted using specific antiserum. There was a marked reduction in mean granuloma size and number in neutrophil-depleted animals when compared with neutrophil-sufficient controls. To determine potential mechanisms through which neutrophils may participate in granuloma formation, the antioxidant enzymes superoxide dismutase and catalase were administered to neutrophil-sufficient animals that had received glucan. Superoxide dismutase treatment did not reduce granuloma formation, whereas catalase treatment resulted in decreased granuloma size, suggesting that H2O2 plays an important role in this process. The local expression of MCP-1 mRNA and protein, as determined by in situ hybridization and immunohistochemical analysis, respectively, was decreased in both neutrophil-depleted and catalase-treated animals but not in superoxide dismutase-treated rats. Quiescent human umbilical vein endothelial cells incubated with either H2O2 or activated neutrophils secreted MCP-1. These data indicate that neutrophils and H2O2 are required for both full granuloma development and early blood vessel wall-associated MCP-1 expression after glucan infusion. These in vivo data, coupled with in vitro data that indicate that both catalase-sensitive reagent H2O2 and neutrophil-derived reactive oxygen intermediates (ie, H2O2) can induce MCP-1 secretion by human umbilical vein endothelial cells, support the hypothesis that neutrophils and neutrophil-derived products (H2O2) influence granuloma formation through induction of local MCP-1 expression.