A patient with bacteraemia and possible endocarditis caused by a recently-discovered genomospecies of Capnocytophaga: Capnocytophaga genomospecies AHN8471: a case report

<p>Abstract</p> <p>Introduction</p> <p><it>Capnocytophaga </it>are a genus of bacteria that have been found to be the causative organisms in a range of infections, including serious conditions such as bacteraemia, endocarditis and meningitis. This has been especially true amongst those with serious comorbidities and the immunocompromised populations. Although several species are known to cause human disease, historically, laboratories have often not identified isolates to species level due to the unreliable, laborious techniques needed. With the advent of Polymerase Chain Reaction-Restriction Fragment Length Polymorphism Analysis, identification to species level is now frequently possible and desirable, as it may provide clues as to the source of infection and its treatment.</p> <p>Case presentation</p> <p>Here we describe a case of bacteraemia and possible endocarditis in a 64-year-old white British man caused by a newly identified genomospecies of <it>Capnocytophaga </it>in a patient subsequently diagnosed with metastatic adenocarcinoma of the oesophagus. The source of the bacteraemia was presumed to be from the patient's own oral flora.</p> <p>Conclusion</p> <p>Our case further confirms the potential for <it>Capnocytophaga </it>to cause systemic infections, highlights the availability and need for identification of isolates to species level and re-emphasises the difficulty in diagnosing <it>Capnocytophaga </it>infections due to their slow growth in the laboratory.</p

Acquisition of Complement Inhibitor Serine Protease Factor I and Its Cofactors C4b-Binding Protein and Factor H by Prevotella intermedia

Infection with the Gram-negative pathogen Prevotella intermedia gives rise to periodontitis and a growing number of studies implies an association of P. intermedia with rheumatoid arthritis. The serine protease Factor I (FI) is the central inhibitor of complement degrading complement components C3b and C4b in the presence of cofactors such as C4b-binding protein (C4BP) and Factor H (FH). Yet, the significance of complement inhibitor acquisition in P. intermedia infection and FI binding by Gram-negative pathogens has not been addressed. Here we show that P. intermedia isolates bound purified FI as well as FI directly from heat-inactivated human serum. FI bound to bacteria retained its serine protease activity as shown in degradation experiments with 125I-labeled C4b. Since FI requires cofactors for its activity we also investigated the binding of purified cofactors C4BP and FH and found acquisition of both proteins, which retained their activity in FI mediated degradation of C3b and C4b. We propose that FI binding by P. intermedia represents a new mechanism contributing to complement evasion by a Gram-negative bacterial pathogen associated with chronic diseases