Legionella Native Valve Endocarditis Case Report and Review of Literature
Title: Legionella native valve endocarditis case report and review of literature
Legionella native valve endocarditis is exceedingly rare, and to the best of our knowledge, this is the first case complicated by a septic spleen infarction.
The incidence of infectious endocarditis worldwide is estimated at 30/100.000 cases per year. In Western Europe and North America endocarditis on native valves show an incidence of 2–6/100.000 per year [1, 2]. Streptococcus and Staphylococcus species are the cause for endocarditis in about 80%, another 10% are caused by Enterococcus species or bacteria of the HACEK-group. According to Barnes et al. culture negative endocarditis accounts for 2.5 to 31% of all cases . Negative blood cultures often result from previous antimicrobial therapy or fastidious bacteria (mostly Coxiella burnetti, Bartonella spp. And Tropheryma whippeli). Legionella species are very rarely found as causative agent of infectious endocarditis; only 2 patients with involvement of a native valve are mentioned in literature so far.
Methods and Findings:
The current case is, to the best of our knowledge, the first report of an endocarditis due to Legionella complicated by a spleen abscess. Altogether, it represents the third report of a native valve endocarditis attributable to Legionella pneumophila.
Legionella species are fastidious gram-negative bacilli. Today 57 species are known incorporating at least 79 different serotypes. According to Murder and Yu 20 different Legionella species are considered as pathogens for humans, of which Legionella pneumophila is responsible for 90% of infections . Legionella pneumophila has 16 serotypes, with serotype 1 being the most significant, other Legionella serotypes are found in nosocomial infections.
Legionella mostly causes pneumonia by direct inhalation of contaminated aerosol . Extrapulmonary manifestations are rare and described predominantly in surgical patients as prosthetic valve endocarditis, joint-prosthesis- or wound-infections , where the infection pathway is via inoculation with the bacteria during surgery.
Legionella endocarditis has rarely been described in literature. Only 16 cases have been reported from which the first is dated to 1984 . In almost all cases patients had experienced valve surgery, only two other cases had native valves [8, 9]. In one patient, the diagnosis was confirmed with PCR and sequencing from aortic tissue , in the other, Legionella pneumophila serotype 1 was detected in the urine sample and cultures on buffered charcoal-yeast extract (BCYE)–Agar using blood and bronchial fluid .
Gold standard for diagnosis of Legionella pneumonia is a positive culture on a Legionella- BCYE-Agar or a Legionella specific PCR. Since these diagnostic methods are complex and not always available, the most commonly performed testing is the detection of Legionella antigen in the urine, even though the test is only able to detect Legionella pneumophila serotype 1. Serological testing is not useful for diagnosing acute infection since seroconversion often occurs only after several weeks. Final proof of a Legionella endocarditis is a positive histology with typical bacteria seen on electronic microscopy or a positive PCR for Legionella.
Admission diagnosis of our patient was pneumonia and antibiotic treatment with Ceftriaxone and Clarithromycin was started. Since ceasing the therapy with Clarithromycin was followed by serious deterioration of the patient´s state, we assumed systemic spreading of the bacteria. Diagnosis of endocarditis was established by Duke criteria fulfilling 1 major criteria by positive transesophageal echocardiography (Figure 1) with a floating mass on the aortic valve, as well as 4 minor criteria: fever (temperature > 38°C), vascular phenomena (lung and spleen infarction), immunological phenomena (nephritic syndrome) and microbiological evidence (positive urinary antigen for Legionella pneumophila serotype 1 and positive blood serology).
Embolic events due to Legionella endocarditis seem to be very rare and have been reported in only two other cases with valve-prosthesis infection [10, 11]. Our patient showed two fresh spleen infarctions diagnosed in thoraco-abdominal CT scan. Whether they were caused by septic or thrombotic cardiac embolism triggered by the paroxysmal atrial fibrillation is not certain, the lack of other thrombotic material in transthoracic and transesophageal echocardiography other than the floating thrombus on the aortic valve as well as the presence of immunological phenomena (e.g. nephritic syndrome) seem to favor septic embolism as a cause.
Regarding the duration of therapy for Legionella endocarditis evidently no guidelines exists. Therapy regimens ranging from six weeks for native valves  to 5–14 months for prosthetic valves [10, 12] have been described in literature (Table 1).
In conclusion In case of culture negative endocarditis Legionella species has to be thought of as possible causative agent, particularly in patients with prosthetic valves. Embolic events in Legionella endocarditis are extremely rare, but have been reported. Molecular proof of the bacteria with PCR respectively silver impregnation stains from histological material are desirable, but unfortunately histological material is not always available.
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