Eur J Clin Microbiol Infect Dis (2003) 22:106–107 DOI 10.1007/s10096-002-0874-2
CONCISE ARTICLE
J. Benes · O. Dzupova · P. Krizova · H. Rozsypal
Tricuspid Valve Endocarditis due to Neisseria cinerea
Published online: 15 February 2003 Springer-Verlag 2003
Abstract Reported here is a case of infective endocarditis caused by the saprophytic species Neisseria cinerea. To the best of our knowledge, this etiology has not been documented in the medical literature previously. The patient was an intravenous drug addict who developed tricuspid endocarditis with lung embolism. The disease was cured after treatment with ampicillin/clavulanate that was changed to ceftriaxone after an embolic event.
Introduction Neisseria cinerea is known as one of the commensal microbes colonizing the oral cavity and, occasionally, other mucous membranes of the human body. Nevertheless, it possesses some pathogenic ability and has been described as an etiologic agent in the following infections: conjunctivitis and other ocular infections, mainly in early infancy [1, 2]; proctitis [3]; lymphadenitis [4]; urinary tract infection [5]; pneumonia [6, 7]; peritonitis following peritoneal dialysis [8]; meningitis [9]; or bacteremia [7, 10]. We report here a case of endocarditis due to Neisseria cinerea. To the best of our knowledge, this is the first report of a case with this etiology.
J. Benes ()) · O. Dzupova Department of Infectious Diseases, 3rd Faculty of Medicine, Charles University, Ruska 87, 10000 Prague, Czech Republic e-mail:
[email protected] Tel.: +420-266082707 Fax: +420-266082707 P. Krizova National Reference Laboratory for Meningococcal Infections, National Institute of Public Health, Srobarova 48, 10042 Prague, Czech Republic H. Rozsypal Department of Infectious Diseases, 1st Faculty of Medicine, Charles University, Katerinska 32, 12108 Prague, Czech Republic
Case Report A 34-year-old man was referred to the Department of Infectious Diseases for treatment of moderate diarrhea and fever up to 40C of 6 days’ duration; he also complained of chills, shiver, nonproductive cough, breathlessness, and malaise. His medical history had been insignificant until he became an intravenous drug addict 2 years previously. His preferential drug was methamphetamine (pervitin), which is commonly used by addicts in the Czech Republic [11]. Soon after his first experience with intravenous drugs, he had a myocardial infarction and was hospitalized in a local hospital. He had been treated with a beta-blocker (betaxolol) and low-dose acetylsalicylate since that episode. On admission, he was soiled, fatigued and dehydrated. His blood pressure was 90/60 mm Hg and his pulse rate was 120/min. Physical examination of the oral cavity, chest, and abdomen did not reveal any significant pathological changes. Examination of the skin revealed only multiple scars resulting from needle punctures. The laboratory findings were as follows: leukocyte count, 19,300/mm3; hemoglobin, 12.3 g/dl; platelet count, 155,000/mm3; erythrocyte sedimentation rate, 90 mm/h; C-reactive protein, 32 mg/ l; albumin, 30 g/l. Serum aminotransferases, urea, and creatinine were normal, as was urine. Chest radiograph showed two small tipshaped shadows in the middle and lower lobe of the right lung; no cardiac pathological changes were found. On day 3 of hospitalization the patient developed a marked systolic murmur at the left border of the sternum. Transthoracic echocardiography revealed hypokinesis of the posteroseptal part of the left ventricle (consistent with the previous myocardial infarction) and holosystolic regurgitation of the tricuspid valve. All of the three blood cultures drawn within the first 5 days of hospitalization yielded gram-negative coccobacilli with good sensitivity to penicillin, cephalothin, chloramphenicol, tetracycline, cotrimoxazole, and ciprofloxacin. After blood cultures were collected the patient was given ampicillin 3 g and clavulanic acid 200 mg intravenously every 6 h; he became afebrile within 3 days. Transesophageal echocardiography revealed two vegetations of 62 mm on the anterior and septal cusp of the tricuspid valve. The minimum inhibitory concentrations (MIC) of agents tested against the microbe were as follows: penicillin, 0.50 mg/l; ampicillin, 0.25 mg/l; ofloxacin, 0.016 mg/l; ceftriaxone, 0.094 mg/l; and gentamicin, 4 mg/l. After 10 days of treatment the patient developed fever (38.1C) and chest pain. Pleural rub and breath sounds of decreased intensity were heard at the right lung base. The antibiotic therapy was consequently changed to ceftriaxone 4 g daily. Right lung embolism was subsequently confirmed by chest radiograph. Within 5 days of the treatment change, the patient became afebrile. Neither disintegration of lung tissue nor lung congestion was seen on chest radiograph. After finishing the 14-day ceftriax-
107 one regimen the patient insisted on treatment termination and was discharged; oral amoxicillin 750 mg thrice daily was prescribed for the following 10 days. The patient refused standard follow up and reverted to drug use; nevertheless, we ascertained that the patient did not relapse or develop any late complication of endocarditis within the 2 years following hospitalization. The isolated microbe was identified as Neisseria cinerea by the following characteristic biochemical findings: glucose negative, maltose negative, fructose negative, saccharose negative, tributyrin negative, ornithine decarboxylase negative, urease negative, lipase negative, alcalic phosphatase negative, beta-galactosidase negative, proline arylamidase positive, indole negative, synthesis of polysaccharides negative, reduction of nitrates negative, reduction of nitrites positive. The strain grew on Mueller-Hinton agar but did not grow on Thayer-Martin medium. Knowing the difficulties in differentiating Neisseria cinerea from Neisseria gonorrhoeae [12], we confirmed the identification with two commercial biochemical tests (apiNH; bioMrieux, France and Neisseria 4H; Bio-Rad, France).
Discussion Endocarditis caused by non-gonococcal, non-meningococcal neisseriae has been reported with increasing frequency in recent decades. Thirteen cases were documented in the years 1914–1967 [13]; however, a search of the Medline database revealed 29 case reports in the medical literature in the 1990–2001 period. In the latter reports, endocarditis was caused by Neisseria elongata, Neisseria mucosa, Neisseria sicca, Neisseria subflava, and Neisseria flavescens. The present case fulfills the Duke criteria of the disease [14] and serves to add Neisseria cinerea to the list of possible pathogens. Endocarditis due to these saprophytic neisseriae is often associated with severe complications, especially valve destruction and major embolism [15, 16, 17, 18]. Toxicomania seems to be an important predisposing condition for the disease. Indeed, among the 29 patients in the above-mentioned reports seven were intravenous drug users [19, 20, 21, 22, 23]. In a review of 13 cases of endocarditis due to Neisseria mucosa [17], three patients were intravenous drug users (23%). The effect of treatment with penicillin and/or gentamicin was relatively slow and unconvincing in several patients with endocarditis due to saprophytic neisseriae [16, 17, 20]; the MIC of penicillin was found to range up to 4 mg/l [17]. Third-generation cephalosporins, such as ceftriaxone, seem to be more effective than penicillin both in vitro and in vivo [23, 24]. One report also demonstrated a promising effect of ciprofloxacin [25].
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