Eur J Clin Microbiol Infect Dis (2002) 21:480–482 DOI 10.1007/s10096-002-0744-y
CONCISE ARTICLE
M. F. Tripodi · L. E. Adinolfi · P. Rosario · E. Ragone R. Utili
First Definite Case of Aortic Valve Endocarditis due to Moraxella phenylpyruvica Published online: 11 June 2002 © Springer-Verlag 2002
Abstract Described here is the first definite case of endocarditis due to Moraxella phenylpyruvica, which occurred in a 50-year-old male with a bicuspid aortic valve. The diagnosis was delayed because of the confounding positivity of the Widal and Wright tests. The patient was cured with surgical valve replacement and antibiotic treatment.
Introduction Moraxella species cause a wide range of infections in humans, especially in the respiratory tract, but endocarditis due to these organisms has seldom been reported. Infections caused by Moraxella spp. other than Moraxella catarrhalis are relatively rare [1, 2, 3]. Moraxella phenylpyruvica is usually considered a nonpathogenic bacterium, with only one case of endocarditis possibly caused by this organism having been reported in the literature to date [4]. Here, we describe the first case of definite infective endocarditis due to Moraxella phenylpyruvica, according to Duke’s criteria [5].
Case Report A previously healthy 50-year-old male developed remittent fever and arthromyalgia in May 1999 and was treated with erythromycin (1.2 g/day) for 5 days with no improvement. Due to persisting fever (up to 40°C), he was admitted to hospital. A chest radiograph and an ultrasound examination of the abdomen were both normal. A transthoracic echocardiograph showed a thickened biM.F. Tripodi (✉) · L.E. Adinolfi · P. Rosario · R. Utili Institute of Medical Therapy, Faculty of Medicine, Second University of Naples, Via D. Cotugno 1 (c/o Ospedale Gesù e Maria), 80135 Naples, Italy e-mail:
[email protected] Tel.: +39-81-5666229, Fax: +39-81-5666230 E. Ragone Dottorato di ricerca in Scienze Cardiologiche e Cardiochirurgiche, Second University of Naples Medical School, Naples, Italy
cuspid aortic valve with moderate aortic regurgitation and no vegetation. Two blood cultures performed at the time were negative. The patient was treated empirically with intravenous (i.v.) imipenem (1.5 g/day) and the symptoms ameliorated. The Widal and Wright serology tests for Salmonella and Brucella spp. performed shortly after admission were positive for Salmonella typhi (O-antigen, 1:400) and negative for Brucella spp. In light of these findings, imipenem was discontinued and the patient began treatment with chloramphenicol (2 g/day). Stool cultures performed daily resulted negative for Salmonella spp. After 7 days of chloramphenicol treatment, fever recurred. Antimicrobial treatment was then switched to i.v. ceftriaxone (2 g once daily) plus oral ciprofloxacin (500 b.i.d.) for 13 days, and the fever resolved. A second Widal test, performed 2 weeks after the first one, showed a negative O-agglutinin test and a positive H-agglutinin test for Salmonella typhi, with a titer of 1:200. At this time, standard tube agglutination for Brucella spp. yielded a titer of 1:200 for Brucella melitensis. The patient was discharged with apyrexia, and no further treatment was administered. One month later, the patient’s fever recurred. A transthoracic echocardiogram revealed thickened aortic valve leaflets. He was treated at home for 21 days with cefotaxime (1 g q12 h) and tobramycin (100 mg od), and the fever resolved after 5 days of therapy. One week after discontinuing therapy the patient had a new recurrence of fever accompanied by fatigue, malaise and dyspnea, for which he was hospitalized in our institution. On admission, the patient was pale and febrile (38.6°C). On cardiovascular examination, a grade II diastolic murmur was heard at the lower left and upper right sternal borders. Dental caries were noted. Laboratory examinations revealed the following: a leukocyte count of 5.4×103/mm3; erythrocyte count, 4.79×106/mm3; hemoglobin, 11.3 g/dl; hematocrit, 36.4%; platelets, 197×103/mm3; fibrinogen, 183 mg/dl; erythrocyte sedimentation rate, 60 mm/h; urea, 14 mg/dl; creatinine, 1.15 mg/dl; C-reactive protein, 7 mg/dl; blood iron level, 13 µg/dl; and serum ferritin, 524 µg/l. A Widal test was negative and an agglutination test for Brucella spp. yielded a titer of 1:80 for Brucella melitensis. Urinalysis was normal. Transesophageal echocardiography showed a bicuspid aortic valve with large vegetations and an aortic root abscess (size, 1.7×2.3 cm) with severe aortic regurgitation. Two sets of blood cultures were performed on admission, and empirical treatment with i.v. ceftriaxone (2 g q12 h) and i.v. netilmicin (150 mg q12 h) was started. Fever disappeared after 24 h. Four days after admission, all blood cultures yielded gram-negative, oxidase-positive and catalase-positive cocco-bacilli. The biochemical profile determined by the API 20 NE system (bioMèrieux, France) identified Moraxella phenylpyruvica (code 120004). Because the serum agglutination results were positive for Brucella, however, we tested the isolated strain with antisera specific for different Brucella spp., but no agglutination was observed.
481 The antimicrobial susceptibility of the Moraxella phenylpyruvica isolate was determined using the Kirby-Bauer disk-diffusion method. We used breakpoints specific for Neisseria spp., since no approved breakpoints for Moraxella spp. are currently available [6]. The isolate was resistant to penicillin and aztreonam and susceptible to ampicillin, ampicillin-sulbactam, amoxicillin, amoxicillin-clavulanate, ticarcillin-clavulanate, imipenem, meropenem, cefotaxime, ceftazidime, ceftriaxone, cefepime, erythromycin, rifampin, ciprofloxacin, ofloxacin, tetracycline, chloramphenicol, trimethoprim-sulfamethoxazole, and all of the aminoglycosides tested. Based on these results, the antimicrobial therapy was not modified, except the ceftriaxone dose was reduced to 3 g once daily on day 7. The patient received the prescribed antibiotic treatment for 6 weeks, and he remained afebrile during the whole period. In week 3 of treatment, the patient underwent aortic valve replacement due to hemodynamic instability. Bacteriologic cure was based on the negative culture results of the excised valve and the negative results of blood cultures performed after therapy was completed. At 2-year follow-up, the patient was alive with no recurrence of the disease.
Discussion Several fastidious gram-negative bacterial species are emerging as causes of infection, including members of the family Moraxellaceae. Moraxella catarrhalis in particular has been recognized as a significant pathogen of the respiratory tract and the causative pathogen in sporadic cases of endocarditis [1, 2, 3]. The pathogenicity of the other members of this family has been debated. To the best of our knowledge, our patient represents the first definite case of endocarditis caused by Moraxella phenylpyruvica. In a search of the literature using Medline, we found only one case of possible endocarditis that may have been caused by this organism; this patient had Moraxella phenylpyruvica bacteremia and a negative transthoracic echocardiograph result but refused to undergo transesophageal echocardiography [4]. In contrast, seven cases of endocarditis due to Moraxella catarrhalis and one by Moraxella lacunata have been described [1, 2, 3]. Few data exist on the antibiotic susceptibility of Moraxella phenylpyruvica. The strain isolated from our patient as well as the strain causing bacteremia in the other patient [4] were both beta-lactamase producers. This characteristic is shared by most Moraxella spp., which renders these organisms susceptible to beta-lactamase-resistant cephalosporins and aminoglycosides. The course of endocarditis in our patient was progressive, and the severity was mitigated, in part, by repeated short-term courses of appropriate antibiotic therapy at inadequate doses. Despite the remission of fever, extensive aortic valve destruction occurred, which required surgical intervention and a prosthetic implant. The patient with Moraxella phenylpyruvica bacteremia reported previously in the literature was cured by a 4-week regimen of antimicrobial therapy with cefotaxime and gentamicin [4]. Progressive disease has also been described in seven patients with endocarditis due to Moraxella catarrhalis [2, 3]. Four of these patients died, although two of the deaths occurred in the preantibiotic era [1]. In the case of our patient, the diagnosis was delayed by the confounding positivity of the Widal and Wright
tests. It has been reported previously that Brucella spp. can be misidentified as Moraxella phenylpyruvica by commercially available rapid identification systems (such as API 20NE) [7]. Our strain did not agglutinate Brucella antisera despite the positive agglutination test for Brucella spp. observed 2 months prior to the patient’s admission to our center. Although the patient never received specific treatment for Brucella spp., the Brucella titer subsequently declined. Therefore, we explain the transient positivity of the agglutination tests for both Salmonella and Brucella spp. as the consequence of an aspecific cross-reaction. Indeed, serological cross-reactions have been demonstrated between Salmonella or Brucella spp. and several members of the Enterobacteriaceae family as well as Stenotrophomonas maltophilia and Yersinia enterocolitica [8, 9, 10]. Moraxella phenylpyruvica belongs to one of the four phylogenetic groups of the family Moraxellaceae. However, Moraxella phenylpyruvica is distantly related to the species of the other three groups of the Moraxellaceae family [11]. It is therefore conceivable that Moraxella phenylpyruvica may share common antigens that evoke a serological cross-reaction with both Salmonella typhi and Brucella spp. Moraxella endocarditis is rare, but the course of disease may be severe [2, 3]. Accordingly, patients with bacteremia due to Moraxella spp. require prompt and vigorous treatment with appropriate drugs, since endocarditis with severe organ complication may occur. When demonstrated, Moraxella spp. should be treated with a second- or third-generation cepholosporin plus an aminoglycoside, and treatment should be administered for 4–6 weeks. Surgical valve replacement may also be required. Acknowledgements This study was supported by a research grant from the Second University of Naples and by a Ministero dell’Università e della Ricerca (MIUR) grant for research for the Center for Cardiovascular Diseases, Second University of Naples, Naples, Italy.
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