212 surgery. Prophylactic treatment with antibiotics can prevent complications. In surgery antibiotic prophylaxis is only indicated for patients at risk of infectious endocarditis and for patients with reduced host-response, when surgery is performed in infected sites, in cases of extensive and prolonged surgical interventions and when large foreign materials are implanted.5 In a recent Cochrane review no reliable evidence of the effects of preoperative antibiotics for patients receiving dental implants was found.6 We conclude that there is no reason to either recommend or discourage the use of antibiotics to prevent infections when having inserted a dental implant. However, it is conceivable that people carrying S. pyogenes in throat are at risk to develop subsequent infection. Therefore, a practical approach to decrease the risk of streptococcal invasive disease would be probably a throat culture prior to dental implant surgery and, if the culture is positive for streptococcus, subsequent elimination of the streptococcus with antibiotics. We describe a fatal infection that demonstrates the clinical and laboratory features of STSS with early onset of shock and organ failure and isolation of S. pyogenes from normally sterile sites. The onset of the illness occurred after dental implant surgery with major presenting symptoms malaise and severe back pain. This fatal case of STSS highlights the need for more caution after dental implant surgery to prevent potentially life threatening complications. Moreover, it raises the question whether patients should routinely be screened for carrying S. pyogenes or should routinely receive antibiotic prophylaxis.
References 1. Stevens DL. Streptococcal toxic-shock syndrome: spectrum of disease, pathogenesis, and new concepts in treatment. Emerg Infect Dis 1995;1:69e78. 2. The Working Group on Severe Streptococcal Infections. Defining the group A streptococcal toxic shock syndrome. Rationale and consensus definition. JAMA 1993;269: 390e1. 3. Bisno AL, Stevens DL. Streptococcus pyogenes. In: Mandell, Douglas, Bennett, editors. Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. Elsevier, Churchill Livingstone; 2005. p. 2362e79. 4. Stevens DL, Tanner MH, Winship J, Swarts R, Ries KM, Schlievert PM, et al. Severe group A streptococcal infections associated with a toxic shock-like syndrome and scarlet fever toxin A. N Engl J Med 1989;321:1e7. 5. Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. Clin Infect Dis 1997;25:1448e58.
Letters to the Editor 6. Esposito M, Coulthard P, Oliver R, Thomsen P, Worthington HV. Antibiotics to prevent complications following dental implant treatment. Cochrane Database Syst Rev 2003;3 [CD004152].
B.M.W. Diederen* Anton G. Buiting Laboratory of Medical Microbiology and Immunology, St Elisabeth Hospital, PO Box 747, 5000 AS Tilburg, The Netherlands *Corresponding author. Tel.: þ31 13 539 2655; fax: þ31 13 544 1264. E-mail address:
[email protected] (B.M.W. Diederen) Pieter F.M.J. Spooren Department of Internal Medicine, Tweesteden Hospital, Tilburg, The Netherlands Accepted 1 November 2005 Available online 19 December 2005
0163-4453/$30 ª 2005 The British Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jinf.2005.11.001
Pneumonia and bacteremia due to Serratia odorifera Sir, Serratia species are known to cause human infections, the vast majority of which are due to S. marcescens. Other species are occasional colonizers but rarely cause disease. We report the first case of pneumonia and bacteremia due to S. odorifera, review the literature, and discuss the microbiologic characteristics of this organism. A 57-year-old undomiciled man was admitted to the hospital with a cough productive of blood tinged sputum. He had a history of alcoholic liver disease, chronic Hepatitis C virus infection, paranoid schizophrenia, chronic bronchitis and a remote history of injection drug use. On admission, the patient was anxious and ill-appearing. He had a rectal temperature of 35.7 C, pulse of 88 beats per minute, respiratory rate of 18 breaths per minute, and systolic blood pressure of 103 mmHg. Lung exam revealed crackles in bilateral lower lobes. Heart sounds were normal. Abdominal examination was benign. There was pitting edema of the lower extremities.
Letters to the Editor The hematocrit was 16.9% and the white blood cell (WBC) count was 13,100/mm3 with 61% neutrophils. He was in acute renal failure with a blood urea nitrogen of 116 mg/dL, creatinine of 5.7 mg/dL, and potassium of 7.9 mEq/L. Aspartate aminotransferase was 70 U/L, alanine aminotransferase was 28 U/L and total bilirubin was 1.6 mg/dL. Blood, urine and sputum cultures were obtained. Chest radiograph showed predominantly central airspace consolidation with bilateral moderate pleural effusions and electrocardiogram revealed peaked T waves with QRS widening. The patient was treated with insulin, dextrose 50%, sodium polystyrene sulfonate (Kayexalate), sodium bicarbonate and hemodialysis. Treatment with ticarcillin/clavulanate 2 grams intravenously every 12 h and tobramycin 150 milligrams intravenously every 24 h was initiated. Four hours after admission, the patient developed melena and hypotension with a blood pressure of 80/60 mmHg, requiring intensive care. On the second hospital day, sputum and blood cultures grew gram-negative bacilli, which were subsequently identified as S. odorifera. The patient improved within 48 h, tobramycin was discontinued, and ticarcillin/clavulanate was continued for a total of 21 days. The patient did well and was discharged from the hospital. The organism grew on 5% sheep blood agar and had a characteristic strong potato-like odor. It was biochemically identified as S. odorifera by both the VITEK System (Biomerieux products, Marcy I’Etoile, France) and API 20E System (Biomerieux products, Marcy I’Etoile, France). The isolate was susceptible to ticarcillin/clavulanate, tobramycin, ciprofloxacin, piperacillin and gentamicin and was resistant to cephalothin and ampicillin/sulbactam. The New York City Department of Health and Mental Hygiene confirmed the identity of the organism with the Biolog system (Biolog Products, Hayward, CA) and further identified the isolate as S. odorifera biogroup 1 on the basis of its fermentation of raffinose and sucrose, a positive reaction with L-ornithine decarboxylase and negative reactions with L-lysine and arginine decarboxylase. The genus Serratia, a member of the family Enterobacteriaceae, includes several species. S. marcescens is the most commonly isolated species and is routinely associated with human disease. Less commonly isolated is S. liquefaciens and there have been rare reports of nosocomial infections due to other species, including S. rubidaea, S. plymuthica and S. odorifera.1 First described by Grimont et al. in 1978, S. odorifera are gram-negative, non-spore-forming bacilli that have flagella distributed over the cell surface.2 The natural reservoir of
213 S. odorifera is unknown. Most strains have been isolated from cultivated mushrooms and from clinical specimens (bile, blood, pus and most commonly, sputum), but its presence in clinical specimens has generally been felt to represent colonization.2,3 However, S. odorifera has been occasionally reported to cause serious and, in some cases, fatal infections.4 Only 13 cases of invasive disease (including this report) due to S. odorifera have been reported in the literature.5e9 S. odorifera was isolated from both sputum and blood cultures in our patient, making this the first reported case of S. odorifera bacteremic pneumonia. It is unclear whether the primary portal of entry was the lungs or whether pneumonia was secondary to bacteremia. Ten of the previous cases of S. odorifera infections were clearly nosocomial. A cluster of eight cases occurred in a group of neonates who developed bacteremia due to contaminated total parenteral nutrition infusions.8 Two cases occurred in adults with catheter-related bacteremia.5,9 Cook and Lopez considered two of the previously reported four adult cases to be community acquired; however, each of the adult cases of S. odorifera infection developed in patients who had had repeated health care contacts and had underlying conditions, such as chronic hepatic disease, diabetes mellitus, splenectomy and chronic renal failure.6,7 S. odorifera isolates are generally naturally resistant to tetracyclines, chloramphenicol, spectinomycin and macrolides, and are generally susceptible to sulfamethoxazole-trimethoprim, aminoglycosides, ticarcillin, piperacillin, cefotaxime, ceftriaxone, ceftazidime, cefepime, carbapenems, monobactams, and the quinolones.3 The isolate from our patient, however, was resistant to ampicillin. In summary, S. odorifera can cause serious disease, including septic shock, especially in patients with chronic underlying medical illnesses. When isolated from non-sterile sites such as sputum, it should not be presumed to be a colonizer or nonpathogen but rather its significance should be interpreted in the clinical context, particularly in compromised hosts and those with frequent health care contacts.
References 1. Eisenstein BL, Zaleznik DF. Enterobacteriaceae. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 5th ed. Philadelphia: Churchill Livingstone; 2000. p. 2303. 2. Grimont PAD, Grimont F, Richard C, Davis BR, Steigerwalt AG, Brenner DJ. Deoxyribonucleic relatedness between Serratia plymuthica and other Serratia species,
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5. 6. 7. 8.
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with a description of Serratia odorifera sp. nov. (type strain: ICPB 3995). Int J Syst Bacteriol 1978;28:453e63. Stock I, Burak S, Sherwood KJ, Gruger T, Wiedemann B. Natural antimicrobial susceptibilities of strains of ‘unusual’ Serratia species: S. ficarcia, S. fonticola, S. odorifera, S. plymuthica and S. rubidaea. J Antimicrobial Chemother 2003;51:865e85. Bouza E, Garcia de la Torre M, Erice A, Cercenado E, Loza E, Rodriguez-Creixerns M. Serratia bacteremia. Diagn Microbiol Infect Dis 1987;7:237e47. Mermel LA, Spiegel CA. Nosocomial sepsis due to Serratia odorifera biovar 1. Clin Infect Dis 1992;14:208e10. Chmel H. Serratia odorifera biogroup 1 causing an invasive human infection. J Clin Microbio 1988;26:1244e5. Cook MA, Lopez JJ. Serratia odorifera biogroup 1: an emerging pathogen. J Am Osteopath Assoc 1998;98:505e7. Frean JA, Arntzen L, Rosekilly I, Isaacson M. Investigation of contaminated parenteral nutrition fluids associated with an outbreak of Serratia odorifera septicaemia. J Hosp Infect 1994;27:263e73. Glustein JZ, Rudensky B, Abrahamov A. Catheter-associated sepsis caused by Serratia odorifera Biovar 1 in an
Letters to the Editor adolescent patient. Eur J Clin Microbiol Infect Dis 1994; 13:183e4.
Jungmin Lee Jeanne Carey* David C. Perlman Department of Medicine, Beth Israel Medical Center, 20 Baird Hall, First Avenue at 16th Street, New York, NY 10003, USA *Corresponding author. Tel.: þ1 212 420 2690; fax: þ1 212 420 4615. E-mail address:
[email protected] (J. Carey) Accepted 17 November 2005 Available online 3 January 2006 0163-4453/$30 ª 2005 The British Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jinf.2005.11.016