Primary lung abscess caused by Staphylococcus lugdunensis

Primary lung abscess caused by Staphylococcus lugdunensis

J Infect Chemother xxx (2017) 1e3 Contents lists available at ScienceDirect Journal of Infection and Chemotherapy journal homepage: http://www.elsev...

1MB Sizes 0 Downloads 69 Views

J Infect Chemother xxx (2017) 1e3

Contents lists available at ScienceDirect

Journal of Infection and Chemotherapy journal homepage: http://www.elsevier.com/locate/jic

Case Report

Primary lung abscess caused by Staphylococcus lugdunensis* Deng-Wei Chou a, *, Chao-Tai Lee b a b

Department of Critical Care Medicine, Tainan Municipal Hospital, 670 Chungde Road, East District, Tainan, Taiwan Department of Clinical Laboratory, Tainan Municipal Hospital, 670 Chungde Road, East District, Tainan, Taiwan

a r t i c l e i n f o

a b s t r a c t

Article history: Received 10 May 2017 Received in revised form 23 June 2017 Accepted 10 July 2017 Available online xxx

Staphylococcus lugdunensis, a strain of coagulaseenegative staphylococci, is part of the normal flora of human skin but can cause multiple infections at various sites. This microorganism has emerged as a major human pathogen. However, no study has reported primary lung abscess caused by S. lugdunensis. A 54-year-old alcoholic man without relevant past medical history was admitted because of primary lung abscesses. Empirical amoxicillin/clavulanate therapy was initially administered; however, the patient had persistent pleuritic chest pain and fever. He subsequently underwent resection of the lung abscess and removal of exudative pleural effusion on the fourth hospital day. Histopathologic examination confirmed the diagnosis of lung abscess, and colonies of gram-positive bacteria were identified. The culture specimen from the abscess was positive for S. lugdunensis, which was susceptible to amoxicillin/clavulanate, cefazolin, ciprofloxacin, clindamycin, erythromycin, oxacillin, teicoplanin, tetracycline, and vancomycin. Following resection and 3 weeks of amoxicillin/clavulanate therapy, the patient eventually recovered well without relapse. This case report is the first to describe S. lugdunensis as a cause of primary lung abscess; this microorganism should be considered a potential monomicrobial pathogen in primary lung abscess. © 2017 Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.

Keywords: Staphylococcus lugdunensis Coagulase-negative staphylococci Primary lung abscess Alcoholism Minimal inhibitory concentration

1. Introduction

1.1. Case report

Staphylococcus lugdunensis, a strain of coagulase-negative staphylococci (CoNS), is part of the normal flora of human skin [1] but can cause clinically significant infections [2]. A study of clinically reviewed specimens of S. lugdunensis revealed that only 15% of the specimens were evidently a culture contaminant or colonizing organism [1]. S. lugdunensis should not be considered a contaminant without careful investigation [2]; it is more aggressive than other CoNS [3] and has emerged as a major human pathogen [2]. This microorganism can cause multiple infections at various sites, including valve endocarditis; infections of the skin and soft tissue, bloodstream, oral, urinary tract, bone and joint, and central nervous system; peritonitis [2]; ocular infection [4], and acute necrotizing sinusitis [5]. However, according to our review of relevant literature, this study is the first to report primary lung abscess caused by S. lugdunensis.

A 54-year-old alcoholic man without a relevant past medical history was admitted with complaints of fever and cough with purulent sputum for 7 days. He had consumed more than 2 standard drinks (28 g) per day during the previous 2 years. He did not have a habit of smoking. On examination, he was clear, febrile (38.2  C), tachycardic (121 beats/minute), and tachypneic (22 breaths/minute). Lung examination revealed mild crackle sounds and tenderness aggravated by deep breaths in the right lower zone. The remainder of the physical examination was unremarkable. Neither dental nor periodontal infection was found. Laboratory tests yielded a white cell count of 14.7  109/L, with a predominance of neutrophils (80%). Furthermore, hemoglobin, blood sugar, and electrolyte levels; platelet count; and renal and liver function were determined; all results were within the reference range. A chest radiograph (Fig. 1A) revealed a round opacity in the posterior right lower lung. Computed tomography (CT; Fig. 1B) showed a round consolidation of 5 cm in diameter, with central abscess and gas bubbles formation at the posterior region of the right lower lung. Lung abscess was diagnosed based on clinical and radiological findings. Intravenous amoxicillin/clavulanate (1000/200 mg,

*

All authors meet the above ICMJE authorship criteria. * Corresponding author. E-mail addresses: [email protected] (D.-W. Chou), [email protected] (C.-T. Lee).

http://dx.doi.org/10.1016/j.jiac.2017.07.004 1341-321X/© 2017 Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.

Please cite this article in press as: Chou D-W, Lee C-T, Primary lung abscess caused by Staphylococcus lugdunensis, J Infect Chemother (2017), http://dx.doi.org/10.1016/j.jiac.2017.07.004

2

D.-W. Chou, C.-T. Lee / J Infect Chemother xxx (2017) 1e3

Fig. 1. (A) Chest radiograph showing a round opacity in the posterior right lower lung (arrow). (B) Contrast-enhanced computed tomography shows a round consolidation of 5 cm in diameter with central abscess and gas bubbles formation at the posterior region of the right lower lung (arrow), which indicates a lung abscess. Pleural effusion is evident (curved arrow).

respectively) was initiated every 8 hours. A sputum smear showed gram-positive coryneform rods and gram-positive cocci in clusters. No pathogens were found in the sputum and blood cultures collected on the first and third hospital day. Fever and right-sided pleuritic chest pain persisted despite antimicrobial therapy. The patient subsequently underwent video-assisted thoracoscopic surgery, with wedge resection of the right lower lobe for the abscess on the fourth hospital day. Approximately 500 mL of exudative pleural effusion was drained from the right pleural space. Histopathological examination confirmed the diagnosis of lung abscess (Fig. 2), and colonies of gram-positive bacteria were identified. No evidence of malignancy or fungal elements was observed. The culture specimen from the abscess revealed cream-colored colonies with b-hemolysis on a blood agar plate after 24 h of incubation at 35  C in 5% CO2. The isolate was gram-positive cocci in clusters. Biochemical tests revealed that isolate was positive results for catalase, pyrrolidonyl arylamidase, and ornithine decarboxylase

reactions. Furthermore, the isolate yielded a negative result for rapid slide latex agglutination performed using the Staphaurex Plus test latex kit (Remel, Lenexa, KS, USA). The isolate was identified to be S. lugdunensis, and minimal inhibitory concentration (MIC) was investigated using the Phoenix automated microbiology system (Becton Dickinson Microbiology Systems, Sparks, MD, USA). The isolate produced b-lactamase, as determined using Cefinase paper disc (Becton Dickinson Microbiology Systems, Sparks, MD, USA). The organism was susceptible to amoxicillin/clavulanate, cefazolin, ciprofloxacin, clindamycin, erythromycin, oxacillin, teicoplanin, tetracycline, and vancomycin, but resistant to trimethoprim/sulfamethoxazole. Table 1 shows the MIC and antibiotic susceptibilities. No anaerobic bacteria were isolated from the abscess. Transesophageal echocardiogram did not reveal valvular vegetations. Abdominal ultrasonography confirmed no cirrhosis of the liver. Surgery followed by antimicrobial therapy improved the patient's clinical condition. He was discharged on the 10th hospital day and

Fig. 2. Histopathological examination reveals marked acute inflammation with abscess formation in lung tissues. Gram's staining reveals a gram-positive bacterial colony (arrow). Magnification,  200.

Please cite this article in press as: Chou D-W, Lee C-T, Primary lung abscess caused by Staphylococcus lugdunensis, J Infect Chemother (2017), http://dx.doi.org/10.1016/j.jiac.2017.07.004

D.-W. Chou, C.-T. Lee / J Infect Chemother xxx (2017) 1e3 Table 1 Minimal inhibitory concentration and antibiotic susceptibility of Staphylococcus lugdunensis. Antimicrobial agent

MIC (mg/mL)

Interpretation

Amoxicillin/clavulanate Cefazolin Ciprofloxacin Clindamycin Daptomycin Erythromycin Fusidic acid Gentamicin Linezolid Oxacillin Rifampin Teicoplanin Tetracycline Trimethoprim/sulfamethoxazole Vancomycin

1/0.5 2 0.5 0.5 1 0.5 1 2 2 0.5 0.5 1 0.5 >2/38 1

S S S S S S S S S S S S S R S

MIC, minimal inhibitory concentration; S, susceptible; R, resistant.

prescribed 2 weeks of oral amoxicillin/clavulanate (875/125 mg, respectively) twice daily. No complication or relapse was detected at the 1-year follow-up. 2. Discussion Primary lung abscess is caused by the aspiration of oropharyngeal secretions, including those during dental or periodontal infection; paranasal sinusitis; altered consciousness; gastroesophageal reflux disease; frequent vomiting; and alcoholism [6]. The pathogenesis of the aspiration of oropharyngeal secretions in alcoholic patients may be multifactorial. The combination of impaired gastric acid secretion (because of alcohol-associated chronic atrophic gastritis) and alcohol's relaxing effect on the lower esophageal sphincter may contribute to the inoculation of pathogens in the mouth [7]. Furthermore, ethanol adversely affects many critical components of pulmonary host defense essential for eradicating infection and maintaining homeostasis in the host [7]. S. lugdunensis has been isolated from saliva in the oral cavity [8,9]. Thus, it causes lung abscesses via the route involving aspiration of oropharyngeal secretions in alcoholism. The patient had been healthy previously without lung diseases. Furthermore, transesophageal echocardiography did not reveal valvular vegetations, and chest CT scans did not indicate septic pulmonary embolism. There was no evidence of any other route of infection to cause the abscess; thus, primary lung abscesses was diagnosed. S. lugdunensis is part of the normal flora of human skin; therefore, it is a diagnostic challenge to distinguish a clinically significant pathogen from a culture contaminant. S. lugdunensis infection should be highly suspected if the clinical course suggests an infection and correlates with positive S. lugdunensis on culture, particularly from a specimen isolated from a sterile site. Unlike S. aureus, many clinical laboratories do not routinely identify CoNS to the species level for lower respiratory tracts cultures [10]. This is probably the reason why S. lugdunensis has not previously been reported as a pathogen of the pulmonary system. Our case suggests considering S. lugdunensis a potential pathogen in primary lung abscess. Unlike other CoNS species, S. lugdunensis shares certain virulence characteristics with S. aureus, which facilitate causing diseases similar to S. aureus [11,12]. Our case reveals that, similar to S. aureus, S. lugdunensis is potentially a monomicrobial pathogenic cause of lung abscess [13]. b-lactamase, the enzyme that confers resistance on b-lactam antimicrobials, has been reported in S. lugdunensis in America and Europe [3]. The empirical antimicrobial therapy for S. lugdunensis should be a combination of b-lactam and b-lactamase inhibitor.

3

Vancomycin is an alternative in patients allergic to penicillin [3]. Because b-lactamase was detected in our case, amoxicillin/clavulanate was appropriate as the empirical antimicrobial therapy for primary lung abscess. The standard intravenous dosage of amoxicillin/clavulanate is 1000/200 mg every 8 hours for the treatment of community-acquired lower respiratory tract infections [14]. To treat drug-resistant Streptococcus pneumoniae or b-lactamaseproducing bacteria (e.g., Haemophilus influenzae and Moraxella catarrhalis), a high-dosage of 2000/125 mg twice daily for adults has been developed with an extended-release amoxicillin component that enhances the pharmacokinetics of this formulation and covers of more bacterial strains than does conventional dosing [14,15]. In our case, b-lactamase was detected in S. lugdunensis. Therefore, initial administration of a high-dosage of amoxicillin/ clavulanate (2000/125 mg, respectively) twice daily may be more appropriate. Because of the presence of approximately 500 mL of exudative pleural effusion, the patient had persistent pleuritic chest pain and fever despite antimicrobial therapy. Thus, resection of the abscess and removal of exudative pleural effusion were performed. After resection and 3 week of antibiotics therapy, the patient eventually recovered well without relapse. In conclusion, S. lugdunensis should be considered as a potential monomicrobial pathogen in primary lung abscess. Treatments include antimicrobial therapy with a combination of b-lactam and b-lactamase inhibitor as well as surgery in patients who do not respond to antimicrobial therapy.

Conflict of interest None.

References [1] Herchline TE, Ayers LW. Occurrence of Staphylococcus lugdunensis in consecutive clinical cultures and relationship of isolation to infection. J Clin Microbiol 1991;29:419e21. [2] Klotchko A, Wallace MR, Licitra C, Sieger B. Staphylococcus lugdunensis: an emerging pathogen. South Med J 2011;104:509e14. [3] Babu E, Oropello J. Staphylococcus lugdunensis: the coagulase-negative staphylococcus you don't want to ignore. Expert Rev Anti Infect Ther 2011;9:901e7. [4] Frank KL, Del Pozo JL, Patel R. From clinical microbiology to infection pathogenesis: how darling to be different works for Staphylococcus lugdunensis. Clin Microbiol Rev 2008;21:111e33. [5] Matthews PC, Lazarus R, Protheroe A, Milford C, Bowler IC. Acute necrotizing sinusitis caused by Staphylococcus lugdunensis. J Clin Microbiol 2011;49:2740e2. [6] Kuhajda Ivan, Zarogoulidis Konstantinos, Tsirgogianni Katerina, Tsavlis Drosos, Kioumis Ioannis, Kosmidis Christoforos, et al. Lung abscessetiology, diagnostic and treatment options. Ann Transl Med 2015;3:183. [7] Happel KI, Nelson S. Alcohol, immunosuppression, and the lung. Proc Am Thorac Soc 2005;2:428e32. [8] Ohara-Nemoto Y, Haraga H, Kimura S, Nemoto TK. Occurrence of staphylococci in the oral cavities of healthy adults and nasal oral trafficking of the bacteria. J Med Microbiol 2008;57:95e9. [9] You YO, Kim KJ, Min BM, Chung CP. Staphylococcus lugdunensisea potential pathogen in oral infection. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:297e302. [10] Garcia Lynne S. Clinical microbiology procedures handbook. 3rd ed. Washington, DC: ASM; 2010. €cher S, Tønning B, Skov RL, Prag J. Staphylococcus lugdunensis, a common [11] Bo cause of skin and soft tissue infections in the community. J Clin Microbiol 2009;47:946e50. [12] Shah NB, Osmon DR, Fadel H, Patel R, Kohner PC, Steckelberg JM, et al. Laboratory and clinical characteristics of Staphylococcus lugdunensis prosthetic joint infections. J Clin Microbiol 2010;48:1600e3. [13] Fisher AM, Trever RW, Curtin JA, Schultze G, Miller DF. Staphylococcal pneumonia; a review of 21 cases in adults. N Engl J Med 1958;258:919. [14] White AR, Kaye C, Poupard J, Pypstra R, Woodnutt G, Wynne B. Augmentin® (amoxicillin/clavulanate) in the treatment of community-acquired respiratory tract infection: a review of the continuing development of an innovative antimicrobial agent. J Antimicrob Chemother 2004;53:i3e20. [15] Kaye CM, Allen A, Perry S, McDonagh M, Davy M, Storm K, et al. The clinical pharmacokinetics of a new pharmacokinetically-enhanced formulation of amoxicillin/clavulanate. Clin Ther 2001;23:578e84.

Please cite this article in press as: Chou D-W, Lee C-T, Primary lung abscess caused by Staphylococcus lugdunensis, J Infect Chemother (2017), http://dx.doi.org/10.1016/j.jiac.2017.07.004