Journal of Infection (2005) 50, 236–239
www.elsevierhealth.com/journals/jinf
CASE REPORT
Fusobacteriosis presenting as community acquired pneumonia Sanjay Bhattacharyaa, Shaun A. Livseya, Martin Wiselkab, Sayed S. Bukharia,* a
Department of Clinical Microbiology, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Sandringham Building, Level 5, Leicester LE1 5WW, UK b Department of Infectious Diseases, Leicester Royal Infirmary, University Hospitals of Leicester NHS Trust, Leicester LE1 5WW, UK Accepted 27 November 2003 Available online 22 January 2004
KEYWORDS Fusobacterium; Pneumonia; Septicaemia; Antibiotics
Summary Fusobacterium species are anaerobic Gram-negative bacilli, which colonise the mucus membranes of man and animals and can cause a number of clinical manifestations including Lemierre’s disease (postanginal septicaemia), abdominal infection and deep-seated abscesses. The incidence of fusobacterium infections appears to be increasing, and we present three cases of fusobacteriosis who presented with features of community acquired pneumonia (CAP). Cases were treated with benzyl penicillin and metronidazole, co-amoxiclav and metronidazole and amoxicillin and clarithromycin. Since some of the Fusobacterium species are resistant to penicillin and erythromycin, treatment with these antibiotics in cases of fusobacteriosis presenting as CAP may lead to treatment failure. A high index of clinical suspicion is required to recognise this rare cause of CAP. Q 2003 The British Infection Society. Published by Elsevier Ltd. All rights reserved.
Fusobacterium species are long thin spindle shaped anaerobic Gram-negative bacilli (Fig. 1), which colonise the mucus membranes of man and animals and can cause a number of clinical manifestations including oral and dental infection, abdominal infection and deep seated abscesses. The specific condition of Lemierre’s disease is a rare form of upper airways infection with a life threatening secondary septic thrombophlebitis of internal jugular vein and frequent metastatic dissemination. It was first described *Corresponding author. Tel.: þ 44-116-258-6542; fax: þ 44116-255-1949. E-mail address:
[email protected]
in 1900 by Courmont and Cade followed by Lemierre’s extensive case review and detailed description of the syndrome.1 This anaerobic infection is caused by either of the two most common pathogenic species of Fusobacterium (Fusobacterium necrophorum and Fusobacterium nucleatum). The condition usually presents in previously healthy young adults who develop fever, systemic toxicity and tenderness to palpation along the jaw and sternocleidomastoid muscle. The most common site of metastatic infection is the lung. The typical clinical triad consists of pharyngitis, a tender and swollen neck and non-cavitating pulmonary infiltrates.2
0163-4453/$30.00 Q 2003 The British Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jinf.2003.11.007
Fusobacteriosis presenting as community acquired pneumonia
The complications of this infection include persistent bacteraemia and cavitating septic pulmonary emboli. In this report we discuss three cases of fusobacteriosis masquerading as community acquired pneumonia (CAP).
Case report 1 A 57-year-old man was admitted with a 10-day history of shortness of breath (SOB), rigors, cough and haemoptysis. The patient suffered sharp, stabbing, pleuritic chest pains before the SOB developed and had a short history of weight loss. He had, fever (39.8 8C), hypotension (93/63 mmHg), clubbing, tachypnoea (40/min), O2 saturation of 91% and mild leucocytosis (WCC 12.1 £ 109/l). The CXR showed right lower lobe consolidation. Bilateral basal crackles were present. The patient was initially thought to have CAP and was treated for such. However, three days later he had a positive blood culture for F. nucleatum sensitive to penicillin and metronidazole. The inpatient stay was complicated by the development of an acute cerebellar event and malaena. Upper GI endoscopy showed prepyloric antral erosions. No abnormality was detected in CT and MRI scan of the brain. The patient was treated with co-amoxiclav (1.2 g IV tds) and metronidazole (500 mg IV tds). He improved gradually and was discharged.
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Case report 2 A 21-year-old man with a 2-week history of sore throat and productive cough was admitted with tachypnoea, hypoxia and renal dysfunction. His condition deteriorated to the point where he required urgent intubation and haemodynamic monitoring. On admission he was hypotensive (systolic BP 80 – 90 mmHg), hypoxic (PaO2 10 kPa), and tachypnoeic (RR 40/min). CXR showed signs of right upper lobe and right middle lobe consolidation. He was put on activated Protein C. Over the next 48 h his sepsis resolved. Approximately 18 h later his oxygenation significantly deteriorated as a consequence of progressive pulmonary involvement. The aetiology of the condition was uncertain, as routine microbiological tests for CAP were negative. He was treated on full spectrum antibiotic cover with amoxicillin (later changed to cefotaxime) and clarithromycin. After four days F. necrophorum sensitive to penicillin was isolated from his blood culture. He was put on benzyl penicillin 1.2 g qds IV and metronidazole 500 mg bd IV and made a complete recovery.
Case report 3 A 29-year-old veterinary nurse was admitted with a one-week history of flu-like symptoms, becoming increasingly short of breath with pleuritic chest pain. On examination she was pyrexial (38.3 8C),
Figure 1 Gram stained smear of Fusobacterium species (by courtesy of Professor Louis De Vos).
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haemodynamically stable but oxygen saturation was 92% with a respiratory rate of 36/min and coarse crepitations in the right mid and lower chest. Investigations revealed a white cell count of 10.0 £ 109/l, platelets 11 £ 109/l with normal clotting screen, D -dimers were 1000 ng/ml and a subsequent bone marrow indicated peripheral destruction of platelets. Renal and hepatic function, were mildly deranged and a CXR revealed patchy consolidation in the right mid and lower zone. She was treated with intravenous amoxicillin and clarithromycin for severe CAP and given intravenous immunoglobulin. She was transferred to the intensive care unit and required continuous positive airways pressure (CPAP) support. Blood cultures revealed the presence of F. necrophorum and metronidazole was added to her regimen. Recovery was complicated by the development of an empyema requiring drainage. The source of infection was never established but she was noted to be fond of kissing her pet dogs.
Discussion Fusobacterium species have been implicated in the pathogenesis of several diseases, which include cervicofacial infections including jugular vein septic thrombophlebitis, pleuropulmonary infections, abscesses of abdomen, pelvic cavity, bones and CNS, infections of soft tissue, surgical wounds, bite wounds, endocarditis, and otitis media.3 Fusobacteriosis is usually seen in adolescents and young adults but may affect other age groups. It has been associated with blood stream infections in immunocompromised patients including bone marrow transplant recipients.4 There is evidence that the organism itself can initiate local or systemic immunosuppression, which in turn can enhance its pathogenicity.3 Some strains of F. nucleatum have been reported to produce beta-lactamase and would, therefore, exhibit resistance to penicillin and amoxicillin.5 Reports from Health Protection Agency (HPA) suggest that although all isolates of F. necrophorum were sensitive to metronidazole, 2% were penicillin resistant and 18% erythromycin resistant.6 A recent review of Fusobacterium species bacteraemia by the HPA Anaerobe Reference Unit in Cardiff for the period 1990 – 2001 showed that there has been a marked increase in the cases over the past decade. During this period there were 237 reports of F. necrophorum bacteraemia. It is postulated that the reason for this rise may be related to the UK primary care antimicrobial
S. Bhattacharya et al.
Table 1 Management of fusobacteriosis 1. Intravenous antimicrobial therapy for 7–10 days with agents such as: Metronidazole 500 mg IV tds Or Clindamycin 600 mg IV qds Or Co-amoxiclav 1.2 g IV tds Or Piperacillin-Tazobactam 4.5 g IV tds 2. Drainage of metastatic abscess 3. Ligation and resection of the infected internal jugular vein may be necessary in unrelenting cases
guidelines which recommended to the general practitioners not to use antibiotics for presumed viral upper respiratory infections such as pharyngitis which is a common presenting feature of fusobacteriosis.6 The usual aetiological agents associated with CAP include Streptococcus pneumoniae, Haemophilus influenzae and atypical agents such as Legionella pneumophila, Chlamydia pneumoniae and Mycoplasma pneumoniae. First-line empirical antibiotic therapy for these organisms includes amoxicillin and erythromycin. These antibiotics may be ineffective for Fusobacteriosis due to the emergence of resistance. However, metronidazole remains the treatment of choice, as resistance has not been reported6 (Table 1). In addition, it is important to keep in mind that rare pathogens may present with common disease syndromes and may increase the risk of inappropriate therapy. Fusobacteriosis is an uncommon but serious cause of respiratory tract infection, which may be mistaken for CAP. However, it may respond poorly to oral penicillin and amoxicillin partly due to its tendency to disseminate and partly due to the emergence of betalactamase producing strains of Fusobacterium species. A high index of suspicion, and close liaison with the microbiology laboratory are important for accurate diagnosis and optimal therapy.
Acknowledgements The photograph of Fusobacterium sp. was made available with kind permission of Prof. Louis De Vos U.L.B. CP160/11 Te ´l.: 00-32-2-650-24-08; fax: 0032-2-650-22-64; e-mail: http://
[email protected].
References 1. Weesner CL, Cisek JE. Lemierre’s syndrome: the forgotten disease. Ann Emerg Med 1993;22:256—258.
Fusobacteriosis presenting as community acquired pneumonia
2. Chirinos JA, Lichtstein DM, Garcia J, Tamariz LJ. The evolution of Lemierre syndrome: report of 2 cases and review of the literature. Medicine (Baltimore) 2002;81:458—465. 3. Shenker BJ, Datar S. Fusobacterium nucleatum inhibits human T-cell activation by arresting cells in the mid-G1 phase of the cell cycle. Infect Immun 1995;63:4830—4836. 4. Lark RL, McNeil SA, VanderHyde K, Noorani Z, Uberti J, Chenoweth C. Risk factors for anaerobic bloodstream infections in bone marrow transplant recipients. Clin Infect Dis 2001;33:338—343.
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5. Nyfors S, Kononen E, Syrjanen R, Komulainen E, JousimiesSomer H. Emergence of penicillin resistance among Fusobacterium nucleatum populations of commensal oral flora during early childhood. J Antimicrob Chemother 2003;51:107—112. 6. Brazier JS, Duerden BI, Hall V, Morris TE, Yusuf E. A review of Lemierre’s disease and reports of Fusobacterium necrophorum infections in England and Wales 1990—2001. Abstract 27th Annual Scientific Conference, University of Warwick, 9th—11th September, Public Health Laboratory Service, 2002; p. 15.
