Anaerobe xxx (2013) 1e3
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Primary lumbar epidural abscess without spondylodiscitis caused by Fusobacterium necrophorum diagnosed by 16S rRNA PCR Jose Luis Sanmillán a, *, Iván Pelegrín b, David Rodríguez c, Carmen Ardanuy d, Carmen Cabellos b a
Neurosurgery Department, Hospital Universitari de Bellvitge, Feixa Llarga s/n, 08907 Hospitalet de Llobregat, Barcelona, Spain Infectious Diseases Department, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain Neurosurgery Department, Greater Manchester Neuroscience Centre, Salford Royal Foundation Trust, Stott Lane, Salford, UK d Microbiology Department, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona, Spain b c
a r t i c l e i n f o
a b s t r a c t
Article history: Received 27 April 2013 Received in revised form 26 June 2013 Accepted 29 June 2013 Available online xxx
We report the case of a 71-year-old woman who presented a primary spinal epidural abscess caused by Fusobacterium necrophorum. This is the second report in the medical literature to associate this organism with a primary spinal epidural abscess without spondylodiscitis. After treatment with emergency laminectomy followed by 8 weeks of antibiotic treatment the patient was cured. Oral metronidazole (500 mg every 8 h) was the definitive choice of treatment. F. necrophorum spinal epidural abscess is rare, although samples for anaerobic culture should be collected in order to improve detection of anaerobic spinal infections. PCR amplification and sequencing of the 16S rRNA permits early diagnosis in anaerobic infections. Ó 2013 Published by Elsevier Ltd.
Keywords: Spinal epidural abscess Fusobacterium necrophorum
1. Introduction Spinal epidural abscess (SEA) is a condition that requires early diagnosis and adequate treatment to avoid or reduce permanent neurological deficits. The estimated incidence of SEA is 0.2e2.8/ 100,000 hospital admissions. Staphylococcus aureus is the most commonly isolated organism in SEA. Anaerobic SEA is uncommon (0.03%), and Fusobacterium necrophorum, a frequent finding in oral flora and the gastrointestinal tract, rarely causes meningeal involvement [1]. SEA is caused by hematogenous spread of bacteria or local extension associated with spondylodiscitis [2]. However, the source of infection remains unclear in many cases of primary SEA. We report the case of a 71-year-old female with lumbar SEA without spondylodiscitis caused by F. necrophorum. This is the second report of SEA caused by this anaerobic bacterium. 2. Case report A 71-year-old woman presented a 1-week history of acute low back pain, fever, and progressive symmetric weakness of both * Corresponding author. Tel.: þ34 933357011. E-mail addresses:
[email protected] (J.L. Sanmillán), ivan_pelegrin@ hotmail.com (I. Pelegrín),
[email protected] (D. Rodríguez), cardanuy@ bellvitgehospital.cat (C. Ardanuy),
[email protected] (C. Cabellos).
lower limbs. She had a previous history of chronic atrial fibrillation and osteoporosis, but no diabetes mellitus, cancer, drug abuse, corticosteroid treatment, or other conditions. Four months prior to admission she had undergone traditional needle acupuncture on her lower back due to left knee pain. On examination she was febrile (38 C). Chest, cardiovascular, and abdominal examinations were normal, and palpation of the back revealed no tenderness. There was marked weakness of the lower extremities (rated as 3/5 on the Medical Research Council scale), but without sensory impairment or sphincter dysfunction. Her leukocyte count was 10,600 109/L with 85.7% of neutrophils. Initial full-body computed tomography (CT) scan showed several abscesses affecting the liver and left psoas muscle, and air was also evidenced inside the spinal canal (Fig. 1). Lumbar magnetic resonance imaging (MRI) of the lumbosacral spine confirmed the presence of abscesses affecting the left psoas muscle, paraspinal muscles, and posterior spinal epidural space from L2 to S1, with associated dural sac compression (Fig. 2). Emergency laminectomy of L3, evacuation of epidural abscess, and dural sac decompression was therefore performed. Empirical antibiotic treatment consisted of intravenous imipenem 500 mg every 6 h and vancomycin 1000 mg every 12 h. A Gram-stained smear of the abscess material revealed numerous polymorphonucleate cells, but no bacteria were observed. The 16S rRNA PCR was positive and, after sequencing, the presence of F. necrophorum was detected. After that, in blood and anaerobic
1075-9964/$ e see front matter Ó 2013 Published by Elsevier Ltd. http://dx.doi.org/10.1016/j.anaerobe.2013.06.014
Please cite this article in press as: Sanmillán JL, et al., Primary lumbar epidural abscess without spondylodiscitis caused by Fusobacterium necrophorum diagnosed by 16S rRNA PCR, Anaerobe (2013), http://dx.doi.org/10.1016/j.anaerobe.2013.06.014
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Fig. 1. CT scan showing air inside the spinal canal. On the right, rounded hypodense lesions suggestive of left psoas abscess.
abscess fluid, culture grew F. necrophorum. It was susceptible to metronidazole, clindamycin, penicillin, cefoxitin, and imipenem, tested by disk-diffusion. Therefore, empirical endovenous antibiotic treatment was discontinued and switched to oral metronidazole (500 mg every 8 h). Three weeks after admission the left psoas abscess was drained by CT-scan guided needle aspiration, it having failed to resolve with antibiotic therapy. Oral and paranasal sinus infection, as well as other possible hematogenous foci such as endocarditis and Lemierre’s syndrome, were ruled out. Spondylodiscitis was not observed in the MRI and CT scans obtained during and after admission. The patient made a satisfactory recovery after surgery and she was discharged after 4 weeks in hospital, without sequelae. The
Fig. 2. T1WI MRI shows a hypointense posterior collection inside the spinal canal with peripheral contrast enhancement after administration of gadolinium, extending from L2 to S1 and with a major compression of the spinal cord at L3.
abscess volume reduction was confirmed by follow-up full-body CT scan and MRI. The patient completed an 8-week course of metronidazole, and at 1-year of follow-up she remained asymptomatic with no sequelae.
3. Discussion Anaerobic SEA is very unusual, with only one published report in the medical literature to date [3]. In that 1978 paper Guerrero et al. reported the case of a 20-year-old man who presented typical clinical signs and symptoms for SEA, along with a clinical history suggesting a hematogenous spread from an infected frontal sinus. Emergency laminectomies were performed and an abscess of the posterior epidural space, extending from L3 to S1, was drained. Blood and abscess cultures grew F. necrophorum. After 2-week course of penicillin the patient was discharged. At follow-up examination he presented minimal sequelae in his right leg. Our paper therefore constitutes only the second reported case of primary SEA without spondylodiscitis in the literature. It seems to be more common for F. necrophorum to cause vertebral osteomyelitis than primary meningeal involvement, although even then it is rare. Specifically, about 20 cases have been reported in the literature, most of them related to bacteremia preceded by oral infection [4]. The most common locations of SEA are the lower thoracic and upper lumbar segments, specifically in the posterior spinal cord. This can be explained by the anatomical widening of the spinal epidural space at the thoracolumbar level, the presence of more extensive epidural venous plexus (Batson’s plexus), and the tight ventral adherence of the dura to the posterior longitudinal ligament at that levels. Vertebral osteomyelitis is also present in between 12.5% and 44% of SEA cases, and it is usually associated with anterior SEA [2]. F. necrophorum is a Gram-negative anaerobic rod, commonly found as normal oral flora once teeth have erupted, as well as in the gastrointestinal and genitourinary tract. Although invasive fusobacterial infections are rare F. necrophorum has been isolated from a wide variety of infections including dental infections, brain abscesses, endocarditis, obstetric infections, soft tissue infection, and osteomyelitis. The annual incidence of bacteremic Fusobacterium infections has been reported to be 0.55e0.67 cases per 100,000 population. Fusobacterium bacteremia can occur in healthy patients without predisposing conditions or vein thrombosis,and it can be explained by several virulent factors related to certain Fusobacterium strains [5]. In our patient we could find no risk factors for
Please cite this article in press as: Sanmillán JL, et al., Primary lumbar epidural abscess without spondylodiscitis caused by Fusobacterium necrophorum diagnosed by 16S rRNA PCR, Anaerobe (2013), http://dx.doi.org/10.1016/j.anaerobe.2013.06.014
J.L. Sanmillán et al. / Anaerobe xxx (2013) 1e3
infection, nor any source of infection. No history of previous oropharyngeal infection was identified, and bacteremia soon disappeared after empirical antibiotic treatment. Our patient underwent needle acupuncture on her lower back four months before clinical presentation. We believe that local trauma in the epidural space could have acted as a predisposing local factor for infection in the context of a spontaneous bacteremia. In our opinion, the clinical history, location of SEA, lack of spondylodiscitis, and presence of liver abscesses strongly suggests that the mechanism of epidural infection of our patient might be a hematogenous spread of unknown source. Microbiological diagnosis of anaerobic bacteria is sometimes challenging. In this case PCR amplification and sequencing of the 16S rRNA gene improved the diagnosis course which otherwise would be retarded by the slow growth of F. necrophorum. Its final growth in anaerobic cultures confirmed this result. PCR amplification and sequencing of the 16S rRNA was useful to detect the causative microorganism. The most widely accepted therapeutic approach in a patient with SEA and progressive neurologic deterioration is early laminectomy, culture of drained material, and systemic antibiotic treatment. The definitive antibiotic should be chosen carefully, taking into account the microbiology and type of infection. For SEA, definitive antibiotic treatment should be bactericidal and have good penetration in the central nervous system (CNS). Sequential intravenous-oral therapy should be administered, if possible, because a long course of treatment is required (4e6 weeks). The
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treatment of choice in our case was metronidazole, which remains the mainstay of therapy due to its CNS penetration and bactericidal properties in F. necrophorum CNS infections. In conclusion, F. necrophorum SEA is rare, although samples for anaerobic culture should be collected in order to improve the detection of anaerobic spinal infections. PCR amplification and sequencing of the 16S rRNA permits early diagnosis in anaerobic infections.
Conflict of interests The authors declare that they have neither conflict of interest nor fundings from any organization.
References [1] Zimmerer SME, Conen A, Müller AA, Sailer M, Taub E, Flückiger U, et al. Spinal epidural abscess: aetiology, predisponent factors and clinical outcomes in a 4year prospective study. Eur Spine J 2011;20:2228e34. [2] Mackenzie AR, Laing RBS, Smith CC, Kaar GF, Smith FW. Spinal epidural abscess: the importance of early diagnosis and treatment. J Neurol Neurosurg Psychiatr 1998;65:209e12. [3] Guerrero IC, Slap GB, MacGregor RR, Lawner P, Ruggeri S, Gennarelli T. Anaerobic spinal epidural abscess. J Neurosurg 1978;48:465e9. [4] Le Moal G, Juhel L, Grollier G, Godet C, Azais I, Roblot F. Vertebral osteomyelitis due to Fusobacterium species: report of three cases and review of the literature. J Infect 2005;51:e5e9. [5] Nohrström E, Mattila T, Pettilä V, Kuusela P, Carlson P, Kentala E, et al. Clinical spectrum of bacteraemic Fusobacterium infections: from septic shock to nosocomial bacteraemia. Scand J Infect Dis 2011;43:6e7.
Please cite this article in press as: Sanmillán JL, et al., Primary lumbar epidural abscess without spondylodiscitis caused by Fusobacterium necrophorum diagnosed by 16S rRNA PCR, Anaerobe (2013), http://dx.doi.org/10.1016/j.anaerobe.2013.06.014