|Year : 2017 | Volume
| Issue : 1 | Page : 19-21
The fatal case of spinal epidural abscess caused by Fusobacterium necrophorum complicated by meningitis
Grzegorz Miekisiak1, Wojciech Szymański1, Paweł Jarmużek2, Dariusz Łątka3
1 Department of Neurosurgery, Specialist Medical Center, Polanica-Zdroj, Poland
2 Department of Neurosurgery, Regional Medical Center, Opole, Poland
3 Department of Neurosurgery, Lubuskie Center of Neurosurgery and Neurotrauma, Zielona Góra, Poland
|Date of Web Publication||29-May-2017|
Department of Neurosurgery, Specialist Medical Center, ul. Jana Pawła II 2, 57-320 Polanica-Zdroj
Source of Support: None, Conflict of Interest: None
Fusobacterium necrophorum is an anaerobic Gram-negative bacillus classically associated with the Lemierre syndrome. Although it can cause a localized infection, it is rarely a culprit of a spinal epidural abscess. We report a case of a spinal epidural abscess caused by Fusobacterium necrophorum complicated by meningitis. The patient, two years earlier treated surgically for cervical spondylotic myelopathy with corpectomy, presented with a new-onset severe neck pain and progressive tetraparesis. Based on imaging studies spinal epidural abscess was diagnosed. Despite intensive surgical treatment and subsequent antibiotic therapy the patient gradually deteriorated and eventually died. Fusobacterium necrophorum was identified as a culprit. Fusobacterium necrophorum is a very rare cause of spinal epidural abscess (SEA). Because of high virulence of this pathogen localized infection can progress rapidly into a generalized septicemia and life-threatening neuroinfection.
Keywords: Fusobacterium necrophorum, meningitis, spinal epidural abscess, ventriculitis
|How to cite this article:|
Miekisiak G, Szymański W, Jarmużek P, Łątka D. The fatal case of spinal epidural abscess caused by Fusobacterium necrophorum complicated by meningitis. J Spinal Stud Surg 2017;1:19-21
|How to cite this URL:|
Miekisiak G, Szymański W, Jarmużek P, Łątka D. The fatal case of spinal epidural abscess caused by Fusobacterium necrophorum complicated by meningitis. J Spinal Stud Surg [serial online] 2017 [cited 2022 Dec 2];1:19-21. Available from: https://www.jsss-journal.com/text.asp?2017/1/1/19/207210
| Introduction|| |
Fusobacterium necrophorum is a Gram-negative anaerobe classically associated with Lemierre's syndrome (LS) presenting with a characteristic clinical pattern: thrombophlebitis of the internal jugular vein secondary to infections of the head and neck, usually the oropharynx. This bacteria is also capable of causing multiple other local infections, such as otitis, pharyngitis, tonsillitis, mastoiditis, or systemic infections such as necrobacillosis. Despite its high virulence, it is very rarely the culprit of the spinal epidural abscess or meningitis. We present a fatal case of a 60-year-old man with an epidural abscess caused by F. necrophorum, which rapidly progressed into a general septicemia followed by meningitis and ventriculitis.
| Case Report|| |
The 60-year-old male was admitted to our department with 2 weeks' history of severe neck pain and progressive spastic tetraparesis. Two years earlier, he was surgically treated due to fast progressing cervical spondylotic myelopathy, exaggerated by fall from height. The patient underwent corpectomy with an iliac autograft, and on rehabilitation, he improved significantly but remained moderately neurologically impaired. On admission, the patient was awake and oriented, the muscle strength was 4/5 in all limbs, slightly weaker on the right side. He was febrile (39.7°C), the level of C-reactive protein (CRP) was 152.9 mg/L (normal range: 0–5). A magnetic resonance imaging (MRI) scan revealed an epidural collection of heterogeneous fluid identified as pus [Figure 1]. His recent medical history was significant for a mild pharyngitis which resolved spontaneously. Because of fast neurologic deterioration, the decision was made to perform a laminectomy, attempt to reach and debride the lesion and fix the spine with lateral mass screws. During surgery no pus was noted, intraoperative cultures obtained from an anterolateral part of the spinal canal were negative. Noteworthy is a healthy appearance of the dura and adjacent tissues. Immediately after surgery, despite negative exploration, the muscle strength improved significantly. On postoperative day 5, the patient started to deteriorate again, and within the next 2 days, the muscle strength was down to 3/5. At the same time, his general condition worsened rapidly, the purulent discharge from the wound was noticed. This deterioration was reflected in changes of serum CRP level. The patient underwent an emergency surgery with the goal of debridement and evacuation of pus. During surgery, a large quantity of foul-smelling, Café au lait-colored, thick pus was evacuated. The entire surface of dura, as well as all surrounding tissues, was coated with a thick, hard white membrane which was strongly adherent to underlying tissues. Two drains were placed in the wound for continuous-flow drainage. The smear was taken and the isolate was later identified as F. necrophorum using the BBL Crystal Identification System Anaerobe ID Kit (Becton Dickinson Microbiology Systems, Cockeysville, USA). Postoperatively, empiric treatment with intravenous ceftriaxone was initiated, yet the patient failed to improve, his consciousness deteriorated. He was transferred to the Intensive Care Unit, where he was treated with metronidazole, ceftazidime, and fluconazole. Despite antibiotic treatment, he deteriorated further to a Glasgow coma scale of 3. On day 6 after the second surgery, the head computed tomography scan revealed a distention of the entire ventricular system [Figure 2] with periventricular edema; ventriculitis was diagnosed. The patient underwent another surgery: An external ventricular drainage was placed. The cerebrospinal fluid (CSF) collected directly from the ventricle was cloudy with high protein content and high cytosis, consistent with the diagnosis of ventriculitis. The patient then went into multiorgan failure, and on day 8 after the second spine surgery, he was pronounced brain dead.
|Figure 1: The initial magnetic resonance imaging revealing pus collection in the epidural space (arrows). The site of corpectomy if marked with an asterisk.|
Click here to view
|Figure 2: Nonenhanced head computed tomography scan showing the enlargement of lateral ventricles with surrounding periventricular edema.|
Click here to view
| Discussion|| |
F. necrophorum is a highly virulent, nonspore forming Gram-negative bacteria belonging to the Bacteroidaceae. It may cause local infections, such as otitis or pharyngitis sometimes leading to septicemia. It has been traditionally associated with an uncommon but potentially life-threating LS. This condition classically begins with an acute oropharynx infection, which then spreads into the retropharyngeal space and causes septic thrombosis of the internal jugular vein, whereas the otogenic variant may originate from the mastoid cells with subsequent suppurative thrombophlebitis of the lateral and/or cavernous sinuses and meningitis. Other forms of Fusobacterium local infections have been described, including rare cases of the spinal epidural abscesses (SEAs) and rarer still, meningitis. In our case, the patients' medical history was significant for a recent pharyngitis, however, there was no evidence of subsequent vascular involvement necessary for the diagnosis of learning disabilities. Instead, the SEA was found in an MRI study.
This type of infection is usually caused by Gram-positive cocci of the Staphylococcus genus. In an article by Reihsaus et al. analyzing a large series of 830 patients with SEA, just five cases were caused by anaerobic, Gram-negative bacteriodaceae, including one case of F. necrophorum. The authors have identified several risk factor of SEA, including a recent history of trauma and surgery. In our case, almost 2 years passed since the index surgery, yet the abscess was located exactly at the level of corpectomy. It is hypothesized that trauma favors local infection by breaching natural anatomic barriers especially in the presence of hematoma. A direct introduction of bacteria during index surgery with subsequent pus collection was ruled out with the follow-up MRI scan performed 12-month postoperatively.
Unusual course of infection with a rapid acceleration after the laminectomy is difficult to explain, especially considering negative intraoperative cultures (both for aerobes and anaerobes). While this operation was uneventful with no evidence of the ongoing infection, during the second surgery copious amount of pus was evacuated, and thick membranes covering all tissues in contact with the purulent fluid were noticed. Although F. necrophorum is known to be very virulent and capable of causing a fulminating infection, it is difficult to explain how a decompressive surgery could trigger a violent cascade ending with meningitis and ventriculitis. The latter complication could theoretically be caused by a direct inoculation of bacteria into the CSF through a dural defect, however, no dural laceration was identified during either operation. Regardless of the source of infection Fusobacterum spp. is a very rare cause of meningitis. Review of the literature showed that most of the reported cases have been in children, in more than 50% caused by an uncontained otogenic infection. Only a handful of cases in adults has been reported to date., In any case, this form of necrobacillosis is always a serious condition with a high mortality.
SEAs are usually treated surgically with the subsequent prolonged administration of antibiotics, the solely conservative treatment with antibiotics is an option for selected patients. As in all other infections, the empirical antibiotic therapy should cover the most common pathogen. The commonly accepted regimen includes a selection of agents effective against the staphylococci together with antimicrobial drugs targeting Gram-negative bacilli. Metronidazole is usually added when anaerobic infection is suspected. This antibiotic is considered to be one of the most efficient antimicrobial drugs against F. necrophorum, although the optimum treatment regimen has not been established.
| Conclusion|| |
F. necrophorum is a very rare cause of SEA. Because of high virulence of this pathogen localized infection can progress rapidly into a generalized septicemia and life-threatening neuroinfection. The addition of an antianaerobic antibiotic such as metronidazole in the absence of cultures can prevent these serious sequelae.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Park D, Rezajooi K, Sabin I. Lemierre's syndrome: An unusual manifestation of spinal infection. J Bone Joint Surg Br 2006;88:261-2.
Angelino G, Cantarutti N, Chiurchiù S, Amodio D, De Luca M, Lancella L, et al.
Fulminant Fusobacterium necrophorum
meningitis in an immunocompetent adolescent. Pediatr Emerg Care 2012;28:703-4.
Garimella S, Inaparthy A, Herchline T. Meningitis due to Fusobacterium necrophorum
in an adult. BMC Infect Dis 2004;4:24.
Le Monnier A, Jamet A, Carbonnelle E, Barthod G, Moumile K, Lesage F, et al. Fusobacterium necrophorum
middle ear infections in children and related complications: Report of 25 cases and literature review. Pediatr Infect Dis J 2008;27:613-7.
Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: A meta-analysis of 915 patients. Neurosurg Rev 2000;23:175-204.
Megged O, Assous MV, Miskin H, Peleg U, Schlesinger Y. Neurologic manifestations of Fusobacterium
infections in children. Eur J Pediatr 2013;172:77-83.
Jones TH, Bergvall V, Bradshaw JP. Carotid artery stenoses and thrombosis secondary to cavernous sinus thromboses in Fusobacterium necrophorum
meningitis. Postgrad Med J 1990;66:747-50.
Pradilla G, Nagahama Y, Spivak AM, Bydon A, Rigamonti D. Spinal epidural abscess: Current diagnosis and management. Curr Infect Dis Rep 2010;12:484-91.
Lam S, Nguyen TT. Epidural Abscess. Int. Neurol., Oxford, UK: Wiley-Blackwell; 2010. p. 248-9.
Brazier JS. Human infections with Fusobacterium necrophorum
. Anaerobe 2006;12:165-72.
[Figure 1], [Figure 2]