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Cervical Spondylodiscitis, Osteomyelitis, and Epidural Abscess Mimicking a Vertebral Fracture
The Journal of Emergency Medicine, Vol. 42, No. 3, pp. e43– e46, 2012 Copyright © 2012 Published by Elsevier Inc. Printed in the USA 0736-4679/$–see front matter
doi:10.1016/j.jemermed.2008.09.021
Clinical Communications: Adults
CERVICAL SPONDYLODISCITIS, OSTEOMYELITIS, AND EPIDURAL ABSCESS MIMICKING A VERTEBRAL FRACTURE Jill L. Hanck,
MD*
and Antonio E. Muñiz,
MD, FACEP, FAAP, FAAEM†
*Department of Emergency Medicine, Virginia Commonwealth University Medical Center, Richmond, Virginia and †Departments of Emergency Medicine and Pediatrics, University of Texas Health Science Center at Houston, Houston, Texas Reprint Address: Antonio E. Muñiz, MD, FACEP, FAAP, FAAEM, Departments of Emergency Medicine and Pediatrics, The University of Texas Health Science Center at Houston, 6431 Fannin Street, JJL-451, Houston, TX 77030
e Abstract—Background: Spinal vertebral fractures are common in elderly patients, especially after a significant fall. Neck tenderness or neurologic deficits after a fall should increase the suspicion of cervical spinal fracture. Case Report: A 75-year-old woman complained of 2 weeks of gradually increasing neck and right shoulder pain after a fall. She had an X-ray study that appeared to show an unstable C6 –C7 fracture. A computed tomography scan of the neck revealed no fracture and was consistent with spondylodiscitis and osteomyelitis of C6 and C7, with an adjacent epidural abscess and mild cord compression. Conclusion: It is important to consider this diagnosis in patients with a history of infective endocarditis who develop back pain, to minimize morbidity associated with this disorder. © 2012 Published by Elsevier Inc.
CASE REPORT A 75-year-old woman complained of 2 weeks of gradually increasing neck and right shoulder pain after a fall. The fall occurred after she tripped on a carpeted floor. She went to her primary care physician and initial cervical spine radiographs were unremarkable but did not adequately image from C6 to T1. Another cervical radiograph done on the following day with a swimmer’s view showed what appeared to be an unstable C6 –C7 fracture (Figure 1). No computed tomography (CT) scan was obtained. She was immobilized with a cervical collar and placed on a long spine board and transported by ambulance to our hospital for further neurosurgical evaluation. The patient was in no distress. Her past medical history included methicillin-sensitive Staphylococcus aureus endocarditis, congestive heart failure, myocardial infarction, diabetes mellitus, hypertension, fibromyalgia, kidney stones, Parkinson disease, hypothyroidism, and systemic lupus erythematosus. Her past surgical history included percutaneous transluminal coronary angioplasty, appendectomy, cholecystectomy, hysterectomy, thyroidectomy, tonsillectomy, and lumbar diskectomy for a herniated disk approximately 25 years prior. Her medications included aspirin, betaxolol, diltiazem, furosemide, isosorbide dinitrate, lisinopril, magnesium hydroxide, olanzapine, mirtazapine, carbidopa/levodopa,
e Keywords—spondylodiscitis; epidural Abscess; osteomyelitis; endocarditis
INTRODUCTION Spinal vertebral fractures are common in elderly patients with osteopenia (1). Neck pain after a fall in an elderly patient should increase the suspicion of cervical vertebral fracture (2). However, there are other less common entities that can mimic the radiographic findings of a cervical vertebral fracture. A case is presented of cervical spondylodiscitis in an elderly woman, with review of the literature.
RECEIVED: 11 April 2008; FINAL ACCEPTED: 4 September 2008
SUBMISSION RECEIVED:
20 August 2008; e43
e44
J. L. Hanck and A. E. Muñiz
12 weeks of vancomycin and rifampin. She recovered without complications.
DISCUSSION
Figure 1. Radiograph of the cervical spine. The arrow points to an irregularity of the vertebral body of C6 and C7, with retrolisthesis of C6.
levothyroxine, temazepam, duragesic patch, and hydrocodone/acetaminophen. Her allergies included iodine, metoclopramide, cisapride, penicillin, and compazine. Her vital signs showed a blood pressure of 148/68 mm Hg, heart rate of 62 beats/min, respiratory rate of 22 breaths/min, and temperature of 37°C. Examination of the head revealed no abnormalities. The neck was tender over C6 –C7. There was no swelling, deformity, or crepitus. The lung, heart, abdominal, and extremity examinations were normal. Her neurologic examination showed normal motor, sensory, cranial nerves, and cerebellar function. The deep tendon reflexes were 2⫹ and equal bilaterally. The complete blood cell count showed a white blood cell (WBC) count of 9800/mm3, with 65.6% neutrophils, hemoglobin of 10.7 g/dL, and platelets 540,000/mm3. The erythrocyte sedimentation rate (ESR) was 9.8 mm/h and C-reactive protein (CRP) was 0.6 mg/dL. The electrolytes were normal. A CT scan of the cervical spine demonstrated extensive cortical erosion of the inferior endplate of C6 and superior endplate of C7 with associated disk space loss (Figure 2). These findings were consistent with spondylodiscitis. She was hospitalized, and a CT-guided fine-needle aspiration of C6 –C7 revealed no organisms on Gram’s stain with a negative culture. Magnetic resonance imaging (MRI) showed spondylodiscitis and osteomyelitis of C6 and C7 with an adjacent epidural abscess and mild cord compression. An MRI scan of the right shoulder revealed a disruption of the supraspinatus, infraspinatus, and subscapularis tendon consistent with a chronic rotator cuff tear. She was treated with
Spondylodiscitis is an uncommon infection of the nucleus pulposus, the central portion of the intravertebral disk. It frequently involves the adjacent cartilaginous endplates and vertebral bodies (vertebral osteomyelitis). The intervertebral disk becomes infected in one of the following three ways: hematogenous seeding to the intervertebral disk, contiguous spread of infection to the disk from an adjacent structure such as an epidural abscess or osteomyelitis, or direct inoculation of the intervetebral disk during surgical manipulation or through penetrating injury. Overall, spondylodiscitis is more common in adults than children, with a median age of 69 years; however, spontaneous spondylodiscitis occurs frequently in children because the disks are still vascularized (3). In children, the intervertebral disks are supplied with nutrients by intermetaphyseal arteries. By the 20th year of life, these arteries degenerate and the avascular disk receives its nutrients via direct diffusion from the adjacent vertebral endplates. Risk factors associated with spondylodiscitis include systemic infection, immunocompromise, and recent penetrating trauma. In adults, spondylodiscitis has a slow and insidious onset, often delaying the diagnosis for months. Clinical manifestations include pain over the affected disk that increases with movement. Symptoms are usually not relieved with conservative therapy such as analgesics and bed rest. There may be a low-grade fever. Neurologic deficit may occur in 10 –50% of patients. The neurologic findings in radiculopathy occur in 50 –90% (4 – 6). There is rarely an initial neurologic deficit, but a
Figure 2. Computed tomography scan. The arrow indicates extensive erosion of the inferior endplate of C6 and superior endplate of C7.
Spondylodiscitis
delay in the diagnosis can lead to neurologic deficits. Localized tenderness over the involved segment with concomitant paraspinal muscle spasm is the most common physical sign. The disks of the lumbar region are most frequently involved, followed by cervical spine and thoracic spine. Laboratory studies are of limited diagnostic utility. The ESR and CRP are frequently elevated, but are nonspecific. The WBC count may be elevated by associated systemic illness, but is usually normal in isolated spondylodiscitis. The diagnosis can be confirmed by radiographs, nuclear medicine studies, CT scan, or MRI. Radiographs are initially negative. It can take up to 2– 4 weeks before they demonstrate changes suggestive of spondylodiscitis. These changes include disk space destruction and loss of disk space height, followed by irregular cortical bone destruction of the endplate adjacent to the affected disk and calcification of the annulus. Gallium-67 and Technetium 99m diphosphonate scans have been useful in the diagnosis. CT scan has the ability to detect spondylodiscitis earlier than plain film, and findings may include hypodensity of the intervertebral disk with destruction of the adjacent endplate and bone. MRI is the optimal study, as it will demonstrate disk enhancement as well as adjacent soft tissue abscess or inflammation and can differentiate conditions in the differential diagnosis, such as neoplasia or tuberculosis of the spine (7). Although less effective than CT scan, MRI can demonstrate erosion and destruction of the adjacent vertebral endplate. In addition, in patients suspected of endocarditis, a two-dimensional echocardiogram will be helpful to determine if the origin of the embolic infection is from the heart. The most common bacterial agent causing spondylodiscitis is Staphylococcus aureus. Organisms that cause urinary tract infections, pneumonia, or soft tissue infections have been shown to spread to the intervetebral disk. Therefore, Escherichia coli and Proteus species are common causative agents in patients with urinary tract infections, whereas Pseudomonas and Klebsiella are more common in intravenous drug users. Other organisms isolated from patients with spondylodiscitis have included Staphylococcus epidermidis, streptococcus, other Gram-negative organisms, fungal organisms, and tuberculosis (8,9). Group D Streptococcus is a common offending organism when infection is due to endocarditis (3,10). Spondylodiscitis can be managed with intravenous antibiotics targeted at the most likely responsible organism. Ideally, a CT-guided disk space biopsy should be obtained before the initiation of antibiotics, to aid in the proper selection of antibiotics. Even in this situation, the organism is identified in only 50% of the cases. Some have shown that open biopsy has a higher yield but is
e45 Table 1. Antibiotic Choices for Treating Spondylodiscitis Vancomycin and third-generation cephalosporin Vancomycin and rifampin Vancomycin and aminoglycoside
more invasive (11). Use of amplification of DNA by polymerase chain reaction may improve the yield over routine microbiological cultures (12). Broad-spectrum antibiotics used to treat spondylodiscitis are shown in Table 1. These are administered for 6 –12 weeks. Immobilization may be required to minimize pain. However, the pain may last 8 –24 months and typically resolves with spontaneous intervetebral fusion. Surgical intervention is indicated if there is an abscess requiring drainage, if the patient fails to improve despite antibiotic therapy, or if there is progression of neurologic deficits (13).
CONCLUSION Spondylodiscitis can present with vertebral pain and may mimic an acute fracture. It may occur spontaneously, as spread from a contiguous source or from hematogenous spread from an infection away from the intervertebral disk. It is important to consider this diagnosis in patients with a history of systemic infection who develop spinal pain, to minimize morbidity associated with this disorder.
REFERENCES 1. Sakuma M, Endo N, Oinuma T, et al. Incidence and outcome of osteoporotic fractures in 2004 in Sado City, Niigata Prefecture, Japan. J Bone Miner Metab 2008;26:373– 8. 2. Malik SA, Murphy M, Connolly P, O’Byrne J. Evaluation of morbidity, mortality and outcome following cervical spine injuries in elderly patients. Eur Spine J 2008;17:585–91. 3. Le Moal G, Roblot F, Paccalin M, et al. Clinical and laboratory characteristics of infective endocarditis when associated with spondylodiscitis. Eur J Clin Microbiol Infect Dis 2002;21: 671–5. 4. Khan IA, Vaccaro AR, Slotolow DA. Management of vertebral diskitis and osteomyelitis. Orthopedics 1992;22:758 – 65. 5. Gasbarrini AL, Bertoldi E, Mazzetti M, et al. Clinical features, diagnostic and therapeutic approaches to haematogenous vertebral osteomyelitis. Eur Rev Med Pharmacol Sci 2005;9:53– 66. 6. Al-Nammari S, Lucas JD, Lam KS. Hematogenous methicillinresistant Staphylococcus aureus spondylodiscitis. Spine 2007;32: 2480 – 6. 7. Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR imaging in spinal infections: rules and myths? Radiology 2003; 228:506 –14. 8. Lenzi J, Agrillo A, Santoro A, Marotta N, Cantore GP. Postoperative spondylodiscitis from Aspergillus fumigatus in immunocompetent subjects. J Neurosurg Sci 2004;48:81–5. 9. Ugarriza LF, Cabezudo JM, Lorenzana LM, Rodriguez-Sanchez JA. Candida albicans spondylodiscitis. Br J Neurosurg 2004;18: 189 –92.
e46 10. Luz A, Castro A, Ribeiro R, et al. Viridians streptococcus endocarditis associated with spondylodiscitis. Rev Port Cardiol 2004;23:723– 8. 11. Fouquet B, Goupille P, Gobert F, Cotty P, Roulot B, Valat JP. Infectious discitis diagnostic contribution of laboratory tests and percutaneous discovertebral biopsy. Rev Rheum Engl Ed 1996;63: 24 –9.
J. L. Hanck and A. E. Muñiz 12. Lecouvet F, Irenge L, Vandercam B, Nzeusseu A, Hamels S, Gala JL. The etiologic diagnosis of infectious discitis is improved by amplification-based DNA analysis. Arthritis Rheum 2004;50: 2985–94. 13. Schinkel C, Gottwald M, Andress HJ. Surgical treatment of spondylodiscits. Surg Infect (Lrchmt) 2003;4:387–91.
doi:10.1016/j.jemermed.2008.09.021
Clinical Communications: Adults
CERVICAL SPONDYLODISCITIS, OSTEOMYELITIS, AND EPIDURAL ABSCESS MIMICKING A VERTEBRAL FRACTURE Jill L. Hanck,
MD*
and Antonio E. Muñiz,
MD, FACEP, FAAP, FAAEM†
*Department of Emergency Medicine, Virginia Commonwealth University Medical Center, Richmond, Virginia and †Departments of Emergency Medicine and Pediatrics, University of Texas Health Science Center at Houston, Houston, Texas Reprint Address: Antonio E. Muñiz, MD, FACEP, FAAP, FAAEM, Departments of Emergency Medicine and Pediatrics, The University of Texas Health Science Center at Houston, 6431 Fannin Street, JJL-451, Houston, TX 77030
e Abstract—Background: Spinal vertebral fractures are common in elderly patients, especially after a significant fall. Neck tenderness or neurologic deficits after a fall should increase the suspicion of cervical spinal fracture. Case Report: A 75-year-old woman complained of 2 weeks of gradually increasing neck and right shoulder pain after a fall. She had an X-ray study that appeared to show an unstable C6 –C7 fracture. A computed tomography scan of the neck revealed no fracture and was consistent with spondylodiscitis and osteomyelitis of C6 and C7, with an adjacent epidural abscess and mild cord compression. Conclusion: It is important to consider this diagnosis in patients with a history of infective endocarditis who develop back pain, to minimize morbidity associated with this disorder. © 2012 Published by Elsevier Inc.
CASE REPORT A 75-year-old woman complained of 2 weeks of gradually increasing neck and right shoulder pain after a fall. The fall occurred after she tripped on a carpeted floor. She went to her primary care physician and initial cervical spine radiographs were unremarkable but did not adequately image from C6 to T1. Another cervical radiograph done on the following day with a swimmer’s view showed what appeared to be an unstable C6 –C7 fracture (Figure 1). No computed tomography (CT) scan was obtained. She was immobilized with a cervical collar and placed on a long spine board and transported by ambulance to our hospital for further neurosurgical evaluation. The patient was in no distress. Her past medical history included methicillin-sensitive Staphylococcus aureus endocarditis, congestive heart failure, myocardial infarction, diabetes mellitus, hypertension, fibromyalgia, kidney stones, Parkinson disease, hypothyroidism, and systemic lupus erythematosus. Her past surgical history included percutaneous transluminal coronary angioplasty, appendectomy, cholecystectomy, hysterectomy, thyroidectomy, tonsillectomy, and lumbar diskectomy for a herniated disk approximately 25 years prior. Her medications included aspirin, betaxolol, diltiazem, furosemide, isosorbide dinitrate, lisinopril, magnesium hydroxide, olanzapine, mirtazapine, carbidopa/levodopa,
e Keywords—spondylodiscitis; epidural Abscess; osteomyelitis; endocarditis
INTRODUCTION Spinal vertebral fractures are common in elderly patients with osteopenia (1). Neck pain after a fall in an elderly patient should increase the suspicion of cervical vertebral fracture (2). However, there are other less common entities that can mimic the radiographic findings of a cervical vertebral fracture. A case is presented of cervical spondylodiscitis in an elderly woman, with review of the literature.
RECEIVED: 11 April 2008; FINAL ACCEPTED: 4 September 2008
SUBMISSION RECEIVED:
20 August 2008; e43
e44
J. L. Hanck and A. E. Muñiz
12 weeks of vancomycin and rifampin. She recovered without complications.
DISCUSSION
Figure 1. Radiograph of the cervical spine. The arrow points to an irregularity of the vertebral body of C6 and C7, with retrolisthesis of C6.
levothyroxine, temazepam, duragesic patch, and hydrocodone/acetaminophen. Her allergies included iodine, metoclopramide, cisapride, penicillin, and compazine. Her vital signs showed a blood pressure of 148/68 mm Hg, heart rate of 62 beats/min, respiratory rate of 22 breaths/min, and temperature of 37°C. Examination of the head revealed no abnormalities. The neck was tender over C6 –C7. There was no swelling, deformity, or crepitus. The lung, heart, abdominal, and extremity examinations were normal. Her neurologic examination showed normal motor, sensory, cranial nerves, and cerebellar function. The deep tendon reflexes were 2⫹ and equal bilaterally. The complete blood cell count showed a white blood cell (WBC) count of 9800/mm3, with 65.6% neutrophils, hemoglobin of 10.7 g/dL, and platelets 540,000/mm3. The erythrocyte sedimentation rate (ESR) was 9.8 mm/h and C-reactive protein (CRP) was 0.6 mg/dL. The electrolytes were normal. A CT scan of the cervical spine demonstrated extensive cortical erosion of the inferior endplate of C6 and superior endplate of C7 with associated disk space loss (Figure 2). These findings were consistent with spondylodiscitis. She was hospitalized, and a CT-guided fine-needle aspiration of C6 –C7 revealed no organisms on Gram’s stain with a negative culture. Magnetic resonance imaging (MRI) showed spondylodiscitis and osteomyelitis of C6 and C7 with an adjacent epidural abscess and mild cord compression. An MRI scan of the right shoulder revealed a disruption of the supraspinatus, infraspinatus, and subscapularis tendon consistent with a chronic rotator cuff tear. She was treated with
Spondylodiscitis is an uncommon infection of the nucleus pulposus, the central portion of the intravertebral disk. It frequently involves the adjacent cartilaginous endplates and vertebral bodies (vertebral osteomyelitis). The intervertebral disk becomes infected in one of the following three ways: hematogenous seeding to the intervertebral disk, contiguous spread of infection to the disk from an adjacent structure such as an epidural abscess or osteomyelitis, or direct inoculation of the intervetebral disk during surgical manipulation or through penetrating injury. Overall, spondylodiscitis is more common in adults than children, with a median age of 69 years; however, spontaneous spondylodiscitis occurs frequently in children because the disks are still vascularized (3). In children, the intervertebral disks are supplied with nutrients by intermetaphyseal arteries. By the 20th year of life, these arteries degenerate and the avascular disk receives its nutrients via direct diffusion from the adjacent vertebral endplates. Risk factors associated with spondylodiscitis include systemic infection, immunocompromise, and recent penetrating trauma. In adults, spondylodiscitis has a slow and insidious onset, often delaying the diagnosis for months. Clinical manifestations include pain over the affected disk that increases with movement. Symptoms are usually not relieved with conservative therapy such as analgesics and bed rest. There may be a low-grade fever. Neurologic deficit may occur in 10 –50% of patients. The neurologic findings in radiculopathy occur in 50 –90% (4 – 6). There is rarely an initial neurologic deficit, but a
Figure 2. Computed tomography scan. The arrow indicates extensive erosion of the inferior endplate of C6 and superior endplate of C7.
Spondylodiscitis
delay in the diagnosis can lead to neurologic deficits. Localized tenderness over the involved segment with concomitant paraspinal muscle spasm is the most common physical sign. The disks of the lumbar region are most frequently involved, followed by cervical spine and thoracic spine. Laboratory studies are of limited diagnostic utility. The ESR and CRP are frequently elevated, but are nonspecific. The WBC count may be elevated by associated systemic illness, but is usually normal in isolated spondylodiscitis. The diagnosis can be confirmed by radiographs, nuclear medicine studies, CT scan, or MRI. Radiographs are initially negative. It can take up to 2– 4 weeks before they demonstrate changes suggestive of spondylodiscitis. These changes include disk space destruction and loss of disk space height, followed by irregular cortical bone destruction of the endplate adjacent to the affected disk and calcification of the annulus. Gallium-67 and Technetium 99m diphosphonate scans have been useful in the diagnosis. CT scan has the ability to detect spondylodiscitis earlier than plain film, and findings may include hypodensity of the intervertebral disk with destruction of the adjacent endplate and bone. MRI is the optimal study, as it will demonstrate disk enhancement as well as adjacent soft tissue abscess or inflammation and can differentiate conditions in the differential diagnosis, such as neoplasia or tuberculosis of the spine (7). Although less effective than CT scan, MRI can demonstrate erosion and destruction of the adjacent vertebral endplate. In addition, in patients suspected of endocarditis, a two-dimensional echocardiogram will be helpful to determine if the origin of the embolic infection is from the heart. The most common bacterial agent causing spondylodiscitis is Staphylococcus aureus. Organisms that cause urinary tract infections, pneumonia, or soft tissue infections have been shown to spread to the intervetebral disk. Therefore, Escherichia coli and Proteus species are common causative agents in patients with urinary tract infections, whereas Pseudomonas and Klebsiella are more common in intravenous drug users. Other organisms isolated from patients with spondylodiscitis have included Staphylococcus epidermidis, streptococcus, other Gram-negative organisms, fungal organisms, and tuberculosis (8,9). Group D Streptococcus is a common offending organism when infection is due to endocarditis (3,10). Spondylodiscitis can be managed with intravenous antibiotics targeted at the most likely responsible organism. Ideally, a CT-guided disk space biopsy should be obtained before the initiation of antibiotics, to aid in the proper selection of antibiotics. Even in this situation, the organism is identified in only 50% of the cases. Some have shown that open biopsy has a higher yield but is
e45 Table 1. Antibiotic Choices for Treating Spondylodiscitis Vancomycin and third-generation cephalosporin Vancomycin and rifampin Vancomycin and aminoglycoside
more invasive (11). Use of amplification of DNA by polymerase chain reaction may improve the yield over routine microbiological cultures (12). Broad-spectrum antibiotics used to treat spondylodiscitis are shown in Table 1. These are administered for 6 –12 weeks. Immobilization may be required to minimize pain. However, the pain may last 8 –24 months and typically resolves with spontaneous intervetebral fusion. Surgical intervention is indicated if there is an abscess requiring drainage, if the patient fails to improve despite antibiotic therapy, or if there is progression of neurologic deficits (13).
CONCLUSION Spondylodiscitis can present with vertebral pain and may mimic an acute fracture. It may occur spontaneously, as spread from a contiguous source or from hematogenous spread from an infection away from the intervertebral disk. It is important to consider this diagnosis in patients with a history of systemic infection who develop spinal pain, to minimize morbidity associated with this disorder.
REFERENCES 1. Sakuma M, Endo N, Oinuma T, et al. Incidence and outcome of osteoporotic fractures in 2004 in Sado City, Niigata Prefecture, Japan. J Bone Miner Metab 2008;26:373– 8. 2. Malik SA, Murphy M, Connolly P, O’Byrne J. Evaluation of morbidity, mortality and outcome following cervical spine injuries in elderly patients. Eur Spine J 2008;17:585–91. 3. Le Moal G, Roblot F, Paccalin M, et al. Clinical and laboratory characteristics of infective endocarditis when associated with spondylodiscitis. Eur J Clin Microbiol Infect Dis 2002;21: 671–5. 4. Khan IA, Vaccaro AR, Slotolow DA. Management of vertebral diskitis and osteomyelitis. Orthopedics 1992;22:758 – 65. 5. Gasbarrini AL, Bertoldi E, Mazzetti M, et al. Clinical features, diagnostic and therapeutic approaches to haematogenous vertebral osteomyelitis. Eur Rev Med Pharmacol Sci 2005;9:53– 66. 6. Al-Nammari S, Lucas JD, Lam KS. Hematogenous methicillinresistant Staphylococcus aureus spondylodiscitis. Spine 2007;32: 2480 – 6. 7. Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR imaging in spinal infections: rules and myths? Radiology 2003; 228:506 –14. 8. Lenzi J, Agrillo A, Santoro A, Marotta N, Cantore GP. Postoperative spondylodiscitis from Aspergillus fumigatus in immunocompetent subjects. J Neurosurg Sci 2004;48:81–5. 9. Ugarriza LF, Cabezudo JM, Lorenzana LM, Rodriguez-Sanchez JA. Candida albicans spondylodiscitis. Br J Neurosurg 2004;18: 189 –92.
e46 10. Luz A, Castro A, Ribeiro R, et al. Viridians streptococcus endocarditis associated with spondylodiscitis. Rev Port Cardiol 2004;23:723– 8. 11. Fouquet B, Goupille P, Gobert F, Cotty P, Roulot B, Valat JP. Infectious discitis diagnostic contribution of laboratory tests and percutaneous discovertebral biopsy. Rev Rheum Engl Ed 1996;63: 24 –9.
J. L. Hanck and A. E. Muñiz 12. Lecouvet F, Irenge L, Vandercam B, Nzeusseu A, Hamels S, Gala JL. The etiologic diagnosis of infectious discitis is improved by amplification-based DNA analysis. Arthritis Rheum 2004;50: 2985–94. 13. Schinkel C, Gottwald M, Andress HJ. Surgical treatment of spondylodiscits. Surg Infect (Lrchmt) 2003;4:387–91.