Spinal Diseases: Bacterial Causes
 

In the past year, we’ve talked about possible causes of spine disease and associated pain syndromes. I don’t always share much of what I am learning or researching, as these sciences are complicated and my understanding of the pathologies are quite iterative. My summary statement: there is simply not enough attention in the area of spinal disease diagnostics!

So, to break with the guarded position I’ve (previously) maintained, here are some abstracts found from Medline. The search strategy was based on a pathogenic cause of spinal disc disease. You will notice that many abstracts are international or simply dated. Like diseased discs, the funding for U.S. funded research on spinal disc disease appears to have dried up! Why is it that a disease that is so prevalent in America has so few research dollars behind it?! This is crazy.

The first abstract is the one that contains the proverbial “needle in a haystack.” I’ll leave this tome with you for now, and chime back in soon. Please be as candid & verbose as you can with this feedback. If it’s helpful to you all, I’ll keep digging.

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Am J Med. 1996 Jan;100(1):85-9. SPONTANEOUS INFECTIOUS DISCITIS IN ADULTS. Honan M, White GW, Eisenberg GM. Division of Rheumatology, Lutheran GeneralHospital, Park Ridge, Illinois, USA.

PURPOSE: In adults, discitis most frequently follows spinal surgery. We report 16 adult patients with spontaneously occurring infectious discitis and compare them with an additional 52 patients abstracted from the literature. Infecting organisms, predisposing factors, imaging modalities, and response to therapy are described.

PATIENTS AND METHODS: The medical records of adult patients treated for infectious discitis of a community hospital during the past 10 years were reviewed. Postoperative spine patients and patients with primary osteomyelitis were excluded. Sixteen patients were identified with spontaneous primary infection of the disc space. The particulars of comorbid conditions, infection organisms, site of culture, and response to antibiotic therapy were noted and compared to 52 additional cases of spontaneous discitis reported in the literature since 1980.

RESULTS: A wide variety of infecting organisms was identified as causing spontaneous discitis, in contrast to previous reports of both postoperative discitis and spontaneous discitis. Nine of 10 patients with positive disc cultures had negative blood cultures. Appropriate antibiotics were curative in all patients but 1, regardless of the duration of symptoms. Nuclear imaging, computed tomography, and magnetic resonance imaging were all useful, although the last appears to be the most sensitive and specific imaging modality for detecting discitis.

CONCLUSIONS: Spontaneous infectious discitis is an uncommon cause of low back pain in adults. Nevertheless, it should be considered in any patient with acute or subacute pain. Elevated acute-phase reactants with appropriate imaging modality suggest the diagnosis. Given the wide variety of infecting organisms identified, culture of blood and/or disc for the specific causative organism is critical to successful treatment outcome.
PMID: 8579092 [PubMed - indexed for MEDLINE]

Infection. 1992 Mar-Apr;20(2):97-8. LUMBAR PAIN CAUSED BY MYCOPLASMA INFECTION Kayser S, Bhend HJ.Klinik für Rheumatologie und Rehabilitation, Stadtspital Triemli, Zürich, Switzerland.

A 45-year-old woman was admitted to hospital following acute onset of lower back pain. Clinical and laboratory investigations established a lumbar paraspinal soft tissue infection with Mycoplasma hominis associated with severe spondylarthrosis at L5/S1. A relationship to a recently performed hysterectomy must be considered.
PMID: 1533852 [PubMed - indexed for MEDLINE]

Rev Neurol. 2000 Feb 16-29;30(4):326-8. SUBDURAL EMPYEMA DUE TO MYCOPLASMA HOMINIS FOLLOWING EPIDURAL ANESTHESIA[Article in Spanish] Escamilla F, Fernández MD, Espigares A, Arnal C, Ortega A, García T. Servicio de Neurología, Hospital Universitario Virgen de las Nieves, Granada, España. neuro2000@hvn.sas.cica.es

INTRODUCTION: In the literature there are sporadic reports of spinal epidural abscesses after epidural anaesthesia (Staphylococcus aureus in 82%), whilst subdural empyemas are more often related to ear and sinus conditions.

CLINICAL CASE: A 32 year old woman with a clinical history of migraine and symmetrical frontal atrophy on a previous cerebral CT scan, after Caesarean section under epidural anaesthesia, presented with orthostatic headache two days later. On the fourth day it had become constant and she had a high temperature which was considered to be caused by infection of the surgical wound. Neurological examination was found to be normal, the CT scan was inconclusive and the CSF showed a lymphocytic pleocytosis without consumption of glucose. In view of her worsening clinical condition on the ninth day, in the absence of a cutaneous focus and on suspicion of a para-meningeal infective focus, lumbar MR was done and found to be normal, and cerebral MR which showed images compatible with a right fronto-parietal subdural empyema. After a parietal craniotomy and culture of the surgical specimen, colonies of Mycoplasma hominis were grown, similar to those grown from the exudates of the abdomical surgical wound. Treatment was started with ciprofloxacine.

CONCLUSION: We consider that following epidural anaesthesia the patient developed hypotension of the CSF with a secondary subdural hematoma or hygroma and this became infected by hematogenous spread of Mycoplasma hominis.

Spine. 2006 Sep 15;31(20):E770-3. INFECTED VERTEBROPLASTY DUE TO UNCOMMON BACTERIA SOLVED SURGICALLY: A RARE AND THREATENING LIFE COMPLICATION OF A COMMON PROCEDURE: REPORT OF A CASE AND A REVIEW OF THE LITERATURE. Alfonso Olmos M, Silva González A, Duart Clemente J, Villas Tomé C.Department of Orthopaedic Surgery, University Clinic of Navarra, Navarra, Spain. malfonsool@unav.es

STUDY DESIGN: Case report. OBJECTIVE: The aim of this work is to describe a case of infected vertebroplasty due to uncommon bacteria solved surgically with 2 years of follow-up and to discuss 6 other cases found in literature.

SUMMARY OF BACKGROUND DATA: Vertebroplasty is a well-known and useful technique for the treatment of painful osteoporotic vertebral fractures. Complications, such as cord or root compression or pulmonary embolisms, are infrequent and are mainly related with the frequent escape of cement throughout the vertebral veins. Infection is even more rare, but when it occurs is difficult to manage and can be a life-threatening complication.

METHODS: A 63-year-old-man had a spondylitis of L2 after vertebroplasty. The patient was initially managed with antibiotics without clinical improvement. Surgical treatment by anterior debridement and anterior and posterior stabilization was done. The bacteria isolated from the intraoperative cultures were Serratia marcescens, Stenotrophomonas maltophilia, and Burkholderia cepacia. After surgery, the patient was treated with antibiotics for 3 months.

RESULTS: After 2 years of follow-up, the patient was free of pain, without signs of infection, and a correct fusion was achieved.

CONCLUSION: When facing an infected vertebroplasty, initial conservative treatment with needle biopsy culture and antibiotic administration are a rational option to start. If this treatment fails, surgical debridement is then indicated in order to remove the infected tissue and the acrylic cement and to stabilize the spine. Although this can be an effective treatment, it could be a difficult and hazardous surgical procedure.
PMID: 16985448 [PubMed - indexed for MEDLINE]

BMC Fam Pract. 2004 Oct 6;5:21. AN UNUSUAL CASE OF CHRONIC MENINGITIS. Boos C, Daneshvar C, Hinton A, Dawes M. Department of General Medicine, Portsmouth Hospitals NHS Trust, Milton Rd, Portsmouth, UK. christopherboos@hotmail.com

BACKGROUND: Chronic meningitis is defined as symptoms and signs of meningeal inflammation and persisting cerebrospinal fluid abnormalities such as elevated protein level and pleocytosis for at least one month.

CASE PRESENTATION: A 62-year-old woman, of unremarkable past medical history, was admitted to hospital for investigation of a four-week history of vomiting, malaise an associated hyponatraemia. She had a low-grade pyrexia with normal inflammatory markers. A CT brain was unremarkable and a contrast MRI brain revealed sub-acute infarction of the right frontal cortex but with no evidence of meningeal enhancement. Due to increasing confusion and patient clinical deterioration a lumbar puncture was performed at 17 days post admission. This revealed gram-negative coccobacilli in the CSF, which was identified as Neisseria meningitidis group B. The patient made a dramatic recovery with high-dose intravenous ceftriaxone antibiotic therapy for meningococcal meningitis.

CONCLUSIONS: 1) Chronic bacterial meningitis may present highly atypically, particularly in the older adult. 2) There may be an absent or reduced febrile response, without a rise in inflammatory markers, despite a very unwell patient. 3) Early lumbar puncture is to be encouraged as it is essential to confirm the diagnosis.4) Despite a delayed diagnosis appropriate antibiotic therapy can still lead to a good outcome.
PMID: 15469610 [PubMed - indexed for MEDLINE]

Enferm Infecc Microbiol Clin. 2005 Feb;23(2):71-5. SPONDYLODISCITIS AND SACROILIITIS DUE TO STREPTOCOCCUS AGALACTIAE IN ADULTS: CLINICAL CASE AND LITERATURE REVIEW. [Article in Spanish] Díaz-Gonzálvez E, Zarza B, Abreu P, Cobo J, Orte J, Dronda F. Servicio de Enfermedades Infecciosas, Hospital Ramón y Cajal, Ctra. Colmenar, km 9, 28034 Madrid, Spain.

INTRODUCTION: Streptococcus agalactiae is a well-known pathogen related with infection in newborns, and in women during pregnancy and the puerperium. In recent years it has been described as a causal agent in invasive disease in immunodepressed adults and those with other severe underlying pathologies.

METHODS: We describe a case of S. agalactiae spondylodiscitis and concomitant bilateral sacroiliitis in an adult with no known underlying diseases. A systematic review of the related literature was performed (MEDLINE and EMBASE, up to December 2003).

RESULTS: The literature search retrieved only 33 cases of spondylodiscitis (predominance in men, 55-70 years old) and 13 cases of sacroiliitis (higher frequency in women, 30-40 years old) due to S. agalactiae. Simultaneous involvement of both locations of the axial skeleton is unusual.

CONCLUSION: Spondylodiscitis and sacroiliitis due to S. agalactiae is uncommon. S. agalactiae is an emerging pathogen in adults outside of the gestational and perinatal period. This micro-organism produces spondylodiscitis in the adult population over 50 years old. In contrast, sacroiliac involvement is described mainly in women in the reproductive age.

Ned Tijdschr Geneeskd. 2007 Nov 10;151(45):2485-90. SPONDYLODISCITIS AS CAUSE OF UNEXPLAINED FEVER - [Article in Dutch] Van der Wal WA, Oner FC. Universitair Medisch Centrum Utrecht, Postbus 85,500, 3508 GA Utrecht.

An 83-year-old woman was admitted to hospital with complaints of fever, abdominal pain and other complaints suggesting urosepsis. Additional analyses did not reveal the cause of her complaints. After cessation of antibiotic therapy, there was a spontaneous decrease in the infection parameters and she was subsequently discharged. Two and a half months later she was presented in our hospital with low back pain with radiating to the legs. MRI showed signs ofa spondylodiscitis at the level of LIII-LIV existing for some time. Finally, a gram-positive streptococcus infection was found and she was treated with antibiotics for 13 weeks. 6 months later she was free of symptoms. A 57-year-old man was admitted to the intensive care with a double-sided olecranon bursitis and sepsis. An endocarditis caused by Staphylococcus aureus was thought to be the cause of the sepsis and the patient was treated with surgical intervention and antibiotics. Because of persistent sepsis, different CT-scans were performed, and after one and a half months an extensive spondylodiscitis with abscess formation was diagnosed and subsequently treated surgically. A delay in diagnosing spondylodiscitis is the rule rather the exception. The diagnosis should be considered in any patient with localised back pain, especially when accompanied by fever, high ESR, and the presence of risk factors such as high age, diabetes mellitus, immunosuppression, and/or rheumatoid arthritis.
PMID: 18062589 [PubMed - in process]
Pediatrics. 2001 Feb;107(2):E26.

TWO CASES OF DISKITIS ATTRIBUTABLE TO ANAEROBIC BACTERIA IN CHILDREN. Brook I. Department of Pediatrics, Georgetown UniversitySchool of Medicine, Washington, DC, USA. dribrook@yahoo.com

Diskitis, an inflammation of the intervertebral disk, is generally attributable to Staphylococcus aureus and rarely Staphylococcus epidermidis, Kingella kingae, Enterobacteriaciae, and Streptococcus pneumoniae. In many cases, no bacterial growth is obtained from infected intervertebral discs. Although anaerobic bacteria were recovered from adults with spondylodiscitis, these organisms were not reported before from children. The recovery of anaerobic bacteria in 2 children with diskitis is reported. Patient 1. A 10-year-old male presented with 6 weeks of low back pain and 2 weeks of low-grade fever and abdominal pain. Physical examination was normal except for tenderness to percussion over the spine between thoracic vertebra 11 and lumbar vertebra 2. The patient had a temperature of 104 degrees F.

Laboratory tests were within normal limits, except for erythrocyte sedimentation rate (ESR), which was 58 mm/hour. Blood culture showed no growth. Magnetic resonance imaging with gadolinium contrast revealed minimal inflammatory changes in the 12th thoracic vertebra/first lumbar vertebra disk. There was no other abnormality. A computed tomography (CT)-guided aspiration of the disk space yielded bloody material, which was sent for aerobic and anaerobic cultures.

Gram stain showed numerous white blood cells and Gram-positive cocci in chains. Cultures for anaerobic bacteria yielded heavy growth of Peptostreptococcus magnus, which was susceptible to penicillin, clindamycin, and vancomycin. The patient was treated with intravenous penicillin 600 000 units every 6 hours for 3 weeks, and then oral amoxicillin, 500 mg every 6 hours for 3 weeks. The back pain resolved within 2 weeks, and the ESR returned to normal at the end of therapy. Follow-up for 3 years showed complete resolution of the infection.

Patient 2. An 8-year-old boy presented with low back pain and low-grade fever, irritability, and general malaise for 10 days. He had had an upper respiratory tract infection with sore throat 27 days earlier, for which he received no therapy. The patient had a temperature of 102 degrees F, and physical examination was normal except for tenderness to percussion over the spine between the second and fourth lumbar vertebrae. Laboratory tests were normal, except for the ESR (42 mm/hour). Radiographs of the spine showed narrowing of the third to fourth lumbar vertebra disk space and irregularity of the margins of the vertebral endplates. A CT scan revealed a lytic bone lesion at lumbar vertebra 4, and bone scan showed an increase uptake of (99m)technetium at the third to fourth lumbar vertebra disk space. CT-guided aspiration of the disk space yielded cloudy nonfoul-smelling material, which was sent for aerobic and anaerobic cultures. Gram stain showed numerous white blood cells and fusiform Gram-negative bacilli. Anaerobic culture grew light growth of Fusobacterium nucleatum. The organism produced beta-lactamase and was susceptible to ticarcillin-clavulanate, clindamycin, metronidazole, and imipenem. Therapy with clindamycin 450 mg every 8 hours was given parenterally for 3 weeks and orally for 3 weeks. Back pain resolved within 2 weeks. A 2-year follow-up showed complete resolution and no recurrence. This report describes, for the first time, the isolation of anaerobic bacteria from children with diskitis. The lack of their recovery in previous reports and the absence of bacterial growth in over two third of these studies may be caused by the use of improper methods for their collection, transportation, and cultivation. Proper choice of antimicrobial therapy for diskitis can be accomplished only by identification of the causative organisms and its antimicrobial susceptibility. This is of particular importance in infections caused by anaerobic bacteria that are often resistant to antimicrobials used to empirically treat diskitis. This was the case in our second patient, who was infected by F nucleatum, which was resistant to beta-lactam antibiotics. The origin of the anaerobic bacteria causing the infection in our patient is probably of endogenous nature. The presence of abdominal pain in the first child may have been attributable to a subclinical abdominal pathothology. The preceding pharyngitis in the second patient may have been associated with a potential hematogenous spread of F nucleatum. P magnus has been associated with bone and joint infections. This report highlights the importance of obtaining disk space culture for aerobic and anaerobic bacteria from all children with diskitis. Future prospective studies are warranted to elucidate the role of anaerobic bacteria in diskitis in children.
PMID: 11158500 [PubMed - indexed for MEDLINE]

South Med J. 2005 Feb;98(2):144-8. ANAEROBIC SPONDYLODISCITIS: CASE SERIES AND SYSTEMATIC REVIEW. Saeed MU, Mariani P, Martin C, Smego RA Jr, Potti A, Tight R, Thiege D. Department of Medicine, University of North Dakota School of Medicine and Health Sciences, Fargo, ND 58122, USA. musabsaeed@meritcare.com

BACKGROUND: Bacterial spondylodiscitis is rarely caused by anaerobic organisms. We describe two patients with lumbar vertebral osteomyelitis and discitis caused by anaerobic bacteria, including an unusual occurrence after an endodontic procedure, and review the salient clinical features and outcomes of 31 previously reported cases. METHODS: Case reports and review of the literature.

RESULTS: Median age at presentation was 65 years, with a male-to-female ratio of 2:1. The most common presenting symptoms were back pain, fever, and neurologic deficits. The lumbar spine was most frequently involved (43%); an equal number of cases involved contiguous extension or hematogenous spread. Causative anaerobes were recovered from disk space or vertebrae (13), blood (4), and/or soft tissue abscess and included Bacteroides species (12), Propionibacterium acnes (7), Peptococcus species (4), Peptostreptococcus species and Clostridium species (3 each), Corynebacterium diphtheroides and Fusobacterium species (2 each), and unspecified anaerobes (3).

CONCLUSIONS: Apart from specific antibiotic selection, medical treatment and outcomes for anaerobic spondylodiscitis are similar to those for aerobic vertebral disk infection.
PMID: 15759942 [PubMed - indexed for MEDLINE]

QJM. 2001 Sep;94(9):465-70.A CASE ASCERTAINMENT STUDY OF SEPTIC DISCITIS: CLINICAL, MICROBIOLOGICAL AND RADIOLOGICAL FEATURES. Hopkinson N, Stevenson J, Benjamin S.
Department of Rheumatology, Royal Bournemouth and Christchurch Hospitals, Bournemouth, UK.

We studied the spectrum of septic discitis presenting to two busy district general hospitals over 2.5 years (November 1996 to April 1999), surveying the case notes of all patients attending Royal Bournemouth and PooleHospitals with probable septic discitis on magnetic resonance imaging (MRI). Twenty-two cases of septic discitis were identified, suggesting an annual incidence of 2/100 000/year. Seventy-three percent of patients were aged > or =65 years. In 91% of patients, back pain was the presenting symptom, with neurological signs evident in 45% of patients. Fever >37.5 degrees C was present in 68% of patients, and a marked elevation of erythrocyte sedimentation rate (ESR) in 91%. Diagnosis was originally by MRI in 86% of patients, with plain radiographs not diagnostic of discitis in the early stages of the infection. Staphylococcus aureus was the commonest pathogen (41%), but in 18% of patients, no organism was identified. The major predisposing factors to septic discitis were invasive procedures (41%), underlying cancer (25%) and diabetes (18%). Pre-existing degenerative spinal disease was found in 50% of patients. Four patients whose causative organism was not isolated had a poorer outcome: one death and three with increased morbidity. Our estimated incidence rate (2/100 000/year) is higher than that in previous studies and may be due to a higher detection rate with MRI and/or a genuine increase in the number of cases. Septic discitis should be considered in any patient who has severe localized pain at any spinal level, especially if accompanied by fever and elevated ESR, or in the immunosuppressed.
PMID: 11528009 [PubMed - indexed for MEDLINE]

Am J Med. 1993 Jan;94(1):21-8. Am J Med. 2001 Aug1;111(2):161.
ANAEROBIC OSTEOMYELITIS AND ARTHRITIS IN A MILITARYHOSPITAL: A 10-YEAR EXPERIENCE.

Brook I, Frazier EH.Department of Pediatrics and Infectious Diseases, Naval MedicalCenter, Bethesda, Maryland.

PURPOSE: The methods of collecting, transporting, cultivating, and identifying aerobic bacteria in bone and joint infections have improved markedly since the early 1980s. In addition, many of the anaerobes have been reclassified and renamed. The purpose of this study was to provide more current information regarding the incidence of recovery of anaerobic bacteria from clinical specimens of infected bone and joint.

MATERIALS AND METHODS: Specimens from 73 infected bone specimens and 65 infected joints inoculated on media supportive for aerobic and anaerobic bacteria showed bacterial growth.

RESULTS: One hundred fifty-seven organisms (2.2 isolates/specimen), consisting of 122 anaerobic bacteria (1.7 isolates/specimen) and 35 facultative or aerobic bacteria (0.5 isolate/specimen), were recovered from the 73 bone specimens.

Anaerobic bacteria were recovered with aerobe or facultative bacteria in 24 (33%) instances. The predominant anaerobes were Bacteroides species (49 isolates), anaerobic cocci (45), Fusobacterium species (11), Propionibacterium acnes (7), and Clostridium species (6). Conditions predisposing to bone infections were vascular disease, bites, contiguous infection, peripheral neuropathy, hematogenous spread, and trauma. Pigmented Prevotella and Porphyromonas species were mostly isolated in skull and bite infections (7 of 19), members of the Bacteroides fragilis group in hand and feet infection (12 of 16), and Fusobacterium species in skull, bite, and hematogenous long bone infections. Seventy-four organisms (1.1 isolates/specimen), consisting of 67 anaerobic bacteria (1.0 isolate/specimen) and 7 facultative or aerobic bacteria (0.1 isolate/specimen), were isolated from 65 joint specimens. The predominant anaerobes were P. acnes (24 isolates), anaerobic cocci (17), Bacteroides species (10), and Clostridium species (5). Predisposing conditions to joint infection were trauma, prior surgery, presence of a prosthetic joint, and contiguous infection. P. acnes isolates were associated with prosthetic joints, members of the B. fragilis group with hematogenous spread, and Clostridium species with trauma. The clinical presentation of these cases is discussed.

CONCLUSION: These data highlight the importance of anaerobic bacteria in bone and joint infection.
PMID: 8420297 [PubMed - indexed for MEDLINE]

Pediatr Rehabil. 2002 Jan-Mar;5(1):11-9. JOINT AND BONE INFECTIONS DUE TO ANAEROBIC BACTERIA IN CHILDREN. Brook I.

The current review describes the microbiology, diagnosis and management of septic arthritis and osteomyelitis due to anaerobic bacteria in children. Staphylococcus aureus, Haemophilus influenzae type-b, and Group A streptococcus, Streptococcus pneumoniae, Kingela kingae, Neisseria meningiditis and Salmonella spp are the predominant aerobic bacteria that cause arthritis in children. Gonococcal arthritis can occur in sexually active adolescents. The predominant aerobes causing osteomyelitis in children are S. aureus, H. influenzae type-b, Gram-negative enteric bacteria, beta-hemolytic streptococci, S. pneumoniae, K. kingae, Bartonella henselae and Borrelia burgdorferi. Anaerobes have rarely been reported as a cause of these infections in children. The main anaerobes in arthritis include anaerobic Gram negative bacilli including Bacteroides fragilis group, Fusobacterium spp., Clostridium spp. and Peptostreptococcus spp. Most of the cases of anaerobic arthritis, in contrast to anaerobic osteomyelitis, involved a single isolate. Most of the cases of anaerobic arthritis are secondary to hematogenous spread. Many patients with osteomyelitis due to anaerobic bacteria have evidence of anaerobic infection elsewhere in the body, which is the source of the organisms involved in osteomyelitis. Treatment of arthritis and osteomyelitis involving anaerobic bacteria includes symptomatic therapy, immobilization in some cases, adequate drainage of purulent material and antibiotic therapy effective to these organisms.
PMID: 12396847 [PubMed - indexed for MEDLINE]

Br J Neurosurg. 2007 Oct;21(5):473-7. SPONDYLODISCITIS (DISC SPACE INFECTION) ASSOCIATED WITH NEGATIVE MICROBIOLOGICAL TESTS: COMPARISON OF OUTCOME OF SUSPECTED DISC SPACE INFECTIONS TO DOCUMENTED NON-TUBERCULOUS PYOGENIC DISCITIS. Bhagat S, Mathieson C, Jandhyala R, Johnston R.
Department of Neurosurgery, Institute of Neurological sciences, Southern General Hospital, Glasgow, UK. shaishav_bhagat@rediffmail.com

Discitis, an infection of the disc space, is an uncommon diagnosis that, if missed, can lead to spinal deformity and neurological deterioration, although as many as 30% of these patients will have negative microbiological cultures. It was unclear, however, whether the prognosis differed between patients who had positive or negative cultures. A retrospective case note review was carried out to assess the differences in presentation and outcome between these two groups. There were 26 and 43 patients in the negative and positive groups, respectively. Those with a positive culture were more likely to present with pyrexia, have a neurological deficit and not be independently mobile at presentation. The mean CRP recorded at the time of presentation was 96 and 157 in the negative and positive groups respectively (p = 0.004). Similarly, the mean ESR in the positive group was 88 compared with 69 in the negative group (p = 0.02). In conclusion, these patients may be at different ends of a clinical spectrum: those patients with a positive culture having a greater local and systemic inflammatory reaction to the disc space infection.
PMID: 17852101 [PubMed - in process]

A CASE OF BRUCELLA SPONDYLODISCITIS WITH EXTENDED, MULTIPLE-LEVEL INVOLVEMENT
Mehmet Ozden, MD; Kutbettin Demirdag, MD; Ahmet Kalkan, MD; Huseyin Ozdemir, MD; Pinar Yuce, MD
South Med J. 2005;98(2):229-231. ©2005 Lippincott Williams & Wilkins
Posted 03/11/2005

Brucellosis is a zoonosis that affects several organs and has a protean presentation. The authors report the case of a 61-year-old male patient with brucellar spondylodiscitis involving several vertebrae and a paravertebral abscess localized in the erector spinae muscle. Diagnosis was made by positive blood culture and MRI. No relapse was seen with a combined treatment (doxycycline/rifampin) for 3 months, followed by doxycycline alone for 6 months. Almost all radiologic findings disappeared at the end of a 1-year follow-up without any further treatment.

Introduction

Brucellosis is an endemic zoonotic disease, especially in the Middle East and Mediterranean regions. Because it affects several organs and tissues, it may present in a variety of ways.[1-4] Spondylodiscitis is a frequent and important complication of brucellosis, affecting the lumbar vertebrae, followed by thoracic and cervical involvement.[5,6]
We report the case of a male patient with brucellosis and spondylodiscitis who had a lesion at multiple levels-thoracic, lumbar, and sacral-and a paravertebral abscess localized in the erector spinae muscle.

Case Report

A 61-year-old man was admitted to our hospital with a 2-month history of fever, chills, and profuse sweating, especially at night. He complained of fatigue, lack of appetite, weight loss, and back and low back pain for the past 6 weeks. He had a 4-week history of anti-inflammatory treatment for suspected spondylolisthesis. He also had a history of consumption of unpasteurized dairy products and performed stockbreeding.
On physical examination, his body temperature was 37.5°C. Tenderness was present on thoracic and lumbar vertebrae and left lumbosacral region. No neurologic abnormality was noted. He had hepatomegaly and splenomegaly.The patient's laboratory tests included white blood cell count, 6,200/mm3; hemoglobin, 12.2 g/dL; hematocrit, 33.7%; erythrocyte sedimentation rate, 69 mm/h; C-reactive protein, 44 mg/L [normal, 0 to 6 mg/L]; and a normal blood biochemistry profile. The Rose Bengal test was positive. The Wright agglutination test and 2-mercaptoethanol test for brucella were positive at titers of 1/320 and 1/160, respectively. Brucella melitensis was isolated from the blood culture. MRI of the thoracolumbar vertebrae showed loss of height in the intravertebral disks of T12-L1, L2-L3, L4-L5, and L5-S1, signal abnormality in vertebral end plates, and corpus and intervertebral disks consistent with spondylodiscitis (Fig. 1, A and B). A paravertebral abscess extending from the S1 left transverse processus to the erector spinae muscle with epidural involvement was identified. In addition, a soft tissue abscess was observed in both psoas muscles (Fig. 1, C and D).

A and B , MRI of the lumbar spine (sagittal view). T2-weighted image shows high signal intensity of the T12-L1, L2-L3, L3-L4, and L5-S1 vertebral end plate and intervertebral disks. C , precontrast image shows abscess of paravertebral and erector spinae muscle and epidural involvement (axial view). D , postcontrast image shows peripheral enhancement of the left erector spinae muscle and paravertebral abscess. On the basis of these findings, a diagnosis of brucellar spondylodiscitis with multiple vertebral involvement was made. The patient was administered 600 mg/d rifampin and 200 mg/d doxycycline for 3 months, followed by doxycycline alone for another 6 months. The patient's condition gradually improved.

At the end of the 9-month treatment period, the back and low back pain and other symptoms disappeared, and there was no tenderness in the thoracic and lumbar vertebrae and left paravertebral muscles. Laboratory tests demonstrated that erythrocyte sedimentation rate was 7 mm/h; C-reactive protein, 6 mg/L; and Wright agglutination, 1/40. All other blood values were normal. In the thoracolumbar MRI taken 1 year after the discontinuation of the treatment for the radiologic assessment, pathologic contrast was observed to decrease significantly in T12-L1 and disappeared totally in L2-S1. Also, the paravertebral and epidural abscesses disappeared (Fig. 2, A and B). Figure 2.
A , T2-weighted sagittal image shows no high signal intensity of the T12-L1, L2-L3, L3-L4, and L5-S1 vertebral endplates and corpus. B , there is no paravertebral soft tissue and epidural involvement on T2-weighted axial image.

Discussion

Spondylitis is one of the most common and important forms of osteoarticular involvement seen in brucellosis. The most common type of involvement is lumbar vertebra, which is followed by dorsal and cervical involvement.[7,8] Lumbar vertebral involvement among brucella spondylitis cases is reported between 44 and 76%. Involvement of vertebral segments is mostly unifocal, but multifocal and multilevel involvements may also be seen, though rarely.[9,10] A study that included 35 brucellar spondylitis cases reported multifocal spinal involvement in 3 cases.[9] Cases that have both lumbar and cervical vertebral involvement are seldom reported.[11] This case of brucella spondylodiscitis had a total of seven vertebrae, thoracic (1), lumbar (5), and sacral (1), and disks at four levels, T12-L1, L2-L3, L4-L5, and L5-S1. To the best of our knowledge, no case with such an involvement has been hitherto reported.
Spondylodiscitis may be accompanied by paravertebral and/or epidural abscess, which may imitate disk herniation.[2-5,12] However, as far as we know, only one case with a paravertebral abscess in the erector spinae muscle caused by brucellosis has been reported.[13] To the best of our knowledge, this is the first brucella case that had a paravertebral abscess localized in erector spinae muscle with multiple vertebral thoracic, lumbar, and sacral involvement.

Delays in diagnosis and treatment may lead to important neurologic and vascular complications in patients.[3,7] Brucellar spondylitis may be confused with other diseases affecting vertebra, especially with tuberculosis. MRI plays a significant role in diagnosis and follow-up because it is more sensitive than other imaging methods and has an important place in the identification of paravertebral and epidural formations. In brucellar spondylodiscitis, pathologic MRI findings become apparent about 1 month after the onset of clinical symptoms.[8]
Some randomized, double-blinded studies document that in brucellar spondylitis, the doxycycline and streptomycin combination was more effective than the doxycycline/rifampin combination.[14] Other reports suggest that there are no significant differences between the treatment regimens.[9]

The duration of treatment is determined by the clinical and radiologic response. In cases of paravertebral/epidural mass, the duration may be extended up to 12 months. Some studies report treatment being continued for as long as 535 days, and one study reported a mean therapy duration of 120 days for a series of 35 cases.[9] Short-term treatments increase the risk of relapse.

Conclusion

The present case illustrates three important features: First, the multiple-level and extended vertebral involvement; second, the combined treatment for 3 months, followed by doxycycline alone for 6 months, which was not associated with a relapse; and third, nearly all radiologic findings improved at the end of 1 year.

References

1. Young EJ. An overview of human brucellosis. Clin Infect Dis 1995;21:283-290.
2. Tekkok IH, Berker M, Ozcan OE, et al. Brucellosis of the spine. Neurosurgery 1993;33:838-844.
3. Colmenero JD, Reguera JM, Martos F, et al. Complications associated with Brucella melitensis infection: a study of 530 cases. Medicine 1996;75:195-211.
4. Colmenero JD, Cisneros JM, Orjuela DL, et al. Clinical course and prognosis of Brucella spondylitis. Infection 1992;20:38-42.
5. Mousa AR, Muhtaseb SA, Almudallal DS, et al. Osteoarticular complications of brucellosis: a study of 169 cases. Rev Infect Dis 1987;9:531-543.
6. Ariza J, Gudiol F, Valverde J, et al. Brucellar spondylitis: a detailed analysis based on current findings. Rev Infect Dis 1985;7:656-664.
7. Mousa AM, Bahar RH, Araj GF, et al. Neurological complications of brucella spondylitis. Acta Neurol Scand 1990;81:16-23.
8. Khateeb MI, Araj GF, Majeed SA, et al. Brucella arthritis: a study of 96 cases in Kuwait. Ann Rheum Dis 1990;49:994-998.
9. Solera J, Lozano E, Martinez-Alfaro E, et al. Brucellar spondylitis: review of 35 cases and literature survey. Clin Infect Dis 1999;29:1440-1449.
10. Sharif HS, Aideyan OA, ClarkDC, et al. Brucellar and tuberculous spondylitis: comparative imaging features. Radiology 1989;171:419-425.
11. Zormpala A, Skopelitis E, Thanos L, et al. An unusual case of brucellar spondylitis involving both the cervical and lumbar spine. Clin Imaging 2000;24:273-275.
12. Lifeso RM, Harder E, McCorkell SJ. Spinal brucellosis. J Bone Joint Surg Br 1985;67:345-351.
13. Ozgocmen S, Ardicoglu A, Kocakoc E, et al. Paravertebral abscess formation due to brucellosis in a patient with ankylosing spondylitis. Joint Bone Spine 2001;68:521-524.
14. Ariza J, Gudiol F, Pallares R, et al. Treatment of human brucellosis with doxycycline plus rifampin or doxycycline plus streptomycin: a randomized, double-blind study. Ann Intern Med 1992;117:25-30.
Sidebar: Key Messages
· Brucellosis is a zoonosis that is commonly seen throughout the world and is endemic in Turkey. Since it affects several organs and tissues, it may appear in various clinical pictures.
· This report describes a rare case of spondylodiscitis with extended involvement at seven consecutive levels.
· No relapse was observed with a combined treatment for 3 months, followed by doxycycline alone for 6 months.
· All radiologic findings improved at the end of 1 year of follow-up without any treatment in this case.

Reprint Address
Reprint requests to Dr. Mehmet Ozden, FiratUniversity, Faculty of Medicine, Department of Infectious Diseases and Clinical Microbiology, TR-23119 Elazıg, Turkey. Email: ozdenm44@hotmail.com

Mehmet Ozden, MD , Kutbettin Demirdag, MD , Ahmet Kalkan, MD , Huseyin Ozdemir, MD ,and Pinar Yuce, MD , Department of Infectious Diseases and Clinical Microbiology and the Department of Radiology, FiratUniversity, Faculty of Medicine, Elazig, Turkey


Res Vet Sci. 1976 May;20(3):334-9.
PATHOGENICITY STUDIES IN POULTRY WITH AN UNDEFINED SEROTYPE OF MYCOPLASMA.
Wise DR, Fuller MK.
Pathogenicity trials in poultry are reported with an isolate of mycoplasma, designated 'W8', which is serologically unrelated to Mycoplasma gallisepticum, M synoviae or M meleagridis. W8 killed fowl and turkey embryos when injected into the yold sacs of embryonating eggs. Infection of one-day-old fowls, turkeys and pheasants by the air sac route caused marked growth depression and a high incidence of osteomyelitis of the vertebral column in all species. A large proportion of infected turkeys and a smaller proportion of infected pheasants also developed chondrodystrophic changes of the long bones similar to those of turkey syndrome '65. Infection did not cause mortality or macroscopic air sacculitis. No obvious pathological changes occurred in fowls following W8 infection by the air sac route at two weeks of age and only minimal changes when infection was given at one week. Infection did not appear to spread to in-contact controls. W8 was recovered most frequently and in greatest profusion from the air sacs, tracheas, kidneys and vertebral columns of fowls and turkeys following air sac infection at one day of age.

Infection. 2000 Jan-Feb;28(1):46-8.
RETROPERITONEAL ABSCESS AND BACTEREMIA DUE TO MYCOPLASMA HOMINIS IN A POLYTRAUMATIZED MAN.
Brunner S, Frey-Rindova P, Altwegg M, Zbinden R.
Dept. of Medical Microbiology, University of Zurich, Switzerland.
We report a case of a retroperitoneal abscess due to Mycoplasma hominis in a young polytraumatized man who developed septicemia under treatment with rifampin and flucloxacillin. M. hominis was recovered from blood cultures as well as from the abscess near the left iliac spine. After 10 days of therapy with clindamycin the patient improved, and intraoperatively taken swabs were culture negative but still positive by PCR.
PMID: 10697792 [PubMed - indexed for MEDLINE]

Acta Paediatr. 2005 Sep;94(9):1339-41.
ACUTE SEVERE SPINAL CORD DYSFUNCTION IN A CHILD WITH MENINGITIS: STREPTOCOCCUS PNEUMONIAE AND MYCOPLASMA PNEUMONIAE CO-INFECTION.
Manteau C, Liet JM, Caillon J, M'Guyen S, Quere MP, Roze JC, Gras-Le Guen C.Paediatric Intensive Care Unit, Mothers' and Children's Hospital, Nantes Teaching Hospital, Nantes, France.

Tetraplegia developed abruptly in an 11-y-old with pneumococcal meningitis. Magnetic resonance imaging showed multiple hyperintensities at the brainstem-spinal cord junction. Serological tests were positive for Mycoplasma pneumoniae (microparticle agglutination and specific IgMs). Erythromycin and dexamethasone were started promptly, and 10 d later the patient was discharged with normal neurological function. CONCLUSION: Tetraplegia during the course of pneumococcal meningitis in an 11-y-old girl disappeared after treatment with ceftriaxone, erythromycin and dexamethasone.
PMID: 16279003 [PubMed - indexed for MEDLINE]

J Clin Neurosci. 2007 Jan;14(1):61-4. Epub 2006 Nov 7.
REVERSIBLE MYELORADICULOPATHY DUE TO MYCOPLASMA PNEUMONIAE. Hsing J, Welgampola M, Kiernan MC.
Institute of Neurological Sciences, Prince of Wales Hospital, Sydney, Australia.

A 22-year-old man presented with flaccid paraparesis and a thoracic sensory level in the context of a recent respiratory illness. Investigations established cerebrospinal pleocytosis with elevated protein, and subsequent serological testing confirmed raised antibody titres to Mycoplasma pneumoniae. Nerve conduction studies established that H-reflexes were prolonged and somatosensory evoked responses were delayed from the lower limbs bilaterally. Although imaging of the spinal cord revealed no abnormality, clinical and neurophysiological findings were consistent with a myeloradiculopathy. The patient was treated with pulse intravenous methylprednisone and underwent complete recovery over a 4-week period.
PMID: 17092721 [PubMed - indexed for MEDLINE]

I've having html issues, so the Word version for now for the rest of the abstracts...
________

Am J Med. 1993 Jan;94(1):21-8. Am J Med. 2001 Aug1;111(2):161.
ANAEROBIC OSTEOMYELITIS AND ARTHRITIS IN A MILITARY HOSPITAL: A 10-YEAR EXPERIENCE.
Brook I, Frazier EH.

Department of Pediatrics and Infectious Diseases, Naval Medical Center, Bethesda, Maryland.
PURPOSE: The methods of collecting, transporting, cultivating, and identifying aerobic bacteria in bone and joint infections have improved markedly since the early 1980s. In addition, many of the anaerobes have been reclassified and renamed. The purpose of this study was to provide more
obic cocci (45), Fusobacterium species (11), Propionibacterium acnes (7), and Clostridium species (6). Conditions predisposing to bone infections were vascular disease, bites, contiguous infection, peripheral neuropathy, hematogenous spread, and trauma. Pigmented Prevotella and Porphyromonas species were mostly isolated in skull and bite infections (7 of 19), members of the Bacteroides fragilis group in hand and feet infection (12 of 16), and Fusobacterium species in skull, bite, and hematogenous long bone infections. Seventy-four organisms (1.1 isolates/specimen), consisting of 67 anaerobic bacteria (1.0 isolate/specimen) and 7 facultative or aerobic bacteria (0.1 isolate/specimen), were isolated from 65 joint specimens. The predominant anaerobes were P. acnes (24 isolates), anaerobic cocci (17), Bacteroides species (10), and Clostridium species (5). Predisposing conditions to joint infection were trauma, prior surgery, presence of a prosthetic joint, and contiguous infection. P. acnes isolates were associated with prosthetic joints, members of the B. fragilis group with hematogenous spread, and Clostridium species with trauma. The clinical presentation of these cases is discussed.

CONCLUSION: These data highlight the importance of anaerobic bacteria in bone and joint infection
PMID: 8420297 [PubMed - indexed for MEDLINE]

Pediatr Rehabil. 2002 Jan-Mar;5(1):11-9.
JOINT AND BONE INFECTIONS DUE TO ANAEROBIC BACTERIA IN CHILDREN.
Brook I.

The current review describes the microbiology, diagnosis and management of septic arthritis and osteomyelitis due to anaerobic bacteria in children. Staphylococcus aureus, Haemophilus influenzae type-b, and Group A streptococcus, Streptococcus pneumoniae, Kingela kingae, Neisseria meningiditis and Salmonella spp are the predominant aerobic bacteria that cause arthritis in children. Gonococcal arthritis can occur in sexually active adolescents. The predominant aerobes causing osteomyelitis in children are S. aureus, H. influenzae type-b, Gram-negative enteric bacteria, beta-hemolytic streptococci, S. pneumoniae, K. kingae, Bartonella henselae and Borrelia burgdorferi. Anaerobes have rarely been reported as a cause of these infections in children. The main anaerobes in arthritis include anaerobic Gram negative bacilli including Bacteroides fragilis group, Fusobacterium spp., Clostridium spp. and Peptostreptococcus spp. Most of the cases of anaerobic arthritis, in contrast to anaerobic osteomyelitis, involved a single isolate. Most of the cases of anaerobic arthritis are secondary to hematogenous spread. Many patients with osteomyelitis due to anaerobic bacteria have evidence of anaerobic infection elsewhere in the body, which is the source of the organisms involved in osteomyelitis. Treatment of arthritis and osteomyelitis involving anaerobic bacteria includes symptomatic therapy, immobilization in some cases, adequate drainage of purulent material and antibiotic therapy effective to these organisms.
PMID: 12396847 [PubMed - indexed for MEDLINE]

Br J Neurosurg. 2007 Oct;21(5):473-7.
SPONDYLODISCITIS (DISC SPACE INFECTION) ASSOCIATED WITH NEGATIVE MICROBIOLOGICAL TESTS: COMPARISON OF OUTCOME OF SUSPECTED DISC SPACE INFECTIONS TO DOCUMENTED NON-TUBERCULOUS PYOGENIC DISCITIS.
Bhagat S, Mathieson C, Jandhyala R, Johnston R.

Department of Neurosurgery, Institute of Neurological sciences, Southern General Hospital, Glasgow, UK. shaishav_bhagat@rediffmail.com

Discitis, an infection of the disc space, is an uncommon diagnosis that, if missed, can lead to spinal deformity and neurological deterioration, although as many as 30% of these patients will have negative microbiological cultures. It was unclear, however, whether the prognosis differed between patients who had positive or negative cultures. A retrospective case note review was carried out to assess the differences in presentation and outcome between these two groups. There were 26 and 43 patients in the negative and positive groups, respectively. Those with a positive culture were more likely to present with pyrexia, have a neurological deficit and not be independently mobile at presentation. The mean CRP recorded at the time of presentation was 96 and 157 in the negative and positive groups respectively (p = 0.004). Similarly, the mean ESR in the positive group was 88 compared with 69 in the negative group (p = 0.02). In conclusion, these patients may be at different ends of a clinical spectrum: those patients with a positive culture having a greater local and systemic inflammatory reaction to the disc space infection.
PMID: 17852101 [PubMed - in process]

Res Vet Sci. 1976 May;20(3):334-9.
PATHOGENICITY STUDIES IN POULTRY WITH AN UNDEFINED SEROTYPE OF MYCOPLASMA.
Wise DR, Fuller MK.

Pathogenicity trials in poultry are reported with an isolate of mycoplasma, designated 'W8', which is serologically unrelated to Mycoplasma gallisepticum, M synoviae or M meleagridis. W8 killed fowl and turkey embryos when injected into the yold sacs of embryonating eggs. Infection of one-day-old fowls, turkeys and pheasants by the air sac route caused marked growth depression and a high incidence of osteomyelitis of the vertebral column in all species. A large proportion of infected turkeys and a smaller proportion of infected pheasants also developed chondrodystrophic changes of the long bones similar to those of turkey syndrome '65. Infection did not cause mortality or macroscopic air sacculitis. No obvious pathological changes occurred in fowls following W8 infection by the air sac route at two weeks of age and only minimal changes when infection was given at one week. Infection did not appear to spread to in-contact controls. W8 was recovered most frequently and in greatest profusion from the air sacs, tracheas, kidneys and vertebral columns of fowls and turkeys following air sac infection at one day of age.
Infection. 2000 Jan-Feb;28(1):46-8.

RETROPERITONEAL ABSCESS AND BACTEREMIA DUE TO MYCOPLASMA HOMINIS IN A POLYTRAUMATIZED MAN.
Brunner S, Frey-Rindova P, Altwegg M, Zbinden R.
Dept. of Medical Microbiology, University of Zurich, Switzerland.
We report a case of a retroperitoneal abscess due to Mycoplasma hominis in a young polytraumatized man who developed septicemia under treatment with rifampin and flucloxacillin. M. hominis was recovered from blood cultures as well as from the abscess near the left iliac spine. After 10 days of therapy with clindamycin the patient improved, and intraoperatively taken swabs were culture negative but still positive by PCR.
PMID: 10697792 [PubMed - indexed for MEDLINE]
Acta Paediatr. 2005 Sep;94(9):1339-41.

ACUTE SEVERE SPINAL CORD DYSFUNCTION IN A CHILD WITH MENINGITIS: STREPTOCOCCUS PNEUMONIAE AND MYCOPLASMA PNEUMONIAE CO-INFECTION.
Manteau C, Liet JM, Caillon J, M'Guyen S, Quere MP, Roze JC, Gras-Le Guen C.
Paediatric Intensive Care Unit, Mothers' and Children's Hospital, Nantes Teaching Hospital, Nantes, France.
Tetraplegia developed abruptly in an 11-y-old with pneumococcal meningitis. Magnetic resonance imaging showed multiple hyperintensities at the brainstem-spinal cord junction. Serological tests were positive for Mycoplasma pneumoniae (microparticle agglutination and specific IgMs). Erythromycin and dexamethasone were started promptly, and 10 d later the patient was discharged with normal neurological function. CONCLUSION: Tetraplegia during the course of pneumococcal meningitis in an 11-y-old girl disappeared after treatment with ceftriaxone, erythromycin and dexamethasone.
PMID: 16279003 [PubMed - indexed for MEDLINE]
J Clin Neurosci. 2007 Jan;14(1):61-4. Epub 2006 Nov 7.

REVERSIBLE MYELORADICULOPATHY DUE TO MYCOPLASMA PNEUMONIAE.
Hsing J, Welgampola M, Kiernan MC.
Institute of Neurological Sciences, Prince of Wales Hospital, Sydney, Australia.
A 22-year-old man presented with flaccid paraparesis and a thoracic sensory level in the context of a recent respiratory illness. Investigations established cerebrospinal pleocytosis with elevated protein, and subsequent serological testing confirmed raised antibody titres to Mycoplasma pneumoniae. Nerve conduction studies established that H-reflexes were prolonged and somatosensory evoked responses were delayed from the lower limbs bilaterally. Although imaging of the spinal cord revealed no abnormality, clinical and neurophysiological findings were consistent with a myeloradiculopathy. The patient was treated with pulse intravenous methylprednisone and underwent complete recovery over a 4-week period.
PMID: 17092721 [PubMed - indexed for MEDLINE]

I am new but wouold like to comment. Should i intoruce myself here? thank you

Welcome Messy Spine. You sure can introduce yourself in The Big File. Just click on the icon over to the left that says "new," then click on "discussion" and you can give your topic a title and take it away. Sometimes it takes a little experimenting to figure the forums out. Again, welcome and let us be of help to you!

Particular Form of Septic Arthritis: Septic Arthritis of Facet Joint.
Michel-Batôt C, Dintinger H, Blum A, Olivier P, Laborde F, Bettembourg-Brault I, Pourel J, Loeuille D, Chary-Valckenaere I. Rheumatology Department, Brabois Teaching Hospital, CHU Brabois, 54000 Nancy, France.

Only about 40 cases of septic arthritis of the facet joints have been reported to date. We report 6 new cases including 2 at the cervical spine, which is rarely involved. Mean age was 61.5 years; there were 5 men and 1 woman. Spinal pain and stiffness, fever, and asthenia were the presenting manifestations. Laboratory tests consistently showed inflammation. Among classical risk factors for infection, only noninsulin-dependent diabetes was noted, in a single patient. Mean time to the diagnosis was 42 days.

Discitis, a far more common condition, was considered initially, and early radiographs were of limited diagnostic assistance. Radionuclide bone scans identified the site of the infection and served to look for other foci. Magnetic resonance imaging was effective in confirming the diagnosis at an early stage and in looking for local spread (muscles, epidural space, and disk). L3-L4 was involved in 3 patients, C4-C5 in 2, and L4-L5 in 1. Direct inoculation during mesotherapy sessions was the cause in 1 patient. Cultures of blood and needle biopsy samples were positive in all 6 cases; Staphylococcus aureus was the causative agent in 3 patients. The risk of local and systemic complications governs the prognosis of facet joint infection.

Of our 6 patients, 4 experienced complications: there was 1 case each of discitis, epidural infection, endocarditis, and septic arthritis of the acromioclavicular joint. Fatal multiple organ dysfunction occurred in 1 patient. In the other 5 patients, antimicrobial therapy and protection from weight-bearing for 3 months ensured a favorable outcome.
PMID: 18093863 [PubMed - as supplied by publisher]
Rev Rhum Engl Ed. 1997 Jun;64(6):386-95.


Rev Rhum Engl Ed. 1997 Dec;64(12):859-60.
Septic Arthritis Of Lumbar Facet Joints. A Review Of Six Cases. Ergan M, Macro M, Benhamou CL, Vandermarcq P, Colin T, L'Hirondel JL, Marcelli C.Rheumatology Department, Côte de Nacre Teaching Hospital, Caen, France.

Hematogenous infection of the facet joints by pyogenic organisms is exceedingly rare. We report six cases of lumbar facet joint septic arthritis due to hematogenous spread of a pyogenic organism. A review of the literature identified ten anecdotal reports of similar cases. An analysis of these 16 cases showed that the diagnosis was based mainly on imaging study findings and that clinical data failed to discriminate between facet joint septic arthritis and infectious discitis. Increased uptake on the radionuclide bone scan was an early finding and the pattern of uptake was different from that seen in discitis.

Computed tomography was the investigation that best delineated the facet joint lesions. Magnetic resonance imaging of the lumbar spine was superior over computed tomography in demonstrating spread of the infection to the epidural space and/or soft tissues and in some instances demonstrated enhancement of the infected facet joint on T1 images after gadolinium injection. Aspiration of the facet joint under fluoroscopic guidance was required only when blood cultures were negative or when the diagnosis of the septic nature of the arthritis was in doubt. Blood cultures yielded a Staphylococcus aureus in the six cases in our series. Appropriate antimicrobial therapy was successful in most cases. In our series, four of the six patients had posterior epiduritis, pyomyositis, or an abscess in the paraspinal muscles or psoas muscle, suggesting that some epidural infections or psoas muscle abscesses believed heretofore to be primary may in fact be complications of facet joint septic arthritis. Facet joint septic arthritis is a new aspect of pyogenic spinal infections that deserves to be considered in patients with febrile spinal syndromes not explained by discitis. PMID: 9513611 [PubMed - indexed for MEDLINE]

J Spinal Disord Tech. 2003 Jun;16(3):285-7.
Delayed Presentation Of Septic Arthritis Of A Lumbar Facet Joint After Diagnostic Facet Joint Injection. Orpen NM, Birch NC.

Department of Trauma and Orthopaedics, WycombeGeneralHospital, High Wycombe, UK.

We report the case of a 46-year-old, otherwise healthy, man with chronic lower back pain and no evidence of nerve root compression who underwent diagnostic facet joint injections to assist in establishing where his pain sources were located and to try to help his spinal rehabilitation program. He presented with a facet joint infection 2 months after injection, in a manner that was indistinguishable from an acute intervertebral disc herniation. The diagnosis was confirmed on magnetic resonance imaging, and he was successfully treated with surgical debridement and antibiotics. Septic arthritis of a lumbar facet joint with an associated paraspinal abscess is a rare complication of facet joint infiltration with only two similar cases reported in the literature. We propose that this diagnosis be considered in patients who have undergone diagnostic facet joint injection who subsequently deteriorate with back and leg pain without another apparent cause.PMID: 12792344 [PubMed - indexed for MEDLINE]

Pain Med. 2006 Jan-Feb;7(1):52-6.

Septic Facet Joint Arthritis After A Corticosteroid Facet Injection.
Weingarten TN, Hooten WM, Huntoon MA. Department of Anesthesiology, MayoClinicCollege of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota55905, USA.

Lumbar facet joint injections are commonly employed in the treatment of low back pain and are considered to be relatively safe with few known complications. We report the case of septic facet arthritis following a periarticular facet injection in a patient with recurrent urinary tract infections. The literature is reviewed to identify epidemiological and clinical features of patients in whom septic facet arthritis developed after lumbar facet injection. The diagnosis of iatrogenic septic facet arthritis is often delayed because neurologic and constitutional signs and symptoms develop slowly. Serologic nonspecific markers of infection and appropriate imaging studies may be more sensitive for the early diagnosis of septic facet arthritis. Recalcitrant or worsening back pain after facet injections should prompt an investigation to rule out infectious causes. PMID: 16533197 [PubMed - indexed for MEDLINE]

Semin Arthritis Rheum. 2006 Apr;35(5):272-83.
Spontaneous Pyogenic Facet Joint Infection.
Narváez J, Nolla JM, Narváez JA, Martinez-Carnicero L, De Lama E, Gómez-Vaquero C, Murillo O, Valverde J, Ariza J. Rheumatology Department, Hospital Universitari de Bellvitge-IDIBELL, Barcelona, Spain.

OBJECTIVE: To analyze the clinical features, approaches to management, and outcome of spontaneous pyogenic facet joint infection (PFJI) in adults.

PATIENTS AND METHODS: Case series of 10 adults with microbiologically proven PFJI diagnosed during a 10-year period in a teaching hospital, plus a review of 32 additional cases previously reported (PubMed 1972 to 2003). Patients with prior spinal instrumentation or surgery and injection drug users were excluded. Only cases that were sufficiently detailed to be individually analyzed were included. These 32 cases, together with our 10 patients, form the basis of the present analysis.

RESULTS: PFJI represented nearly 20% of all spontaneous pyogenic spinal infection diagnosed in our hospital during a 10-year period. This data suggest that PFJI is more common than was previously thought. This data suggest that PFJI is more common than was previously thought. Of the 42 patients with PFJI, 26 (62%) were men and 16 (38%) were women, with ages ranging from 20 to 86 years (mean age, 59+/-15 years); 55% of patients were older than 60 years. The most common location of infections was the lumbosacral region (86%). All patients presented with severe back pain; fever was noted in 83% of the cases and neurological impairment in nearly 48%. In 38% of patients a systemic predisposing factor for infection was present; the most common conditions were diabetes mellitus, malignancies, and alcoholism.

In almost 36% of cases, one or more concomitant infectious processes due to the same microorganism was found, mainly arthritis, skin and soft-tissue infections, endocarditis, and urinary tract infections. Staphylococcus aureus was the most common etiologic microorganism (86% of cases). Bacteremia was documented in 81% of the cases. The diagnosis of PFJI was based mainly on imaging study findings. Paraspinal and/or epidural extension was frequent (81% of cases), but its presence did not indicate a worse prognosis. Medical treatment alone was usually successful. The overall prognosis of PFJI was good, with a mortality rate of only 2%. The great majority of patients were cured without functional sequelae.

CONCLUSION: Incidence data from our institution reveal that PFJI is not a rare condition, representing approximately 20% of all pyogenic spinal infections. This entity should be considered in the differential diagnosis of patients with low back pain, especially in the presence of fever, whatever the patient's immunological status. PMID: 16616150 [PubMed - indexed for MEDLINE]

A while back, I found this amazing article (attached). After reading it again today, I found more gems of intelligence that helped me connect more dots, while also validating some of my grandiose conclusions about health issues facing many patients within this community.

Following the general theme of "pathologies of spine disease," I attached an article that is now ten years old. It is not only well-researched, but it seems to be the most analytical document I’ve read that ties so many disparate pieces of pathologies and disease together – so that even patients can understand the implications of the evidence presented!

It’s not a spine-centric article, per se, but here are a few points I found interesting:

- An excerpt: “…80% of joint infections in England & Wales (1990-92) were due to mycobacteria…there is a predilection for weight bearing joints and the spine.”

- The author, Dr. Goldenberg, is based in Mass., but did not include any clinical data from the U.S. Furthermore, the paper was published in The Lancet, a UK journal.

- Note the algorithm(s) for evaluating an infected joint; which includes blood, synovial fluid AND tissue. Try getting your ortho to test all these -- most will not except in very rare circumstances.

I am sure there are many other points that patients will find valuable and interesting. Please read it a few times, share it with someone and talk about it. Then read it again in a few weeks!

Again, I find it amazing that this was written a decade ago – with so few other like this published since then. Why is that?!

We are still very much in the dark on these important issues. I hope that helps others connect the dots too! There are many... http://adrsupport.org/groupee_common...n_rolleyes.gif

Oops...almost forgot this eight-year-old article! As I've lamented earlier -- all the studies & article specific to joint disease originate from other countries. You do the math!
______________________________________

J Clin Microbiol. 2000 January; 38(1): 90–93. American Society for Microbiology

Identification of Mycoplasma fermentans in Synovial Fluid Samples from Arthritis Patients with Inflammatory Disease

Sheena Johnson,* David Sidebottom, Felix Bruckner, and David Collins†
St. George's Hospital and Medical School, Cranmer Terrace, London SW17 0RE, United Kingdom
*Corresponding author. Biochemistry Department, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, United Kingdom. Phone: 44 181 725 5779. Fax: 44 181 725 2992. E-mail: sjohnson@sghms.ac.uk.

†Present address: Princess Margaret Hospital, Swindon SN1 4JU, United Kingdom.
Received July 13, 1999; Revisions requested August 26, 1999; Accepted September 22, 1999.
Small right arrow pointing to: This article has been cited by other articles in PMC.

Abstract

Since 1970 Mycoplasma fermentans has been suspected of being associated with rheumatoid arthritis. However, this association has been difficult to prove, and this has been our goal. The distribution of M. fermentans was studied in the synovial fluid of patients suffering from different arthritides. Samples of synovial fluid were taken from patients with well-defined disease and a clear diagnosis. After removal of the inflammatory cells and hyaluran, they were treated with proteinase K and tested by a single or fully nested PCR with primers directed against part of the two 16S rRNA genes of M. fermentans.

The product was sequenced automatically, by using an ALF Express automatic sequencer, to confirm the mycoplasma species and to identify the strain since the two genes were usually found to be polymorphic. This was also true of the type strain, strain PG18. M. fermentans was detected in 23 of 26 (88%) rheumatoid arthritis patients, and four different strains were found. It was also found in 7 of 8 (88%) of the nonrheumatoid inflammatory arthritis patient group, which consisted of one patient with reactive arthritis, one patient with pauciarticular juvenile chronic arthritis, two patients with gout, two patients with ankylosing spondylitis, and two patients with psoriatic arthritis, only one of whom was infected with M. fermentans. It was not detected in any of the 10 osteoarthritis patients. M. fermentans was therefore found to be a variable and very common organism in arthritic patients with inflammatory joint exudates and may well prove to be important in the etiology of the diseases.

Full article at:

http://www.pubmedcentral.nih.gov/art...gi?artid=86027

A patient who recently had 2 level cervical ADR sent me this article. He also tested positive for Lyme disease, erlichiosis and bartonella. It's an old article, but it is worth repeating since these diseases are so rampant. Many spine patients from our community are from New York, New Jersey and Connecticut!
______________________________________

Sciatica, disk herniation, and neuroborreliosis. A report of four cases Sciatica, disk herniation, and neuroborreliosis. A report of four cases

Arnaud Dupeyron , , a, Jehan Lecocqa, Benoît Jaulhacb, Marie-Eve Isner-Horobetia, Philippe Vautraversa, Julien Cohen-Solalc, Christelle Sordetc and Jean-Louis Kuntzc
a Physical Medicine and Rehabilitation Unit, Strasbourg Teaching Hospitals, Avenue Molière, 67098, Strasbourg cedex, France
b School of Medicine, Bacteriology Institute, Louis Pasteur University and Strasbourg Teaching Hospitals, 67000, Strasbourg, France
c Rheumatology and Clinical Immunology Department, Strasbourg Teaching Hospitals, Avenue Molière, 67098, Strasbourg cedex, France

Available online 25 September 2003. Abstract

We report four cases of sciatica in patients with same-level disk herniation confirmed by computed tomography and a final diagnosis of acute radiculitis caused by Borrelia burgdorferi, with a favorable response to ceftriaxone therapy. The neurological manifestations of Lyme disease are protean, and a potential contribution of concomitant disk disease to sciatica can lead to diagnostic wanderings. Disk lesions and infectious conditions that can cause sciatica are discussed. Whether a favorable response to antibiotic therapy should be taken as proof of B. burgdorferi radiculitis deserves discussion. In practice, in a patient with clinical manifestations suggesting disk-related nerve root pain and residing or having traveled to an endemic area, B. burgdorferi infection should be looked for, as both etiologies can coexist.

I was wondering how many disks that are removed for fusion or ADR are ever investigated, so the cause of the degeneration is known and can be used as a treatment. I bet nearly zero% are ever studied. It a pitiful shame that medicine treats symptoms, not causes. Every doctor will matter of factly claim they don't know what causes these diseases, but do they investigate them to find a cause?

If or when I have surgery, I will ask if they are going to do anything with the disks.

Thanks for the articles Harrison.

Rich,
When I finish my project for tomorrow night's class, I'll read thru what you have here & comment. I caught something about osteomyelitis which hits home. http://adrsupport.org/groupee_common...on_biggrin.gif

Don

I asked if mine could be saved for perhaps possible future tissue engineering/cultures. No was the answer, they are thrown away.

Lynda

Ive had spine problems since I was in junor high. I now believe lymes is the cause. Some people may want to see the movie on lymes coming out soon. See http://youtube.com/watch?v=sxWgS0XLVqw Listen for the spine degenerative disease in the video.

Messy Spine, thanks for the link. I briefly talked to the producer of this film last year, so I appreciate the link & reminder. It will be interesting to see how the film is received. For me, any reference by a doctor linking spine problems and Lyme is an especially interesting event!

BTW: It's "Lyme" disease, based on where the disease was discovered in CT, 35 years ago. Concerned parents got together to discuss the arthritis-like symptoms had afflicted their children. Their common complaints? Back and joint pain!

A patient referred me to this interesting research paper that specifically implicates some of these little buggers in everything from joint disease to arthritis. Surprisingly, this document is eleven years old and not easily found. The research was funded by the NIH, it is found on the CDC site: http://www.cdc.gov/ncidod/eid/vol3no1/baseman.htm

It is notable that the NIH now provides little funding for this kind of research; I heard its actually none. I'll see if I can confirm this. Here’s an excerpt relating to a recent post in another forum:
_________________________________

Rheumatoid Arthritis and Other Human Arthritides

The occurrence of various Mycoplasma and Ureaplasma species in joint tissues of patients with rheumatoid arthritis, sexually transmitted reactive arthritis, and other human arthritides can no longer be ignored (8). A clinical trial of long-term (6 to 12 months) antibiotic (doxycycline) therapy before cartilage destruction might prove beneficial in managing such frequent and often debilitating infections.

Extensive clinical and microbiological evidence indicates that mycoplasmas alone can elicit a spectrum of illness for which no other agents are incriminated. The eradication of these pathogenic mycoplasmas from various tissue sites requires an intact and functional immune system, although persons with fully competent immune systems may have difficulty eliminating mycoplasmas, even with recommended prolonged drug therapy. Nonetheless, mycoplasmas are still viewed as subordinates to other infectious agents and are relegated to a category of commensals that unwittingly cause disease in patients whose immune systems offer little resistance to microbial stress and overload.

Harrison,

Great paper and very interesting. Too bad finding a doctor to accept these theories or investigate them is so difficult. I can't find one.

Thanks-

Don, just to nitpick...these aren't theories. I know you this, but it's interesting that the "standard of care" disregards these facts as such...

thanks richard... this is definitely disconcerting. since having some bloodwork done to test for these various "bugs" is much less invasive and less expensive than all the epidurals, facet injections, and discograms we all receive in trying to nail down pain generators for our degenerative spines, if one could find a good doctor to work with why not test for these bugs?

when i had surgery i asked about saving my discs for tissue engineering but i was told at this time they couldn't do that. i should have asked about sending then to a lab for analysis. these are our discs! and they are just getting thrown away? i'm sure there is some fear about what our discs would reveal and how this may change future treatment.

i'm only 32 yrs old and yet i have 4 level DDD. yes, i had an injury and presumably tore L3-S1 from it and preceded to run, backpack and ski until i had nothing left at L5-S1 but still. i have the spine of an old woman. L2-3 now shows radiographic signs of DDD. my scoliosis could be pinching it but there may be another cause. i consider myself to have a strong immune system as i almost never get sick but it's worth investigating if anything else is causing this degenerative cascade.

Some of the doctors i saw said I had MS and i do not. Before i got sick with spine pain and lymes I never got colds. Now i know why some people have hyperimmune systems and never get colds.

Messy, thanks for posting..but it's "Lyme," where it was discovered (see previous post).

I've also heard that some patients can & do have "hyper-vigilant" immune systems; I've also read about it recently for the Nth time in reference to "never getting colds." I can dig up references if anyone cares.

Harrison, what I meant was that for any doctor to accept this, there would need to be acceptance of the theory that the particular person's disease or symtoms were caused by these bacteria. Many doctors think the immune response is due to genetic predisposition or some other factors, including viruses, and won't quickly accept new ideas unless research is done.

There are so many competing theories of causes of DDD and many are probably right depending on the case.

Lots of questions, but at least they are being asked and eventually something will be done. I'd like to see someone get a grant and do a study of about 200 Marshal Protocol patients and get some real numbers. As you know, I definitely think I had some little bugger make me sick and it is what affects my spine and joints. But it can't get beyond the theory stage without real research being done and published.

More abstracts to share on this complex issue. As I mentioned before, the more provocative studies originate from outside of the U.S., particularly the U.K. and Germany.
__________________________________________________ ___

IS SCIATICA DUE TO BACTERIAL INFECTION?
Journal of Bone and Joint Surgery - British Volume, Vol 87-B, Issue SUPP_III, 291.
Copyright © 2005 by British Editorial Society of Bone and Joint Surgery

Combined Orthopaedic Associations
Sydney, Australia – 24–29 October, 2004 Chairman – Kalev Wilding
A.J. Stirling; M. Jiggins; T.S.J. Elliott; T. Worthington; and P.A. Lambert
The Royal Orthopaedic Hospital Birmingham, UK. The Royal Orthopaedic Hospital Birmingham, UK. Dept of Clinical Microbiology, University Hospital, Birmingham, UK. Dept of Pharmaceutical & Biological Science, Aston University, Birmingham, UK

Introduction and Aims: To confirm whether bacteria were present in disc material harvested at the time of discectomy; and to determine whether the presence of bacteria correlated with elevation of Anti Lipid S antibody levels; and to compare these results with antibody levels and disc specimens from patients undergoing surgery for indications other than radiculitis.

We have previously demonstrated significantly elevated IgG titers (ELISA) to a glycolipid antigen found in the cell wall of most gram-positive bacteria in patients with discogenic sciatica. This raised the possibility that the inflammation associated with disc protrusion might be initiated or accelerated by bacteria.
Method: A prospective study was performed using disc material harvested with stringent aseptic precautions from 207 microdiscectomy and 27 trauma, tumor or scoliosis patients (controls). Serology was obtained for all patients.

Results: In the Microdiscectomy group 76/207 (37%) had positive cultures after seven days incubation, of which 26 (34%) had positive serology. Forty-nine patients had Propionibacteria, 11 Coagulase-negative-Staphylococci (CNS), eight Propionibacteria and CNS, four other organisms and four mixed growth.
One hundred and thirty one (63%) patients had negative cultures of whom 15% had positive serology. There was a significant difference between patients with positive serology and culture, compared with those with negative serology and culture (Fischer exact test P<0.01). In some patients, organisms were visible on microscopy prior to culture. Two of the patients undergoing surgery for other indications had positive cultures (P.acnes) of whom one had positive serology. Of those with negative cultures, six had positive serology. There was a significant difference between positive cultures in those with sciatica and controls (P<.001).

Conclusion: A significant proportion of patients with discogenic radiculitis have positive cultures with low-virulence Gram-positive organisms (predominantly Propionibacteria) and in proportion, a corresponding appropriate antibody response.

These abstracts were prepared by Editorial Secretary, George Sikorski. Correspondence should be addressed to Australian Orthopaedic Association, Ground Floor, The William Bland Centre, 229 Macquarie Street, Sydney, NSW 2000, Australia.

One or more of the authors are receiving or have received material benefits or support from a commercial source.
Modic changes, possible causes and relation to low back pain.
1: Med Hypotheses. 2007 Jul 9; [Epub ahead of print]
Albert HB, Kjaer P, Jensen TS, Sorensen JS, Bendix T, Manniche C.
All The Back Research Center, Part of Clinical Locomotion Science, University of Southern Denmark, Lindevej 5, 5750 Ringe, Denmark.

In patients with low back pain (LBP) it is only possible to diagnose a small proportion, (approximately 20%), on a patho-anatomical basis. Therefore, the identification of relevant LBP subgroups, preferably on a patho-anatomical basis, is strongly needed. Signal changes on MRI in the vertebral body marrow adjacent to the end plates also known as Modic Changes (MC) are common in patients with LBP (18-58%) and is strongly associated with LBP. In asymptomatic persons the prevalence is 12-13%. MC is divided into three different types. Type 1 consists of fibro vascular tissue, type 2 is yellow fat, and type 3 is sclerotic bone. The temporal evolution of MC is uncertain, but the time span is years. Subchondral bone marrow signal changes associated with pain can be observed in different specific infectious, degenerative and immunological diseases such as osseous infections, osteoarthritis, ankylosing spondylitis and spondylarthritis.

In the vertebrae, MC is seen in relation to vertebral fractures, spondylodiscitis, disc herniation, severe disc degeneration, injections with chymopapain, and acute Schmorl's impressions. The aim of this paper is to propose two possible pathogenetic mechanisms causing Modic changes. These are: A mechanical cause: Degeneration of the disc causes loss of soft nuclear material, reduced disc height and hydrostatic pressure, which increases the shear forces on the endplates and micro fractures may occur. The observed MC could represent oedema secondary to the fracture and subsequent inflammation, or a result of an inflammatory process from a toxic stimulus from the nucleus pulposus that seeps through the fractures. A bacterial cause: Following a tear in the outer fibers of the annulus e.g. disc herniation, new capilarisation and inflammation develop around the extruded nuclear material. Through this tissue it is possible for anaerobic bacteria to enter the anaerobic disc and in this environment cause a slowly developing low virulent infection. The MC could be the visible signs of the inflammation and oedema surrounding this infection, because the anaerobic bacteria cannot thrive in the highly aerobic environment of the MC type 1.

Perspectives: One or both of the described mechanisms can - if proven - be of significant importance for this specific subgroup of patients with LBP. Hence, it would be possible to give a more precise and relevant diagnosis to 20-50% of patients with LBP and enable in the development of efficient treatments which might be antibiotics, special rehabilitation programmes, rest, stabilizing exercise, or surgical fixation, depending on the underlying cause for the MC.
PMID: 17624684 [PubMed - as supplied by publisher]

1: Clin Orthop Relat Res. 1992 Jul;(280):175-8.
Case report of an unusual cause of low back pain. Intervertebral diskitis caused by Eikenella corrodens.
Noordeen MH, Godfrey LW. Department of Orthopaedic Surgery, Stoke Mandeville Hospital, Aylesbury, Buckinghamshire, England.

A 42-year-old man suffered from low back pain caused by intervertebral diskitis. The condition was diagnosed on plain roentgenogram and computed tomography scans. The infected area was biopsied and grew Eikenella corrodens, a gram-negative anaerobic rod, which grows slowly only after culture on blood agar in 5-10% carbon dioxide. This is the first reported case of E. corrodens intervertebral diskitis causing acute low back pain. Recognition of this organism in this condition emphasizes the importance of aerobic and anaerobic cultures of infected disks. The organism has unusual antibiotic sensitivities. The infection, once appropriately treated, responded rapidly.
Bacterial Pathogenesis and Genomics Research Grouphttp://www.ciir.qub.ac.uk/bpg/bpgfront.htm

Research within this group centres on infection caused by obligately anaerobic bacteria. There are two main areas of interest. Firstly bone and joint infection, focusing on prosthetic joint failure, fracture healing and the possible role of bacterial infection in sciatica and back pain. Previous studies from this group indicate that the bacterium Propionibacterium acnes is frequently associated with failed artificial hips. Therefore studies of the virulence determinants of this bacterium may give key insights into the relationship between infection and the osteolysis that leads to artificial hip failure. The second main area of interest relates to opportunistic infection arising from the normal intestinal microbiota, such as peritonitis, the risk of which requires prophylactic antibiotic treatment prior to bowel surgery. Bacteroides fragilis is a major cause of this type of infection. The Wellcome Trust have recognised the importance of this pathogen and are funding the complete genome sequencing programme, which is a joint project between the Sanger Centre, Cambridge UK and Dr Patrick’s laboratory. This opens up exciting possibilities with respect to the study of B. fragilis pathogenesis.

'This group is a member of the Research and Development Office of the HPSS Northern Ireland, Infectious Diseases Recognised Research Group from whom S Patrick has a 5 year Programme Grant. Additional current funding sources include the British Orthopaedic Wishbone Trust, the Royal College of Surgeons of England and the Department of Employment and Learning NI. Current collaborative links include the Schools of Biology & Biochemistry, Agriculture & Food Science and Pharmacy at QUB; Orthopaedic Surgery, Musgrave Park Hospital & the Royal Victoria Hospital NI; the Sanger Wellcome Institute, Cambridge; the Institute of Cell and Molecular Biology, University of Edinburgh and the University of Capetown, SA.'

Doctors stumble on infection clue to sciatica cure

By Lorraine Fraser, Medical Correspondent
Last Updated: 11:54pm BST 14/07/2001

DOCTORS believe that half of all cases of the excruciating back pain known as sciatica could be caused by an infection which is easily cured by antibiotics.Specialists in Birmingham have found slow-growing bacteria of the kind that normally lives on the surface of the skin in spinal tissue from nearly 50 per cent of patients with sciatica.

The finding suggests that a course of antibiotics could be all that is needed to solve the problem for millions of sufferers, revolutionising the way that doctors treat back pain. A clinical trial involving hundreds of patients is being set up to test the hypothesis and the results should be known in 18 months' time. The NHS spends £500 million a year on investigations and therapy for patients with back pain, which is one of the most difficult complaints to treat.

The cost to industry in terms of lost working time is an estimated £4 billion annually and the potential savings, should the doctors be proved right, would be enormous.

Tom Elliott, the professor of clinical microbiology at the University Hospital in Edgbaston, told The Telegraph that the finding of infection in patients with sciatica was "very exciting".
He said: "In terms of future therapy it may mean we could treat this with antibiotics. It could have a tremendous impact in terms of the management of patients with back pain and that has large implications for the NHS as a whole."

Sixteen million people suffer at least one bout of back pain in the UK in any one year and sciatica - pain in the sciatic nerve which extends down the leg from the base of the spinal cord - is one of the most common symptoms.

It has traditionally been explained as pressure on the sciatic nerve from a bulging or "slipped" vertebral disc.
However, until now there has been no explanation for the inflammation which is frequently present.
Professor Elliot and four colleagues from Aston University and the Royal Orthopaedic Hospital in Birmingham stumbled across the answer when trying out a blood test for deep-seated infections in patients, intended to identify infections of the heart or bone.

They applied the test to sciatica sufferers as a "control" group expecting negative results in these individuals - only to find that in a third of them it was positive.

They have examined disc tissue from 180 patients with sciatica so severe that they needed surgery and found bacterial infection in 46 per cent of them.

The most frequently occurring microbe was Proprionibacterium acnes, a normal skin bacterium linked to acne.
Professor Elliot said: "We think the organisms are getting into the blood and settling in this part of the body, perhaps in already damaged discs, setting up a low-grade infection."

The theory would explain why some people have slipped discs but do not have sciatic pain. The bacteria concerned are all sensitive to common antibiotics. Tests are under way to see if it is possible to get sufficient drug into the infected discs to kill the bacteria.

Professor Elliot said: "We suspect that short courses of antibiotics won't work and sciatica patients may need six weeks of antibiotics, as is the case for example in bone infection."
In future it might also be possible to use the blood test to spot those who might benefit from antibiotic treatment, he added.

A spokesman for the charity BackCare, which helped to fund the research, said: "This is extremely interesting work and we will be very excited to see the results of the clinical trial, but we must wait and see."

http://www.telegraph.co.uk/news/main.jhtml?xml=/news/20...1/07/15/ixhomef.html
Language: German English title: Neuro-borreliosis or intervertebral disk prolapse?
Authors: Dieterle, et al

Abstract: Between September 1986 and November 1988, 17 patients were hospitalized and treated for neuro-borreliosis. Ten of them had been admitted with suspected lumbar or cervical root or compression syndrome. Only four patients recalled a tick bite, only three an erythema migrans. Uni- orbilateral facial paresis was a prominent feature in six patients. Three of 14 patients had no IgG antibodies against Borrelosis, either in serum or cerebrospinal fluid at the initial examination, two had positive serum in titers only. Despite antibiotic treatment (usually 10 mega U penicillin threetimes daily) six patients had recurrence by April, 1989. treated with penicillin again or with twice daily 100 mg doxycycline or2 g ceftriaxon. In four of them a residual painful polyneuropathy remains.

Author: Meier, et al
title : Meningoradiculitis mimicking vertebral disc herniation . A "neurosurgical " complication of Lyme-borreliosis.
source: Acta Neurochir: (Wien) 1989;98(1-2):42-6

Abstract: We report on 3 patients with meningoradiculoneuritis (MRN) due to Lyme-borreliosis (LB)., which presented clinically as vertebral disc herniation. In 2 cases the undelying infection was discovered only after UNSUCESSFUL NEUROSURGICAL TREATMENT. In the differential diagnosis between MRN and disc herniation the following criteria are suggestive of MRN and should raise suspicion of a non-discogenic aetiology: History of tick bite or erythema chronicum migrans, fever or general malaise, mono-or ligoradiculopathy with absent or insignificant lumbar pain and complaints of a burning character of the radiating pain. In suspicious cases we recommend blood investigations including antibody determination against borrelia burgdorferi and CSF investigations including cell count and cytology, protein and glucose determination, nephelometry and isoelectric focusing to exclude MRN and other conditions that may mimic disc herniation.

Neurologic Manifestations of Lyme Disease, the New Great Imitator
author: Andrew Pachner
source: Review of Infectious Diseases Vol. 11, supplement 6 Sept-Oct 1989

"....A Washington D.C. business executive had developed pain in both his shoulders and arms. The pain described as aching or gnawing and sometimes electrical, was worse on the left side. A diagnosis of cervical disk disease was made, and a number of remedies appropriate for such a diagnosis were attempted. None was sucessful. Subsequent computed tomography and magnetic resonance imaging of the cervical spine revealed a small right C5 disk. The patient's discomfort was attributed to this disk despite the fact that he had bilateral symptoms that were more severe on the contralateral.......serologic studies for Lyme disease
were performed. The result was positive....A positive Lyme serology was confirmed in my lab...therapy with intravenous penicillin..was begun. The patient has done well, with resolution of his pain and no progression of his disease...."

Incidence of nervous system Borrelia burgdorferi infection in patients with lumboradicular syndrome.

Authors:Schmutzhard E, Mohsenipour I, Stanek G
Source:Eur Neurol 1993;33(2):149-51
Organization: Department of Neurology, University Hospital Innsbruck, Austria.

We investigated 103 consecutive patients primarily admitted to our Department of Neurosurgery (36 women, age: median 44, range 21-79; 67 men, age: 47, range 19-77) suffering from low back pain radiating into one or both legs. Neurological examination combined with computer tomography and lumbar myelography revealed lumbar-disc herniation in 74, vertebrostenosis in 10 and relapsed disc herniation in 9 patients. In 9 patients the diagnosis of pseudoradicular syndrome was established without definite neuroradiological morphological evidence. Two patients were diagnosed as having polyneuropathy, and 1 patient suffered from a nervus ischiadicus lesion due to a gluteal abscess. CSF of all patients was examined according to a fixed routine schedule (cells, protein, sugar, immunoglobulins, IgG index). Antibodies to Borrelia burgdorferi were found in the serum and CSF of 5.8%, and in the serum alone of 2% of patients. Intrathecally produced specific antibodies were detected in 3 patients (2.9%) with neuroradiological evidence of disc or spinal-canal disease, indicating the coexistence of previous CNS infection by B. burgdorferi with lumbar-disc herniation. None of the patients showed CSF pleocytosis; thus, in no case was acute radiculitis due to B. burgdorferi infection diagnosed.

Language: Eng Unique ID: 93223723

Meningoradiculoneuritis mimicking vertebral disc herniation. A "neurosurgical"
complication of Lyme-borreliosis.

Authors:Meier C, Reulen HJ, Huber P, Mumenthaler M
Source:Acta Neurochir (Wien) 1989;98(1-2):42-6
Organization:University Department of Neurology, Inselspital, Bern,
Switzerland.

We report on 3 patients with meningoradiculoneuritis (MRN) due to Lyme-borreliosis (LB), which presented clinically as vertebral disc herniation. In 2 cases the underlying infection was discovered only after unsuccessful neurosurgical treatment. In the differential diagnosis between MRN and disc herniation the following criteria are suggestive of MRN and should raise suspicion of a non-discogenic aetiology: History of tick bite or erythema chronicum migrans, fever or general malaise, mono- or oligoradiculopathy with absent or insignificant lumbar pain and complaints of a burning character of the radiating pain. In suspicious cases we recommend blood investigations including antibody determination against borrelia burgdorferi and CSF investigations including cell count and cytology, protein and glucose determination, nephelometry and isoelectric focusing to exclude MRN and other conditions that may mimic disc herniation.

Language: Eng Unique ID: 89300369
_________________

Meningopapillitis disclosing Lyme disease
Authors:Gerard P, Canaple S, Rosa A
Source:Rev Neurol (Paris) 1996 Jun-Jul;152(6-7):476-8
Organization:Service de Neurologie, CHU Amiens.

Abstract:
A 65 old year woman was admitted to the hospital for a low back pain, a fever and an elevated sedimentation rate. Four months later she noted a progressive visual loss first affected the right eye (visual acuity: 6/10) and then the left (visual acuity : 6/10). Fundus examination showed a bilateral papilledema.

CT Scan and MRI were normal. A lumbar puncture disclosed a lymphocytic pleocytosis (68 leukocytes/mm3), an increase in protein level (1,9 g/l) and oligoclonal bands. A serologic test for B. Burgdorferi was positive both in blood (1/64 degrees) and n cerebrospinal fluid (> or = 1/128). The patient was treated with intravenous ceftriaxone 2 g daily for 2 weeks. Fifteen days later the low back pain had disappeared and the CSF cellular count had decreased to
20 leukocytes/mm3. Seven months later, CSF was normal (2 leukocytes/mm3, protein level: 0.65 g/l.); Titer against B. Burgdorferi had improved to 1/160 in serum and 1/16 in CSF; visual acuity had improved to 8/10 on left, and was the same on right.

Language: French Unique ID: 97099678

Clinical And Electrophysiologic Findings In Chronic Neuropathy Of Lyme Disease.
Authors:Logigian EL, Steere AC
Source:Neurology 1992 Feb;42(2):303-11
Organization: Department of Neurology New England Medical Center Boston MA.

We evaluated 25 patients with Lyme disease and chronic peripheral neuropathy. All had immunologic evidence of exposure to Borrelia burgdorferi and no other identifiable cause of neuropathy. Neuropathic symptoms began a median of 8 months (range, 0 to 165) after erythema migrans and had been present for a median of 12 months (range, 2 to 168) prior to evaluation. Twelve patients (48%) had generally symmetric distal, nonpainful paresthesia, and another 12 (48%) had generally asymmetric radicular pain. One patient (4%) had
asymptomatic neuropathy. The most common physical finding was multimodal sensory loss, which was observed in 13 patients (52%); weakness and hyporeflexia were less common. Motor or sensory nerve conduction was slightly slow in 16 patients (64%). The paresthesia group more often had abnormalities on physical examination and on nerve conduction testing than did the radicular group. In 75% to 80% of patients from both groups, however, needle examination showed denervation in paraspinal and limb muscles. Among 20 patients who
underwent lumbar puncture, only one had a slight spinal fluid pleocytosis. Six months after treatment with intravenous ceftriaxone, 19 patients (76%) were clinically improved. We conclude that Lyme disease can be associated with a reversible, mild chronic axonal sensorimotor polyradiculoneuropathy or polyradiculopathy.

Language: German Unique ID: 92140650

Persistent Leg Pain (clinical conference)
Authors:Satz N, Dvorak J, Reich C, Knoblauch M
Source:Schweiz Rundsch Med Prax 1990 Jul 3;79(27-28):886-8
Organization:Medizinische Abteilung Kreisspital M:annedorf, Z:urich.

A 72 year old patient suddenly experienced severe lumbar pain irradiating into the right leg. Later on, weakness of the muscles thigh appeared. A thorough radiological investigation which showed degenerative alterations of the vertebral column did not supply an explanation. After a pathological titer against Borrelia burgdorferi was found in serum and radiculitis was detected on EMG, the diagnosis of Lyme-Borreliosis of the nervous system could be confirmed by analysis of the cerebrospinal fluid. Under intravenous antibiotic treatment with Ceftriaxone (2 to 4 g daily for three weeks) the symptoms regressed completely, and the pathological findings in the CSF regressed. The significance of some findings in CSF in relation to Borreliosis of the CNS.
Localization of Borrelia Burgdorferi in the Nervous System And Other Organs In A Nonhuman Primate Model Of Lyme Disease.
Cadavid D, O'Neill T, Schaefer H, Pachner AR.
Department of Neuroscience, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103, USA.

Lyme borreliosis is caused by infection with the spirochete Borrelia burgdorferi. Nonhuman primates inoculated with the N40 strain of B. burgdorferi develop infection of multiple tissues, including the central (CNS) and peripheral nervous system. In immunocompetent nonhuman primates, spirochetes are present in low numbers in tissues. For this reason, it has been difficult to study their localization and changes in expression of surface proteins. To further investigate this, we inoculated four immunosuppressed adult Macaca mulatta with 1 million spirochetes of the N40 strain of B. burgdorferi, and compared them with three infected immunocompetent animals and two uninfected controls. The brain, spinal cord, peripheral nerves, skeletal muscle, heart, and bladder were obtained at necropsy 4 months later. The spirochetal tissue load was first studied by polymerase chain reaction (PCR)-ELISA of the outer surface protein A (ospA) gene. Immunohistochemistry was used to study the localization and numbers of spirochetes in tissues and the expression of spirochetal proteins and to characterize the inflammatory response. Hematoxylin and eosin and trichrome stains were used to study inflammation and tissue injury. The results showed that the number of spirochetes was significantly higher in immunosuppressed animals. B. burgdorferi in the CNS localized to the leptomeninges, nerve roots, and dorsal root ganglia, but not to the parenchyma. Outside of the CNS, B. burgdorferi localized to endoneurium and to connective tissues of peripheral nerves, skeletal muscle, heart, aorta, and bladder. Although ospA, ospB, ospC, and flagellin were present at the time of inoculation, only flagellin was expressed by spirochetes in tissues 4 months later. Significant inflammation occurred only in the heart, and only immunosuppressed animals had cardiac fiber degeneration and necrosis. Plasma cells were abundant in inflammatory foci of steroid-treated animals. We concluded that B. burgdorferi has a tropism for the meninges in the CNS and for connective tissues elsewhere in the body.

Curr Treat Options Neurol. 2006 May;8(3):179-84
Ehrlichia Infection of The Central Nervous System. Hongo I, Bloch KC.
Division of Infectious Diseases, Vanderbilt University School of Medicine, A-2200 Medical Center North, 1161 21st Avenue South, Nashville, TN 37232, USA. igen.hongo@vanderbilt.edu
Ehrlichiosis in the United States is caused by three closely related bacterial species (Ehrlichia chaffeensis, Ehrlichia ewingii, and Anaplasma phagocytophilum), all transmitted through tick bite. Although there is variation with respect to geography and tick vector, the clinical manifestations are similar, and treatment of these infections is identical. Ehrlichiosis can present with a spectrum of neurologic manifestations, ranging in severity from headache to meningoencephalitis. Treatment is straightforward if the diagnosis is suspected, but antibiotic therapy should not be delayed pending laboratory confirmation. Doxycycline, the treatment of choice for adults and children with suspected ehrlichiosis, has high bioavailability and can be administered orally in most cases. Therapy is typically continued at least 3 days after the last documented fever. Although there have been no studies specifically evaluating duration or dosing of doxycycline for Ehrlichia meningoencephalitis, anecdotal reports suggest 100 mg doxycycline administered twice daily is effective, despite limited penetration into the cerebrospinal fluid. Because doxycycline interacts with CYP3A4 enzymes, there is potential for drug interactions with a number of medications. In endemic areas, documentation of coinfection with Borrelia burgdorferi, the etiologic agent of Lyme disease, may require prolonging the duration of doxycycline therapy.
PMID: 16569376 [PubMed]

1: Przegl Epidemiol. 2006;60 Suppl 1:125-30.
Diagnosis and Treatment of Lyme Arthritis [Article in Polish]
Przytuła L, Gińdzieńska-Sieśkiewicz E, Sierakowski S.
Klinika Reumatologii i Chorób Wewnetrznych AM w Białymstoku.

Lyme disease is a multisystem disease that affects primarily skin, nervous system, heart and joins. Lyme disease is caused by Borrelia burgdorferi and spread by Ixodes ticks. Arthritis is a well-known manifestation of Lyme disease (LD). Joint symptoms associated with B. burgdorferi infection range from arthralgias, to brief attacks of arthritis, to chronic erosive synovitis. Arthritis may present as oligo- or monoarthritis and typically causes intermittent attacks of oligoarticular arthritis in a few large joints, especially the knee. A small percentage of patients may develop chronic arthritis. The diagnosis is usually based on the clinical picture, exposure in an endemic area, and detection of IgG antibody against B. burgdorferi by ELISA and Western blotting. Spirochetal DNA may be detected in joint fluid by PCR. Antibiotic treatment during early stages normally prevents development of late manifestations. Joint involvement is treated successfully with a 1-month course of doxycycline or ceftriaxone. However, about 10% of Lyme arthritis patients do not respond sufficiently to antibiotic treatment. If patients have persistent arthritis despite a second course of antibiotics with negative results of PCR testing, treatment with anti-inflammatory agents or arthroscopic synovectomy is possible. In this article, we discuss clinical features, diagnosis and treatment.
PMID: 16909789 [PubMed - indexed for MEDLINE]

Scand J Infect Dis. 2007 Jul 6;:1-3 [Epub ahead of print]
Group G Streptococcus Spinal Epidural Abscess: Case Report and Review of The Literature. Saeed MU, Gottmukkula R, Kennedy DJ.
From the Department of Infectious Diseases, Saint Louis University Hospital, St. Louis, Missouri, USA.
Group G streptococci have been identified as a recently emerging pathogen. Spinal epidural abscess is an infrequent but well described infection of the central nervous system that may present with non-specific clinical symptoms and physical examination findings. Group G streptococci are a rare cause of spinal epidural abscess that should be considered in the clinical picture so that appropriate therapy can be initiated in a timely fashion.
PMID: 17852916 [PubMed - as supplied by publisher]

Neurologia. 2007 Jun 28; [Epub ahead of print]
Past Hepatitis B Virus Infection And Demyelinating Multiphasic Disease: Casual or Causal Relationship? [Article in Spanish]
Santos D, Arias-Rivas S, Dapena D, Arias M.
Servicio de Neurología. Hospital Clínico Universitario. Santiago de Compostela.
Introduction. The relationship between hepatitis B virus and hepatitis B vaccine with central nervous system demyelinating diseases is controversial. Case reports. We describe two male patients, who in their 70's developed recurrent pictures of acute demyelinating diseases. The first one had recurrent acute disseminated encephalomyelitis (diplopia, paraparesis and urinary retention) and the second one recurrent transverse myelitis (paraparesis and urinary retention).
Results. The cerebrospinal fluid test showed mononuclear pleocytosis with negative oligoclonal bands in both patients. Visual evocated potentials were normal. Magnetic resonance imaging (T2-WI and FLAIR) showed hyperintense lesions located in the brain and spinal cord in the first case and only in the spinal cord in the second. With negative antigenemia, antibodies against hepatitis B core and hepatitis B surface antigens were positive in both patients. No patient had been vaccinated for nor had suffered symptomatic hepatic disease. In the second patient, there was an almost total remission of the symptoms with periodic treatment with immunoglobulin.
Conclusions. We recommend hepatitis B virus infection investigation in all patients with central nervous system demyelinating disease. Neurología 2007;22(0):0-0.
PMID: 17602335 [PubMed - as supplied by publisher]

PMID: 17554701 [PubMed - indexed for MEDLINE]
Spinal Brucellosis: Turkish Experience Based On 452 Cases Published During The Last Century.
Turgut M, Turgut AT, Koşar U.
Department of Neurosurgery, Adnan Menderes University School of Medicine, Aydin, Turkey. drmturgut@yahoo.com
BACKGROUND: Spinal brucellosis continues to be the leading cause of morbidity from infectious disease in the infested regions of the world, particularly in the rural areas including Turkey. The purpose of this review was to present the Turkish experience by analyzing the literature on the management of spinal brucellosis during the last century.
MATERIALS AND METHOD: To establish new guidelines for the diagnosis and treatment of this disabling health problem, publications reported from Turkey in national (n = 27) and international (n = 37) journals during the last century and databases containing medical literature were analysed.
RESULTS: It was observed that the number of articles produced by Turkish authors regarding spinal brucellosis has tremendously increased throughout the study period. Although the total number of reported cases with spinal brucellosis from a total of 34 secondary or tertiary referral centers in Turkey was 452, only cases having detailed information were evaluated for further analysis according to inclusion/exclusion criteria. Despite the inherent limitations, this type of study clearly indicates that the incidence of brucellosis has not decreased in Turkey over recent years. The clinical and radiological findings of brucellosis involving the spine were mostly atypical and it was difficult to diagnose this infectious disease owing to its nonspecific and variable clinical picture. Therefore, it may easily lead to a misdiagnosis of lumbar disc herniation or other spinal infections and a high index of suspicion is required to diagnose this condition in endemic parts of the world. In addition to serological tests, CT and/or MRI techniques were found to be sensitive for diagnosis and follow-up because they provide early diagnosis of lesions involving the spine and more accurate localization of intraspinal and paraspinal infestation by means of multiplanar images. Histologically, noncaseating granulomatous tissue and chronic inflammation were characteristic features of cases of brucellosis with spinal involvement.
CONCLUSIONS: Based on this critical review of literature from Turkey, it is concluded that early diagnosis and correct management are important to prevent the harmful effects of brucellosis and its complications, and that the treatment of choice is antibiotic therapy alone in most cases of brucellosis involving the spine.

PMID: 16944052 [PubMed - indexed for MEDLINE]
Acta Med Port. 1992 Sep;5(8):419-23.
Spinal Brucellosis. 4 Years Of Experience [Article in Portuguese]
Lopes C, Oliveira J, Malcata L, Pombo V, Da Cunha S, Côrte-Real R, Meliço-Silvestre A.
Clínica de Doenças Infecciosas dos Hospitais, Universidade de Coimbra.
The Authors retrospectively studied 17 patients who have been admitted to the Infectious Diseases Clinic of Coimbra University Hospital during a four year period and whose final diagnosis was brucellar spondylitis. Clinical, epidemiological, laboratory and imaging features are analyzed, as well as those related to the therapeutic schedules and outcome. Females were more often affected (70.58%) and the mean age was 53.35 +/- 13.82 years. Lumbar spine was most frequently involved and an unusual elevated incidence of paravertebral soft tissue swelling was noticed (23.52%). Two patients were also suffering from neurobrucellosis (11.76%). The preferred therapeutic schedule was rifampin and doxycycline and surgery was performed in one patient. Finally, several comments are made regarding basically the incidence, laboratory and imaging diagnosis, therapeutic aspects and evolution of the disease. The imaging similarities and differences between tuberculous, pyogenic and brucellar spondylitis are briefly approached.

PMID: 1442190 [PubMed - indexed for MEDLINE]
Radiologic Findings of the Lumbar Spine in Patients with Rheumatoid Arthritis, and a Review of Pathologic Mechanisms.
Journal of Spinal Disorders & Techniques. 16(1):38-43, February 2003.
Kawaguchi, Yoshiharu; Matsuno, Hiroaki; Kanamori, Masahiko; Ishihara, Hirokazu; Ohmori, Kazuo; Kimura, Tomoatsu

Summary: We have analyzed the radiologic findings on the lumbar spine and the clinical symptoms in patients with rheumatoid arthritis (RA). A total of 106 patients who fulfilled the revised criteria of the American Rheumatism Association were subjected. All of the patients were asked to fill out a questionnaire about the existence of low back pain, leg pain, and leg numbness. Radiologic features of the lumbar spine, including scoliosis, spondylolisthesis, disc space narrowing, endplate erosion, osteophyte, and osteoporosis, were checked. Radiographs of the cervical spine were also taken. The clinical background of RA, such as mutilating disease or not, was assessed. Forty-two patients (40%) had the symptoms of low back pain. Abnormal radiologic findings in lumbar spine were detected in 57%. The prevalence of clinical symptoms tended to be higher in the patients with endplate erosion. Forty-two percent of the patients had both lumbar and cervical lesions. The prevalence of lumbar lesion was not high in the mutilating type of RA, except for facet erosion and severe osteoporosis. The patients with pulse steroid therapy revealed a higher prevalence of vertebral fracture. From these results, we concluded that lumbar lesions were frequently observed in patients with RA. The possibility of lumbar lesions as well as the lesions in the cervical spine and peripheral joints should be examined in patients with RA.

Continuing to update this topic here...a UK spine patient sent me a link to this 12-year-old paper.
_____________________________________

Isolated neuritis of the sciatic nerve in a case of Lyme disease
Journal The Italian Journal of Neurological Sciences

Publisher Springer Milan
ISSN 0392-0461 (Print) 1126-5442 (Online)
Issue Volume 19, Number 2 / April, 1998

Case Report

Isolated neuritis of the sciatic nerve in a case of Lyme disease

S. Avanzi1 G. Messa1, A. Marbini1, G. Pavesi1 and F. Granella1
(1) Institute of Neurology, University of Parma, Strada del Quartiere 4, 1-43100 Parma, Italy
Received: 2 December 1996 Accepted: 14 February 1998

Abstract Lyme disease is an infectious disease caused by the spirochete Borrelia burgdorferi. The course of the disease is divided into three stages, the second of which may include various types of peripheral nervous system disturbances. We report the case of a patient with persistent deficits caused by the prevalent involvement of the sciatic nerve, confirmed by electrophysiological and neuropathological findings. The most significant bioptic results were axonal degeneration and perivascular inflammation. Damage to a single peripheral nerve as the dominant clinical expression during the course of Lyme disease is an unusual finding that has been rarely described in the literature.

Key words Lyme disease - Peripheral neuropathy - Sciatic nerve - Nerve biopsy - Vasculitis

Just bumping this to the top -- especially for the new UK patient I just spoke with a few moments ago...

This is a really interesting article on reactive arthritis. For those of you that may have unusual pain syndromes (before AND/OR after surgery), please read these carefully!

http://www.drmirkin.com/joints/J103.htm

No, not everyone actually has ankylosing spondylitis -- but the overall context of all these articles in this topic illuminate the gaping hole in spinal diagnostics.

http://adrsupport.org/groupee_common...icon_frown.gif

This is most interesting- I need to read more about this - especially since over the years I have had "odd" neurological and pain events - when I did not have a herniated disk and little to no DDD. Now - I do have a herniated disk that is abutting (well- probably compressing to some degree the cord - will know more next week).

I understand stress plays a big role with these "pathogens" to increase the inflammation -my body has "fallen" apart after several major stressful events in my life. I dont want to bore you with my story - but - if gives you an idea why the drs are a bit puzzled:

pain/numbness in my left hand back in 1989 in college (not that this should be stressful) - to the point where I could not use it for a full semester(I am left handed - a problem). Then out of the blue - it cleared up - and it was really challenged in post grad school (which was stressful) - but no problems -thankfully.

In 2002 - just few years after my Mom died and some other very stressful issues at the time- I had 5 mos of a horrible body break down episode - both hands - very numb, severe neck and shoulder pain, facial numbness, and lower back pain, sciatica - with numbness into my left leg - and my left toe would go numb (which I have having again now). All MRIs and emgs wre normal (except for a problem with the left tricep which could explain the left hand problem in 1989. Drs - thought it was carpel tunnel and stress. Finally- the body rebounded - (I think I was on alot of antibiotics at the end of that year due to recurring sinus infection). Felt great - and went back on to life with occasional numbness in the hands - which a good massage would take care of for the shoulders. Many sinus infections and alot of antibiotcis.

Ffast forward to 2005. Just a week after losing my Dad - (again another major stress event) - the body fell apart. Numbness in the face all over the body (including that left big toe....again), chest pain, and pain - in many places, that left toe went numb too, etc. I regret that they did not do an MRI on my neck (which I wanted) but they were worried it was either my heart (I had chest pains) or a brain tumor - MRI on brain was clear - so were heart exams. Body rebounded felt great. Would have neck pain and stiffness - treated by the chiro- and

fast forward to Aug 2007. Alot of stress going on - at the office, and in personal life. Body breakdown again. This time severe numbness - everywhere - mostly on the left side - gait issues, leg pain (left toe would go numb) also the soles of my feet, pain like I have never suffered before, could not use neck very well, facial numbness, jaw pain, etc. MRI on the neck - showed DDD at C5-6 - protruding and abutting the cord right central - mild stenosis. (Some drs did not feel there was any abuttment). Lumbar - small tear at L4-5, throastic - normal. Brain MRI normal. EMG/nerve conduction tests- normal. I went full guns for testing this time! Finally - after 4 mos of intense pain and numbness (mostly on the left side), horrible traction which made the pain worse, PT, accupuncture, and alot of celebrex - the body rebounded again. One dr thought I had fibro....I did not have the range of motion on my neck I used to have - but my body was "calm" and not on high alert/traffic mode. I also was back on antibiotics late last fall....Not sure if that is the link to rebounding...

I know that I now have a spine issue - that if not treated will get worse and lead to more spine damage -which I do not want to get to. But - I went to some of our "top drs" here in Florida last fall searching for answers - and they were mystified at my symptoms. No surgery was recommended last fall. I dont believe I have MS - the MRIs were clean (while I knowthat is not the complete answer for diagnosis - but a good indication from what I have been told). But - it does beg the question - if I had no stenosis in 2002 and 2005 - then why did I have those strange numbness/pain episodes? I was just told last week by a local neurologist that I have an unexplained neurological syndrome. That is not good enough answer! So - perhaps I have 2 issues going on - one with the spine -and this other type of immune issue which may have led to the spine deterioration....

And again - a few stressful episodes of late - and a minor jerk of the neck (I forgot all about my structural instability - I was feeling that great) - and bam - the wave of pain, numbness - and yes - the big toe on the left foot are all back. Back on celebrex, PT, and new cervical MRI....I suspect that there has been a slight deterioraton in the disk....

Off to get a bunch of blood tests I think is the next approach while poundering what to do to correct my current situation. I pray I can hold off on surgery - as I know they are developing some wonderful new technologies but will have to see..

Sorry to bore you with all of this! But reading about those immune issues - I had to share.

Twix, this is not boring at all. On the contrary -- it's validation. This year, about half the patients I've spoken to on the phone recall a time in their lives when they had some other serious health issue that MAY have started the degenerative process in the spine. Of these serious events, the ones that are most often mentioned are meningitis and Lyme disease.

Plain old "vanilla" blood tests usually reveal "boring" results. You may want to consider getting screened for the mycoplasmas and Borrelia, though most doctors will be resistant to such requests. Why they are is a mystery, given the ample clinical evidence presented internationally (some in this topic).

Thank you! It is interesting the correlation between some "triggering event" like stress or another illness and the degeneration.....

Lisa

Lisa, well said. Many spine patients do not have a clear picture of the disease factors causing their pain. And still others don't long after surgery -- as this recent abstract illustrates. Here, we see no less than THREE pathological conditions contributing to the poor patient's problem (IMHO, all bacterial; some are gram negative bugs).

This is sad to read, but may be progress in terms of focusing on the pathology of disease. Can you find the three!?

Once again, the US medical system is being outdone by countries who focus on the cause of disease. Most of these "diagnostic" studies are published from overseas. It really gets me mad!
_______________________

Delayed spinal infection after laminectomy in a patient with rheumatoid arthritis interruptedly exposed to anti-tumor necrosis factor alpha agents.

Mori S, Tomita Y, Horikawa T, Cho I, Sugimoto M. --- Clinical Research Center for Rheumatic Disease and Department of Rheumatology, Kumamoto Saishunsou National Hospital, 2659 Suya, Kohshi, 861-1196, Japan, moris (at) saisyunsou1.hosp.go.jp.

We report a case of spondylodiscitis caused by Staphylococcus aureus 8 months after laminectomy of the lumbar spine, occurring in a rheumatoid arthritis (RA) patient interruptedly treated with anti-tumor necrosis alpha (TNFalpha) agents. The patient had suffered from seropositive RA for 2 years. An intravenous infusion (200 mg) of infliximab, a chimeric antibody against human TNFalpha, was introduced; however, due to Pneumocystis jiroveci pneumonia, this therapy was withdrawn. Four months later, the patient underwent an L3-L4 and L4-L5 laminectomy for spinal stenosis.

Two months after surgery, we started treatment with 25 mg of etanercept, a soluble humanized TNF receptor dimer, subcutaneously twice a week. At that time, wound healing was satisfactory and no evidence of infection was obtained. Eight months after surgery, septic spondylodiscitis of the lumbar spine occurred.

To the best of our knowledge, this is the first case in the literature to show a delayed type of postoperative infection as a complication of non-instrumented orthopedic surgical procedures. Despite interruption of anti-TNFalpha therapy before surgery, patients may remain at risk of developing postoperative infections.

Interesting - thanks for sharing that info.

Ok - here is what I see as the 3:

Pneumocystis jiroveci pneumonia
Staphylococcus aureus
rheumatoid arthritis

There were a few other "fancy" words that may also be contributing factors!

Rich: just my $0.02 regarding minutiae....Staph is a gram positive bacteria, Pneumoncystis is actually an opportunistic fungus. BUT, many of the other bugs mentioned in the other articles are indeed gram negative bacteria. Gram neg bacteria can be difficult to treat, as many have become resistant to common antibiotics, because of overuse of antibiotics in inappropriate situations (eg. the common cold....it's viral, no point to antibiotics, but some people demand it, and some doctors seem to give in...)
Treating a discitis would generally seem to require long term antibiotics, as the blood supply into the disc itself is not fabulous (I'm speaking from my veterinary experience here...). I've got an appt coming up regarding my shoulder (crikey, it never ends!) and am planning on asking my orthopod about such bacterial theories surrounding DDD, sciatica, blah blah blah. We shall see what she thinks. She is the "medical" orthopedist in the practice I see, vs the "surgical" orthopedist, who is her partner. It's a nice combination of folks, eh?

Susan/ERvet

Richard,
Please don't take offense...I think many of us are convinced by the articles and research you have done. I think at this point, what would be most helpful for the community is some research and a list of U.S. physicians for U.S. patients who will do testing for mycoplasmas because I live in one of the bigger metro areas and I have not been able to find a doctor that will even write a prescription to send my blood off for testing for mycoplasmas. It is so frustrating as I am facing a life-threatening revision surgery now and my spine is getting worse and worse as the days go by. Please a list of doctors that will write or do the testing even if it is really small. Names, locations and contact information would be so appreciated. Again, please don't take offense and know I, for one, really do appreciate the time you have put into your research for us.
Thanks,

Hey Linda,

When your docs turned down your request to have mycoplasma tests done what did they say ? I'm trying to decide which of my numerous physicians to discuss this with right now and plan on having tests done soon. I would be interested in the excuse any MD can give for a simple blood test that could change the outcome of the chronic pain we have.. and need to develop my response to them should my docs try to stop me ....

Right now I think three of my medical team would be more than happy to write for the tests.. but I may be sadly mistaken once I give it a go...

I'll let you know how it turns out !!

I'm awaiting results of a whole battery of new tests that we just concluded.. once I get those , if there is no clear cut cause of my continued pain I'm gonna hit the trail with my mycoplasm requests... http://adrsupport.org/groupee_common.../icon_razz.gif

Effect of MALP-2, a Lipopeptide from Mycoplasma fermentans,on Bone Resorption In Vitro

GRAZYNA PIEC,1† JELENA MIRKOVITCH,1 SILVIA PALACIO,1 PETER F. MU¨HLRADT,2
AND ROLF FELIX1*

Department of Clinical Research, Bone Biology, University of Bern, CH-3010 Bern, Switzerland,1 and Immunobiology Research Group, Gesellschaft fu¨r Biotechnologische Forschung,D-38124-Braunschweig, Germany2
Received 8 June 1999/Returned for modification 7 July 1999/Accepted 9 September 1999

Mycoplasmas may be associated with rheumatoid arthritis in various animal hosts. In humans, mycoplasma arthritis has been recorded in association with hypogammaglobulinemia.

Mycoplasma fermentans is one mycoplasma species considered to be involved in causing arthritis. To clarify which mycoplasmal compounds contribute to the inflammatory, bone-destructive processes in arthritis, we used a well-defined lipopeptide, 2-kDa macrophage-activating lipopeptide (MALP-2) from M. fermentans, as an example of a class of macrophageactivating compounds ubiquitous in mycoplasmas, to study its effects on bone resorption. MALP-2 stimulated osteoclast-mediated bone resorption in murine calvaria cultures, with a maximal effect at around 2 nM. Antiinflammatory drugs inhibited MALP-2-mediated bone resorption by about 30%. This finding suggests that MALP-2 stimulates bone resorption partially by stimulating the formation of prostaglandins. Since interleukin-6 (IL-6) stimulates bone resorption, we investigated IL-6 production in cultured calvaria. MALP-2 stimulated the liberation of IL-6, while no tumor necrosis factor was detectable.

Additionally, MALP-2 stimulated low levels of NO in calvaria cultures, an effect which was strongly increased in the presence of gamma interferon, causing an inhibition of bone resorption. MALP-2 stimulated the bone-resorbing activity of osteoclasts isolated from long bones of newborn rats and cultured on dentine slices without affecting their number. In bone marrow cultures, MALP-2 inhibited the formation of osteoclasts. It appears that MALP-2 has two opposing effects: it increases the bone resorption in bone tissue by stimulation of mature osteoclasts but inhibits the formation of new ones.

Full article: http://iai.asm.org/cgi/reprint/67/12/6281.pdf

A recently published book addresses many of these unanswered questions – it’s called "Cure Unknown," written by Pamela Weintraub. Though it focuses on Lyme disease, it also explains:

- Why accurate blood tests for Lyme (and co-infections like mycoplasma) are unavailable;
- Why many Lyme treatment doctors have been targeted and literally run out of town (addressing Linda’s question);
- Why there are so few doctors practicing medicine that can help the hundreds of thousands of people with these kinds of chronic, degenerative infections;
- Why so many people continue to be undiagnosed and untreated.

There is so much information packed into this book, yet written in such a concise manner, you’ll start and finish all 354 pages in a week! I highly recommend it for a long list of reasons.

See the author’s site at http://www.cureunknown.com/ Also note the many links and descriptions on the bottom of that page.

More abstracts: mycobacteria/plasmas and spine
 

J Lab Clin Med. 2005 Aug;146(2):55-63.

Mycoplasma pneumoniae and central nervous system complications: a review.Guleria R, Nisar N, Chawla TC, Biswas NR.

Department of Medicine, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.

Mycoplasma pneumoniae is a common cause of community-acquired pneumonia. Little is known about the extrapulmonary manifestations of this organism. Numerous central nervous system (CNS) manifestations have been described with M. pneumoniae. CNS involvement is probably the most common site of involvement in addition to the respiratory system.

Up to 7% of patients hospitalized with M. pneumoniae may have CNS symptoms. Common CNS presentations include encephalitis, aseptic meningitis, polyradiculitis, cerebellar ataxia, and myelitis. The mechanism behind these CNS manifestations remains unclear. Direct invasion, neurotoxin production, or an immune-mediated mechanism has been proposed. Newer diagnostic techniques for the direct detection of the antigen and the microorganism are proving useful for the detection of extrapulmonary disease. This review comprehensively reviews the CNS complications that have been reported with M. pneumoniae.

PMID: 16099235 [PubMed - indexed for MEDLINE]

Conn Med. 2002 Jul;66(7):387-9.

Atypical mycobacterial osteomyelitis in a non-AIDS patient.

Niazi S, Batra V, Zangrilli JG.
Department of Medicine, Division on Critical Care, Pulmonary, Allergic, and Immunologic Diseases, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.

Disseminated Mycobacterium avium intercellulare (MAI) infection is rare in non-AIDS patients. We report a 60-year-old woman with chronic lung disease who developed vertebral osteomyelitis due to MAI. She was treated successfully with combined therapy consisting of rifampin, ethambutol, and clarithromycin.

Harrison, does this mean that the other countries are taking this seriously, and that their citizens are getting proper treatment, taking this into consideration?

Over this long trek to get treatment, I have often thought about the logistics of moving to Germany or some other country that seems to be miles ahead in terms of medical treatment.

Has anyone tried to do this?

US Regulatory Institutions are Understaffed & Misdirected
 

And the article below is evidence of this unfortunate fact. However, though this is a shocking admission by the CDC, it does represent progress, albeit a few decades late. I believe the outfall from statements like this will have some rather dramatic repercussions -- at least this is my hope.

Just to clarify, these mycobacterial bugs in question are intracellular. They are so small, and so sophisticated, that they literally tunnel into blood cells and live (and love!) there. Their insidious ways make them hard to detect, but also make them tougher for the immune system (and diagnostic technology) to identify. As they "live and love," they compromise the immune system, or disease tissue that tends to be less vascular (e.g., damaged tissue, cartilage, ligaments, joints).

As a sidenote, this spine patient community has a significant number of patients from Michigan, Minnesota and other states with a disproportionate number of tick-reported diseases. Frankly, I am very surprised that the CDC would release this report based on "strong presumptive evidence," as they have maintained a decidedly cautious position on TBDs (tick-borne diseases).

Note: If this is the first time you read this lengthy topic, please start from the beginning and carefully read the whole thing. Go to Thread Tools > Show Printable Version to print the topic.
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CDC Weeklyhttp://www.cdc.gov/mmwr/images/spacer.gifhttp://www.cdc.gov/mmwr/images/spacer.gifOctober 24, 2008 / 57(42);1145-1148

Anaplasma phagocytophilum Transmitted Through Blood Transfusion --- Minnesota, 2007

Anaplasma phagocytophilum, a gram-negative, obligate intracellular bacterium of neutrophils, causes human anaplasmosis, a tickborne rickettsial disease formerly known as human granulocytic ehrlichiosis (1). In November 2007, the Minnesota Department of Health was contacted about A. phagocytophilum infection in a hospitalized Minnesota resident who had recently undergone multiple blood transfusions. Subsequent investigation indicated the infection likely was acquired through a transfusion of red blood cells. This report describes the patient's clinical history and the epidemiologic and laboratory investigations. Although a previous case of transfusion-transmitted anaplasmosis was reported (2), this is the first published report in which transfusion transmission of A. phagocytophilum was confirmed by testing of the recipient and a donor.

Although polymerase chain reaction (PCR) assays provided reliable evidence of transmission in this case, no cost-effective method for screening blood donors for A. phagocytophilum exists. Screening donors for a recent history of tick bite is not likely to be sensitive or specific because such exposures are common and often not recalled by persons with anaplasmosis (3). Physicians should consider the possibility of anaplasmosis in patients who develop posttransfusion acute thrombocytopenia, especially if accompanied by fever, and should report suspected transfusion-associated cases to health authorities.

Case Report

The patient, a male aged 68 years with a medical history of chronic renal insufficiency, psoriatic arthritis, ankylosing spondylitis, and corticosteroid therapy, underwent elective knee arthroplasty and synovectomy on October 12, 2007. Three weeks before his hospitalization, the patient had traveled to an area where blacklegged ticks (Ixodes spp.) were endemic, but he did not spend time outdoors and had no known tick bites. Several hours after the procedure, the patient developed bleeding at the surgical site and associated coagulopathy, indicated by elevated international normalized ratio (INR) and partial thromboplastin time (PTT) and by decreased fibrinogen and platelet counts.

The extensive hemorrhage required two surgical evacuations of hematoma from the knee, popliteal artery embolization, and transfusion of multiple blood components. During October 12--21, the patient received 34 units of nonleukoreduced red blood cells (RBC), 4 units of leukocyte-reduced apheresis platelets, 14 units of fresh frozen plasma (FFP), and 7 units of cryoprecipitate. The components came from 59 individual blood donors; all donations were collected by Memorial Blood Centers (St. Paul, Minnesota). On October 19, the patient developed sepsis and multisystem failure. He was treated empirically with antibiotics (cefazolin, piperacillin/tazobactam, vancomycin, and levofloxacin). Blood cultures were negative on October 18, 20, and 31, and urine cultures were negative on October 19 and 25.

On October 31, the patient was found to have worsening thrombocytopenia. His platelet count declined from 178,000/mm3 on October 31 to 54,000/mm3 on November 5. On November 1, he developed hypotension and fever attributed to urinary tract infection. He was treated with levofloxacin and sulfamethoxazole/trimethoprim and was afebrile by November 3. On November 3, 22 days after admission, a peripheral blood smear from the patient demonstrated inclusions compatible with A. phagocytophilum morulae in neutrophils.

Retrospective review of an October 15 blood smear from the patient showed no evidence of intracellular morulae. Whole blood specimens from November 3--5 were positive for A. phagocytophilum DNA by PCR assays conducted at the Mayo Medical Laboratory, Minnesota Department of Health, and CDC. Serum from November 3--5 was tested at CDC and found to be weakly positive by indirect immunofluorescence assay (IFA) (titer 1:64) for immunoglobulin G (IgG) antibodies to A. phagocytophilum. Doxycycline treatment was begun on November 5. The patient's platelet count steadily improved and returned to a normal level of 163,000/mm3 on November 10. Pretransfusion blood samples and serum from the patient's convalescence period were not available for further testing. The patient improved clinically and was transferred to a rehabilitation unit on November 13. After rehabilitation, the patient was discharged on December 3, 2007.

Epidemiologic and Laboratory Investigation

In early November, Memorial Blood Centers began an investigation to identify whether any of the 59 blood donors associated with the 34 RBC, 4 platelet, 14 FFP, and 7 cryoprecipitate units had evidence of A. phagocytophilum infection. Paired whole blood specimens from the original donations had been retained from all 34 RBC donors and eight of 14 FFP donors and were available for PCR testing. During November 2007--March 2008, Memorial Blood Centers also collected postdonation blood samples for serologic testing and information on recent illness history and potential tick exposure from 53 of the 59 donors. In addition, plasma components from two FFP donors and two cryoprecipitate donors who donated again during December 2007--January 2008 were retained for serologic testing. The whole blood specimens retained from initial donation were tested by PCR, followed by sequencing of the PCR amplicons at CDC. Serum and plasma specimens were tested by IFA for IgG antibodies to A. phagocytophilum.

PCR and IFA tests on samples from a female RBC donor aged 64 years were positive for A. phagocytophilum infection (Table). A. phagocytophilum DNA was found in an RBC product donated by this woman on September 28 and transfused to the patient on October 13. IgG IFA titers to A. phagocytophilum were 1:512 and 1:256, respectively, in subsequent sera collected November 17 and December 18. The donor did not recall being bitten by a tick, but had spent time in wooded areas of northeast Minnesota where anaplasmosis is endemic within the month before her donation. She reported no history of fever during the month before or after her donation. No other patients received blood components from her donation.

No whole blood samples from other tested donors were PCR positive for A. phagocytophilum. Sera from two RBC donors were weakly positive by IFA (titer 1:64), but their respective whole blood samples from the original transfused units were PCR negative. These two donors did not live on wooded property and reported they had no tick exposure or illness during the 2 months before donation. Available postdonation serum samples from other donors were negative for A. phagocytophilum by IFA (titer <1:32).

Reported by:

M Kemperman, MPH, D Neitzel, MS, Minnesota Dept of Health; K Jensen, J Gorlin, MD, E Perry, MD, MemorialBloodCenters, Saint Paul; T Myers, MD, T Miley, MD, ParkNicolletMethodistHospital, Saint Louis Park, Minnesota. J McQuiston, DVM, ME Eremeeva, MD, PhD, ScD, W Nicholson, PhD, J Singleton, National Center for Zoonotic, Vector-Borne, and Enteric Diseases; J Adjemian, PhD, EIS Officer, CDC.

Editorial Note:

A. phagocytophilum, the causative agent of anaplasmosis, typically is transmitted to humans by infected Ixodes spp. ticks. In wooded areas of the United States, A. phagocytophilum is transmitted by the blacklegged tick (Ixodes scapularis) in the Northeast and upper Midwest and by the western blacklegged tick(Ixodes pacificus) on the West Coast. In infected persons who are symptomatic, illness onset occurs 5--21 days after a bite from an infected tick. Initial presentation typically includes sudden onset of fever, headache, malaise, and myalgia, often accompanied by thrombocytopenia, leukopenia, and elevated liver transaminases. Severe infections can include prolonged fever, shock, confusion, seizures, pneumonitis, renal failure, hemorrhages, opportunistic infections, and death (1). Anaplasmosis and other tickborne diseases, including human ehrlichiosis, Rocky Mountain spotted fever, and babesiosis, caused by Ehrlichia chaffeensis or Ehrlichia ewingii, Rickettsia rickettsii, and Babesia spp., respectively, represent a potential risk for transmission via blood transfusion in the United States (2--6).

The case described in this report provides strong presumptive evidence that A. phagocytophilum infection in this patient was acquired through blood transfusion. Pretransfusion blood samples and convalescent serum from the transfusion recipient were not available for PCR or serologic testing to demonstrate conclusively that the patient was free of A. phagocytophilum infection before his hospitalization on October 12.

However, the patient reported limited outdoor exposure that might include potential tick contact during the 3 weeks before hospitalization, and a blood smear collected 3 days after hospital admission showed no evidence of intracellular morulae. The timing of events and the expected incubation period for anaplasmosis (5--21 days) suggest that the patient's exposure most likely occurred during hospitalization. A. phagocytophilum DNA was found in a retained sample from the implicated RBC product that was transfused to the recipient, providing strong evidence that this was the likely route of disease transmission to the blood transfusion recipient. Some blood transfusion recipients (i.e., those who are immune compromised) likely are at increased risk for developing severe complications associated with tickborne diseases.

Both A. phagocytophilum and E. chaffeensis can survive in refrigerated RBCs, and possible transfusion-transmission cases have been reported for anaplasmosis (Minnesota Department of Health, unpublished data, 1998) (2,3,5,6). However, because of the rarity of transfusion-associated cases, concerns regarding the specificity of available tests, (none of which are approved by the Food and Drug Administration), and the economic costs associated with implementation, the U.S. blood supply is not routinely screened for tickborne disease using laboratory methods (7).

As a method to reduce the risk for certain pathogens in blood products, blood banks often defer donations if the potential donor is ill at the time of donation. However, persons infected with tickborne disease might experience mild illness or have asymptomatic infection, as was the case with the implicated donor in this report (1,3). Screening donors for a recent history of tick bite is unlikely to identify high-risk donors, because this type of exposure frequently is not recalled by persons with anaplasmosis (3). In this case, the implicated donor did not recall a tick bite, although she did report contact with wooded habitat in an anaplasmosis-endemic area. Nearly 75% of the other blood donors in this investigation reported similar outdoor contact, making the screening of blood donors for tick-related exposures poorly predictive for possible infection. Because Ehrlichia and Anaplasma are associated with white blood cells, leukoreduction techniques would be expected to reduce the risk for Ehrlichia and Anaplasma transfusion-transmission through RBC components (5,8). In the absence of effective screening tools to identify donors or products infected with the organisms, physicians should weigh the benefits of using leukoreduced blood components, to potentially reduce the risk for Ehrlichia and Anaplasma transmissions.

Although transfusion-associated transmission of A. phagocytophilum appears to be rare, reported incidences of anaplasmosis and other tickborne diseases are increasing in the United States (1). A record 322 cases of anaplasmosis were reported in Minnesota in 2007 (6.2 cases per 100,000 population) (9). As the incidence of tickborne diseases increases, physician vigilance for possible transmission of these agents via transfusions also should increase. In addition to other more common etiologies, physicians should suspect possible rickettsial infection if transfusion recipients develop acute thrombocytopenia posttransfusion, especially if accompanied by fever. Such signs should lead to rapid assessment for rickettsial agents and empiric treatment with doxycycline (1). Although insensitive, blood smear can provide timely support for a presumptive diagnosis of anaplasmosis, followed by IFA or PCR to confirm the diagnosis (1). Similarly, babesiosis should be suspected in patients who develop hemolytic anemia and fever posttransfusion (3,4).

Anaplasmosis and ehrliciosis are nationally notifiable diseases. Suspected cases of tickborne rickettsial diseases should be reported promptly to the state or local health department, and suspected transfusion-associated transmission should be reported to the supplying blood center and appropriate public health authorities.

Acknowledgments

The findings in this report are based, in part, on contributions by G Liu, PhD, and K Smith, DVM, PhD, Minnesota Dept of Health; M Kuehnert, MD, National Center for Preparedness, Detection, and Control of Infectious Diseases, and S Holzbauer, DVM, Coordinating Office for Terrorism Preparedness and Emergency Response, CDC.


References

1. CDC. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichiosis, and anaplasmosis---United States. MMWR 2006;55 No.RR-4).
2. Eastlund T, Persing D, Mathiesen D, et al. Human granulocytic ehrlichiosis after red cell transfusion. Transfusion 1999;39:117S.
3. McQuiston JH, Childs JE, Chamberland ME, Tabor E. Transmission of tickborne agents of disease by blood transfusion: a review of known and potential risks in the United States. Transfusion 2000;40:274--84.
4. Herwaldt BL, Neitzel DF, Gorlin JB, et al. Transmission of Babesia microti in Minnesota through four blood donations from the same donor over a 6-month period. Transfusion 2002;42:1154--8.
5. McKechnie DB, Slater KS, Childs JE, Massung RF, Paddock CD. Survial of Ehrlichia chaffeensis in refrigerated, ADSOL-treated RBCs. Transfusion 2000;40:1041--7.
6. Kalantarpour F, Chowdhury I, Wormser GP, Aguero-Rosenfeld ME. Survival of the human granulocytic ehrlichiosis agent under refrigeration conditions. J Clin Microbiol 2000;38:2398--9.
7. AuBuchon JP. Meeting transfusion safety expectations. Ann Intern Med 2005;143:537--8.
8. Mettille FC, Salata KF, Belanger KJ, Casleton BG, Kelly DJ. Reducing the risk of transfusion-transmitted rickettsial disease by WBC filtration, using Orientia tsutsugamushi in a model system. Transfusion 2000;40:290--6.
9. CDC. Final 2007 reports of nationally notifiable infectious diseases. MMWR 2008;57:901, 903--13.

Article at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5742a1.htm

The microscope...a forgotten tool makes a comeback!
 

Naturally, the NIH does not fund this kind of useful research. I hope this changes!
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Grading of degenerative disk disease and functional impairment: imaging versus patho-anatomical findings.

Quint U, Wilke HJ.
Orthopaedic and Trauma Center, Spine Unit, St Marien-Hospital Hamm, Nassauerstr. 13-19, 59065, Hamm, Germany, ulrich.quint@marienhospital-hamm.de.

Degenerative instability affecting the functional spinal unit is discussed as a cause of symptoms. The value of imaging signs for assessing the resulting functional impairment is still unclear. To determine the relationship between slight degrees of degeneration and function, we performed a biomechanical study with 18 multisegmental (L2-S2) human lumbar cadaveric specimens. The multidirectional spinal deformation was measured during the continuous application of pure moments of flexion/extension, bilateral bending and rotation in a spine tester.

The three flexibility parameters neutral zone, range of motion and neutral zone ratio were evaluated. Different grading systems were used: (1) antero-posterior and lateral radiographs (degenerative disk disease) (2) oblique radiographs (facet joint degeneration) (3) macroscopic and (4) microscopic evaluation. The most reliable correlation was between the grading of microscopic findings and the flexibility parameters; the imaging evaluation was not as informative.

Interesting TV Special Tonight on Lyme – New England Viewers
 

One of the things I try to do as an advocate is to connect with patients, medical researchers and experts in the field(s) of degenerative disease. A few months ago, I personally met a woman who is a patient, researcher, expert, writer…and more.

Pam Weintraub is the author of Cure Unknown, an up-to-date book on Lyme disease (mentioned in my 8-19-08 post). Her amazing body of work will be reviewed on Channel 5 Boston tonight on the Chronicle magazine at 7:30 PM. I believe she is a real “mover and shaker” and agent of change; which explains in part why this enlightening special on Lyme disease(s) will be aired. If you are in New England, do tune in to watch what may be the media’s first in-depth look at this terrible epidemic.

Root Causes of Certain Cervical Spine Disorders
 

While doing some research, I found the following page was expired...but I found an archived (cached) page. There is some useful diagnostic information herein. It's also (er, was) one of the few places on the Internet where you will find a doctor admitting that Lyme disease (et al pathogens) can directly cause a cervical spine disorder! Does anyone else find it significant that a rheumatologist is admitting this?!

Some of the formatting was funky, so I'll attach a PDF of this content too. I am guessing this was written in 2003. It was published the GWU web site in 2004 and removed in 2005.
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Management of Neck Pain: A Primary Care Approach
DAVID G. BORENSTEIN, George Washington University

Among the many disorders that cause neck pain, biomechanical stress is the most common. Nonoperative therapies offer relief in most patients within three months. Those with chronic or radicular pain require additional evaluation and multiple therapies for effective relief. Systemic illness and spinal compression require prompt intervention to prevent serious complications.

Dr. Borenstein is Clinical Professor of Medicine, The George Washington University Medical Center, Washington, D.C.

A common complaint evaluated by primary care physicians, neck pain affects about 10% of the population of the United States every year. Although cervical spine disorders have a diverse etiology (Table 1), biomechanical disorders that occur secondary to overuse, trauma, or deformity are the most common cause of neck pain. Typically, these disorders are characterized by correlating exacerbation or alleviation of symptoms with certain physical activities.










Most biomechanical disorders of the cervical spine have a natural history of improvement. More than 50% of patients will have decreased pain in two to four weeks; 80% will be asymptomatic in two to three months, and most will improve without requiring diagnostic x-rays or laboratory tests. Such studies are reserved for patients with histories or physical findings that suggest cord or nerve root compression or systemic illness. These disorders are uncommon causes of neck pain but require thorough evaluation and immediate treatment.

Spinal Compression

Cervical myelopathy occurs secondary to compression of the spinal cord or nerve roots in the spinal canal. Only one third of patients complain of neck pain. Although cervical myelopathy is rare, one form, spondylitic myelopathy, is the most common cause of spinal cord dysfunction in patients older than age 55. The location, duration, and size of lesions influence the severity and distribution of symptoms. Compression usually results from a combination of osteophyte growth and degenerative disk disease. Symptoms may involve all limbs and include difficulty in walking and urinary or fecal incontinence.

The most frequent presentation is arm and leg dysfunction. Older patients may describe leg stiffness, foot shuffling, and a fear of falling. Common findings include weakness of the appendages, spasticity, fasciculations, and hyperreflexia, clonus, and Babinski's reflex in the lower extremities.

Many imaging techniques can be used for diagnosis. Plain x-rays reveal advanced degenerative disease with narrowed disk spaces, facet joint sclerosis, and osteophytes; computed tomographic (CT) myelograms can distinguish osteophytes from protruding disks, and magnetic resonance imaging (MRI) can detect the extent of spinal cord compression (Figure 1). Plain x-rays are the most convenient test to use but do not reveal nerve compression. CT myelograms are used presurgically to identify bone, disks, and canal space.

Cervical spondylitic myelopathy has a gradual progression; severe myelopathy seldom develops in patients who do not exhibit signs at presentation. Although some patients improve with conservative therapy, those with progressive myelopathy require surgery to prevent further cord compression, vascular compromise, and myelomalacia. Obviously, surgery is most effective when performed before severe neurologic deficits develop.

Systemic Illness

Positive responses to one or more questions about systemic symptoms accompanying neck pain necessitate additional evaluations.

Tumors. Pain with fever or weight loss suggests the presence of a tumor or infection. Pain that is greatest at night or with recumbency is associated with infiltration of the spinal cord and tumors of the vertebral column. Patients with neurologic signs should undergo MRI of the central nervous system. A spinal cord tumor appears as a single mass; in contrast, demyelinating disease produces multiple lesions.

Patients who have nocturnal pain without neurologic signs may have a bone tumor. Benign tumors tend to affect the posterior elements of vertebral bodies. If plain x-rays are unable to detect alterations in vertebral architecture, bone scans are sensitive alternatives for revealing lesions over the entire axial skeleton. CT scans can locate suspected tumors not detected with other imaging methods. All tumors should be biopsied and treated; surgical excision is preferred for accessible tumors.

Spondyloarthropathies and Other Rheumatic Diseases produce early-morning neck stiffness that lasts for hours. Patients usually have extensive disease in other articular locations. Flexion-extension views reveal the presence of C1-C2 subluxation. Women with spondyloarthropathy may have neck disease without low back pain. A Ferguson view of the pelvis is a useful test to detect sacroiliitis if neck x-rays do not reveal syndesmophytes or squaring of vertebral bodies. Patients with polyarthritis can be identified with bone scans and erythrocyte sedimentation rate (ESR) measurement; treatment requires maximum doses of nonsterodial anti-inflammatory drugs (NSAIDs). Joint instability warrants bracing or surgical fusion if neural dysfunction is documented.

Polymyalgia rheumatica occurs predominantly in women older than 60 years. In such patients, pain is often localized to the proximal muscles of the shoulders and thighs. An elevated ESR is the most common laboratory finding. Treatment with daily low-dose corticosteroids is often effective.

Visceral Source of Pain. Patients may have neck pain secondary to cardiovascular, gastrointestinal, or neurologic disorders. Vascular lesions in the neck (carotodynia) can cause localized pain. Esophageal disorders should be considered if neck pain occurs when patients are eating; posterior esophageal lesions may affect the prevertebral space to produce pain. An esophagram can identify abnormalities of peristalsis or structure; endoscopy may detect intrinsic esophageal lesions. Neurologic disorders may involve cranial nerve lesions that cause cervical spine and facial pain.

Nonoperative Therapies
Patients without systemic disorders should be treated with nonoperative therapy for three to six weeks. Among the available therapies, NSAIDs can decrease the pain and inflammation that is associated with localized disease. Although agents with rapid onset and good analgesic effect are preferred, those with sustained-release properties may offer better relief with fewer tablets per day. Muscle relaxants do not affect peripheral muscles but do offer additional relief for patients with increased paracervical muscle contractions; physicians should in- form patients of these drugs' potential sedative effect. Temperature modalities may also be useful. Ice massage for 10 minutes provides additional analgesia in some cases, whereas application of heat may decrease muscle tightness and improve range of motion in others. Injection of a mixture of 1 mL of semisoluble corticosteroid and 3 to 5 mL of lidocaine into the area of maximum tenderness in the paravertebral musculature or trapezii may be another way to decrease pain.

Patients should understand that the eventual goal of therapy is a return to normal neck motion. This may be difficult to accomplish. Patients often prefer to wear a cervical collar and limit motion. Short-term immobilization is useful--particularly at night, when movement during sleep causes pain. A soft collar that supports but does not extend the neck is an appropriate treatment; however, its use should decrease as neck pain diminishes. The use of a collar with cervical hyperextension should be severely limited; in contrast, patients with disk herniations will require full-time collar immobilization to limit radicular pain for longer periods.

Most patients, including those with cervical radiculopathy, improve and return to normal activity within two months. Patients who are still symptomatic after six weeks of nonoperative treatment are separated into two groups--those with neck pain and those with arm pain as the major complaint.

Neck Pain as the Major Complaint

Patients with pain only in the cervical area, trapezii, and shoulders may have one of many disorders. The different types of relevant biomechanical neck pain may be differentiated by characteristics summarized in Table 2.

Table 2. Selected Characteristics of Biomechanical Neck Pain (See PDF)

Strain causes pain in the middle or lower portion of the posterior neck. The pain may be diffuse or localized to both sides of the spine. Physical examination reveals local tenderness in the paracervical muscles, decreased range of motion, and loss of cervical lordosis. No abnormalities are found with neurologic or shoulder examinations. X-rays of the spine may be normal or reveal a loss of lordosis. Laboratory test results are normal.

Therapy for chronic cervical strain includes NSAIDs, muscle relaxants, local injections, and exercises (including strengthening and range-of-motion). The choice and dosage of NSAIDs may be modified for patients with severe chronic pain.

Cervical Spondylosis (Osteoarthritis) is associated with disk degeneration and approximation of articular surfaces. Instability causes osteophyte formation in the uncovertebral and zygapophyseal joints, and diffuse pain may radiate from the neck to the shoulders, occipital area, or the interscapular muscles. Physical examination may reveal midline tenderness and pain at the limit of motion with extension and lateral flexion.

Radiographic findings are significant only if they correlate with the patient's clinical signs and symptoms. Plain x-rays of the cervical spine typically demonstrate intervertebral narrowing and facet joint sclerosis. MRI reveals degenerative cervical disk disease in more than 50% of patients 40 years of age or older. Scans are indicated in patients who have persistent pain that radiates to the shoulders; imaging serves to locate nerve impingement for subsequent treatment.

Patient education is essential for pain management. Most patients have a relapsing course with recurrent exacerbations of acute neck pain; hence, therapy requires a balance between stability and maintenance of motion. Range-of-motion exercises maximize neck flexibility; cervical collars decrease pain by restricting neck movement. NSAIDs and local injections may help to diminish neck and referred pain.

Cervical Hyperextension (Whiplash) is an acceleration-deceleration injury to the soft tissue structures in the neck. Common causes include rear-impact motor vehicle accidents, falls, and diving accidents and other sports injuries. Paracervical muscles are stretched or torn, and the sympathetic ganglia may be damaged, resulting in Horner's syndrome, nausea, hoarseness, or dizziness; intervertebral disk injuries occur with severe trauma.

The first symptoms occur 12 to 24 hours after trauma. Patients experience stiffness and pain with motion; they may also have difficulty in swallowing or chewing. Physical examination reveals soreness, paracervical muscle contraction, and decreased range of motion. Neurologic examination is often unremarkable, but radiographs can reveal loss of cervical lordosis. In severely injured patients, structural damage identified on x-rays mandates immediate stabilization.

Nonnarcotic analgesics, NSAIDs, and muscle relaxants reduce pain and facilitate neck movement. Treatment of most whiplash injuries includes use of a cervical collar for a minimal period of time. The collar is removed as soon as pain relief is obtained. Longer use of collars has resulted in delayed recovery. The Quebec Task Force on whiplash-associated disorders showed that prolonged use of cervical collars resulted in increased pain, decreased range of motion, and a longer recovery. Patients whose symptoms last for more than six months usually have a zygapophyseal joint injury and rarely experience significant improvement.

When fever or weight loss develops during nonoperative management, patients should undergo x-ray evaluation to assess bone integrity. If x-rays are negative, MRI or CT scans may locate the lesion and guide placement of biopsy needles.
Elevated ESR or C-reactive protein values identify patients with inflammatory lesions. The ESR may also be monitored during therapy to document improvement. Antibiotics are the treatment of choice for osteomyelitis and diskitis in the absence of neural compromise or paracervical abscess.

Fractures. Pain directly over the bony structures (vertebral arch or body) of the cervical spine is usually a sign of fracture or expansion of bone; physical examination can locate the point of maximum tenderness. Conditions that replace bone with abnormal cells or increase mineral loss from trabeculae predispose patients to fractures that occur spontaneously or with minimal trauma and result in localized pain.
Imaging techniques can identify the location of fractures if the physical examination is equivocal. Bone scans are helpful when x-rays of the neck are normal. MRI can identify the presence of malignant cells that do not stimulate osteoblast activity (e.g., myeloma). Biochemical and hematologic tests may detect perturbations of calcium meta- bolism or the presence of hemo- globinopathies; as noted, an elevated ESR is common with inflammation.

Fibromyalgia. Patients without systemic disorders should be examined for tender or trigger points. Such patients will have normal ESRs but experience localized pain with pressure (tender point) or radiation of muscle pain distal to the area of pressure (trigger point). Tender points are associated with a generalized pain syndrome, fibromyalgia; trigger points are associated with myofascial pain syndrome.
Patients with fibromyalgia benefit from aerobic exercise and antidepressants; those with myofascial disorders improve with injections of combined anesthetic and semisoluble corticosteroid. If patients do not have muscle tenderness, they should undergo a complete psychosocial evaluation. In patients with psychiatric disturbances, conversion reactions or substance dependence often are the cause of neck pain.

Arm Pain as the Major Complaint

Disk Herniation. In patients with arm pain refractory to nonoperative management, the underlying cause often is pressure from a herniated disk or hypertrophic bone and secondary inflammation of the nerve roots. Herniation can result from sudden exertion, as in heavy lifting. Neck pain is minimal or absent, and the injury causes pain that spreads from the shoulder to the forearm and hand and is sometimes severe enough to limit arm use.

Physical examination will detect increased radicular pain with any maneuver that narrows the intervertebral foramen and places tension on the affected nerve, such as compression, extension, or lateral flexion of the cervical spine (Spurling's sign).
Neurologic examination will reveal sensory abnormalities, reflex asymmetry, or motor weakness correlated with the affected spinal nerve root and degree of impingement. The characteristics of radicular pain caused by nerve root compression are summarized in Table 3.



MRI is the best technique to locate disk herniation and nerve root impingement; electromyography and nerve conduction tests will document nerve dysfunction and differentiate peripheral entrapment syndromes (e.g., carpal tunnel syndrome) from spinal nerve impingement.

Therapy includes controlled physical activity, firm cervical collars, NSAIDs, and traction. Patients may require full-time collar immobilization to limit radicular pain for weeks at a time. Those with recalcitrant pain may also obtain relief from epidural corticosteroid injections at the level of nerve impingement documented by MRI. Low-dose oral corticosteroids (10 mg to 15 mg/day) may be considered for patients who refuse epidural injections. Corticosteroids should be used for a limited period; dosage is tapered slowly once radicular symptoms have resolved. Many patients' arm symptoms resolve within three months.

When there is unequivocal evidence of nerve root compression (i.e., physical findings corroborated by MRI or CT findings), surgical decompression should be considered. Some studies suggest that patients who undergo such surgery do better than those who do not. Although nonoperative management of patients with radicular pain may prevent progression to cervical myelopathy, some patients nevertheless experience persistent arm pain. When performed in selected patients with good technique, surgery is successful for more than 90% of cases. In one study, for example, anterior diskectomy with fusion achieved excellent outcomes in 94% of patients.

Other Causes. Patients with arm pain that occurs with exertion should undergo a vascular evaluation. If chest pain occurs in conjunction with arm pain, coronary artery disease (CAD) should be investigated with an electrocardiogram and a stress test; positive stress test results (reproduction of arm pain) confirm the presence of CAD. Exertional pain limited to the arm suggests thoracic outlet syndrome. Adson's test can detect the impingement. The test is performed by taking the patient's pulse at the wrist. While the pulse is continuously palpated, the arm is then abducted, extended, and externally rotated. The patient takes a deep breath and turns the head toward the arm being tested. Compression of the subclavian artery results in a marked diminution of the radial pulse. Patients with thoracic outlet syndrome may benefit from isometric shoulder girdle exercises, improved posture, and restriction of arm movement above the head. Surgery is helpful in a minority of patients who do not respond to other therapy.

Patients with persistent arm pain, numbness, and weakness require an apical view chest x-ray to rule out Pancoast's tumor, which invades the inferior portions of the brachial plexus and causes pain by compression of local neural tissues. Such patients require palliative radiation therapy.

Chronic Neck Pain

Patients without a specific diagnosis are considered to have chronic neck pain. Education, patience, and encouragement are important components of therapy. Chronic pain management requires convincing the patient that the goal of therapy is to maximize physical function. A combination of therapies is necessary to reach this goal. Exercise programs that improve aerobic conditioning and range of motion are helpful. Patients may benefit from an increased NSAID dosage or switching to a different NSAID. Tricyclic antidepressants offer additional pain relief mediated through the central nervous system. Narcotic analgesics are generally discouraged but may be used at a specified effective dose to treat patients who experience an acute exacerbation of pain. The goal for these patients is gradual decrease of dosage and eventual discontinuance of narcotic analgesics.

Patients with chronic pain should be encouraged to return to some form of work. Movement aids the adaptive process by improving function and countering the inactivity that can exacerbate pain. The appearance of new symptoms or marked exacerbation of preexisting complaints are indications for reevaluation.

Conclusion

Many disorders are implicated in neck pain, but biomechanical problems of the cervical spine are the most common cause. Diseases affecting the cervical spine are rare but important causes of pain; certain symptoms and signs help to identify the more serious clinical conditions. Most patients improve with nonoperative therapy within three months; only about 10% of patients require surgical intervention.
Selected Reading

Aker PD et al: Conservative management of mechanical neck pain: Systemic overview and meta-analysis. BMJ 313:1291, 1996
Bell GR, Ross JS: The accuracy of imaging studies of the degenerative cervical spine: Myelography, myelo-computed tomography, and magnetic resonance imaging. Semin Spine Surg 7:9, 1995
Bernhardt M et al: Cervical spondylitic myelopathy. J Bone Joint Surg 75A:119, 1993
Borenstein DG, Wiesel SW, Boden SD: Neck Pain: Medical Diagnosis and Comprehensive Management, WB Saunders, Philadelphia, 1996, pp 161-437
Brodsky AE: Cervical angina: A correlative study with emphasis on the use of coronary arteriography. Spine 10:699, 1985
Ferrante FM et al: Clinical classification as a predictor of therapeutic outcome after cervical epidural steroid injection. Spine 18:730, 1993
Herkowitz HN, Kurz LT, Overholt DP: Surgical management of cervical soft disc herniation: A comparison between the anterior and posterior approach. Spine 15:1026, 1990
Lehto IJ et al: Age-related MRI changes at 0.1 T in cervical discs in asymptomatic subjects. Neuroradiol 36:49, 1994
Lindgren K, Oksala I: Long-term outcome of surgery for thoracic outlet syndrome. Am J Surg 169:358, 1995
Martel W: The occipito-atlanto-axial joints in rheumatoid and ankylosing spondylitis Am J Roentgenol 86:223, 1961
Praemer A, Furner S, Rice DP: Musculoskeletal Conditions in the United States. American Academy of Orthopaedic Surgeons, Park Ridge, Ill., 1992, pp 23-33.
Redford JB, Patel AT: Orthotic devices in the management of spinal disorders. Phys Med Rehabil 9:709, 1995
Spitzer WO et al: Scientific monograph of the Quebec Task Force on whiplash-associated disorders: Redefining "whiplash" and its management. Spine 20(suppl 8):1S, 1995
Watt I, Cummins B: Management of rheumatoid neck. Ann Rheum Dis 49:805,1990


Was originally published here: http://www.uphs.upenn.edu/medicine/Medicine/Jaeger_Archive/neck_pain.htm