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Spinal infection and discitis

67 citationsUpdated Sep 2026

Overview

Spondylodiscitis is a significant source of morbidity, particularly when diagnosis is delayed [11]. In the context of lumbar disc operations, discitis occurred in 15 of 502 cases, representing a 2.8 per cent incidence [5]. Risk factors for surgical site infection encompass the nature of the spinal pathology and the surgical procedure, as well as the systemic health of the patient [13]. Clinicians must remain aware of the pathogenic potential of Propionibacterium acnes, particularly following invasive spine procedures [3]. Because multifocal spondylodiscitis is found in approximately 13% of cases, MRI imaging of the total spine is recommended to avoid overlooking additional infection levels that can impact therapeutic strategy [12]. The presence of an epidural abscess on MRI is crucial in the decision-making process for early surgical treatment in patients with pyogenic spondylitis to improve clinical outcomes [24].

Most patients with spondylodiscitis are successfully treated by conservative means, where appropriate antibiotics and a back support usually lead to a satisfactory outcome [6, 16]. Treatment of fungal spinal infections relies on the prompt institution of appropriate pharmacotherapy and constant monitoring of clinical progress [29]. However, surgical intervention is usually reserved for infections resistant to medical management, the need for open biopsy/culture, evolving spinal instability or deformity, and neurologic deficit or deterioration [1]. Specific indications for surgery include doubtful diagnosis, progressive neurological deficits, progressive spinal deformity, failure to respond to treatment, and unresolved pain [6]. The authors recommend a surgical approach for patients with ventral vertebral body destruction, progressive neurological impairment, septicaemia, or antibiotic-resistant infections [4]. For spinal epidural abscess associated with neurologic compromise, the treatment of choice is emergent surgical decompression and débridement (with or without spinal stabilization), followed by long-term antimicrobial therapy [7]. In fungal infections, resistance to medical therapy, spinal instability, and neurologic deficits serve as indications for débridement and stabilization with spinal fusion [29]. Among patients with negative initial nonoperative culture results, spinal decompression and abscess drainage can be used for those with substantial or aggravating neurological deficits or intractable pain, while additional early spinal instrumentation can be applied when mechanical instability is present [15]. The authors suggest that future cases of Pseudomonas vertebral osteomyelitis may require surgical intervention for removal of infected tissue and fusion, even without abscess [26].

Surgical debridement with or without stabilization may be required for effective eradication of chronic spinal infections when nonoperative treatment fails or specific indications such as abscess, neurologic deficit, or instability are present [2]. Surgical treatment of lumbar spinal tuberculosis in selected cases gives satisfactory results [8]. Patients with cervical and lumbar osteomyelitis can successfully have instrumented-combined, one-stage surgery [17]. Instrumented treatment showed the highest recurrence-free survival rate and the lowest proportion of major medical complications, suggesting surgeons can use instrumentation in an infected spinal environment [27]. For patients with significant spinal instability or abscess formation, a two-stage anterior debridement-fusion may be required [28]. Surgical treatment for MRSA spondylodiscitis with posterior spinal instrumentation provided patients with satisfactory final outcomes [45]. Patients treated with early surgery had significantly lower ODI and VAS scores at 12 months compared to those treated with antibiotics alone [54]. Single-stage anterior debridement and fusion with autografting and internal fixation may be a safe and effective operative procedure for appropriate pyogenic lumbar spondylodiscitis [78].

Anatomy & Pathophysiology

Anatomical Basis of Infection Spread

Osteomyelitis almost always affects the anterior spinal column and rarely involves the posterior elements [36]. The intervertebral disk has limited blood supply, with the majority of nutrient delivery occurring via diffusion from the vertebral body [36]. Consequently, for an infection to invade the disk space, it usually originates from the vertebral body [36]. Once a vertebral body is inoculated with a bacterial pathogen, the pathogen may spread to the adjacent disk space via diffusion and cause diskitis [104]. The multiple and redundant sources of vascularity to the spinal column provide a ready avenue for bacterial pathogens to seed vertebrae [104]. Direct inoculation of the spinal column can occur secondary to skin compromise, such as in patients with chronic sacral decubitus ulcers [104]. Direct inoculation of the spinal column can also occur in patients undergoing spinal surgery or spinal procedures due to iatrogenic contamination of the surgical site [104]. In children, bloodborne infection can primarily invade the disc space [42].

Pathogenesis and Microbiology

The pathogenesis of spinal osteomyelitis/diskitis involves either direct inoculation of the spinal column or hematogenous spread from another organ site [104]. Hematogenous spread is more common than direct inoculation and accounts for the majority of cases of osteomyelitis/diskitis [104]. Pyogenic vertebral osteomyelitis is usually from hematogenous spread and involves Staphylococcus aureus in 50% to 75% of cases [33]. Staphylococcus aureus is the most common source of bacterial osteomyelitis/diskitis [104]. In a systematic review of 1,008 patients with pyogenic vertebral osteomyelitis, S. aureus was the most frequently found organism, with Streptococcus being the next most common pathogen [104]. Gram-negative species are also a frequent source of osteomyelitis, including Escherichia coli and Klebsiella pneumonia [104]. Pseudomonas aeruginosa has been described as a common pyogenic vertebral osteomyelitis pathogen in patients with intravenous drug abuse [104]. In older patients with osteodiscitis, gram-negative organisms are common [42].

Clinical Presentation and Progression

Patients with osteomyelitis/diskitis of the spine often have an indolent clinical course in which low-grade back pain increases in severity over several weeks to months [10]. Back pain is the most common presenting report for osteomyelitis/diskitis, followed by fever [10]. Pyogenic vertebral osteomyelitis is commonly associated with a significant 6- to 12-week delay in diagnosis [20]. The lumbar spine is the most common region involved in pyogenic vertebral osteomyelitis, accounting for 50% of cases [20]. In a systematic review of 1,008 patients with pyogenic vertebral osteomyelitis, the lumbar vertebrae were affected in 59% of patients, followed by the thoracic vertebrae in 30% and the cervical vertebrae in 11% [36]. The median age of patients with pyogenic vertebral osteomyelitis is 59 years [36]. There is a male predominance (62%) among individuals affected by pyogenic vertebral osteomyelitis [36]. In patients with pyogenic vertebral osteomyelitis, 24% had diabetes mellitus and 11% used intravenous drugs [36].

In a systematic review by Mylona et al, 34% of patients with pyogenic vertebral osteomyelitis presented with some type of neurologic issue, ranging from radiculopathy to urinary incontinence [10]. As pyogenic infection spreads, it can cause neurologic compromise secondary to bony retropulsion or extension into the epidural space, causing an epidural abscess [10]. Resultant central or foraminal stenosis from bony retropulsion or epidural abscess can result in neurologic deficits [10]. Neurologic deficits in pyogenic vertebral osteomyelitis are seen in older patients, patients with infections at more cephalic levels of the spine, patients with debilitating systemic illnesses such as diabetes or rheumatoid arthritis, and those with delayed diagnoses [20]. Bloodwork for osteomyelitis/diskitis can show a normal or elevated white blood cell count [10]. Patients with osteomyelitis/diskitis will have an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) secondary to the inflammatory response [10]. Blood cultures should be obtained to assess for disseminated infection and identification of microbial pathogen [10].

Patients with spinal epidural abscess are typically more systemically ill than patients with osteodiscitis and osteomyelitis [33]. Spinal epidural abscess is a serious condition with high morbidity and mortality if left untreated [50]. The close proximity of infectious material to neural elements in spinal epidural abscess can lead to devastating complications such as quadriparesis and paraparesis [50]. The incidence of spinal epidural abscess is estimated to be 2 to 5/10,000 hospital admissions [50]. The most common age for spinal epidural abscess is 50 to 70 years, and males are more frequently affected than females [50]. In a review of 128 patients with spinal epidural abscess, the most common location was the lumbar spine (54.7%) followed by the thoracic spine (39.1%) [50]. In a systematic review by Arko et al of 1,099 patients with spinal epidural abscess, the lumbar spine was the most common location (48%), males were affected more frequently (62.5%), and S. aureus was the most common pathogen (63.6%) [50]. Staphylococcus aureus is the most common bacterial pathogen that causes spinal epidural abscess [50]. In a review of 128 patients with spinal epidural abscess, MSSA was the most frequently isolated bacterial pathogen, followed by MRSA (30%) [50].

Risk factors for spinal epidural abscess include intravenous drug use, which is a significant risk factor [50]. Recent trauma and alcohol use have been shown to increase the risk of spinal epidural abscess [50]. Patients who have undergone a recent spinal epidural or facet injection or spine surgery are at risk for spinal epidural abscess secondary to direct bacterial inoculation [50]. Medical comorbidities that cause immunocompromise, such as diabetes and HIV, place patients at elevated risk for spinal epidural abscess [50]. In a review of 128 patients with spinal epidural abscess, the most common risk factors were IV drug use (39.1%) and diabetes (21.9%) [50].

Tuberculosis Pathophysiology

Spinal tuberculosis is the most common extrapulmonary location of tuberculosis [39]. Tuberculosis is the second most common cause of infectious mortality worldwide, behind HIV [117]. A recent WHO report estimated that there were 10.4 million new cases of tuberculosis worldwide (142 cases per 100,000 people) [117]. Extrapulmonary tuberculosis affects the musculoskeletal system in 10% of cases, with the spinal column being the most common site of osseous involvement [117]. The spinal column is involved in 50% of tuberculosis cases that spread to the musculoskeletal system [117]. The thoracic and lumbar spine are the most commonly infected areas of the spinal column in tuberculosis [117]. Spinal tuberculosis may be seen in the HIV-positive population with CD4+ counts of 50 to 200 cells/µL [39]. There is a synergistic relationship between HIV and TB, where suppressed CD4-related immunity in HIV patients increases the ability of TB to penetrate immune defenses [117]. In regions such as Sub-Saharan Africa, 50% of all TB cases were estimated to occur in patients who also had HIV [117].

Spinal tuberculosis originates in the metaphysis of the vertebral body and spreads under the anterior longitudinal ligament [39]. The spread of spinal tuberculosis leads to destruction of several contiguous levels or results in skip lesions (15%) or abscess formation (50%) [39]. On early plain radiographs, anterior vertebral body destruction with preservation of the disc distinguishes tuberculosis from pyogenic infection [39]. About two-thirds of patients with spinal tuberculosis have abnormal chest radiographs, and 20% have a negative test result for purified protein derivative of tuberculin or are anergic [39]. Severe kyphosis, sinus formation, and (Pott) paraplegia are late sequelae of spinal tuberculosis [39]. Spinal cord injury in spinal tuberculosis may occur secondary to direct pressure from the abscess, bony sequestra, or (rarely) meningomyelitis [39].

The diagnosis of spinal TB should be suspected in any individual with a diagnosis of tuberculosis who develops worsening back pain [70]. The back pain in spinal TB is often insidious in nature and progresses over the course of several months [70]. A kyphotic deformity of the spinal column on physical examination should raise suspicions for spinal TB [70]. Patients with spinal TB can present with motor and/or sensory neurologic deficits, depending on the extent and location of the infection [70]. Cervical TB patients can develop quadriplegia and have been noted to suffer from retropharyngeal abscesses [70]. Lumbar TB patients can have restriction of hip flexion secondary to large psoas abscesses rather than true neurologic compromise [70]. Radiographs of the spinal column in a patient with spinal TB will demonstrate kyphotic deformity of the vertebral body with osteolysis of the affected vertebrae [70]. In spinal TB, there is often involvement of multiple vertebrae, and the posterior elements are rarely affected [70]. Associated soft-tissue abscesses in spinal TB are frequently calcified or produce shadowing, both of which can be visualized on radiographs [70]. MRI with and without gadolinium contrast is the study of choice for the diagnosis of spinal TB [70]. MRI demonstrates epidural and paravertebral abscesses, myelopathic cord signal changes, involvement of multiple vertebral bodies, and sparing of the disk space in spinal TB [70]. Disc spaces are typically preserved with tuberculosis spondylitis [33]. Associated spinal deformity is more common with tuberculosis spondylitis, typically kyphosis [33]. Tuberculosis spondylitis is more typically associated with large paravertebral abscess/phlegmon [33]. Tuberculosis spondylitis is more likely to spread along the anterior longitudinal ligament to involve adjacent vertebral bodies [33].

Imaging Pathophysiology and Mimics

Radiographic examination of patients with osteomyelitis of the spine usually demonstrates changes in the architecture of the vertebral body, such as scalloping of end plates and sclerosis of the subchondral bone [10]. Changes in the osteology of the posterior elements of the spine are rarely seen in osteomyelitis because of the predilection of infectious pathogens for the vertebral body [10]. Radiographic changes in the vertebrae usually take several weeks to develop and may not be seen in a patient with acute vertebral osteomyelitis [10]. In patients with chronic osteomyelitis, loss of bone commonly causes focal kyphosis [10]. Plain radiographic findings for pyogenic vertebral osteomyelitis include osteopenia, paraspinous soft tissue swelling (loss of a psoas shadow), erosion of the vertebral end plates, and disc destruction [20]. Disc space is preserved in metastatic disease, distinguishing it from pyogenic vertebral osteomyelitis [20]. Radiographic findings for osteodiscitis include loss of normal lumbar lordosis (range 20–80 degrees) as the earliest finding, followed by disc space narrowing and end plate erosion [42]. Radiographic findings for osteodiscitis do not occur until 10 days to 3 weeks after onset, and their absence is unreliable [42]. Radiographic changes in infectious spondylitis usually lag behind clinical findings, with loss of lumbar lordosis, disc space narrowing, loss of vertebral height, and end plate changes occurring in that order [46].

Noncontrast CT scan can show bony morphologic changes in greater detail, including bony retropulsion into the spinal canal, subchondral sclerosis, and erosion of the vertebral end plates [10]. MRI of the affected area of the spine with and without gadolinium contrast allows for detailed imaging of the soft-tissue structures of the spine [10]. On T1-weighted imaging, a patient with vertebral osteomyelitis/diskitis will have hypointense signal at the affected end plate and disk [10]. On T2-weighted imaging, a patient with vertebral osteomyelitis/diskitis will demonstrate hyperintense signal in the vertebral body and disk space [10]. If the infectious process has spread to the spinal canal, MRI will demonstrate any associated epidural phlegmon or epidural abscess [10]. The addition of gadolinium contrast allows for improved visualization of the infectious process, as the contrast will be taken up at the site of the infection [10]. MRI is sensitive for detecting infection and specific in differentiating infection from tumor in pyogenic vertebral osteomyelitis [20]. Gadolinium enhances MRI sensitivity in pyogenic vertebral osteomyelitis [20]. MRI with gadolinium is the diagnostic modality of choice for osteodiscitis [42]. Bone scan may be useful in the diagnosis of osteodiscitis [42]. Bone scanning is sensitive for a destructive process in pyogenic vertebral osteomyelitis [20]. MRI is highly sensitive and specific for infectious spondylitis [46]. Tissue diagnosis via blood cultures or aspiration of the infection is mandatory for pyogenic vertebral osteomyelitis [20].

In spinal epidural abscess, abscess and CSF have high signal intensity on T2-weighted images [20]. Gadolinium enhances the pus on T1-weighted images, whereas CSF remains low-signal in spinal epidural abscess [20]. MRI is the modality of choice for spinal epidural abscess, and supplementation with gadolinium allows differentiation between epidural abscess and CSF [20].

Many degenerative and inflammatory spinal disorders may mimic spinal infections and it is necessary to be able to differentiate them from infectious spondylitis [18]. Modic type I degenerative changes can mimic infectious spondylitis as it can have endplate bone marrow edema with areas of contrast enhancement [18]. Lack of abnormally increased signal in the disc on T2 weighted images and lack of soft tissue involvement including epidural abscess favors a degenerative disease over an infection [18]. Acute traumatic schmorl's node is the extrusion of a disc into the endplate [18]. Due to associated vascularization and inflammation, bone marrow edema and contrast enhancement may be identified in acute traumatic schmorl's node, and imaging features may be indistinguishable from those of infectious spondylitis [18]. The presence of a high-signal-intensity concentric ring surrounding a cartilaginous node and involvement of only one endplate without disc signal abnormality favor acute traumatic schmorl's node over infection [18]. A common complication of advanced ankylosing spondylitis is spinal fractures which can be either spontaneous or following a trauma [18]. These fractures in ankylosing spondylitis are commonly caused by osteoporosis in a patient with spinal fusion [18]. These fractures typically are three-column fractures involving juxtadiscal endplate or the disk space [18]. Pseudoarthrosis may develop at the site of the fracture resulting in endplate erosion and bone marrow edema mimicking imaging findings of infectious spondylitis [18]. A history of ankylosing spondylitis, proper clinical context and extension of the fracture line into the posterior elements help in differentiating ankylosing spondylitis related pseudoarthrosis from infectious spondylitis [18].

Classification

Etiology and Pathogen Classification

Vertebral osteomyelitis arises from diverse pathogenic organisms depending on host factors and procedural history. Propionibacterium acnes is a recognized pathogen, particularly following invasive spine procedures [3]. Mycobacterium phlei is a described etiology for vertebral osteomyelitis of the spine [22]. In specific populations, Pseudomonas serves as an etiology for vertebral osteomyelitis in heroin addicts [26], while Candida is also identified as an etiology for vertebral osteomyelitis [53]. Spinal brucellosis manifests variably as spondylitis, spondylodiscitis, discitis, epidural abscess, paraspinal abscess, and vertebral collapse [9]. Additionally, lumbar vertebral osteomyelitis can be associated with mycotic aortic aneurysm [19].

Anatomical and Demographic Classification

Paediatric spondylodiscitis predominantly affects children between 6 and 48 months old, with the lumbar spine being the most at-risk location [23]. In adult pyogenic spondylodiscitis, the lumbar spine remains the dominant site; in a cohort of 172 surgically treated patients, 54.0% underwent lumbar spine surgery [75]. Specific level involvement varies by pathology. In a study of 25 patients with infected lumbar interbody cages, the most common infected level was L4–L5 (52%), followed by L5–S1 (19%) and L3–L4 (15%) [114]. Regarding spinal tuberculosis, a study of 35 patients with thoracic and lumbar involvement found 15 cases involving thoracic vertebrae and 20 cases involving the lumbar spine [119].

Imaging and Diagnostic Classification

Multifocal spondylodiscitis is found in approximately 13% of cases, necessitating MRI imaging of the total spine to detect multifocal infection in pyogenic spondylodiscitis [12]. Several non-infectious conditions can mimic infectious spondylitis on MRI. Modic type I degenerative changes mimic infection due to endplate bone marrow edema and contrast enhancement [18]. Acute traumatic schmorl's nodes also mimic infectious spondylitis due to associated vascularization and inflammation [18]. Furthermore, pseudoarthrosis at the site of spinal fractures in ankylosing spondylitis can mimic imaging findings of infectious spondylitis [18]. Diagnostic discrimination between vertebral osteomyelitis and degenerative diseases is improved by the combination of soluble urokinase-type plasminogen activator receptor (suPAR) and C-reactive protein (CRP) [51]. The presence of an epidural abscess on MRI is a crucial factor in the decision-making process for early surgical treatment in patients with pyogenic spondylitis [24].

Severity and Structural Classification

Kulowski: This classification evaluates the degree of end-plate destruction in infectious spondylitis. Grade I is defined as only disk space narrowing. Grade II involves bony destruction limited only in the end-plate. Grade III indicates vertebral body destruction of less than 50% of vertebral height. Grade IV indicates vertebral body destruction over 50% of vertebral height [114]. In a study of infected lumbar interbody cages, cases were classified from Kulowski Grade II to Grade IV [114].

SINS: The spinal instability neoplastic score (SINS) has been investigated for evaluating instability in spinal tuberculosis, though certain parameters are inapplicable to spondylodiscitis [32]. Spondylodiscitis results in the chronic instability of the spine, distinguishing it from the acute instability induced by traumatic injuries [32]. In a study of 58 patients with multi-level pyogenic spondylodiscitis, 19% had distant discitis and 81% had adjacent levels involved [75].

Clinical Presentation Classification

The clinical diagnosis of concomitant lumbar osteomyelitis and a mycotic aneurysm can be difficult due to insidious onset and overlapping symptoms [19]. Clinical manifestations of spinal tuberculosis include back pain, anorexia, fatigue, low-grade fever, and sweats [119]. In a study of 35 patients with spinal tuberculosis, 10 cases presented with spinal cord injury, classified as 4 cases of Frankel grade C and 6 cases of Frankel grade D [119].

Clinical Presentation

General Presentation and Epidemiology

Pyogenic vertebral osteomyelitis is characterized by a significant diagnostic delay, typically ranging from 6 to 12 weeks [20]. Recent epidemiological data indicate a median diagnostic delay for pyogenic spondylodiscitis between 30 and 69.4 days [41], while the average duration from initial symptoms to diagnosis for spondylodiscitis has been reported as two to six months [38]. This delay often results from the nonspecific nature of initial signs and symptoms [38], particularly when patients present with back pain but no fever, leading to atypical spinal radiographs [31]. Consequently, discitis and osteomyelitis remain underdiagnosed due to this nonspecific presentation [41].

The condition exhibits a male predominance, with 62% of affected individuals being male [36]. Anatomically, the lumbar vertebrae are affected in 59% of patients, followed by the thoracic vertebrae in 30% and the cervical vertebrae in 11% [36].

Risk Factors and Predisposing Conditions

Risk factors for spinal osteomyelitis include diabetes, smoking, immunocompromise secondary to infections such as HIV or hepatitis C, infections in other body sites, previous spine surgery, and skin compromise [36]. Specifically, 24% of patients with pyogenic vertebral osteomyelitis have diabetes mellitus, and 11% use intravenous drugs [36]. Intravenous drug users are at increased risk for pyogenic vertebral osteomyelitis [20]. The condition is more common in patients with a history of pneumonia, urinary tract infection, skin infection, or immunologic compromise [20]. Immunologic compromise encompasses transplantation, rheumatoid arthritis, diabetes mellitus, and HIV positivity with CD4+ counts <200 cells/μL [20]. Fungal spondylitis can also be seen in patients with immunologic compromise [20].

In paediatric infectious spondylitis, patients with discitis are often younger, with a mean age of 2.8 years compared to 7.5 years for vertebral osteomyelitis [46]. This condition is most commonly seen at the L3 to L4 and L4 to L5 disc spaces [46].

Neurologic Findings

Although many patients with osteomyelitis or discitis do not present with neurologic deficits, 34% of patients present with some type of neurologic issue, ranging from radiculopathy to urinary incontinence [10]. The number of patients with neurological deficits in spondylodiscitis ranges from 35% to 40% [41]. Neurologic deficits are seen in older patients, patients with infections at more cephalic levels of the spine, patients with debilitating systemic illnesses such as diabetes or rheumatoid arthritis, and those with delayed diagnoses [20].

Severe neurological deficits are more common in the cervical and thoracic spine, in infection with S. aureus, in the presence of epidural abscess, and when C-reactive protein is higher than 150 mg/L [41]. The presence of epidural empyema shows a correlation with neurological deficits [41]. Short-term mortality in spondylodiscitis is related to empyema and neurologic deficits [41]. Patients with spinal epidural abscess associated with neurologic compromise require emergent surgical decompression and débridement [7].

Laboratory Findings

Laboratory findings for pyogenic vertebral osteomyelitis include elevated ESR, CRP, and WBC count, which is often high normal or mildly elevated [20]. Most commonly, osteodiscitis presents with pain and elevated erythrocyte sedimentation rate and C-reactive protein levels [33]. C-reactive protein should be used to monitor the response to treatment in osteodiscitis [33].

Physical Examination and Specific Signs

A history of unremitting spinal pain at any level is characteristic of pyogenic vertebral osteomyelitis, accompanied by tenderness, spasm, and loss of motion [20]. In paediatric infectious spondylitis, presentation includes acute back pain and refusal to sit or bear weight [46].

A kyphotic deformity of the spinal column on physical examination should raise suspicions for spinal tuberculosis [70]. Lumbar tuberculosis patients can have restriction of hip flexion secondary to large psoas abscesses rather than true neurologic compromise [70]. Cervical tuberculosis patients can develop quadriplegia and have been noted to suffer from retropharyngeal abscesses [70]. Clinical manifestation of spinal brucellosis can include spondylitis, spondylodiscitis, discitis, epidural abscess, paraspinal abscess, and vertebral collapse [9].

Imaging Characteristics

Radiographs: Radiographs are often normal in osteodiscitis, with loss of lumbar lordosis and disc space narrowing being the earliest findings [33]. In paediatric infectious spondylitis, radiographic changes usually lag behind clinical findings, with loss of lumbar lordosis, disc space narrowing, loss of vertebral height, and end plate changes occurring in that order [46]. In spinal tuberculosis, early plain radiographs demonstrate anterior vertebral body destruction with preservation of the disc [39]. Associated soft-tissue abscesses in spinal TB are frequently calcified or produce shadowing, which can be visualized on radiographs [70].

CT Scan: Noncontrast CT scan of the affected part of the spine can show bony morphologic changes in greater detail than radiographs [10]. Bony retropulsion into the spinal canal, subchondral sclerosis, and erosion of the vertebral end plates are better delineated with CT scan imaging than with MRI [10].

MRI: MRI of the affected area of the spine with and without gadolinium contrast allows for detailed imaging of the soft-tissue structures and should be obtained in all patients with suspected osteomyelitis of the spine [10]. Gadolinium enhances MRI sensitivity for detecting pyogenic vertebral osteomyelitis [20]. On T1-weighted MRI, a patient with vertebral osteomyelitis/diskitis will have hypointense signal at the affected end plate and disk [10]. T2-weighted MRI will demonstrate hyperintense signal in the vertebral body and disk space in vertebral osteomyelitis/diskitis [10]. MRI is highly sensitive and specific for paediatric infectious spondylitis [46]. Due to multifocal spondylodiscitis being found in approximately 13% of cases, MRI imaging of the total spine is recommended to avoid overlooking additional infection levels [12].

Differential Diagnosis on Imaging: Disc space is preserved in metastatic disease, distinguishing it from infectious disc destruction [20]. Spinal tuberculosis is associated with large paravertebral abscess/phlegmon and is more likely to spread along the anterior longitudinal ligament to involve adjacent vertebral bodies [33]. Disc spaces are typically preserved with tuberculosis spondylitis, distinguishing it from pyogenic infections [33]. Associated spinal deformity, typically kyphosis, is more common in tuberculosis spondylitis than in pyogenic infections [33]. There is often involvement of multiple vertebrae in spinal TB, and the posterior elements are rarely affected [70].

Many degenerative and inflammatory spinal disorders may mimic spinal infections. Modic type I degenerative changes can mimic infectious spondylitis with endplate bone marrow edema and contrast enhancement [18]. Acute traumatic schmorl's node may have imaging features indistinguishable from infectious spondylitis due to associated vascularization and inflammation [18]. Spinal fractures in advanced ankylosing spondylitis can result in pseudoarthrosis with endplate erosion and bone marrow edema mimicking imaging findings of infectious spondylitis [18]. Cervical spinal gout involving the disc and adjacent vertebral endplates is uncommon and may be misdiagnosed as infectious spondylodiscitis [71].

Microbiology and Pathogen Identification

The organism in pyogenic vertebral osteomyelitis is usually hematogenous, with S. aureus involved in 50%–75% of cases [20]. Staphylococcus aureus is the most common pathogen in spondylodiscitis [41]. Staphylococcus aureus is the most common offender in paediatric discitis, though gram-negative organisms are common in older patients [42]. In paediatric infectious spondylitis, S. aureus is most commonly seen, though K. kingae, Mycobacterium tuberculosis, Bartonella henselae, and Salmonella are also seen [46]. Mycobacterium phlei osteomyelitis of the spine has been described, serving as a reminder that proper diagnosis of infectious etiologies is necessary for adequate treatment [22].

Culture results in paediatric infectious spondylitis are positive in only 60% of cases [46]. Image-guided biopsy has a reasonably high diagnostic yield in patients with suspected infectious spondylodiscitis [65]. A meta-analysis found moderate-to-high diagnostic performance of molecular methods on direct patient specimens for the diagnosis of native vertebral osteomyelitis [72]. Improvement in the diagnostic power for discrimination of vertebral osteomyelitis and degenerative diseases of the spine can be achieved by a combination of both suPAR and CRP [51].

Investigations

Clinical Presentation and History: Patients with spinal osteomyelitis or diskitis typically present with an indolent course characterized by low-grade back pain that increases in severity over several weeks to months [10]. Back pain is the most common presenting symptom, followed by fever [10]. In a systematic review by Mylona et al., 34% of patients presented with neurologic issues ranging from radiculopathy to urinary incontinence [10]. Pyogenic vertebral osteomyelitis is commonly associated with a diagnostic delay of 6 to 12 weeks [20, 21]. A history of unremitting spinal pain at any level is characteristic of pyogenic vertebral osteomyelitis, often accompanied by tenderness, spasm, and loss of motion [20, 21]. Paediatric spondylodiscitis predominantly affects children between 6 and 48 months old, with the lumbar spine being the most at-risk location [23]. Diagnostic delay in anaerobic spondylodiscitis may occur when patients report only back pain without fever, potentially leading to atypical spinal radiographs [31].

Laboratory: Bloodwork for spinal osteomyelitis or diskitis can show a normal or elevated white blood cell count [10]. Patients will have an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) secondary to the inflammatory response [10]. Laboratory findings for pyogenic vertebral osteomyelitis include elevated ESR, CRP, and WBC count, which are often high normal or mildly elevated [20, 21]. Blood cultures should be obtained to assess for disseminated infection and identification of the microbial pathogen in suspected spinal osteomyelitis or diskitis [10]. The combination of soluble urokinase-type plasminogen activator receptor (suPAR) and CRP can improve the diagnostic power for discriminating vertebral osteomyelitis from degenerative diseases of the spine [51].

Plain radiography: Radiographic examination usually demonstrates changes in the architecture of the vertebral body, such as scalloping of end plates and sclerosis of the subchondral bone [10]. Changes in the osteology of the posterior elements are rarely seen due to the predilection of infectious pathogens for the vertebral body [10]. In patients with chronic spinal osteomyelitis, loss of bone commonly causes focal kyphosis [10]. Standing full-length scoliosis radiographs can be obtained to assess sagittal spinal alignment in greater detail [10]. Disc space is preserved in metastatic disease, which helps differentiate it from infectious disc destruction on plain radiographs [20, 21].

CT: Noncontrast CT scan of the affected part of the spine is commonly performed and can show bony morphologic changes in greater detail than plain radiographs [10]. CT-guided bone biopsy can be performed to obtain a sample of the affected vertebral body to allow for guidance of antibiotic therapy [10]. CT is superior for performing success control after treatment of spondylodiscitis [115]. A reduction in the Hounsfield units (HU) of the affected intervertebral disc by approximately 25% and/or an increase in the HU of the affected vertebral bodies by approximately 30% compared to adjacent structures indicates spondylodiscitis even in early stages without destruction [147].

MRI: MRI allows the clinician to assess for local spread of the infection, the development of epidural abscess or diskitis, and the chronicity of the infectious process [10]. T2-weighted imaging will demonstrate hyperintense signal in the vertebral body and disk space in vertebral osteomyelitis or diskitis [10]. The addition of gadolinium contrast allows for improved visualization of the infectious process, as the contrast is taken up at the site of infection, providing increased visualization of the boundaries [10]. For spinal epidural abscess, MRI is the modality of choice, and supplementation with gadolinium allows differentiation between epidural abscess and cerebrospinal fluid (CSF) [20, 21]. Abscess and CSF have high signal intensity on T2-weighted images [20, 21]. Gadolinium enhances the pus on T1-weighted images, whereas CSF remains low-signal [20, 21]. MRI is the radiological method of choice for establishing the diagnosis of spondylodiscitis, particularly for differentiating cases with and without abscess formations [115]. The presence of an epidural abscess on MRI should be regarded as crucial in the decision-making process for early surgical treatment in patients with pyogenic spondylitis [24]. Follow-up MRI findings of pyogenic spondylodiscitis show variable tissue responses [57].

Nuclear Medicine: The diagnostic effect of fluorine-18 fluorodeoxyglucose positron emission tomography (PET) for pyogenic spondylitis without previous spine surgery seems to be better than that for postoperative cases [124].

Differential Diagnosis and Mimics: Many degenerative and inflammatory spinal disorders may mimic spinal infections, and it is necessary to differentiate them from infectious spondylitis [18]. Modic type I degenerative changes can mimic infectious spondylitis as they can have endplate bone marrow edema with areas of contrast enhancement [18]. The presence of a high-signal-intensity concentric ring surrounding a cartilaginous node and involvement of only one endplate without disc signal abnormality favors acute traumatic Schmorl's node over infection [18]. Pseudoarthrosis at the site of spinal fractures in advanced ankylosing spondylitis can result in endplate erosion and bone marrow edema mimicking imaging findings of infectious spondylitis [18].

Tissue Diagnosis and Microbiology: A meta-analysis found moderate-to-high diagnostic performance of molecular methods (16S PCR followed by Sanger sequencing or next-generation sequencing) on direct patient specimens for the diagnosis of native vertebral osteomyelitis [72]. Salmonella spondylodiscitis usually responds favorably to appropriate antibiotics; consequently, a tissue diagnosis is important [67]. This case serves as the first description of Mycobacterium phlei osteomyelitis of the spine and as a reminder that proper diagnosis of infectious etiologies is necessary for adequate treatment [22].

Treatment

Non-Operative

Isolated vertebral osteomyelitis or diskitis in patients without neurologic deficits is initially managed with nonsurgical treatment [68]. This regimen typically involves intravenous antibiotics administered for at least six weeks, followed by a transition to oral antibiotics, alongside patient mobilization [68]. For non-MRSA gram-positive infections, IV cefazolin is commonly used, while IV vancomycin remains the standard for MRSA osteomyelitis [68]. Bracing provides additional spinal stability, with lumbosacral orthoses used for lumbar cases and thoracolumbar orthoses or Jewett extension braces for thoracic cases [68]. Appropriate antibiotics and back support usually yield satisfactory outcomes for pyogenic vertebral osteomyelitis [16]. In spinal epidural abscess without neurologic deficit, conservative management includes IV antibiotics for at least six weeks, close monitoring of inflammatory markers, blood cultures, and neurologic status, and mobilization with external bracing [44]. In pediatric spondylodiscitis, early therapy with immobilization, antibiotics, and clinical monitoring achieves good long-term results without instability or deformity [55]. Candida vertebral osteomyelitis requires appropriate antimicrobial agents and relative immobilization of the affected vertebrae [53].

Operative

Indications: Surgical intervention is reserved for infections resistant to medical management, the need for open biopsy or culture, evolving spinal instability or deformity, and neurologic deficit or deterioration [1]. Specific indications include doubtful diagnosis, progressive neurological deficits, progressive spinal deformity, failure to respond to treatment, and unresolved pain [6]. Surgery is recommended for ventral vertebral body destruction, progressive neurological impairment, septicaemia, or antibiotic-resistant infections [4]. For spinal epidural abscess, surgery is indicated for neurologic compromise [7], as well as for patients with neurologic deficits, positive blood cultures with systemic illness despite antibiotics, significant ongoing pain despite medical management, and progressive deformity or fracture at the infection site [44]. Vertebral osteomyelitis surgery is commonly performed when infection progresses despite nonsurgical treatment, associated epidural abscesses or diskitis develop, neurologic deficits occur, or bony instability and significant kyphotic deformity arise [68]. Open biopsy is indicated when tissue diagnosis has not been established for pyogenic vertebral osteomyelitis [20]. Anterior débridement and strut grafting are reserved for refractory cases involving neurologic deterioration, extensive bony destruction, or marked deformity [20]. Surgical irrigation, débridement, and bone grafting are reserved for osteodiscitis refractory to medical management [33]. Indications for osteodiscitis surgery include systemic illness, evidence of epidural abscess, failure of medical treatment, inability to obtain percutaneous biopsy, unknown diagnosis, mechanical instability, and neurologic deficits [42]. In pediatric infectious spondylitis, surgery is indicated for abscess and failure of nonoperative management [46]. Timely surgery is advisable for spondylodiscitis with progressive neurological deficits, deformities, and spinal instability, irrespective of pain or antimicrobial therapy status [32]. Surgery is also advised for persistent or recurrent bloodstream infections without an alternative source, or escalating pain despite appropriate pharmacotherapy, with or without spinal instability [32]. Spinal decompression and abscess drainage are used for native culture-negative pyogenic vertebral osteomyelitis with substantial or aggravating neurological deficits or intractable pain [15]. Early spinal instrumentation is applied when mechanical instability is present in these patients [15]. For fungal spinal infections, débridement and stabilization with spinal fusion are indicated for resistance to medical therapy, spinal instability, and neurologic deficits [29]. Successful treatment of granulomatous infection requires surgical intervention for neural decompression and correction of spinal malalignment [14]. The main indications for surgery in vertebral osteomyelitis are extensive bone destruction, epidural abscess, instability, severe neurologic impairment, or failure of nonsurgical treatment [113]. For monosegmental pyogenic spondylodiscitis with significant spinal instability or abscess formation, a two-stage anterior debridement-fusion may be required [28].

Surgical Approach / Technique: Surgical intervention for spinal epidural abscess typically consists of laminectomy at the infection site(s) and irrigation/débridement of the infectious collection [44]. Fusion is performed if significant instability results from bony resection [44]. Laminectomy is performed if the epidural abscess is predominantly posterior [20]. If concomitant vertebral osteomyelitis exists with an epidural abscess, anterior and posterior decompression is performed [20]. Posterior surgery is usually ineffective for débridement of pyogenic vertebral osteomyelitis, though posterior stabilization may occasionally be required after anterior débridement and strut grafting [20]. The goals of surgical treatment for vertebral osteomyelitis are débridement of infectious pathology, preservation of neurologic function, and stabilization of the spinal column [68]. Secondary goals include correction of sagittal or coronal plane deformities caused by the infectious process [68]. Resection often requires subtotal or total corpectomy with reconstruction using autograft, allograft, or cage placement [68]. Pedicle screw instrumentation is typically performed to stabilize at least two levels above and below the affected level [68]. If a concomitant epidural abscess is present, laminectomy can be performed to evacuate the collection [68]. Both single-segment and short-segment fixation combined with debridement and fusion are effective for mono-segmental lumbar or lumbosacral pyogenic vertebral osteomyelitis [123]. Unilateral percutaneous endoscopic debridement and drainage with physiological saline or empirical antibiotics did not disrupt lumbar stability and avoided important intraspinal structures [69].

Outcomes: Patients treated with early surgery for pyogenic spondylodiscitis had significantly lower ODI and VAS scores at 12 months compared to those treated with antibiotics alone [54]. Surgery for vertebral osteomyelitis lowers 1-year mortality and failure rates compared with nonsurgical treatment [113]. Conservative and surgical treatments are safe and effective, producing good clinical outcomes for lumbosacral tuberculosis [105]. Surgical management of spondylodiscitis remains controversial due to the absence of a standardized classification system and universally acknowledged surgical guidelines [32]. Approximately 50% of affected spondylodiscitis patients ultimately undergo surgical treatment [32]. Surgical objectives for spondylodiscitis encompass removal of the infected lesion, identification of the infecting microorganism, stabilization of the affected spinal segment, and facilitation of osseointegration [32]. Surgical intervention enables early postoperative mobilization and offers a more definitive and reliable approach to treating spinal deformities [32]. When indicated, surgical stabilisation of infected segments is mandatory for disease control and immediate mobilisation of patients with spondylodiscitis [38]. Overall, quality of life seems to be more favourable in patients following surgical treatment of spondylodiscitis [38].

Complications

Neurologic Deficits

In a systematic review of 1,008 patients with pyogenic vertebral osteomyelitis, 34% presented with neurologic issues ranging from radiculopathy to urinary incontinence [10]. Prognosis for isolated nerve-root deficits is good with or without surgery [109]. For spinal cord compression, results are generally better with anterior decompression and stabilization than with laminectomy [109]. Early treatment of vertebral osteomyelitis with paralysis should target the prevention of intrinsic spinal-cord damage, which is irreversible [109]. Diabetes mellitus, rheumatoid arthritis, increased age, and a more cephalad level of infection predispose to paralysis [109]. Meningomyelitis as a cause of spinal cord injury in spinal tuberculosis carries a poor prognosis [39].

Spinal Deformity and Instability

Severe kyphosis, sinus formation, and (Pott) paraplegia are late sequelae of spinal tuberculosis [39]. Spinal tuberculosis can lead to destruction of several contiguous vertebral levels or result in skip lesions, which occur in 15% of cases [39]. Abscess formation occurs in 50% of spinal tuberculosis cases [39]. Surgical treatment is indicated for progressive spinal deformity in spondylodiscitis [6]. Surgical intervention is usually reserved for evolving spinal instability or deformity in bacterial spine infections [1]. Surgical debridement with or without stabilization may be required for effective eradication of chronic spinal infections when specific indications such as instability are present [2]. The authors recommend a surgical approach for patients with ventral vertebral body destruction [4].

Abscess and Infection Spread

Spinal tuberculosis is more typically associated with large paravertebral abscess or phlegmon than pyogenic infections [33]. It is more likely to spread along the anterior longitudinal ligament to involve adjacent vertebral bodies [33]. Spinal epidural abscess can lead to devastating complications such as quadriparesis and paraparesis due to the close proximity of infectious material to neural elements [50]. MRI imaging of the total spine is recommended to avoid overlooking additional infection levels in pyogenic spondylodiscitis, which can impact the therapeutic strategy chosen [12].

Morbidity and Mortality

Mortality in spondylodiscitis is high at 8.9% and has been described as ranging from 1.8% to 15% [41]. Short-term mortality is related to empyema and neurologic deficits [41]. The hospital mortality for pyogenic spondylodiscitis is reported to be 2–17% [38]. Osteomyelitis/diskitis are common conditions that can cause significant morbidity and mortality if left untreated [36].

Diagnostic Delay and Misdiagnosis

The median diagnostic delay in pyogenic spondylodiscitis ranges from 30 days to 69.4 days [41]. In one cohort, the time from symptom onset to diagnosis was 17.88 days, with 41.4% of patients receiving antibiotic therapy for unclear infection prior to surgery [41]. The time from symptom onset to first surgical treatment was about 69.4 days and did not change significantly over the past two decades [41]. Diagnostic delay may occur because of atypical spinal radiographs if the patient reports only back pain but no fever in anaerobic spondylodiscitis [31]. Many degenerative and inflammatory spinal disorders may mimic spinal infections, making it necessary to differentiate them from infectious spondylitis [18]. Acute traumatic schmorl's node imaging features may be indistinguishable from those of infectious spondylitis due to associated vascularization and inflammation [18].

Postoperative and Procedural Complications

Discitis occurred in 15 of 502 lumbar disc operations (2.8 per cent) following removal of the lumbar intervertebral disc [5]. Patients who have undergone a recent spinal epidural or facet injection or spine surgery are at risk for spinal epidural abscess secondary to direct bacterial inoculation of the spinal column [50].

Recovery

Non-Operative Management: In children aged 3 years or younger with spondylodiscitis, adequate and early therapy comprising immobilization, antibiotics, and clinical monitoring achieves good long-term results without spine instability or deformity [55]. For pyogenic vertebral osteomyelitis, the success of non-operative treatment is predicted by age under sixty, immune status, Staphylococcus aureus infection, and a decreasing erythrocyte sedimentation rate [48].

Operative Indications and Outcomes: Surgical treatment for spondylodiscitis is indicated for doubtful diagnosis, progressive neurological deficits, progressive spinal deformity, failure to respond to treatment, and unresolved pain [6]. Successful treatment of granulomatous infection requires timely diagnosis, prompt medical management, and potential surgical intervention directed at the decompression of neural elements and the correction of spinal malalignment [14]. In fungal spinal infections, resistance to medical therapy, spinal instability, and neurologic deficits serve as indications for débridement and stabilization with spinal fusion [29]. Long posterior instrumentation with short posterior or posterolateral fusion is effective in the treatment of TB spine, controlling infection, correcting kyphosis, and maintaining correction and neurological improvement over time [76]. Patients treated with early surgery had significantly lower ODI and VAS scores at 12 months compared to those treated with antibiotics alone for pyogenic spondylodiscitis [54].

Complications and Prognosis: The clinical manifestation of spinal brucellosis can include spondylitis, spondylodiscitis, discitis, epidural abscess, paraspinal abscess, and vertebral collapse [9].

Key Evidence

• [L4] Surgical intervention is usually reserved for infections resistant to medical management, the need for open biopsy/culture, evolving spinal instability or deformity, and neurologic deficit or deterioration. [1] (10.5435/jaaos-d-13-00102)
• [L3] Surgical debridement with or without stabilization may be required for effective eradication of chronic spinal infections when nonoperative treatment fails or specific indications such as abscess, neurologic deficit, or instability are present. [2] (10.1097/01.blo.0000203447.44146.55)
• [L4] Clinicians should be aware of the pathogenic potential of this organism, particularly following invasive spine procedures. [3] (10.1097/blo.0b013e318073c25d)
• [L4] The authors recommend this surgical approach for patients with ventral vertebral body destruction, progressive neurological impairment, septicaemia, or antibiotic-resistant infections. [4] (10.1007/bf00393878)
• [L4] Discitis occurred in 15 of 502 lumbar disc operations (2.8 per cent). [5] (10.2106/00004623-196951040-00009)
• [L5] Most patients with spondylodiscitis are successfully treated by conservative means; however, surgical treatment is indicated for doubtful diagnosis, progressive neurological deficits, progressive spinal deformity, failure to respond to treatment, and unresolved pain. [6] (10.1302/2058-5241.2.160062)
• [L5] For spinal epidural abscess associated with neurologic compromise, the treatment of choice is emergent surgical decompression and débridement (with or without spinal stabilization), followed by long-term antimicrobial therapy. [7] (10.5435/00124635-200405000-00003)
• [L4] Surgical treatment of lumbar spinal tuberculosis in selected cases gives satisfactory results. [8] (10.1097/blo.0b013e318067bcd9)
• [L4] Clinical manifestation of spinal brucellosis can include spondylitis, spondylodiscitis, discitis, epidural abscess, paraspinal abscess, and vertebral collapse. [9] (10.1097/01.blo.0000203455.59393.9a)
• [L4] Spondylodiscitis is associated with significant morbidity and a high rate of complications, particularly in cases with delayed diagnosis. [11] (10.1186/s12891-025-08748-z)
• [L3] Due to multifocal spondylodiscitis being found in approximately 13% of cases, MRI imaging of the total spine is recommended to avoid overlooking additional infection levels, which can impact the therapeutic strategy chosen. [12] (10.1186/s12891-020-03928-5)
• [L4] Risk factors for SSI include factors related to the nature of the spinal pathology and the surgical procedure, as well as factors related to the systemic health of the patient. [13] (10.1007/s00264-011-1427-z)
• [L5] Successful treatment of a granulomatous infection requires timely diagnosis, prompt medical management, and potential surgical intervention directed at the decompression of neural elements and the correction of spinal malalignment. [14] (10.5435/jaaos-d-13-00213)
• [L4] Among patients with negative initial nonoperative culture results, spinal decompression and abscess drainage can be used for those with substantial or aggravating neurological deficits or intractable pain, while additional early spinal instrumentation can be applied when mechanical instability is present. [15] (10.1097/corr.0000000000001866)
• [L4] Treatment with appropriate antibiotics and a back support usually leads to a satisfactory outcome. [16] (10.1097/01.blo.0000201172.64764.bb)
• [L2] Patients with cervical and lumbar osteomyelitis can successfully have instrumented-combined, one-stage surgery. [17] (10.1097/01.blo.0000203449.51769.7f)
• [L5] [18] (10.1186/s12891-017-1608-z)
• [L4] The clinical diagnosis of concomitant lumbar osteomyelitis and a mycotic aneurysm can be difficult due to insidious onset and overlapping symptoms. [19] (10.2106/00004623-199511000-00014)
• [L5] This case serves as the first description of M. phlei osteomyelitis of the spine and as a reminder that proper diagnosis of infectious etiologies is necessary for adequate treatment. [22] (10.5435/jaaosglobal-d-18-00069)
• [L4] Paediatric spondylodiscitis predominantly affects children between 6 and 48 months old with the lumbar spine being the most at-risk location. [23] (10.1530/eor-2025-0224)
• [L4] The presence of an epidural abscess on MRI should be regarded crucial in the decision-making process for early surgical treatment in patients with pyogenic spondylitis in order to improve clinical outcomes. [24] (10.1186/s12891-023-06703-4)
• [L4] The authors suggest that future cases may require surgical intervention for removal of infected tissue and fusion, even without abscess. [26] (10.2106/00004623-197355070-00008)
• [L5] Instrumented treatment showed the highest recurrence-free survival rate and the lowest proportion of major medical complications, suggesting surgeons can use instrumentation in an infected spinal environment. [27] (10.1097/corr.0000000000001907)
• [L4] For patients with significant spinal instability or abscess formation, a two-stage anterior debridement-fusion may be required. [28] (10.1186/s13018-025-05660-z)
• [L5] Treatment relies on the prompt institution of appropriate pharmacotherapy and constant monitoring of clinical progress, with resistance to medical therapy, spinal instability, and neurologic deficits serving as indications for débridement and stabilization with spinal fusion. [29] (10.1097/01.blo.0000203451.36522.4c)
• [L4] Diagnostic delay may occur because of atypical spinal radiographs if the patient reports only back pain but no fever. [31] (10.1186/s12891-022-05749-0)
• [L1] [32] (10.1530/eor-2025-0041)
• [L4] [38] (10.1007/s00264-011-1425-1)
• [L3] [41] (10.3390/brainsci11081019)
• [L5] Surgical treatment for MRSA spondylodiscitis with posterior spinal instrumentation provided patients with satisfactory final outcomes. [45] (10.1007/s00402-006-0114-9)
• [L3] Pyogenic vertebral osteomyelitis is uncommon and affects older, sicker patients; the success of non-operative treatment is predicted by age under sixty, immune status, Staphylococcus aureus infection, and decreasing erythrocyte sedimentation rate. [48] (10.2106/00004623-199706000-00011)
• [L3] Improvement in the diagnostic power for discrimination of vertebral osteomyelitis and degenerative diseases of the spine can be achieved by a combination of both suPAR and CRP. [51] (10.1186/s13018-019-1420-6)
• [L4] Therapy should include appropriate antimicrobial agents and relative immobilization of the affected vertebrae. [53] (10.2106/00004623-197658040-00028)
• [L3] Patients treated with early surgery had significantly lower ODI and VAS scores at 12 months compared to those treated with antibiotics alone. [54] (10.1186/s12891-017-1533-1)
• [L4] With adequate and early therapy of immobilization, antibiotics, and clinical monitoring, good long-term results without spine instability or deformity can be achieved. [55] (10.1007/s00402-007-0316-9)
• [L3] Follow-up MRI findings of pyogenic spondylodiscitis show variable tissue responses. [57] (10.1186/s12891-020-03446-4)
• [L2] Image-guided biopsy has a reasonably high diagnostic yield in patients with suspected infectious spondylodiscitis. [65] (10.1302/0301-620x.104b1.bjj-2021-0848.r2)
• [L4] Salmonella spondylodiscitis usually responds favorably to appropriate antibiotics; consequently, a tissue diagnosis is important. [67] (10.1097/01.blo.0000137561.82099.d5)
• [L4] Unilateral PEDD with physiological saline or empirical antibiotics did not disrupt lumbar stability and avoided important intraspinal structures. [69] (10.1186/s13018-018-1009-5)
• [Case_report] Cervical spinal gout involving the disc and adjacent vertebral endplates is uncommon and may be misdiagnosed as infectious spondylodiscitis. [71] (10.1186/s12891-019-2813-8)
• [L1] This meta-analysis found moderate-to-high diagnostic performance of molecular methods on direct patient specimens for the diagnosis of native vertebral osteomyelitis. [72] (10.1097/corr.0000000000003314)
• [L3] [75] (10.1186/s13018-023-03584-0)
• [L4] Long posterior instrumentation with short posterior or posterolateral fusion is effective in the treatment of TB spine, controlling infection, correcting kyphosis, and maintaining correction and neurological improvement over time. [76] (10.1302/0301-620x.98b6.36472)
• [L4] Based on the limited population studied, this technique may be a safe and effective operative procedure for appropriate pyogenic lumbar spondylodiscitis in patients. [78] (10.1007/s00402-011-1451-x)
• [L4] Conservative and surgical treatments are safe and effective and produce good clinical outcomes for patients with lumbosacral tuberculosis. [105] (10.1371/journal.pone.0130185)
• [L4] [109] (10.2106/00004623-198365010-00004)
• [L3] [113] (10.2106/jbjs.23.00283)
• [L3] [114] (10.1186/s13018-021-02535-x)
• [L4] MRI is the radiological method of choice for establishing the diagnosis of spondylodiscitis, particularly for differentiating cases with and without abscess formations, while CT is superior for performing success control after treatment. [115] (10.1007/s004020050457)
• [L4] [119] (10.1186/s12891-018-2187-3)
• [L3] Both single-segment and short-segment fixation combined with debridement and fusion are effective treatments for mono-segmental lumbar or lumbosacral pyogenic vertebral osteomyelitis. [123] (10.1186/s13018-022-03269-0)
• [L1] The diagnostic effect of this nuclear imaging method for pyogenic spondylitis without previous spine surgery seems to be better than that for the postoperative ones. [124] (10.1186/s13018-023-03507-z)
• [L4] A reduction in the HU of the affected intervertebral disc by approximately 25% and/or an increase in the HU of the affected vertebral bodies by approximately 30% compared to the adjacent intervertebral discs or vertebrae indicates spondylodiscitis even in the early stages without destruction and regardless of the location. [147] (10.1186/s12891-025-09106-9)

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