Version July 2025
INTRODUCTION —
Vertebral osteomyelitis is usually a result of hematogenous seeding. Osteomyelitis of the vertebral bodies and discitis are the most common forms, and they typically occur together. Infection of the posterior elements of the spine (eg, facet joint) can also occur [1].
Issues related to vertebral osteomyelitis will be reviewed here. Issues related to other forms of hematogenous osteomyelitis in adults are discussed separately. (See "Osteomyelitis in the absence of hardware: Approach to diagnosis in adults".)
Epidural abscess and psoas abscess, infections often associated with vertebral osteomyelitis, are discussed separately. (See "Spinal epidural abscess" and "Psoas abscess".)
Tuberculous and Brucella vertebral osteomyelitis are discussed separately. (See "Bone and joint tuberculosis" and "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Brucellosis: Treatment and prevention".)
TERMINOLOGY —
Vertebral osteomyelitis terminology is based on the anatomic site of infection:
●Vertebral osteomyelitis – Infection of any part of the spinal column.
●Discitis (diskitis) – Infection of an intervertebral disc.
●Spondylitis – Infection or noninfectious inflammation of the joints and ligaments of the spine.
●Spondylodiscitis – Infection of intervertebral disc and adjacent vertebral body or bodies. This condition is also called osteodiscitis.
●Septic facet arthritis – Infection of a facet joint of the posterior spine.
●Posterior element osteomyelitis – Infection of bone in the posterior portion of the spine (pedicles, transverse processes, posterior spinous processes, and/or laminae) [2,3].
●Hardware-associated vertebral osteomyelitis – Infection of bone around implanted spinal hardware (also called spinal implant infection).
Vertebral osteomyelitis can also be categorized based on pathologic features, which depend on the type of pathogen [4]:
●Pyogenic – These infections are most common and are caused by pathogens that cause purulence (eg, staphylococci, gram-negative bacilli).
●Nonpyogenic (ie, granulomatous) – Atypical pathogens that create granuloma (eg, tuberculosis, Brucella spp, fungi) characterize this category. These infections are discussed in detail separately. (See "Bone and joint tuberculosis" and "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Brucellosis: Treatment and prevention".)
Additional infections commonly occur adjacent to vertebral osteomyelitis:
●Epidural abscess – Abscess within the epidural space of the spinal canal (figure 1). (See "Spinal epidural abscess".)
●Psoas abscess – Abscess within psoas muscle (figure 2). (See "Psoas abscess".)
EPIDEMIOLOGY AND RISK FACTORS —
Vertebral osteomyelitis is primarily a disease of adults, and the incidence increases with age; most cases occur in patients >50 years old [1,5-7]. Some studies suggest that men are affected more often than women [6-8].
The annual incidence of hospitalization for vertebral osteomyelitis in the United States between 1998 and 2013 rose from 2.9 to 5.4 per 100,000, with lengthy hospital stays and substantial long-term burden for patients and the health system [9]. Similar increases have been reported elsewhere, including in France, where nationwide discharge data revealed an increase from 6.1 to 11.3 per 100,000 from 2010 to 2019 [5].
Increasing incidence is likely due to increases in the number of patients with risk factors for vertebral osteomyelitis [1,6-8]:
●Increasing rates of bacteremia due to intravascular devices and other forms of instrumentation. An increasing proportion of vertebral osteomyelitis is healthcare-related and/or post-procedural (up to one-third of new cases) [10,11].
●Increasing age of the population.
●Increasing number of patients who inject drugs.
●Increasing number of immunocompromised patients, including those with diabetes mellitus or who are on corticosteroids or other immunosuppressive medications.
PATHOGENESIS
Mechanisms of infection — Bacteria can reach the bones of the spine by three basic routes (figure 1):
●Hematogenous spread from a distant site or focus of infection. (See 'Hematogenous spread' below.)
●Contiguous spread from adjacent soft tissue infection. (See 'Contiguous spread' below.)
●Direct inoculation from trauma, invasive spinal diagnostic procedures, or spinal surgery (image 1). (See 'Direct inoculation' below.)
Hematogenous spread — Hematogenous spread is by far the most common mechanism leading to vertebral osteomyelitis. Any infection that can cause bacteremia can be the source, including infections of heart valves (ie, infective endocarditis), skin and soft tissue, intravascular devices, genitourinary tract, and teeth. Injection drug use may also lead to hematogenous inoculation from unsafe injection practices. In many cases, the primary source is not identified [12].
Adult vertebral bone has abundant, highly vascular marrow with a sluggish but high-volume blood flow within nutrient vessels of the posterior spinal artery. With aging, these vessels progressively develop a characteristic "corkscrew" anatomy that may predispose to bacterial hematogenous seeding.
Bloodborne organisms that transit the vertebral marrow cavity can produce a spontaneous local suppurative infection. Initiation of infection may be facilitated by recent or prior bone trauma (eg, osteoarthritis) with disruption of normal architecture.
Hematogenous vertebral osteomyelitis almost exclusively involves two vertebral bodies and the disc between. Segmental arteries supplying the vertebrae usually bifurcate to supply two adjacent end plates of the vertebrae. Thus, hematogenous vertebral osteomyelitis often causes bone destruction in two adjacent vertebral bodies and the infection may then spread contiguously to the intervertebral disc between them. Alternatively, infection involving one vertebral endplate quickly involves the adjacent avascular disc and spreads to the adjacent vertebral endplate.
Lumbar vertebral bodies are most often involved, followed by thoracic and, less commonly, cervical vertebrae. Skip lesions (ie, areas of normal bone between infected sites) occur in less than 5 percent of reported cases of pyogenic vertebral osteomyelitis [13]. Hematogenous osteomyelitis of the sacrum is rare.
It was previously postulated that spread of infection might occur via vertebral veins known as Batson plexus [14,15]; this theory has been discounted.
Contiguous spread — Contiguous spread to the spine may occur from infected adjacent tissues, such as ruptured esophagus, diverticular or renal abscess, and infected pleural space or aorta (image 2) [16]. Post-operative wound infections may also spread to the spine.
Sacral osteomyelitis most commonly occurs as a complication of a sacral pressure ulcer, although it can follow pelvic infection, trauma, and/or surgery. Typically, it is polymicrobial and restricted to cortical bone [17,18]. Detailed discussion of pressure ulcer-associated infection is found separately. (See "Infectious complications of pressure-induced skin and soft tissue injury", section on 'Osteomyelitis'.)
Direct inoculation — Vertebral osteomyelitis has been reported as a complication of spine surgery [19], trauma, lumbar puncture, myelography, translumbar aortography, chemonucleolysis, discography, facet joint corticosteroid injection [20], epidural catheter placement, and epidural corticosteroid injection [21].
Extension of infection — Extension of infection can lead to epidural abscess, subdural abscess, or meningitis (image 1). (See "Spinal epidural abscess".)
Extension of infection anteriorly or laterally can lead to psoas, paravertebral, retropharyngeal, mediastinal, subphrenic, or retroperitoneal abscess, or pleural empyema (image 3 and table 1) [22]. (See "Psoas abscess".)
Development of epidural or paravertebral abscess is more common in the setting of gram-positive infection than gram-negative infection [23].
MICROBIOLOGY —
Hematogenous vertebral osteomyelitis is usually caused by a single pathogen.
The most commonly reported pathogens include the following [6-8,24-26]:
●Staphylococcus aureus – This organism is the most common cause of vertebral osteomyelitis in most studies.
Rates of methicillin-resistant S. aureus (MRSA) infections vary geographically. In most reports from resource-abundant countries, MRSA represents a substantial portion of cases. For example, MRSA caused 25 percent of pyogenic vertebral osteomyelitis in a 2019 study of over 350 cases in South Korea [26].
Major risk factors for MRSA infection include known colonization or prior infection by MRSA and injection drug use; other risk factors are listed in the table (table 2).
●Enteric gram-negative bacilli, particularly following urinary tract instrumentation or in patients with malignancy [7].
●Streptococci, including groups B, C, and G streptococci, viridans group, milleri group, Streptococcus bovis, and enterococci [27,28].
Pseudomonas aeruginosa, coagulase-negative staphylococci, and Candida spp occur less frequently and may be especially associated with intravascular access, immunocompromise, sepsis, or injection drug use [25,29]. (See "Candida osteoarticular infections".)
Granulomatous causes of spine infection include tuberculosis and Brucella spp, particularly in areas where these infections are endemic. (See "Bone and joint tuberculosis" and "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
Geography also influences other rarer causes of vertebral osteomyelitis. Burkholderia pseudomallei (melioidosis) is a potential pathogen in patients from peri-equatorial regions, and Salmonella are occasional causes in sub-Saharan Africa or South America. (See "Melioidosis: Epidemiology, clinical manifestations, and diagnosis", section on 'Common manifestations'.)
CLINICAL FEATURES
Clinical history — The major clinical manifestation of vertebral osteomyelitis is back pain. The pain typically localizes to the infected site and is exacerbated by physical activity or palpation of the affected area. Depending on the anatomic level of infection (eg, cervical, thoracic, lumbar), and nerve root impingement, pain may radiate to the arms, shoulders, abdomen, leg, scrotum, groin, or perineum. The pain is often worse at night, although, in the early stages, it may be relieved by bed rest. Pain may be absent in patients with paraplegia.
Spinal pain usually begins insidiously and progressively worsens, and the typical pace of progression is days to weeks [3,6-8,25,30]. However, acute severe pain can be the presenting complaint, and progression can be more rapid [31].
Patients whose infections extend into the epidural space may present with clinical features of an epidural abscess. Signs of epidural abscess often progress from focal and severe back pain, to radiculopathy, then motor weakness and sensory changes (including loss of bowel and bladder control and loss of perineal sensation), then eventual paralysis. The risk of severe neurologic deficit is increased in the presence of epidural abscess, especially with thoracic or cervical spinal involvement [32]. In a review of 50 patients in France, 32 percent had an epidural abscess at the time of diagnosis [6]. (See "Spinal epidural abscess".)
Fever is an inconsistent finding. One review noted a frequency of 52 percent [33]; lower rates have been noted in other studies [34].
A thorough clinical history may reveal specific risk factors for vertebral osteomyelitis, including presence of indwelling devices, recent instrumentation, injection drug use, recent infection at another anatomic site (eg, cellulitis, urinary tract infection), diabetes mellitus, or immunosuppression.
Physical examination — Local tenderness to gentle spinal percussion is the most useful clinical sign but is not specific. Back pain is often accompanied by reduced mobility and/or spasm of nearby muscles. Rarely, a mass or spinal deformity may be visible or palpable.
The physical examination should also include evaluation for a distended bladder (may reflect spinal cord compression), signs of psoas abscess (eg, flank pain and pain with hip extension), neurologic deficits of the upper and/or lower limbs (sensation, strength, reflexes), and saddle anesthesia and loss of anal sphincter. In a case series of 50 patients from France, neurologic deficits were detected in 40 percent at the time of diagnosis and psoas abscess was present in 12 percent [6]; in a United States series of 70 patients, 10 percent had paralysis at the time of diagnosis [7]. (See "Psoas abscess" and "Anatomy and localization of spinal cord disorders".)
A careful physical examination of the entire body is essential to evaluate for potential sources of hematogenous spread; these include injection sites and recent skin or soft tissue infection.
Laboratory findings — The white blood cell count may be elevated or normal.
Elevations in the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are observed in more than 80 percent of patients [35-37]. Elevations in ESR and CRP may be predictive of specific pathogens; in a case series of 133 patients, CRP and ESR were higher in patients whose infections were caused by S. aureus than fungal, tuberculosis, or culture-negative infections [1,38].
Overall, CRP and ESR are not or specific for vertebral osteomyelitis as other diagnostic tests (eg, magnetic resonance imaging [MRI]).
DIAGNOSIS
Clinical suspicion — Vertebral osteomyelitis should be suspected in the setting of new or worsening back or neck pain and fever, recent bloodstream infection, or infective endocarditis [1]. It should also be suspected in patients with fever and new peripheral neurologic symptoms (with or without back pain).
Additionally, it should be considered in patients with new-onset, progressive, severe back pain that does not respond to standard therapy, especially if neurologic deficits are present.
Back pain due to vertebral osteomyelitis may respond initially to bed rest and conservative measures, leading to the erroneous conclusion of minor trauma, muscle strain, or other noninfectious cause. In addition, a history of degenerative spinal disease or recent trauma sometimes obscures or delays the true diagnosis. In such cases a sedimentation rate and/or C-reactive protein (CRP; or serial values of these tests) can be useful; normal results are reassuring. Serial imaging may also serve a role in this setting.
Confirming the diagnosis — In patients with clinical features of vertebral osteomyelitis, diagnostic evaluation typically includes blood and urine cultures, inflammatory markers (erythrocyte sedimentation rate [ESR], CPR, white blood cell count), and imaging studies. A bone biopsy is obtained (either during surgery or percutaneously) if imaging is compatible with the diagnosis and blood cultures are negative (algorithm 1).
Definitive diagnosis requires isolation of bacteria or fungus from a sterilely obtained bone specimen with histologic evidence of inflammation and osteonecrosis [39]. (See 'Importance of biopsy' below.)
The diagnosis may be inferred in patients with clinical and radiographic findings typical of vertebral osteomyelitis and one of the following (see 'Clinical suspicion' above and 'Imaging studies' below):
●Positive blood cultures with a typical pathogen, such as S. aureus. In such cases, bone biopsy is not required but may still be useful if alternative diagnoses are suspected. (See 'Blood cultures' below.)
●Bone histopathology consistent with osteomyelitis in the absence of positive culture data (particularly in the setting of recent antibiotic administration). (See 'Importance of biopsy' below.)
●Persistently elevated inflammatory markers (eg, ESR, CRP) and no suspected alternative diagnosis in patients for whom bone biopsy was not performed or was nondiagnostic. (See 'Laboratory findings' above.)
Specific tests
Imaging studies — Radiologic imaging is an integral component of the evaluation for suspected vertebral osteomyelitis.
Although imaging cannot definitively confirm the diagnosis, imaging results consistent with vertebral osteomyelitis markedly increase the probability in patients with compatible clinical findings.
MRI as preferred study — For patients with suspected vertebral osteomyelitis, the imaging study of choice is MRI with and without gadolinium contrast (algorithm 1). Intravenous contrast (eg, gadolinium) does not improve the detection of osteomyelitis, but it does provide more detailed information about associated soft tissue infection or abscess.
MRI is the most sensitive imaging test for vertebral osteomyelitis and associated soft tissue complications (eg, epidural abscess, psoas abscess) [40,41].
Typical MRI findings in vertebral osteomyelitis include the following (image 1) [42,43]:
●T1-weighted images without contrast – Decreased signal intensity in infected vertebral body and disc, and loss of endplate definition (image 4).
●T1-weighted images following contrast – Enhancement of infected bone, soft tissue, and abscess margins (fluid within abscess does not enhance) (image 5 and image 6 and image 7).
●T2-weighted images – Increased signal intensity of infected disc, abscess fluid, and soft tissue. Infected vertebral body may also show increased signal (image 1 and image 7).
MRI abnormalities consistent with osteomyelitis can be observed long before plain films become abnormal. In a review of 103 patients, MRI demonstrated changes suggestive of osteomyelitis in 91 percent of patients with symptoms of less than two-weeks' duration and in 96 percent of those with symptoms of more than two-weeks' duration [44].
False-negative MRI findings have been reported in patients with vertebral osteomyelitis and epidural abscess, especially in those with concurrent meningitis or with long, linear abscesses lacking discrete margins [45]. MRI may also be falsely negative in very early infection. False-positive results can occur with bone infarction or fracture. (See 'Differential diagnosis' below.)
Radiographic findings in the setting of tuberculous vertebral osteomyelitis overlap with those seen in the setting of bacterial osteomyelitis. Multilevel involvement and extension into surrounding soft tissue with large fluid collections tends to be more prominent in tuberculosis of the spine. Some patients with spinal tuberculosis have vertebral body abnormalities in the absence of disc space involvement (disc-sparing). These issues are discussed further separately. (See "Bone and joint tuberculosis", section on 'Radiography'.)
Further discussion of use of MRI for diagnosis of osteomyelitis is found separately. (See "Imaging studies for osteomyelitis", section on 'MRI'.)
CT — Computed tomography (CT) is a reasonable alternative imaging modality when MRI is not available and in chronic infection. The addition of intravenous contrast is preferred because it helps to define soft tissue infection, particularly psoas abscesses (image 3 and image 8). For epidural abscess, CT has a high false-negative rate, even with contrast [40].
CT demonstrates findings of vertebral osteomyelitis before changes are apparent on plain films (image 9 and image 2). CT is also useful for detecting bony sequestra or involucra and in localizing the optimal approach for a biopsy (image 9 and image 10) [40].
Subtle abnormalities detected by CT, such as end plate irregularities, may not be specific for osteomyelitis, and early destructive changes may be missed.
Further discussion of the use of CT for diagnosis of osteomyelitis is found separately. (See "Imaging studies for osteomyelitis", section on 'CT'.).
Plain x-rays — If neither CT nor MRI is available, plain x-rays are an option.
However, plain films typically demonstrate radiographic findings only after the disease has become advanced. Bone destruction may not be apparent for three weeks or more after the onset of symptoms [24,46].
If a plain x-ray demonstrates vertebral osteomyelitis, additional imaging is still warranted (eg, MRI, CT) to assess the extent of disease and presence of complications (eg, epidural or paraspinal abscess).
Typical findings in vertebral osteomyelitis consist of destructive changes of two contiguous vertebral bodies with collapse of the intervening disc space (image 2 and image 6). Rarely, infection is confined to a single vertebra and produces collapse of the vertebral body, which can cause misdiagnosis as a vertebral compression fracture [47,48]. (See 'Differential diagnosis' below.)
Further discussion of the use of plain x-rays for diagnosis of osteomyelitis is found separately. (See "Imaging studies for osteomyelitis", section on 'Plain radiograph'.)
Nuclear imaging — Nuclear imaging (ie, radionuclide scanning) studies used for diagnosis of osteomyelitis include scintigraphy and positron emission tomography (PET). (See "Imaging studies for osteomyelitis", section on 'Role of nuclear imaging'.)
●Scintigraphy – The main scintigraphic studies used to evaluate vertebral osteomyelitis are bone scans and gallium scans (tagged white blood cell [WBC] scans are not recommended for vertebral osteomyelitis). They are relatively sensitive but their specificity for infection is low [49]. (See "Imaging studies for osteomyelitis", section on 'Scintigraphy'.)
These studies can be useful if MRI is contraindicated (eg, due to implantable device) or findings on CT or plain x-rays are absent or equivocal [1,49]. Given poor specificity, these studies are most useful to rule out infection.
•Three-phase bone scan – Bone scans using labeled technetium are relatively sensitive and specific, but they may produce false-positive results in patients with noninfectious disorders such as fracture. False-negative results also can occur early in infection or in cases in which bone infarction accompanies bone infection. (See "Imaging studies for osteomyelitis", section on 'Three-phase bone scan'.)
•Gallium scans – Gallium imaging is a sensitive and specific radionuclide scanning technique for vertebral osteomyelitis [50]. A typical positive test reveals intense uptake in two adjacent vertebrae with loss of the intervening disc space. In a series of 41 patients with suspected vertebral osteomyelitis, increased gallium uptake was detected in all of the 39 patients with biopsy-proven osteomyelitis; subsequent biopsy showed only degenerative changes in two patients with negative gallium scans [51]. (See "Imaging studies for osteomyelitis", section on 'Gallium and dual tracer studies'.)
•Tagged WBC scan – These scans are not recommended for the diagnosis of vertebral osteomyelitis because abnormalities are nonspecific and regions with substantial quantities of red marrow (such as the vertebral bodies) are not visualized reliably [50,52]. (See "Imaging studies for osteomyelitis", section on 'Tagged wbc scan'.)
●PET scan – PET scanning using 18-fluorodeoxyglucose (FDG), especially when combined with CT (PET-CT), is highly sensitive, with a negative predictive value for vertebral osteomyelitis of close to 100 percent. The specificity is good but may be compromised by the presence of tumor, degenerative spinal disease, and/or spinal implants [53]. In one prospective study including 32 patients with suspected vertebral osteomyelitis who underwent both MRI and fluorine-18-fluorodeoxyglucose-PET/CT (18F-FDG-PET/CT), MRI was more useful for detection of epidural/spinal abscess and 18F-FDG-PET/CT was more useful for detection of metastatic infection [54].
Further discussion of use of PET scans for diagnosis of osteomyelitis is found separately. (See "Imaging studies for osteomyelitis", section on 'PET'.)
Importance of biopsy — In patients with negative blood cultures, biopsy is warranted to confirm clinical and/or radiographic suspicion of vertebral osteomyelitis and to establish a microbiologic and histologic diagnosis.
In patients who have positive blood cultures with a pathogenic organism, biopsy is sometimes deferred because the blood pathogen is usually the cause of bone infection (algorithm 1). (See 'Confirming the diagnosis' above and 'Blood cultures' below.)
Sensitivity of biopsy varies substantially across studies. In a 2009 systematic review of 14 studies including over 1000 patients with vertebral osteomyelitis, the overall sensitivity of biopsy was 77 percent [8]. Factors that may affect the yield of vertebral biopsies include sampling technique, type of tissue sampled, ability to culture the infecting pathogen, and exposure to antibiotics prior to biopsy:
●Biopsy technique – Biopsies are obtained via open surgical procedure (during surgical debridement) or percutaneous sampling by CT or fluoroscopic guidance (image 10) [55-57]. Open surgical biopsies may have higher microbiologic yield than percutaneous biopsies, perhaps due to sampling error and/or lower volume of tissue collection during percutaneous biopsies [7,28,58]. The diagnostic accuracy of CT-guided versus fluoroscopic-guided biopsy is similar [56].
If possible, biopsy tissue is obtained from the infected bone and the infected disc space, and abscess fluid is aspirated [24,57,59]. Cultures from infected disc spaces may have higher microbiologic yield than bone biopsies [57,60]. In one study of 173 individuals with vertebral osteomyelitis and/or discitis, 6 of 43 (14 percent) bone biopsies and 66 of 152 (43 percent) disc specimens were culture positive [57]. Histopathology was positive in 47 (56 percent) of 84 specimens.
●Tests to order – Biopsy samples should be sent for histopathology as well as aerobic and anaerobic cultures. Mycobacterial and fungal cultures should be sent when suspected based on clinical and epidemiologic factors [24]. Inoculation of biopsy specimens into blood culture bottles may increase detection rates [59]. Mycobacterial cultures are especially important in patients with risk factors for tuberculosis [61]. (See "Epidemiology of tuberculosis", section on 'Risk factors'.)
●Effect of recent antibiotic therapy – Clinicians should not be deterred from obtaining a biopsy if the patient recently received antibiotics. Some studies suggest that prior antibiotic exposure reduces yield from culture [59,62], whereas other studies have found no effect [58,63,64]. Guidelines suggest withholding antimicrobial therapy, if possible, until after biopsy is obtained; however, antibiotics should not be delayed if there is concern for neurologic compromise or sepsis [1,65]. The duration for which antibiotics should be withheld is uncertain, as discussed separately. (See "Osteomyelitis in the absence of hardware: Approach to diagnosis in adults", section on 'Timing and technique'.)
Because biopsies can have false-negative results, repeat biopsies can be helpful if the clinical suspicion for vertebral osteomyelitis remains high (based on clinical and radiographic findings) [59,66]. In one retrospective study of 136 patients with vertebral osteomyelitis in the absence of bacteremia, initial percutaneous biopsy was positive in 43 percent of cases and performing a second biopsy in the culture-negative patients increased the culture-yield to 80 percent [66]. However, other studies have found a lower yield from repeat biopsies [67]. Some experts initiate empiric therapy instead of obtaining, or while awaiting the results of, a repeat biopsy. Advanced molecular testing (eg, 16S rRNA PCR, metagenomic next-generation sequencing) is emerging as an alternative to culture for pathogen-detection, but false-positives and limited sensitivity in culture-negative cases have been reported [68-71].
Additional tests
Blood cultures — At least two sets of blood cultures should be obtained in all patients with suspected vertebral osteomyelitis. Blood cultures are positive in up to 50 of cases [8,25,29,58,72].
In patients with clinical and radiographic findings typical of vertebral osteomyelitis, positive blood cultures with a likely pathogen (such as S. aureus, Staphylococcus lugdunensis) may obviate the need for tissue biopsy [1]. Similarly, a positive blood culture due to a gram-negative enteric rod, P. aeruginosa, or other invasive pathogen, is often good evidence that the same pathogen is also the cause of the vertebral osteomyelitis. However, blood culture isolates do not always correlate with culture results from biopsy; therefore, biopsy is warranted for cases in which an alternate source for the bacteremia is present or strongly suspected. (See 'Confirming the diagnosis' above.)
If blood cultures grow S. aureus, streptococci, or enterococci, evaluation for concurrent infective endocarditis is warranted, particularly in patients with underlying valvular disease, a cardiac implantable device, or signs and symptoms consistent with endocarditis (eg, new-onset heart failure). These pathogens are common causes of endocarditis. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis", section on 'Evaluation'.)
Urine culture — In addition to blood cultures, we obtain a urine culture in all patients. Urine cultures may identify urinary tract infection as a potential source, are positive in a significant number of patients with S. aureus bacteremia, and can guide antibiotic therapy if multidrug-resistant bacteria are identified. However, unlike blood cultures, a positive urine culture should never be used as a replacement for bone biopsy to make a diagnosis of vertebral osteomyelitis.
Brucellosis serology — Brucellosis serologic testing and blood cultures are warranted in the setting of unexplained fever, fatigue, and arthralgia in an individual with a possible source of exposure (eg, contact with animal tissues, ingestion of unpasteurized milk or cheese). Major endemic areas include countries of the Mediterranean basin, Persian Gulf, the Indian subcontinent, and parts of Mexico and Central and South America. The microbiology laboratory should be notified if brucellosis is suspected, because the organism is a biohazard to laboratory personnel. (See "Brucellosis: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
Tuberculosis — Diagnostic evaluation for tuberculosis is warranted in the setting of relevant risk factors; these include a family history of tuberculosis, birth or long-term residence in a highly endemic region, HIV/AIDS, chest radiograph suggestive of latent tuberculosis infection, and/or diabetes. (See "Diagnosis of pulmonary tuberculosis in adults".)
Evaluation for endocarditis — Evaluation for concurrent infective endocarditis is warranted in patients with vertebral osteomyelitis caused by certain gram-positive organisms (eg, Staphylococcus, Streptococcus, Enterococcus), particularly in the presence of bacteremia, or in patients with underlying valvular disease, cardiac implantable devices, and/or new-onset heart failure or murmur [27,65,73,74].
Evaluation for infective endocarditis is warranted even though the duration of therapy for vertebral osteomyelitis (at least six weeks) is an adequate duration for treatment of infective endocarditis in most cases. Patients with infective endocarditis require additional follow-up, evaluation for valvular disease, and prophylactic antibiotics for prevention of subsequent infective endocarditis. (See "Prevention of endocarditis: Antibiotic prophylaxis and other measures" and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)
A retrospective review including 91 cases of vertebral osteomyelitis (excluding tuberculosis, brucellosis, and culture-negative and postsurgical cases) identified 28 patients (31 percent) with infective endocarditis [73]. When patients with and without infective endocarditis were compared, the following risk factors were significantly associated with coincident infective endocarditis:
●Age >75 years [27]
●Predisposing heart condition
●Heart failure
●Positive blood cultures
●Infection due to gram-positive organisms, especially nonpyogenic streptococci or staphylococci
Endocarditis was less likely in patients with a urinary tract–presumed source of infection and with infection due to gram-negative organisms.
DIFFERENTIAL DIAGNOSIS —
The differential diagnosis of vertebral osteomyelitis includes the following conditions; they are all distinguished radiographically.
●Spinal epidural abscess – Clinical manifestations of spinal epidural abscess include fever, back pain, and neurologic deficits. It can occur concomitant with or independent of vertebral osteomyelitis. (See "Spinal epidural abscess".)
●Psoas abscess – Clinical manifestations of psoas abscess include back or flank pain, fever, and pain with hip extension; this condition be associated with or independent of vertebral infection. (See "Psoas abscess".)
●Degenerative spine disease – Degenerative spine disease causes chronic, slowly progressive back pain and is common with aging. (See "Lumbar spinal stenosis: Pathophysiology, clinical features, and diagnosis".)
●Herniated disc – Clinical manifestations of disc herniation include back pain and radiculopathy. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis", section on 'Disc herniation'.)
●Metastatic tumor – Metastatic spinal tumor is typically associated with back pain in the setting of known malignancy. Metastatic tumors may be difficult to differentiate from vertebral osteomyelitis on imaging, but features suggestive of metastatic disease are skip lesions and bony destruction that is not centered around the disc space [4].
The most common primary cancers associated with skeletal metastasis include breast, prostate, thyroid, lung, myeloma, and renal cancer. (See "Evaluation of low back pain in adults", section on 'Urgent and acute conditions' and "Epidemiology, clinical presentation, and diagnosis of bone metastasis in adults".)
●Vertebral compression fracture – Clinical manifestations of vertebral compression fracture consist of acute onset of localized back pain in the setting of risk factors for osteoporosis [47,48]. (See "Evaluation of low back pain in adults", section on 'Subacute and chronic conditions'.)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Osteomyelitis and prosthetic joint infection in adults" and "Society guideline links: Outpatient parenteral antimicrobial therapy".)
SUMMARY AND RECOMMENDATIONS
●Terminology – Vertebral osteomyelitis refers to infection of any part of the spinal column, which may include the intervertebral disc, vertebral bodies, facet joints, and/or posterior portions of the spine. (See 'Terminology' above.)
Infections commonly associated with vertebral osteomyelitis include epidural abscess and psoas abscess. (See "Spinal epidural abscess" and "Psoas abscess".)
●Risk factors – Risk factors include older age, prior spine surgery, presence of intravascular device, injection drug use, and immunocompromise. (See 'Epidemiology and risk factors' above.)
●Pathogenesis – Hematogenous spread is by far the most common mechanism leading to vertebral osteomyelitis. Any infection that can cause bacteremia can be the source (eg, endocarditis, skin infection). (See 'Pathogenesis' above.)
●Microbiology – Staphylococcus aureus is the most common cause of vertebral osteomyelitis, but other common bacteria (eg, gram-negative bacilli, Streptococcus spp) can also cause the infection. Atypical causes include tuberculosis, brucellosis, and fungal pathogens. (See 'Microbiology' above.)
●Clinical features – The main symptom is back pain, which may begin insidiously or be more acute in nature. Neurologic deficits may occur from the level of infection (eg, radiculopathy, weakness, sensory changes, bowel or bladder retention, paralysis). Neurologic deficits may be a clue that a patients has an epidural abscess. (See 'Clinical features' above.)
●Diagnostic evaluation – Patients with clinical suspicion for vertebral osteomyelitis should undergo thorough examination (including neurologic examination), imaging (MRI is the preferred study), and laboratory evaluation (including blood cultures, erythrocyte sedimentation rate [ESR], and C-reactive protein [CRP]). (See 'Physical examination' above and 'Imaging studies' above and 'Blood cultures' above and 'Laboratory findings' above.)
For patients suspected of vertebral osteomyelitis due to an atypical pathogen, further studies are often necessary (eg, Brucella serology, mycobacterial and fungal culture). (See 'Brucellosis serology' above and 'Tuberculosis' above.)
●Confirming the diagnosis – Definitive diagnosis requires isolation of bacteria or fungus from a sterilely obtained bone specimen. The bone specimen can be obtained during surgical debridement (if performed) or by radiology-guided percutaneous biopsy.
The diagnosis can be inferred in patients with clinical and imaging findings typical of vertebral osteomyelitis and one of the following:
•Positive blood culture with a typical pathogen (eg, S. aureus)
•Bone histopathology consistent with osteomyelitis
•Persistently elevated ESR and CRP with no alternative diagnosis. This criterion should only be used if bone biopsy is not possible or inconclusive.
(See 'Confirming the diagnosis' above.)
●Evaluation for endocarditis – Evaluation for concurrent infective endocarditis is warranted in patients with vertebral osteomyelitis caused by certain gram-positive organisms (eg, Staphylococcus, Streptococcus, Enterococcus), particularly in the presence of bacteremia, or in patients with underlying valvular disease, cardiac implantable devices, and/or new-onset heart failure or murmur. (See 'Evaluation for endocarditis' above.)
●Differential diagnosis – Syndromes that can have a similar clinical presentation include infections (eg, epidural abscess, psoas abscess) and noninfectious processes (eg, spinal metastases, spinal arthritis, herniated disc, compression fracture). Imaging can help differentiate these syndromes in many cases. (See 'Differential diagnosis' above.)
ACKNOWLEDGEMENT —
The UpToDate editorial staff acknowledges Malcolm McDonald, MD, who contributed to an earlier version of this topic review.
