Vertebral osteomyelitis and discitis in adults

Author: Trisha Peel, MD, MBBS

Section Editor: Denis Spelman, MBBS, FRACP, FRCPA, MPH
Deputy Editor: Keri K Hall, MD, MS

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2024. | This topic last updated: Aug 16, 2022.

INTRODUCTION

Vertebral osteomyelitis most often occurs as a result of hematogenous seeding of

one or more vertebral bodies from a distant focus [1]. Infection may also involve the
adjacent intervertebral disc space, which has no direct blood supply in adults.
Infection can also arise following surgery or injection of the disc space or via
contiguous spread from adjacent soft tissue infection.

Vertebral osteomyelitis and discitis may occur together or independently. The term
pyogenic spondylitis refers to either vertebral osteomyelitis or discitis. The diagnosis
and management of these two entities are similar in most patients.

Issues related to vertebral osteomyelitis will be reviewed here. Issues related to other
forms of hematogenous osteomyelitis in adults are discussed separately. (See
"Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section
on 'Hematogenous osteomyelitis'.)

Issues related to spinal epidural abscess and tuberculous spinal infections are
discussed separately. (See "Spinal epidural abscess" and "Bone and joint
tuberculosis".)

EPIDEMIOLOGY

Vertebral osteomyelitis is primarily a disease of adults; most cases occur in patients

>50 years old [2]. The incidence increases with age. Men are affected approximately
twice as often as women in most case series; the reason for this is not fully
understood. Risk factors for vertebral osteomyelitis include injection drug use,
infective endocarditis, degenerative spine disease, prior spinal surgery, diabetes
mellitus, corticosteroid therapy, or other immunocompromised state. (See
'Pathogenesis' below.)

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 [3]. 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
[4].Reasons for the increase in incidence include [1]:
● Increasing rates of bacteremia due to intravascular devices and other forms of
instrumentation. An increasing proportion of vertebral osteomyelitis is health
care related and/or post-procedural (up to one-third of new cases) [5,6].
● Increasing age of the population
● Increasing number of patients on renal replacement therapy
● Increasing number of patients on immunosuppressive medications

PATHOGENESIS

Mechanisms of infection — Bacteria can reach the bones of the spine by three basic
routes (see "Pathogenesis of osteomyelitis"):
● Hematogenous spread from a distant site or focus of infection
● Direct inoculation from trauma, invasive spinal diagnostic procedures, or spinal
surgery ( image 1)
● Contiguous spread from adjacent soft tissue infection

Potential sources of hematogenous or contiguous spread of infection include the

genitourinary tract, skin and soft tissue (eg, injection drug use), respiratory tract,
infected intravascular devices, postoperative wound infection, infective endocarditis,
and dental infection. In many cases, the primary site of infection cannot be identified
[7]. Less common causes include infected native or prosthetic heart valve infections,
direct spread from a ruptured esophagus, diverticular or renal abscesses, and
infected aortic lesions ( image 2) [8].

Vertebral osteomyelitis has been reported as a complication of lumbar puncture,

myelography, translumbar aortography, chemonucleolysis, discography, facet joint
corticosteroid injection [9], epidural catheter placement, and epidural corticosteroid
injection [10].

Hematogenous spread — Hematogenous spread is by far the most common cause

of vertebral osteomyelitis. Adult vertebral bone has abundant, highly vascular marrow
with a sluggish but high-volume blood flow via 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 with disruption of normal architecture.

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 usually destroys their
intervertebral disc. The lumbar vertebral bodies are most often involved, followed by
thoracic and, less commonly, cervical vertebrae. Hematogenous sacral osteomyelitis
is rare.

Skip lesions with more than one level of spinal infection occur in less than 5 percent of
reported cases. Noncontiguous epidural abscesses appear to be more common (10
percent) [11].

It was previously postulated that spread of infection might occur via vertebral veins
known as Batson plexus [12,13]; this theory has been discounted.

Contiguous spread — Contiguous spread of infection may occur from tissues

adjacent to the spine, such as the aorta, esophagus, or bowel. In such cases,
extension of infection is facilitated by absence of a circumferential cartilage plate or a
layer of subchondral compact bone [14].
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 [15,16]. (See "Infectious complications of
pressure-induced skin and soft tissue injury", section on 'Osteomyelitis'.)

Extension of infection — Extension of infection posteriorly can lead to epidural

abscess, subdural abscess, or meningitis ( image 1). Extension of infection anteriorly
or laterally can lead to paravertebral, retropharyngeal, mediastinal, subphrenic,
retroperitoneal, or psoas abscess ( image 3 and table 1). Development of epidural
or paravertebral abscess is more common in the setting of gram-positive infection
than gram-negative infection [17]. In addition, thoracic vertebral infections can extend
into the pleural space to produce an empyema [18].

Infection can occur in spinal elements other than the vertebral bodies, including the
posterior spinous processes, the facet joints, the pedicles, and, rarely, the odontoid
process [19].

MICROBIOLOGY

Most patients have monomicrobial infection. The most common cause of vertebral
osteomyelitis is Staphylococcus aureus, accounting for more than 50 percent of cases
in most series from developed countries. The relative importance of methicillin-
resistant S. aureus as a cause of vertebral osteomyelitis has increased as the
community and hospital proportion of S. aureus strains that are methicillin resistant
have increased.

Other causes of vertebral osteomyelitis include [20,21]:

● Enteric gram-negative bacilli, particularly following urinary tract instrumentation
● Nonpyogenic streptococci, including viridans group, milleri group, Streptococcus
bovis, and enterococci [22,23]
● Pyogenic streptococci, including groups B and C/G, especially in patients with
diabetes mellitus (see "Group C and group G streptococcal infection" and "Group
B streptococcal infections in nonpregnant adults", section on 'Microbiology')
 ● Pseudomonas aeruginosa, coagulase-negative staphylococci, and Candida spp,
especially in association with intravascular access, sepsis, or injection drug use
[21,24] (see "Candida osteoarticular infections")
● Tuberculous infection (see "Bone and joint tuberculosis")
● Brucellosis, especially Brucella melitensis in North Africa, the Mediterranean rim,
and the Middle East [25] (see "Brucellosis: Epidemiology, microbiology, clinical
manifestations, and diagnosis")

Geography also influences the organisms associated with vertebral osteomyelitis.

Burkholderia pseudomallei (melioidosis) is a potential pathogen in patients from peri-
equatorial regions, and Salmonella and Entamoeba histolytica are occasional causes
in sub-Saharan Africa or South America.

CLINICAL FEATURES

Symptoms and signs — The major clinical manifestation of vertebral osteomyelitis is

pain; pain is typically localized to the infected disc space area and is exacerbated by
physical activity or percussion to the affected area. Pain may radiate to the abdomen,
leg, scrotum, groin, or perineum.

Spinal pain usually begins insidiously and progressively worsens over several weeks
to months. In one series of 64 patients with hematogenous vertebral osteomyelitis,
the mean duration of symptoms was 48±40 days [21]. The pain is often worse at
night; initially, it may be relieved by bed rest. Pain may be absent in patients with
paraplegia.

Patients whose infections extend posteriorly into the epidural space may present with
clinical features of an epidural abscess; this often consists of focal and severe back
pain, followed by radiculopathy, then motor weakness and sensory changes
(including loss of bowel and bladder control and loss of perineal sensation), and
eventual paralysis. The risk of severe neurologic deficit is increased in the presence of
epidural abscess, especially with thoracic or cervical spinal involvement [26]. (See
"Spinal epidural abscess".)
Fever is an inconsistent finding. One review noted a frequency of 52 percent [2]; lower
rates have been noted in other studies [27].

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.

The physical examination should include palpation for a distended bladder (may
reflect spinal cord compression), evaluation for signs of psoas abscess (eg, flank pain
and pain with hip extension), and a careful neurologic assessment of the lower limbs.
(See "Psoas abscess".)

A careful general examination is essential to evaluate for potential sources of

hematogenous spread; these include injection sites and recent skin or soft tissue
infection.

Laboratory findings — The leukocyte count may be elevated or normal. Elevations in

the erythrocyte sedimentation rate (ESR), which can exceed 100 mm/h, and C-reactive
protein (CRP) are observed in more than 80 percent of patients [28-30].

If elevated, the ESR and CRP are useful for following the efficacy of therapy. (See
'Clinical and laboratory monitoring' below.)

DIAGNOSIS

Vertebral osteomyelitis should be suspected in the setting of new or worsening back

or neck pain, especially with fever, and/or presence of bloodstream infection or
infective endocarditis (IE) [1]. It should also be suspected in patients with fever and
new peripheral neurologic symptoms (with or without back pain) and in patients with
new back or neck pain following a recent episode of bacteremia (especially with S.
aureus) or fungemia.
The diagnosis of vertebral osteomyelitis or discitis is established based on positive
culture obtained from image guided biopsy (via computed tomography [CT] or
fluoroscopic guidance) of the involved vertebra(e) and/or disc space [31-33]. The
diagnosis may be inferred in the setting of clinical and radiographic findings typical of
vertebral osteomyelitis and positive blood cultures with a likely pathogen such as S.
aureus. Similarly, the diagnosis may be inferred in the setting of histopathologic
findings consistent with infection in the absence of positive culture data, particularly
in the setting of recent antibiotic administration. For circumstances in which there are
no positive microbiologic cultures or Gram stains and a biopsy cannot be performed,
the diagnosis may be inferred in the setting of suggestive clinical and typical
radiographic findings and persistently elevated inflammatory markers.

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 (or serial sedimentation rates) can be useful; a normal
result is reassuring.

Suggested clinical approach — Initial evaluation of patients with suspected vertebral

osteomyelitis begins with careful history and physical examination; patients should
have a thorough neurologic exam and should be questioned about predisposing
factors including presence of indwelling devices, recent instrumentation, and
injection drug use. Initial diagnostic tests include inflammatory markers (erythrocyte
sedimentation rate [ESR] and C-reactive protein [CRP]) and cultures (blood and urine),
followed by spinal imaging (magnetic resonance imaging [MRI] preferred if available)
( algorithm 1). (See 'Radiographic imaging' below.)

Evaluation for surgery is warranted for patients with neurologic deficits, radiographic
evidence of epidural or paravertebral abscess, and/or cord compression (threatened
or actual). Ongoing monitoring for emergence or progression of neurologic signs is
essential. In one case-control study including 97 patients with vertebral osteomyelitis
and severe neurologic deficit, risk factors for neurologic deficit included epidural
abscess and thoracic vertebral involvement [26]. (See 'Surgery' below.)

In the absence of the above conditions warranting surgical intervention, patients with
radiographic evidence of vertebral osteomyelitis should undergo a CT-guided needle
biopsy of the affected bone and disc space as well as aspiration of abscess if present
[20,33]. The specimens should be sent for bacterial (aerobic and anaerobic), fungal,
and mycobacterial culture as well as histologic examination.
If possible, antimicrobial therapy should be withheld until a microbiologic diagnosis is
confirmed. Clinical exceptions include neurologic compromise and sepsis; in these
circumstances, empiric antibiotic therapy is warranted [1]. (See 'Antimicrobial therapy'
below.)

A needle biopsy may not be necessary in patients with clinical and radiographic
findings typical of vertebral osteomyelitis and positive blood cultures with a likely
pathogen (such as S. aureus, Staphylococcus lugdunensis) or in patients with positive
serology for Brucella (which is warranted for patients with relevant risk factors) [1].
Similarly, a positive blood culture due to a gram-negative enteric rod, P. aeruginosa,
or other invasive pathogen is usually good evidence that the same pathogen is also
the cause of the spinal infection. However, blood culture isolates do not always
correlate with culture results from needle biopsy; therefore, needle biopsy is
warranted for cases in which an alternate source for the bacteremia is present or
strongly suspected [24]. (See "Brucellosis: Epidemiology, microbiology, clinical
manifestations, and diagnosis".)

If cultures of blood and the needle aspirate are negative and the clinical suspicion for
vertebral osteomyelitis remains high (on the basis of clinical and radiographic
findings), we advocate performing a second biopsy. In one retrospective study
including 136 patients with vertebral osteomyelitis in the absence of bacteremia, first
biopsy was positive in 43 percent of cases and a second biopsy in 40 percent of cases;
when combined with blood culture results, this approach led to microbiological
diagnosis in nearly 75 percent of cases [34]. Performing blood cultures immediately
following biopsy does not appear to add any benefit.

If repeat biopsy specimens and initial blood cultures are nondiagnostic, we usually
initiate empiric therapy as discussed below. If such therapy does not result in
objective clinical improvement in three to four weeks, a third percutaneous needle
biopsy or an open surgical biopsy should be performed. Some suggest that, if the first
set of cultures is negative, open biopsy be pursued before starting antibiotic therapy
[20]. (See 'Antimicrobial therapy' below.)

The individual clinical approach must include consideration of the location of the
infection, the underlying health of the patient, and the experience of the local
surgeons.

Diagnostic tools — Diagnostic tools for vertebral osteomyelitis include cultures

(blood and urine), imaging studies, and biopsy.

Microbiology cultures — Blood and urine cultures should be obtained in all

patients with suspected vertebral osteomyelitis; they are positive in up to 50 of cases
[21,24]. (See 'Suggested clinical approach' above.)

In the setting of positive blood cultures for gram-positive organisms, evaluation for
concurrent IE is warranted in patients with underlying valvular disease and/or new-
onset heart failure. (See 'Evaluation for endocarditis' below.)

Radiographic imaging — MRI is the most sensitive radiographic technique for

diagnosis of vertebral osteomyelitis and epidural abscess [35]. CT is a reasonable
alternative imaging modality when MRI is not available. If neither CT nor MRI is
available, plain films should be pursued; however, plain films typically demonstrate
radiographic findings only after the disease has become advanced. If a plain film
demonstrates vertebral osteomyelitis, additional imaging is still warranted to assess
the extent of disease and presence of complications (epidural or paraspinal abscess).
Radionuclide scanning may be useful if MRI is contraindicated because of
claustrophobia or presence of an implantable cardiac or cochlear device [1].
● Magnetic resonance imaging – MRI is the most sensitive radiographic technique
for diagnosis vertebral osteomyelitis [35]. Typical MRI findings in vertebral
osteomyelitis include ( image 4) [36,37]:

• Decreased signal intensity in the vertebral bodies and disc and loss of endplate
definition (T1-weighted images) ( image 5).

• Increased disc signal intensity; less often, increased vertebral body signal
intensity (T2-weighted images) ( image 1).

• Contrast enhancement of the vertebral body and disc ( image 6). Ring
enhancement of paraspinal and epidural processes correlates with abscess
formation, whereas homogeneous enhancement correlates with phlegmon
formation.
 Vertebral osteomyelitis rarely occurs without characteristic involvement of the
intervertebral disc. For cases in which the disc is spared, an erroneous diagnosis
of malignancy or compression fracture may be made [38].

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 [39].

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 [40]. False-positive results
can occur with bone infarction or fracture.

Radiographic findings in the setting of tuberculous vertebral osteomyelitis

overlap with those seen in the setting of bacterial osteomyelitis. Extension into
surrounding soft tissue tends to be more prominent in tuberculosis (TB) of the
spine, and some patients with spinal TB have vertebral body abnormalities in the
absence of disc space involvement. These issues are discussed further separately.
(See "Bone and joint tuberculosis", section on 'Radiography'.)

The role of follow-up MRI is discussed below. (See 'Role of imaging' below.)
● Computed tomography – CT demonstrates findings of vertebral osteomyelitis
before changes are apparent on plain films ( image 7). CT is also useful for
detecting bony sequestra or involucra, adjacent soft tissue abscesses ( image 8),
and in localizing the optimal approach for a biopsy ( image 9) [35].

Subtle abnormalities detected by CT, such as end plate irregularities, may not be
specific for osteomyelitis, and early destructive changes may be missed. CT has a
high false-negative rate for epidural abscess [35].
● Plain radiography – Plain radiographs are often normal in the early phases of
infection. Typical findings in vertebral osteomyelitis consist of destructive
changes of two contiguous vertebral bodies with collapse of the intervening disc
space.
 Bone destruction may not be apparent for three weeks or more after the onset of
symptoms ( image 10) [20,41]. Rarely, infection is confined to a single vertebra
and produces collapse of the vertebral body, mimicking vertebral compression
fracture [42,43].

Chest radiography is warranted in the setting of clinical suspicion for TB, but a
normal chest film does not reduce clinical suspicion of spinal TB. (See "Diagnosis
of pulmonary tuberculosis in adults" and "Bone and joint tuberculosis".)
● Radionuclide scanning – Radioisotope studies may be useful adjuncts to
diagnosis when radiographic changes on plain films or CT scans are absent or
equivocal and the suspicion for osteomyelitis is high. They are relatively sensitive
but their specificity for infection is low. Radionuclide scanning may be useful
when MRI is contraindicated [44].

• Labeled-leukocyte scans are rarely useful for the diagnosis of vertebral

osteomyelitis because abnormalities typically manifest as a nonspecific
photopenic defect with a reduced uptake of isotope [45].

• Three-phase bone scintigraphy using labeled technetium is a relatively

sensitive and specific test, but it 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.

• Gallium imaging is a sensitive and specific radionuclide scanning technique for

vertebral osteomyelitis. 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 [46].

• Positron emission tomography (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 [47]. 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 [48].

Biopsy — In general, biopsy is warranted to confirm clinical and/or radiographic

suspicion of vertebral osteomyelitis and to establish a microbiologic and histologic
diagnosis.

Biopsy material is obtained via an open procedure or needle biopsy by CT or

fluoroscopic guidance ( image 9) [31-33]. The diagnostic accuracy of CT-guided
versus fluoroscopic-guided biopsy is similar [32]. In one study of 92 patients with
vertebral osteomyelitis who had a biopsy, open biopsies had a higher microbiologic
yield than needle biopsies (91 versus 53 percent) [49]. In a subsequent study including
129 patients with vertebral osteomyelitis, open biopsy had a higher diagnostic yield
(70 percent) than fine needle aspirate (41 percent) or core biopsy (30 percent) [23].

Biopsies from infected disc spaces may have higher microbiologic yield than bone
biopsies. 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 [33]. Forty-seven (56 percent) of 84 histopathology (bone or disc)
specimens were positive for osteomyelitis or discitis. In an earlier study of 102
patients, comparison of the yield of cultures from the vertebral endplate disk, disk
space, and adjacent paravertebral soft tissues revealed a trend favoring disk space or
paravertebral soft tissue versus endplate disk cultures [50]. Prior antibiotic therapy
confounded the results of both studies, and the overall yield of positive cultures was
less than 50 percent.

Clinicians should not be deterred from obtaining a biopsy if the patient has received
antibiotics recently [49,51]. Prior antibiotic exposure is likely to reduce the yield but
not critically [33,52].

Samples should be sent for aerobic, anaerobic, mycobacterial, and fungal cultures
and histopathology [20]. The sensitivity (measured by yield of positive cultures or
Gram stain of aspirated material) varies between studies from a low of 50 percent [53]
to a high of 73 to 100 percent [27,54].

Rarely, nucleic acid amplification testing may be useful if initial aerobic and anaerobic
cultures are negative [1]. In one study including 19 patients with discitis,
amplification-based DNA analysis of aspirated disc material correlated well with
traditional culture methods [55]. A subsequent study demonstrated the potential
value of 16S rRNA gene polymerase chain reaction (PCR) assay of biopsy
material/aspirates as an adjunct to culture, although there were some false-positive
results [56]. Contamination with skin flora is a potential problem with DNA-based
diagnostic methods.

Recent studies have also highlighted the potential role of metagenomic next-
generation sequencing in diagnosis of spinal infection. In one study with 30 cases of
spinal infection, the application of metagenomic next-generation sequencing
demonstrated improved sensitivity and preserved specificity when compared to
traditional culture-based approaches [57]. However, costs and access to this approach
limits clinical utility.

Additional tests — Additional diagnostic tests may be warranted based on

epidemiologic factors; these include:
● Brucellosis serology – Brucellosis serologic testing is 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. (See "Brucellosis: Epidemiology, microbiology, clinical manifestations,
and diagnosis".)
● Tuberculosis – Diagnostic evaluation for TB is warranted in the setting of relevant
risk factors; these include a family history of TB, birth or long-term residence in a
highly endemic region, HIV/AIDS, chest radiograph suggestive of latent TB
infection, and/or diabetes. (See "Diagnosis of pulmonary tuberculosis in adults".)

Evaluation for endocarditis — Evaluation for concurrent IE is warranted in patients

with underlying valvular disease and/or new-onset heart failure in the setting of
positive blood cultures for gram-positive organisms [22,58,59]. This is warranted even
though the duration of therapy for vertebral osteomyelitis (at least six weeks) is an
adequate duration for treatment of IE in most cases. Patients with IE require
additional follow-up evaluation for valvular disease as well as prophylactic antibiotics
for prevention of subsequent IE. (See "Clinical manifestations and evaluation of adults
with suspected left-sided native valve endocarditis" and "Prevention of endocarditis:
Antibiotic prophylaxis and other measures".)

A retrospective review including 91 cases of vertebral osteomyelitis (excluding TB,

brucellosis, and culture-negative and postsurgical cases) identified 28 patients (31
percent) with IE [58]. When patients with and without IE were compared, the following
risk factors were significantly associated with coincident IE:
● Age >75 years [22]
● Predisposing heart condition
● Heart failure
● Positive blood cultures
● Infection due to gram-positive organisms, especially nonpyogenic streptococci or
staphylococci

IE 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. (See "Spinal epidural abscess".)
● Psoas abscess – Clinical manifestations of psoas abscess include back or flank
pain, fever, and pain with hip extension. (See "Psoas abscess".)
● Degenerative spine disease – Degenerative spine disease is common with aging,
is associated with back pain, but does not usually result in radiculopathy. (See
"Acute lumbosacral radiculopathy: Etiology, 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".)
● Metastatic tumor – Metastatic spinal tumor is typically associated with back pain
in the setting of known malignancy; the most common primary cancers
associated with skeletal metastasis include breast, prostate, thyroid, lung, and
renal cancer. (See "Evaluation of low back pain in adults", section on 'Serious
etiologies' 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. (See "Evaluation of low back pain in adults", section on 'Less
serious etiologies'.)

TREATMENT

Management of vertebral osteomyelitis consists of antimicrobial therapy and

percutaneous drainage of paravertebral abscess(es) if present. Timely surgical
intervention is usually warranted for patients with neurologic deficits, radiographic
evidence of epidural or paravertebral abscess, and/or cord compression (threatened
or actual).

During the course of treatment for vertebral osteomyelitis, the pace of progression
can change suddenly, with potential for catastrophic complications. Therefore, close
observation (especially in the first two weeks after diagnosis) is essential. New
neurologic manifestation(s), persistent back pain, and/or features of sepsis require
immediate investigation.

Antimicrobial therapy

Clinical approach — Selection of antimicrobial therapy should be tailored to results

of biopsy or blood culture.

If possible, antimicrobial therapy should be withheld until a microbiologic diagnosis is

confirmed. Clinical exceptions include neurologic compromise and sepsis; in these
circumstances, empiric antibiotic therapy is warranted [1].

If blood and biopsy cultures are negative and the clinical suspicion for vertebral
osteomyelitis is high based on clinical and radiographic findings, initiation of empiric
therapy is warranted. (See 'Empiric therapy' below.)

Pathogen-directed therapy — No randomized controlled studies have

compared antibiotic regimens for vertebral osteomyelitis. Choice of antibiotic therapy
should be guided by biopsy or blood culture results:
● Staphylococcal spp – If the organism is found to be methicillin-susceptible
Staphylococcus, we recommend treatment with an anti-staphylococcal penicillin
such as nafcillin or oxacillin (2 g intravenously [IV] every 4 hours) or cefazolin (2 g
IV every 8 hours); flucloxacillin is also an acceptable agent (not available in the
United States).

If the Staphylococcus is methicillin resistant or if the patient is allergic to beta-

lactam antibiotics, we favor beta-lactam desensitization or treatment with
vancomycin ( table 2). We do not use ceftriaxone as an alternative to cefazolin
or antistaphylococcal penicillin in the absence of special circumstances (such as
inability to give multiple daily intravenous doses). For patients who are unable to
tolerate vancomycin due to allergy, daptomycin (6 mg/kg IV once daily) is an
acceptable alternative.
● Streptococcal spp – If the streptococci is fully sensitive to penicillin (minimum
inhibitory concentration [MIC] <0.12 mcg/mL), we recommend treatment with
either ceftriaxone (2 g IV every 24 hours) or penicillin G (12 to 18 million units/day
by continuous infusion or in six divided daily doses).

If the Streptococcus has intermediate susceptibility to penicillin (MIC between

0.12 and 0.5 mcg/mL), we typically treat with ceftriaxone (2 g IV every 24 hours).
Alternatively, penicillin (24 million units/day per continuous infusion or in six
divided daily doses) may be used. Patients with intermediate or fully resistant
streptococci should be treated in collaboration with an infectious disease
specialist. Specialized in vitro testing may be needed to select an appropriate
antibiotic regimen for infections caused by fully resistant streptococci.
 ● Gram-negative bacilli – Choice of a specific agent for empiric therapy of gram-
negative bacilli should be based on knowledge of the prevailing pathogens (and
susceptibility patterns) within the health care setting. Initial treatment with one of
the following is appropriate:

• Third-generation cephalosporin (ceftriaxone 2 g IV daily or ceftazidime 2 g IV

every 8 hours or cefotaxime 2 g IV every 6 hours).

• Fourth-generation cephalosporin (cefepime 2 g IV every 8 to 12 hours). Dosing

every 12 hours is sufficient in most cases; dosing every 8 hours is reasonable in
patients with febrile neutropenia (particularly in the setting of known or
suspected osteomyelitis due to Pseudomonas spp).

• Fluoroquinolone (ciprofloxacin 400 mg IV every 12 hours or 500 to 750 mg

orally every 12 hours).
● Cutibacterium (formerly Propionibacterium) acnes – For treatment of infection
due to C. acnes, we favor penicillin (20 million units IV daily by continuous
infusion or in six divided doses) or ceftriaxone (2 g IV every 24 hours). Patients
allergic to beta-lactams may be treated with vancomycin ( table 2).
● Fungal infection – Treatment of fungal vertebral osteomyelitis is discussed
separately. (See "Candida osteoarticular infections".)

Empiric therapy — Patients with negative Gram stain and culture results should
be treated with an antimicrobial regimen with activity against the common causes of
vertebral osteomyelitis, including staphylococci, streptococci, and gram-negative
bacilli.

An appropriate empiric regimen consists of vancomycin ( table 2) plus one of the

following: cefotaxime (2 g IV every 6 hours), ceftazidime (1 to 2 g IV every 8 to 12
hours), ceftriaxone (2 g IV daily), cefepime (2 g IV every 12 hours), or ciprofloxacin
(400 mg IV every 12 hours or 500 to 750 mg orally twice daily).

Anaerobes are uncommon pathogens in patients with vertebral osteomyelitis, and we

do not routinely add anaerobic coverage to initial empiric therapy. Such coverage is
warranted if clinical features suggest that the infection may be due to anaerobic
organisms (such as in the setting of a concomitant intra-abdominal abscess) or if the
Gram stain is positive but aerobic cultures are negative. In such cases, metronidazole
(500 mg IV every six hours) may be added to the above regimen.

If empiric therapy does not result in objective clinical improvement (decreasing

inflammatory markers, resolving fever and back discomfort) in three to four weeks, a
repeat percutaneous needle biopsy or open surgical biopsy is required
( algorithm 1).

Duration of therapy and follow-up — We routinely treat for a minimum of six

weeks, with careful review to determine if further treatment is required [1,60]. Longer
duration of therapy (eight weeks in some cases) is warranted for patients with
undrained paravertebral abscess(es) and/or infection due to drug-resistant organisms
(including methicillin-resistant S. aureus [MRSA]) [61]. In some cases, up to 12 weeks
of therapy may be necessary, particularly in the setting of extensive bone destruction;
the duration of therapy should be tailored to individual circumstances during the
course of clinical follow-up. (See 'Clinical and laboratory monitoring' below.)

The above approach to duration of therapy is supported by the following studies:

● A randomized trial including 351 patients with vertebral osteomyelitis
demonstrated that six weeks of antibiotic treatment was not inferior to 12 weeks
of antibiotic therapy with respect to the proportion of patients cured at one year
[60]. The number of patients with abscesses in the trial was low (19 percent), and
computed tomography (CT)-guided drainage was needed in only 4 percent of
cases. In addition, a short duration of intravenous therapy was administered
(median 14 days); the most common oral antibiotic regimen was a
fluoroquinolone with rifampin. The trial did not include patients with culture-
negative infections. The most commonly isolated pathogen was S. aureus;
fluoroquinolones are not regarded as ideal drugs for treatment of staphylococcal
infections.
● A retrospective review including 314 patients with vertebral osteomyelitis noted
that independent risk factors conferring an increased likelihood of relapse in
patients treated <8 weeks included presence of undrained paravertebral
abscess(es) and MRSA infection; in the absence of these findings, the likelihood of
relapse in patients treated <8 weeks was much lower [61].
Following at least two weeks of parenteral therapy, completion of treatment with oral
therapy may be reasonable in the following circumstances [1,62,63]:
● The infection is uncomplicated and the patient has no significant comorbidities.
● A favorable clinical response to initial parenteral therapy is observed.
● A suitable drug is available, with proven susceptibility to the causative organism
and excellent bioavailability.
● There is a high chance of reliable absorption of oral medication. Clinicians should
check for concomitant medication that may hinder absorption.
● Compliance with oral therapy can be assured or carefully monitored.

Oral antibiotic regimens for completing treatment of vertebral osteomyelitis are

summarized in the table ( table 3).

Patients with laboratory and radiographic evidence of treatment failure warrant

repeat tissue biopsy (via image-guided aspiration or surgery) for microbiologic and
histologic examination.

Clinical and laboratory monitoring — During antimicrobial therapy, patients

should be followed carefully for clinical signs of soft tissue extension, paraspinal
abscess, and cord compression.

Patients should also be followed with weekly monitoring of inflammatory markers

(erythrocyte sedimentation rate [ESR] and C-reactive protein [CRP]) [1]. In one
retrospective study including 44 patients with vertebral osteomyelitis, those without a
significant decline in the ESR during the first month of therapy were more likely to fail
medical therapy (9 of 18 cases compared with 3 of 26 cases with a >50 percent fall in
ESR) [29]. However, a rapid decline was not common: the ESR either rose or failed to
decline during the first two weeks of treatment in 19 of 32 patients who were
ultimately cured with medical therapy. Similar findings have been reported by others
[64]. CRP normalizes more rapidly than the ESR after successful treatment of spinal
infections and after uncomplicated spinal fusion surgery [35].

Role of imaging — Routine follow-up imaging studies are not necessary. Regular
imaging during treatment and in the presence of clinical improvement will not benefit
the outcome. Magnetic resonance imaging (MRI), CT, and plain films may appear to
worsen for several weeks after the initiation of antibiotic therapy that will be
ultimately successful [39].

Follow-up imaging studies are warranted in patients whose clinical status has not
improved at the planned time for discontinuation of antibiotics in order to evaluate
for the presence of an abscess in need of drainage or to detect spinal instability
amenable to surgical intervention [1].

The utility of obtaining imaging studies four to eight weeks after completion of
treatment of vertebral osteomyelitis was examined in a retrospective study including
79 patients [65]; none of 27 patients who demonstrated improvement in follow-up
MRI studies had evidence of treatment failure after one year of follow-up. In contrast,
5 of 38 patients (13 percent) and 4 of 14 patients (29 percent) whose initial follow-up
images demonstrated equivocal changes or evidence of radiographic worsening
subsequently failed medical treatment during long-term follow-up.

Associated hardware — Development of vertebral osteomyelitis in the presence of

spinal hardware typically reflects a complication of the hardware placement. Most
patients have an associated wound infection, although rarely hematogenous seeding
of hardware can occur. In such cases, treatment should be based on culture data
obtained from wound drainage and/or operative debridement. Typically such
infections are treated with intravenous antimicrobial therapy tailored to culture
results until bone fusion has been achieved (at least six weeks). If removal of the
hardware following union is feasible, repeat cultures should be obtained at the time
of hardware removal to guide subsequent therapy, which typically includes at least
another six weeks of antimicrobial therapy. If hardware removal is not feasible,
antimicrobial suppression (tailored to culture and susceptibility data) may be required
either after or in lieu of a long course of parenteral therapy. Rarely oral therapy can be
used as primary therapy if the causative organism is susceptible to an oral agent such
as fluoroquinolone.

Issues related to treatment of infections associated with hardware are discussed

further separately. (See "Nonvertebral osteomyelitis in adults: Treatment", section on
'Presence of orthopedic hardware'.)

Surgery — Indications for surgery include [1,20]:

 ● Presence of neurologic deficits
● Presence of epidural or paravertebral abscesses in need of drainage (see "Spinal
epidural abscess")
● Threatened or actual cord compression due to vertebral collapse and/or spinal
instability
● Progression, persistence, or recurrence of disease (as documented by persistently
positive blood cultures or worsening pain) despite appropriate antimicrobial
therapy

There are no randomized trials evaluating surgical management of vertebral

osteomyelitis [1]. Placing hardware in the setting of spinal infection has raised
concern regarding recurrent or chronic infection due to adherence of bacteria to
foreign material. It is common practice to administer an additional six-week 'tail' of
oral antibiotics, although there is little evidence to guide management. One
retrospective study has indicated that, when spinal stabilization is required, timely
instrumentation may be safe in the setting of appropriate selection and duration of
antimicrobial therapy [66]. Another study reported outcomes for 100 patients with
vertebral osteomyelitis who underwent a variety of surgical procedures, which were
highly variable; approximately one-quarter of patients had residual pain and a similar
proportion required repeat surgery [67].

In contrast to the preceding study, a report of 42 patients with vertebral osteomyelitis

who required surgery, 40 had complete resolution of their deficits with no recurrences
following a two-stage procedure that included anterior debridement and strut
grafting followed by delayed instrumented posterior fusions [68]. Patients received an
average of 14.4 days of intravenous antibiotics after the anterior debridement and six
weeks of intravenous therapy following the posterior instrumentation (see 'Prognosis'
below). In a systematic review of nine observational studies with 299 patients,
reinfection rates were similar for patients undergoing acute versus delayed
instrumentation (15.7 versus 15.9 percent), although the analysis was limited by lack
of clarity regarding the type of surgery performed in included studies [69].

In general, paravertebral abscess can be managed by CT-guided catheter drainage.

Epidural abscess in the setting of neurologic deficit should be managed with surgical
intervention; this may include open drainage, bone debridement, and interbody
fusion (with or without bone grafting and posterior instrumentation). (See "Spinal
epidural abscess".)

Adjunctive measures — Bed rest and analgesics are generally helpful in managing
pain after the diagnosis is established. A fitted back brace often provides substantial
back relief and enhances mobility for patients with severe pain. Clinicians should have
a low threshold for referral to a specialist pain service.

Early bed rest may be particularly important, especially in lumbar osteomyelitis. When
the patient is upright, the whole weight of the upper body is transmitted to the point
of active infection. It is our practice to put patients with severe pain to bed for at least
10 days and use intensive in-bed, nonweight-bearing physical therapy and long-acting
oral analgesics. In such circumstances, prophylactic measures for prevention of deep
venous thrombosis are warranted. (See "Prevention of venous thromboembolic
disease in acutely ill hospitalized medical adults".)

PROGNOSIS

The most serious complication of vertebral osteomyelitis is neurologic impairment

secondary to either abscess formation or bony collapse. Most patients have gradual
improvement in back pain after therapy is begun, and the pain typically disappears
after bone fusion occurs. However, back pain can persist. The best way to reduce the
morbidity and mortality associated with vertebral osteomyelitis is to minimize the
time between the onset of symptoms and the initiation of appropriate therapy.

The long-term outcome in vertebral osteomyelitis was evaluated in a retrospective

study of 253 patients with vertebral osteomyelitis with median duration of follow-up
6.5 years (range 2 days to 38 years) [70]. Relapse occurred in 14 percent and residual
symptoms occurred in 31 percent; 11 percent died (all-cause mortality). Surgery was
performed in 43 percent of patients and was successful in 79 percent of cases.
Independent risk factors for death or residual symptoms included neurologic
compromise at the time of diagnosis (eg, motor weakness, spinal instability,
paralysis), nosocomial acquisition of infection, and delay in diagnosis. The results of
this study need to be interpreted with caution since cases were collected over a long
time period (1950 to 1994), which means that some cases occurred prior to the
development of modern imaging and diagnostic techniques.

In another study including 260 patients with vertebral osteomyelitis, three-quarters of

treatment failures occurred within 4.7 months of diagnosis [5]. Multivariate analysis
indicated that infection with S. aureus was associated with increased risk of relapse.
Longer-term outcomes included neurological deficit (16 percent) and persistent back
pain (32 percent).

Major depression is a well-recognized complication of chronic back pain (about a third

of patients) and is an important potential long-term consequence [71,72].

Overall morbidity and mortality tends to increase with age [73]; this may be related to
delayed diagnosis (especially when people have background degenerative spinal
disease or have communication difficulties), multiple comorbidities, and age-related
frailty [74]. Older patients are also more likely to have concomitant infective
endocarditis (IE); in one study including 351 patients with vertebral osteomyelitis (85
of whom were ≥75 years of age), IE was diagnosed in 37 percent of patients ≥75 years
compared with 14 percent of patients <75 years [75].

Mortality — Prior to the discovery of antibiotics, vertebral osteomyelitis was fatal in

approximately 25 percent of cases [14]. Mortality due to vertebral osteomyelitis in the
antibiotic era is less than 5 percent, and the rate of residual neurologic deficits among
survivors is less than 7 percent. Delays in diagnosis can lead to disabling
complications [1].

In a large retrospective study including more than 7000 patients with vertebral
osteomyelitis, in-hospital mortality (6 percent) was largely determined by
comorbidities including diabetes, end-stage kidney disease, cirrhosis, and malignancy
[76].

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

● Pathogenesis – Vertebral osteomyelitis occurs by three basic routes:
hematogenous spread from a distant site or focus of infection (this is the most
common mechanism), direct inoculation from trauma or spinal surgery, and
contiguous spread from adjacent soft tissue infection. (See 'Mechanisms of
infection' above.)
● Microbiology – The most important infecting organism in vertebral osteomyelitis
is Staphylococcus aureus, accounting for more than 50 percent of cases. Other
pathogens include nonpyogenic streptococci, pyogenic streptococci including
groups B and C/G, enteric gram-negative bacilli, Candida spp, Pseudomonas
aeruginosa, Brucella spp, and Mycobacterium tuberculosis. (See 'Microbiology'
above.)
● Clinical features – The major clinical manifestation of vertebral osteomyelitis is
back or neck pain, with or without fever. The most common clinical finding is local
tenderness to percussion over the involved posterior spinous processes. The
most common laboratory abnormalities are elevated erythrocyte sedimentation
rate and C-reactive protein. (See 'Clinical features' above.)
● Diagnosis – Vertebral osteomyelitis should be suspected on the basis of clinical
features and radiographic studies (magnetic resonance imaging is the most
sensitive radiographic technique) and confirmed by biopsy of the infected
intervertebral disc space or vertebral bone. Blood cultures are positive in up to 50
to 70 percent of patients; a biopsy may not be necessary in patients with clinical
and radiographic findings typical of vertebral osteomyelitis and positive blood
cultures with a likely pathogen. (See 'Diagnosis' above.)
● Diagnostic evaluation – Every effort should be made to identify the pathogen(s)
before starting antimicrobial treatment. In patients with suspected vertebral
osteomyelitis, we favor the clinical approach described above and summarized in
 the algorithm ( algorithm 1). Evaluation for concurrent infectious endocarditis
may be warranted in select patients. (See 'Suggested clinical approach' above.)
● Role of surgery – Most cases of vertebral osteomyelitis respond to antimicrobial
therapy. Surgery is necessary in a minority of patients with vertebral
osteomyelitis; prompt surgery is warranted for patients with focal neurologic
deficits, epidural or paravertebral abscess, and/or cord compression. (See
'Treatment' above and 'Surgery' above.)
● Antibiotic therapy – If possible, antimicrobial therapy should be withheld until a
microbiologic diagnosis is confirmed. Clinical exceptions include neurologic
compromise and sepsis; in these circumstances, empiric antibiotic therapy is
warranted. Choice of antibiotic therapy should be guided by biopsy or blood
culture results if available. For patients with negative culture results, empiric
treatment is warranted based on the most likely organisms to cause infection.
(See 'Clinical approach' above.)

• Duration of antibiotic therapy – We routinely treat for a minimum duration of

six weeks. Longer duration of therapy (at least eight weeks) is warranted for
patients with undrained paravertebral abscess(es) and/or infection due to
drug-resistant organisms (including methicillin-resistant S. aureus). The
duration of therapy should be tailored to individual circumstances during the
course of clinical follow-up. (See 'Duration of therapy and follow-up' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Malcolm McDonald, MD, who contributed
to an earlier version of this topic review.
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