Accepted Manuscript

Imaging Spinal Infection

Jay Acharya, M.D., Wende Gibbs, M.D.

PII: S2352-6211(16)30006-7
DOI: 10.1016/j.jrid.2016.03.001
Reference: JRID 73

To appear in: Radiology of Infectious Diseases

Received Date: 6 March 2016

Revised Date: 14 March 2016
Accepted Date: 15 March 2016

Please cite this article as: Acharya J, Gibbs W, Imaging Spinal Infection, Radiology of Infectious
Diseases (2016), doi: 10.1016/j.jrid.2016.03.001.

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 ACCEPTED MANUSCRIPT

Imaging Spinal Infection

Jay Acharya, M.D. (Corresponding Author)

University of Southern California
Department of Radiology
1500 San Pablo Street, 2nd Floor
Los Angeles, CA 90033

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323-442-7471
Jay.Acharya@med.usc.edu

Wende Gibbs, M.D.

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University of Southern California
Department of Radiology
1500 San Pablo Street, 2nd Floor
Los Angeles, CA 90033

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Imaging Spinal Infection

1. Introduction:

Infection of the vertebral column may lead to profound neurologic deficits,

structural deformity, and may lead to significant morbidity and mortality. Infection

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of the vertebral column may have a variety of different clinical presentations, which

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in turn, may present with differing imaging characteristics. Furthermore, directed

treatment options of these infections are critical in order to optimize patient

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recovery. The proximity of the spinal column to critical structures including the

spinal cord, mediastinum, and aorta make accurate and early diagnosis integral in

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patient recovery. Less than 2-4% of all cases of osteomyelitis are secondary to

infection involving the vertebral column; however, its importance is key given the
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critical adjacent structures. [1, 2] This article will review the salient imaging

characteristics of vertebral column infection with focus on discitis/osteomyelitis

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and adjacent structures.

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1.1 Spondylitis and spondylodiskitis:

A variety of organisms may result in infection of the vertebral column, including

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bacteria, mycobacteria, and fungus. Patients with infection of the spine may have
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variable clinical presentations, which can make diagnosis difficult. Typically,

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patients present with back pain, tenderness, and focal rigidity in the site of the

infection. Fever may also be a presenting factor although is reported in less than

20% of patients. Neurological symptoms are rare and usually are associated with

infection resulting in regional mass effect. [3, 4] Patients can have radicular nerve

pain if there is inflammation affecting adjacent nerve roots. Additionally, epidural

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extension can lead to more severe neurologic deficits. If untreated, infection may

involve adjacent structures by direct extension, including involvement of the aorta,

esophagus, and paravertebral musculature. A recent literature review by

Buensalido et al discussed the utility of biomarkers for assessment of spinal

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infection. Their literature review concluded that patients with spondylodiskitis and

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a positive culture was associated with significantly higher C-Reactive Protein (CRP)

levels (range: 22-400 mg/L), and correlated better than elevated ESR levels (range:

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30-127 mm/h). Procalcitonin (PCT) has also been used as a biomarker for

osteomyelitis. A serum PCT level of >0.4 ng/mL was reported to be 100% specific

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for diagnosis of acute osteomyelitis; however, PCT levels may decrease once

antibiotics have been implemented and limited studies have been performed to
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assess the utility of PCT as a biomarker in chronic osteomyelitis. [5]

1.2 Pathophysiology:
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The most common hypothesis of infectious involvement of the vertebral column is

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secondary to hematogenous spread with deposition of an infected micro-embolus

lodging into a metaphyseal artery in the vertebra, which causes infarction at this site
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and secondary infection results. The endplates are most frequently involved
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because of the vascular supply is most abundant at this site, in the adult population.
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The metaphyseal artery in adults is an end artery, which results in infarction, then

adjacent extension to the adjacent same level endplate through primary periosteal

arteries. Extension to adjacent level endplates occurs via extension through

intermetaphyseal arteries. [6] The adult disc is nearly avascular, which precludes

blood borne immune defense mechanisms at this site. [7, 8]

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A second route of hematogenous spread is via venous involvement. The Batson

plexus, which forms the epidural venous plexus and serves as a conduit of spread of

infection. Venous spread has been discussed in patients with inflammatory bowel

disease and urinary tract infection, with propagation of the infection through the

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Batson plexus and into the vertebral column, usually involving the lumbar spine. [9]

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Direct extension may also lead to infection, which can be seen in patients in the

setting of penetrating trauma and open wounds. Infection may also occur from

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direct involvement from surgical intervention, from both spine surgery or surgical

intervention of adjacent structures. Procedures including epidural spinal injections,

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lumbar puncture, vertebroplasty, kyphoplasty, facet block, and the use of indwelling

catheters, such as lumbar drain, spinal pain pump catheters, and spinal cord
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stimulator leads may also result in infection. [10, 11] Other risk factors that

predispose spinal infection include, malnutrition, substance abuse, HIV infection,

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malignancy, chronic renal failure, septicemia, liver failure, and diabetes mellitus. [4,
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12]

2. Bacterial Spondylitis/spondylodiskitis:
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The lumbar spine is the most common location for pyogenic spondylodiskitis,
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accounting for 48% of cases. The thoracic spine is involved in approximately 35% of
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cases, with cervical spine involvement comprising 6.5% of cases of pyogenic

spondylodiskitis. [13]

Pyogenic spondylitis is usually caused by hematogenous spread of infection. Sources

of septic embolism are most commonly from the genitourinary tract, followed by

skin and respiratory infections. Bacterial spondylitis may also be caused by direct
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extension from penetrating trauma, surgical intervention, or from adjacent infected

structures. These include invasion from the oropharynx, lung pleura, or from

infection involving the thoracic or abdominal wall. The causative organisms are

predominantly gram-positive, with Staphylococcus aureus as the most common

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bacterium. Enterobacteriaceae comprise approximately 30% of cases, with other

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less common causative organisms including Staphylococcus epidermidis,

Haemophilus influenzae, and Streptococcal species. [14] Escherichia coli is the most

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common gram-negative source. Pseudomonas is commonly seen in intravenous

drug abusers. Salmonella is relatively more commonly encountered in patients with

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Sickle cell disease. [15] Salmonella spondylodiskitis has also been implicated in

disease spread to the aorta and mycotic aneurysm formation. [16] There is a similar
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predilection for males and females. [17]

Patient presentation is variable in patients with pyogenic infections, but typically

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involve focal back pain, myalgia, and muscle spasm, which are reported in more
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than 90% of cases. [18] Fever and elevated white blood cell counts are reported in

approximately 40-50% of patients. [6] Additionally, erythrocyte sedimentation rate

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and CRP are almost always elevated. [19]

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While plain radiography is often the primary imaging examination performed due to
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its availability and cost efficiency, the findings are often not evident until later in

disease course. Radiographic evidence of osseous demineralization requires 30% to

40% loss of the osseous matrix, which may occur two weeks after onset of clinical

symptomology. [20] Evaluation of soft tissue structures on plain radiographic

imaging can also provide a secondary sign of infection and may clue the Radiologist
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and clinician to a suspicious area. Computed tomography is not considered to be of

much utility for diagnosis of intervertebral disk infection. [21, 22] However, CT is

often utilized in image guidance to obtain samples of infected specimens, for both

osseous and non-osseous tissue.

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The mainstay to diagnose and assess the extent of disease involvement is with MR

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imaging. MR is the most sensitive imaging modality to assess for early osteomyelitis

[23]. The earliest imaging finding (across all imaging modalities) is osseous bone

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marrow edema. [24] Marrow edema manifests as ill-defined hypointense signal on

T1-weighted imaging. There is often loss of endplate definition in the vertebral body

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endplates adjacent to the level of the infected intervertebral disk. Bone marrow

edema demonstrates hyperintense signal on T2-weighted imaging. With T2-

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weighted imaging, the intervertebral disk space may show increased signal

intensity, as well as an abnormal configuration of the infected disk. The use of fat
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suppression techniques, specifically short tau inversion recovery (STIR), provides

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the highest sensitivity for increased water content within the infected tissue. It is

important, however, to note that MR imaging findings of osseous infection may lag
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behind the clinical symptoms. Follow-up MR imaging may demonstrate imaging

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findings of diskitis/osteomyelitis in cases with persistent clinical suspicion and a

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negative initial MR imaging examination. Furthermore, MR imaging findings may

lag behind the healing phase of spinal diskitis/osteomyelitis; so follow-up imaging

should be performed judiciously. The Radiologist should maintain careful

consideration of the clinical status of the patient when evaluating follow up studies.

A study conducted by Layton et al demonstrated no specific associations on 4 to 8

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week follow up MR imaging and the clinical status in their population cohort

involving patients with spinal infection. [25] As can be seen in healing infection in

other parts of the body, decreased inflammatory changes in the adjacent soft tissue

correlates as one of the earliest imaging findings of improvement in the infection.

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[26] Healing can also be demonstrated by a return to the expected fatty marrow

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signal within the involved vertebral bodies. This finding is demonstrated with

hyperintense signal in the bone marrow on T1-weighted imaging, which signifies an

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underlying decrease in the edema and inflammation in these areas.

3. Tuberculous Spondylitis/spondylodiskitis:

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The prevalence of tuberculosis has declined across the world secondary to disease

recognition and antibiotic use. However, tuberculosis is still commonly encountered

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in immunocompromised patients, the homeless population, and third world

countries. The initially low-grade and often insidious onset and presentation of
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symptoms allow for a delay in diagnosis. Many patients also often do not have
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readily available primary health care services. Tuberculosis is caused by

Mycobacterium tuberculosis and generally affects the respiratory system, but any
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organ system can be affected.

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The thoracolumbar junction is the most commonly affected segment of the spine
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involved in tuberculous infection. Cervical and sacral spine involvement is less

common. [27] Spinal tuberculosis usually begins in the anterior aspect of the

vertebral body, either at its superior or inferior margin. The infection typically

spreads in a sub-ligamentous fashion, usually deep to the anterior longitudinal

ligament and may traverse multiple vertebral levels. The route of disease spread
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generally occurs anterolaterally. In contradistinction to pyogenic diskitis,

tuberculous disease spares the intervertebral disk, as Mycobacterium tuberculosis

lacks the proteolytic enzymes to break down the disk. Due to the lack of

intervertebral disk involvement, there may be no abnormal T2-weighted signal

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within the disk space. However, as vertebral body disease progresses and results in

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collapse, destruction of the disk space may occur as a finding seen in a late stage of

disease. [4] Vertebral body marrow demonstrates T1-weighted hypointense signal

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and T2-weighted hyperintense signal in the involved levels. T2-weighted

hyperintense signal is also noted within the affected vertebrae and adjacent soft

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tissues. Peripheral enhancement surrounding osseous and paraspinal abscesses is

more common in tuberculous infection, in comparison to other organisms causing

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spinal infections and paraspinal phlegmonous changes. [28] Paravertebral

phlegmonous change is associated with thick enhancement on contrast-enhanced

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imaging. Paravertebral involvement may be secondary to direct spread or via

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paravertebral veins. Paravertebral soft tissue and muscular abscesses are more

commonly seen in tuberculous infection compared to other spinal infectious

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organisms. [29] Fistulous tracts to adjacent structures, such as the aorta and pleural
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space, may also be present. [30]

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4. Fungal infection:

Fungal infection of the spine is most commonly encountered in

immunocompromised patients. These include patients with the human

immunodeficiency virus (HIV), diabetes mellitus, patients on certain

chemotherapeutic agents, or post transplant patients on immunosuppressive

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therapy. The incidence of fungal infections has increased in the past decade. [31]

Candida and Aspergillus are the most common causes of opportunistic fungal

infection. [7] Similarly to bacterial and mycobacterial infection, fungal infections

may lead to diskitis/osteomyelitis. The imaging findings are similar to that of

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pyogenic infection, with hypointense T1-weighted signal in the infected endplates.

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However, the abnormal T2-weighted signal is relatively less commonly identified in

patients with fungal diskitis/osteomyelitis. [31] The imaging findings in patients

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with fungal diskitis/osteomyelitis may be attributed to the relatively blunted

immune response in affected patients. [6]

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Various fungi may lead to spondylitis/spondylodiskitis, and depend on the area in

which the fungus is endemic. Coccidioidomycosis immitis is endemic to the San

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Joaquin Valley in the Southwestern United States, as well as in Mexico, Central and

South America. Histoplasmosis is most commonly encountered in the Ohio River

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Valley in the United States, but is also endemic to Central and South America, Africa,
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Asia, and Australia. [32] Mucormycosis and aspergillosis infections have an

increased incidence in patients with diabetes mellitus. Candida infections have also
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demonstrated an increased incidence in immunocompromised patients.

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Coccidioidomycosis infection typically affects the disk space and demonstrates disk
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space narrowing and often is associated with paraspinal soft tissue infection.

Although osseous manifestations are uncommon, the spine is the most often

involved osseous structure. Osseous destruction is less commonly seen in

coccidioidomyocosis in comparison to pyogenic infections. [33] Even though fungal

spinal infection is less common than pyogenic or tuberculous involvement, it is

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important to consider fungal disease in the differential diagnosis and use clinical

history and the patient presentation to make the imaging diagnosis more accurate.

5. Advanced Imaging

Diffusion weighted imaging (DWI), which is commonly used in the evaluation of

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intracranial pathology, has increasingly been applied to imaging of spine pathology,

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including evaluation of the spinal cord, extra-axial space, in a heterogeneous

magnetic environment, and physiologic motion in and around the spinal cord.

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Technical advances including parallel imaging and more powerful gradient systems,

as well as techniques including multi-shot echo planar imaging (EPI) and restricted

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field of view DWI are practical and more resistant to artifact, which facilitates

diffusion weighted imaging of the spine. [34] [35]

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In the setting of infection, DWI can highlight epidural abscess, osteomyelitis, and

paravertebral abscess. Patel et al. demonstrated that DWI of the spine can be used to
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distinguish Type 1 degenerative endplate signal changes from

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discitis/osteomyelitis; a common diagnostic dilemma in the setting of a T2

hyperintense disc. The “claw sign,” is described as paired regions of well-

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marginated, linear, increased diffusion weighted signal within the adjacent

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endplates, which reflects degenerative change, while diffusely increased signal in

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the vertebral bodies adjacent to the disk suggests diskitis/osteomyelitis. [36]

6. Summary:

Infection involving the vertebral column, including the bone, intervertebral disk,

and paravertebral soft tissues is of critical importance and early detection and

diagnosis is paramount. Utilizing the clinical information in conjunction with the

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imaging findings is necessary to optimize treatment and ultimately improve patient

care and prevent mortality and morbidity.

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Image Captions:

Figure 1: Pyogenic Spondylodiskitis: 71 year old male with prior spinal Tuberculous infection with
subsequent spinal decompression presenting with worsening back pain, fever, and lower extremity
weakness 4 weeks after surgery. Staphylococcus aureus was the causative organism.

A) Sagittal CT demonstrates destructive change of the endplates at the L4-L5 level with

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intervertebral disk height loss and destruction with retrolisthesis of L4 on L5.
B) Sagittal T1-weighted image shows hypointense signal in the L3, L4, and L5 vertebral bodies with
edema infiltrating the expected fatty marrow signal.

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C) Sagittal T2-weighted image demonstrates ill defined hyperintense signal in the L3, L4, and L5
vertebral bodies with hyperintense signal in the L4-L5 intervertebral disk space and surround
paraspinal soft tissues.

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D) Sagittal T2/STIR sequence better demonstrates the edema and inflammatory change within the
L3, L4, and L5 vertebral bodies, L3-L4 and L4-L5 intervertebral disks, and paraspinal musculature.
The suppression of the fatty marrow in the more normal L1 and L2 vertebral bodies allows for

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better sensitivity to detect edema when compared to the T2-weighted sequence (C)

Figure 2: AN
Pyogenic Spondylodiskitis: 71 year old male with prior spinal Tuberculous infection with subsequent
spinal decompression presenting with worsening back pain, fever, and lower extremity weakness 4
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weeks after surgery. Staphylococcus aureus was the causative organism.

A) And (B) Axial T1-weighted and axial T1-weighted fat suppressed contrast-enhanced (B) images
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demonstrate extensive phlegmonous tissue with enhancement in the bone, epidural space,
prevertebral region, and paraspinal musculature.
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Figure 3:

Pyogenic Spondylodiskitis with posterior mediastinal abscess: 35 year old male intravenous drug user
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presenting with right arm weakness, back pain, and chest pain. Methicillin-resistant Staphylococcus
aureus (MRSA) was the causative organism.
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A) Sagittal CT demonstrates osseous destruction of the endplates at the T2-T3 level with reactive
sclerosis of the adjacent vertebral bodies.
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B) And (C) Sagittal T1-weighted fat-saturated post contrast images demonstrate enhancement of
the intervertebral disk space and adjacent vertebral bodies at the T2-T3 level.

Figure 4:

Pyogenic Spondylodiskitis with posterior mediastinal abscess: 35 year old male intravenous drug user
presenting with right arm weakness, back pain, and chest pain. Methicillin-resistant Staphylococcus
aureus (MRSA) was the causative organism.
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A) Axial CT demonstrates destructive changes involving the T2 vertebral body

B) Axial T2-weighted image demonstrates prevertebral phlegmon with abscess formation within
the posterior mediastinum, which anteriorly displaces the esophagus and the aorta.
C) Axial T1-weighted image demonstrates prevertebral phlegmon with abscess formation within
the posterior mediastinum, which anteriorly displaces the esophagus and the aorta.

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D) Axial T1-weighted fat-saturated post contrast image demonstrates prevertebral phlegmon with
abscess formation within the posterior mediastinum, which anteriorly displaces the esophagus

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and the aorta.

Figure 5:

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Pyogenic Spondylodiskitis with massive mycotic aortic aneurysm: 71 year old male presenting with
fever and back pain. Salmonella enteritidis was the causative organism.

A) And (B) Lateral radiographs demonstrate minimal loss of the osseous matrix involving the

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anterior aspect of the L3 and L4 vertebral bodies. Prospective diagnosis of osteomyelitis is very
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difficult on this example and exemplifies the poor sensitivity of radiographs for early
osteomyelitis. Small foci of gas, however, can be seen which may clue in the Radiologist to a site
of infection at these levels. (arrow)
C) Sagittal T2/STIR image demonstrates the edema involving the L2, L3, and L4 vertebral bodies.
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Edema involving the L2-L3, L3-L4, and L4-L5 intervertebral disk spaces is also present.
D) Sagittal T1-weighted fat-saturated post contrast image of the lumbar spine demonstrates
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enhancement of the anterior margins of the L3 and L4 vertebral bodies. An abscess in the
prevertebral soft tissues at the L5 level is also noted.
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Figure 6:

Pyogenic Spondylodiskitis with massive mycotic aortic aneurysm: 71 year old male presenting with
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fever and back pain. Salmonella enteritidis was the causative organism.

A) Sagittal contrast-enhanced CT demonstrates a large aneurysm of the aorta just above its
bifurcation into the common iliac arteries. Foci of gas within the anterior aspect of the L4
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vertebral body and in the prevertebral tissue are present.

B) Axial contrast-enhanced CT demonstrates a large aneurysm of the aorta just above its
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bifurcation into the common iliac arteries. Foci of gas within the anterior aspect of the L4
vertebral body and in the prevertebral tissue are present.
C) Axial T1-weighted fat-saturated contrast-enhanced CT demonstrates a large aneurysm of the
aorta just above its bifurcation into the common iliac arteries. Foci of gas within the anterior
aspect of the L4 vertebral body and in the prevertebral tissue are present.
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Figure 7: Tuberculous spondylitis: 64 year old female with history of low back pain. Image D is the same
patient 19 month later, presenting with severe lower extremity weakness and cauda equina like
symptoms.

A) Sagittal T1-weighted image demonstrates hypointense signal in the L1, L2, and L3 vertebral
bodies with collapse of the L3 vertebral body with osseous retropulsion and a mild gibbus
deformity.

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B) Sagittal T2-weighted image demonstrates mild ill defined hyperintense signal in the L1, L2, and
L3 vertebral bodies with collapse of the L3 vertebral body with osseous retropulsion and a mild
gibbous deformity. Note the relative lack of abnormal signal within the intervertebral disk

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spaces in the lumbar spine due to the lack of proteolytic enzymes in the Tuberculosis
mycobacterium.

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C) Sagittal T1-weighted fat-saturated contrast-enhanced image demonstrates enhancement of the
L1, L2, and L3 vertebral bodies without abnormal enhancement of the intervertebral disks
D) Sagittal T2-weighted image demonstrates destruction and collapse of the L1 vertebral body with
osseous retropulsion and compression of the distal spinal cord/conus medullaris in the same

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patient 19 months later. There is a resultant gibbus deformity.
AN
Figure 8: Tuberculous spondylitis with intravertebral and psoas major abscesses: 57 year old male with
low back pain.
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A) Sagittal T1-weighted fat-saturated contrast-enhanced image demonstrates intraosseous abscess
formation with a well defined border of enhancement around the abscess
B) Axial T1-weighted fat-saturated contrast-enhanced image demonstrates intramuscular abscess
D

involving the right psoas major.

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Figure 9:

Tuberculous spondylitis: 56 year old female with neck pain, difficulty swallowing and arm weakness
bilaterally.
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A) Sagittal T2/STIR image demonstrates edema in the C3, C4, and C5 vertebral bodies with infected
prevertebral and ventral epidural fluid.
C

B) Sagittal T1-weighted fat-saturated contrast-enhanced image demonstrates enhancement of the C3,

C4 and C5 vertebral bodies with enhancement of the prevertebral and ventral epidural phlegmon.
AC

C) Sagittal T2 image demonstrates prevertebral abscess and ventral epidural abscess resulting in spinal
cord compression.

Figure 10:

Coccidioidomycosis: 15 year old female with 2 month history of back pain

A) Lateral radiograph demonstrates destructive change involving the L4 vertebral body and
pedicles. Increased density involving the anterior and inferior aspect of the L3 vertebral body is
compatible with spondylitis as well.
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B) Sagittal T1-weighted fat-saturated contrast-enhanced image demonstrates enhancement

multiple lower thoracic and lumbar vertebral bodies. Note the enhancement of the anterior and
inferior aspect of the L3 vertebral body, which corresponds to the abnormal density on the
corresponding radiograph.

Figure 11:

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Coccidioidomycosis, diffuse hematogenous spread: 16 year old female with progression of fungal
disease after stopping anti fungal medication.

RI
A) Sagittal T2-weighted image demonstrates multiple foci of hyperintense signal in the lower
thoracic and lumbar vertebral bodies with collapse of multiple levels and spinal malalignment.
Collapse of lower thoracic/upper lumbar vertebral bodies result in osseous retropulsion and

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severe spinal stenosis.
B) Sagittal T1-weighted fat-saturated contrast-enhanced image demonstrates multiple foci of
abnormal enhancement in the lower thoracic and lumbar vertebral bodies with collapse of

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multiple levels and spinal malalignement. Note the multiple intraosseous abscesses and the
abscess in the presacral soft tissues.
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C) Axial T1-weighted fat-saturated contrast-enhanced image demonstrates multiple foci of
intraosseous abscesses and the abscesses in the right multifidus and longissimus muscles.

Figure 12:
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Pyogenic paraspinal musculature abscess: 6 year old female with rapidly progressive fever and back
pain.
D

Axial DWI (A), Axial ADC (B), and Axial T2-weighted images demonstrate restricted diffusion and edema
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within an intramuscular left psoas major abscess, as well as phlegmonous tissue and edema in the right
paraspinal musculature.
EP

Figure 13:
C

Pyogenic diskitis/osteomyelitis: 40 year old male presenting with fever and ataxia. Staphylocccus aureus
was the causative organism.
AC

Axial DWI (A), Axial ADC (B) demonstrates restricted diffusion within the T5-T6 intervertebral disk.

(C) Sagittal T1-weighted fat-saturated contrast-enhanced image demonstrates enhancement of the T5

and T6 vertebral bodies with endplate destructive and enhancement of the intervertebral disk at this
level.

(D) Axial T1-weighted fat-saturated contrast-enhanced image demonstrates enhancement of the T5-T6
intervertebral disk with paravertebral enhancement.
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