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Discitis in Adults
Kartik Shenoy, MD
Amit Singla, MBBS, MS
Jonathan D. Krystal, MD
Afshin E. Razi, MD
Yong H. Kim, MD
Alok D. Sharan, MD, MHCDS
Investigation performed at NYU
Langone Orthopedic Hospital, New
York, NY
COPYRIGHT © 2018 BY THE
JOURNAL OF BONE AND JOINT
SURGERY, INCORPORATED
Abstract
» Discitis is a bacterial infection of the intervertebral disc that is
commonly caused by direct inoculation from surgery or hematoge-
nous seeding.
» Rapid diagnosis and treatment are essential to preserve spinal
stability and neurological function.
» Discitis is usually treated nonoperatively with antibiotics. However,
when surgical intervention is indicated, debridement and interverte-
bral fusion are often performed to promote healing, limit neurological
impairment, and restore spinal stability.
D
iscitis continues to be
problematic despite
advances in medicine. A
thorough understanding of
discitis and its presentation is critical for
appropriate management. Aggressive
medical therapy and surgical intervention,
when needed, are critical to achieving a
favorable prognosis.
Spondylodiscitis is a broad term en-
compassing vertebral osteomyelitis, spon-
dylitis, and discitis, which are considered
different manifestations of the same path-
ological process. The epidemiological dis-
tributionofdiscitis isbimodal with2 peaks:
children in the first and second decades of
life and adults in the fifth and sixth decades
of life1-3
. In adults, males are affected twice
as often as females. The lumbar spine is the
most frequently involved area (58%), fol-
lowed by the thoracic spine (30%) and the
cervical spine (11%). This pattern is
attributed to the relative blood flow to each
area of the vertebral column2-5
.
The source of infection in discitis can
be iatrogenic through direct inoculation or
through hematogenous spread, with most
cases arising secondary to a nonspinal
infection. Risk factors associated with an
increased incidence of discitis include dia-
betes mellitus, immunosuppression,
intravenous (IV) drug abuse, chronic
renal disease, alcoholism, infective endo-
carditis, urinary tract infections, and
spinal procedures1,3,6
. Recently, the
incidence of diagnosed discitis has been
increasing because of a marked increase in
the immunocompromised population,
the number of spinal procedures per-
formed, and the sensitivity of radio-
graphic tests4,7,8
. Although the rate of
diagnosis has increased, the treatment and
outcome of discitis are still highly varia-
ble, which reflects the absence of treat-
ment guidelines and the complex nature
of the pathogenesis.
Etiology and Pathogenesis
Causative Pathogens
When possible, identification of a causative
pathogeniscriticaltoguidingthetreatment
process6,7,9-11
. Most cases involve a single
pathogen, although polymicrobial infec-
tion can occur3
.
The microorganism etiology of disci-
tisisdividedintopyogenic,granulomatous,
and fungal. An appropriate workup is
dependent on biopsy and cultures. How-
ever, a review by Cottle and Riordan re-
vealed that blood and biopsy specimens are
positive on culture in 50% and 76% of
cases, respectively1
, and Michel et al.
Disclosure: No funding has been received for this study. On the Disclosure of Potential Conflicts of
Interest forms, which are provided with the online version of the article, one or more of the authors
checked “yes” to indicate that the author had a relevant financial relationship in the biomedical arena
outside the submitted work (http://links.lww.com/JBJSREV/A323).
|
JBJS REVIEWS 2018;6(6):e6 · http://dx.doi.org/10.2106/JBJS.RVW.17.00104 1

reported that as many as 39% of biopsy
specimens from patients with no prior
antibiotic exposure may be negative on
culture12
.
The most commonly isolated
pyogenic pathogen is Staphylococcus
aureus1,3,4,7,9,11,13-15
. The rate of
methicillin-resistant S. aureus (MRSA)
ranges from 10% to 40%, especially in
nosocomially acquired isolates2,4,16
.
Other identified isolates include
coagulase-negative staphylococci such
as Staphylococcus epidermidis (5% to
29%) and members of the Strepto-
coccus genus (5% to 20%)1,2,17
. The
most frequently cultured gram-
negative bacilli include Escherichia coli
(7% to 33%), commonly seen in the
immunocompromised patient18
, and
Pseudomonas (4% to 12%)2,9,17
.
Pseudomonal species, Staphylococcus
aureus, and Staphylococcus epidermidis
are most prevalent in IV drug abusers.
In patients with infectious endocardi-
tis, Streptococcus viridans and Group D
streptococci must be considered
(Table I)18
.
Tuberculous discitis is the most
common infectious etiology worldwide,
but it is less prevalent in the United
States11
. The causative agent is
Mycobacterium tuberculosis (TB), which
produces a granulomatous reaction. In
patients with tuberculous discitis, the
major areas of spinal involvement are
paradiscal (33%), central (11.6%),
anterior (2.1%)19
, and posterior (2% to
10%)20,21
. Atypical forms of spinal
tuberculosis include those associated
with neural arch involvement only and
rare cases in which granulomas occur
in the spinal canal without osseous
involvement. Large paraspinal abscesses
are more common in patients with TB
infections than in those with pyogenic
infections. Because Mycobacterium
lacks proteolytic enzymes, the disc is
typically spared. Consequently, the
pathological changes generally take
longer to develop and are frequently
associated with greater osseous defor-
mity22-25
.
Fungal and brucellar infections
represent a small fraction of cases
worldwide, but in some endemic areas,
they still account for many spinal infec-
tions. Large studies have shown the rate
of fungal discitis to be very low (0.5% to
1.6%) in the general population, but the
rate is higher among those who are im-
munosuppressed. Candida, Aspergillus,
and Cryptococcus have a more global
distribution, but dimorphic fungi such
as Coccidioides and Blastomyces are
seen in the Southwestern U.S. and Ohio
River Valley, respectively26
. Brucellar
discitisisseenmainlyinendemicregions
such as the Mediterranean, Middle East,
and Central and South America, par-
ticularly among people who work with
animals13,27
.
Hematogenous Spread
The nucleus pulposus and anulus fi-
brosus of a child’s intervertebral disc are
both richly vascularized. However, after
the first 2 decades of life, there is a
decline in the blood supply to the disc,
specifically to the nucleus pulposus.
The nucleus relies on diffusion through
the porous central concavity of the
vertebral body, which explains why
discitis rarely occurs without end plate
involvement. The relatively avascular
adult disc is seeded with pathogenic
organisms via end-arteriolar vessel
arcades, neovascularization secondary
to degenerative disc disease, or the
Batson plexus (a valveless venous sys-
tem that drains the pelvic organs into
the vertebral venous plexuses).
Increases in intra-abdominal pressure
can permit retrograde seeding from the
pelvic organs. Many cases (17%) of
hematogenous spread through the
Batson plexus originate from primary
infections of the genitourinary tract1,5
.
In addition, integumentary (11%),
gastrointestinal (5%), respiratory
(2%), and oral (2%) mucosal systems
have been implicated in seeding via
spread through the arterial system.
Iatrogenic Discitis
Despite advances in surgical technique,
iatrogenic discitis is still a relatively
common occurrence, with a reported
postoperative rate as high as 4%28
. Iat-
rogenic causes form the bulk of non-
hematogenous infections, accounting
for 25% to 30% of all cases. Discitis has
been reported after nearly every type of
invasive spinal procedure, including
both open and minimally invasive
operations, presumably as a result of
direct inoculation of the disc space29
.
Discectomy and laminectomy carry the
lowest risk of iatrogenic discitis, whereas
bone-grafting and procedures involving
instrumentation are associated with a
higher rate of infection4
. Rarely, geni-
tourinary procedures can indirectly
cause discitis despite adequate use of
prophylactic antibiotics30
. Intra-
operative damage to the vertebral end
plates and adjacent vessels and the re-
sulting creation of necrotic tissue lead to
inflammation, which serves as a nidus
for infection4
.
Clinical Presentation
The clinical findings associated with
discitis are variable, but the majority of
patients report severe back pain at the
TABLE I Summary of Discitis Pathogens Specific to Different
Patient Populations
Patient Population Common Pathogens
General S. aureus, coagulase-negative staphylococci,
streptococci
Immunocompromised E. coli, S. aureus
IV drug abusers S. aureus, Pseudomonas aeruginosa,
S. epidermidis
Patients with endocarditis Group D streptococci, Streptococcus viridans,
otherstreptococcalspecies, coagulase-negative
staphylococci
| D i s c i t i s i n A d u l t s
2 JUNE 2018 · VOLUME 6, ISSUE 6 · e6

affected levels. Early signs include ten-
derness to palpation, paraspinal muscle
spasm, or reduced spinal range of
motion. The patient may have difficulty
walking orstanding as well as night pain.
Fever has been reported in up to 50% of
cases7
. Localized back pain with fever
always warrants a workup for discitis,
especially if it occurs after spinal surgery.
Other constitutional symptoms such as
chills, malaise, and weight loss may also
be present. If the infection spreads to the
epidural space, radiculopathy or mye-
lopathy can develop as a result of direct
spinal cord compression by suppurative
material or a protruding osseous frag-
ment. If left untreated, radiculopathy
or myelopathy can result in severe
neurological deficit3,18
.
Tuberculous discitis has an insidi-
ous and indolent course. In addition to
local warmth, swelling, and tenderness,
constitutional symptoms such as fever
and weight loss may be present; how-
ever, fever and chills are reported less
often with tuberculous discitis as com-
pared with pyogenic discitis13
. Consti-
tutional symptoms may be present long
before the onset of back pain, so a
thorough history is critical. In cases of
thoracic spine involvement, especially
those involving $3 vertebral levels,
tuberculosis discitis should be
suspected11
.
Some authors have grouped bru-
cellar and pyogenic discitis together, but
the presentations can be different27
.
Similar to pyogenic discitis, brucellar
discitis can manifest with nonspecific
complaints such as fatigue, fever, or
night sweats, but patients with this form
of discitis also may have elevated trans-
aminases and hepatosplenomegaly.
Fungal discitis also presents with
nonspecific symptoms and findings. A
thorough travel and medical history can
help in making the diagnosis. Early on,
patients may have constitutional signs,
backpain,andneurological deficits.The
spine is rarely affected alone, and sys-
temic symptoms and involvement of
other joints are common26
.
In all types of discitis, the variabil-
ity in presentation and the nonspecific
signsandsymptomscanleadtoadelayed
diagnosis. Therefore, whenever discitis
is suspected, an immediate workup
should be performed. Early diagnosis
has proven to improve outcome.
Therefore, in addition to understanding
the clinical presentation, clinicians must
rely on changes in laboratory values and
neurodiagnostic tests.
Diagnosis
Laboratory Evaluation
Distinguishing discitis from other spine
conditions remains a challenge. In the
setting of discitis, laboratory testing can
reveal a normal to elevated white blood-
cell (WBC) count, with elevation
occurring in only 13% to 60% of
cases1,2,7
. The erythrocyte sedimenta-
tion rate (ESR) and C-reactive protein
(CRP) level are elevated in .90% of
cases, and therefore those laboratory
values are more sensitive than WBC
counts. Carragee et al.31
investigated the
ESR trend in predicting response after
1 month of medical management. A
75% decline in the ESR was considered
to be a good prognostic marker, but the
authors found that an unchanged or
rising ESR was difficult to interpret on
its own and required evaluation in con-
junction with other parameters. CRP
has higher sensitivity for an active
inflammatory process. It usually peaks
on the second or third day after spine
surgery and should normalize within 2
weeks. However, a persistently elevated
CRP level is highly correlated with the
presence of infection32
. In addition,
bloodculturesmaybepositivein20%to
60% of cases2,7
. The gold standard for
diagnosing discitis is computed tomog-
raphy (CT)-guided biopsy and culture,
which is positive in about 70% to 90%
of cases33,34
.
Imaging
Diagnostic imaging for discitis may
include radiographs, nuclear bone scans,
CT scans, and magnetic resonance
imaging (MRI).
Radiography has a sensitivity of
82% and a specificity of 57%. The low
specificity is due to non-discitis-related
degenerative changes that can result in a
false-positive result2
. In the setting of
discitis,theearliestradiographic changes
include loss of lordosis, loss of the psoas
shadow, disc space narrowing, and end
plate irregularities35
. Although radio-
graphs have diagnostic limitations, they
are still useful for evaluating stability.
The preferred nuclear study involves the
use of gallium-67, which yields high
sensitivity (90%) and specificity
(100%). Indium-111 scans have low
sensitivity and are not diagnostic.
Technetium-99m scans are highly
sensitive (90%) but are not specific
(78%). The combination of technetium
and gallium is often used to increase
diagnostic accuracy2,35
. CT scans pro-
vide higher sensitivity than radiographs
but still lack specificity. Despite its
sensitivity, CT falls short of the
diagnostic accuracy of MRI3
.
The imaging modality of choice in
the diagnosis of discitis is MRI, which
has a sensitivity of 93% to 96% and a
specificity of 92% to 97%. MRI has
been demonstrated to be as effective as
combined technetium and gallium
nuclear imaging1-3
. MRI of the entire
spine should be performed, with acqui-
sition of fat-suppressed T2-weighted
and post-gadolinium T1-weighted
series. Gadolinium enhancement is
essential for visualizing involvement of
the bone marrow and paraspinal tissues.
MRI showing paraspinal or
epidural inflammation and T1 hypo-
intensity at the vertebral body or T2 hy-
perintensity in the intervertebral disc has
a high sensitivity for discitis (Fig. 1)36
. It
is difficult to distinguish between pyo-
genic, tuberculous, brucellar, and fungal
discitis with use of MRI, so a history,
laboratory evaluation, and biopsy are
critical for definitive diagnosis. Never-
theless, each pathogen type has subtle
features that can be appreciated on MRI.
In pyogenic cases, there is a confluent
hypointense signal from the vertebral
bodies and adjacent disc on T1-weighted
sequences, making the margin between
the 2 structures indistinct. On
T2-weighted sequences, there is hyper-
intense signal of the vertebral bodies and
D i s c i t i s i n A d u l t s |
JUNE 2018 · VOLUME 6, ISSUE 6 · e6 3

the involved disc, and the intranuclear
cleftnormallyseenwithintheadultdiscis
not generally visible.
In cases of tuberculous spondy-
lodiscitis, there is no disc space
involvement because of the lack of
proteolytic enzymes, but meningeal
involvement is characteristic and
paraspinal or intraosseous abscesses
are commonly seen8,35
. Additional
findings that suggest tuberculous
spondylodiscitis include sub-
ligamentous spread and multilevel
involvement in the thoracic spine8,37
.
Jung et al., in a study that investigated
characteristics that specifically
distinguish tuberculous from pyogenic
spondylodiscitis,found thattubercular
infections more commonly were asso-
ciated with a well-defined paraspinal
abnormal signal and a thin, smooth
abscess wall, whereas pyogenic discitis
was associated with a poorly defined
paraspinal abnormal signal and a thick,
irregular abscess wall38
.
Brucellar discitis is usually less
aggressive in comparison with tubercu-
lar discitis and tends to affect the lumbar
spine, with fewer cases affecting the
thoracic and cervical spine36
. Like other
forms of discitis, brucellar discitis is
associated with low signal intensity on
T1-weighted images and high signal
intensity on T2-weighted images27
.
MRI also demonstrates preservation of
the vertebral body and a lack of posterior
element involvement or abscess
formation35
.
Fungal discitis is often difficult to
diagnose because of its lower incidence,
but it is characterized by a lack of hy-
perintensity in the disc on T2-weighted
images. As with tuberculous discitis,
Aspergillus discitis can show multilevel
involvement and subligamentous
spread36
. Fungal infections rarely show
contrast enhancement, but they may be
associated with anterior and/or posterior
disc bulging with enhancement of the
anterior and posterior longitudinal
ligaments and subligamentous spaces.
Whereas the intranuclear cleft is gener-
ally not visible on MRI scans in cases of
pyogenic discitis, it is often visible in
cases of fungal discitis35
.
More recently developed imaging
modalities such as 18-
fluorodeoxyglucose positron emission
tomography (FDG-PET) have yielded
higher sensitivity and specificity than
MRI33
. Smids et al. suggested that
FDG-PETissuperiortoMRIduringthe
first 2 weeks of the infection, with a
sensitivity and specificity of 96% and
95%, respectively, but that FDG-PET
and MRI have similar diagnostic utility
after 2 weeks39
. Other investigators have
soughttodeterminewhetherFDG-PET
can be used to distinguish between the
various pathogens associated with dis-
citis. Bassetti et al. suggest that cases
of tuberculous spondylodiscitis show
significantly higher maximum stan-
dardized uptake values when compared
with controls with known pyogenic
spondylodiscitis (p 5 0.003)40
. This is
an area of promising future research to
distinguish between the various causes
of discitis.
Treatment
Aggressive antibiotic management, early
immobilization,andclosemonitoringof
inflammatory markers and the clinical
status are the mainstays of initial,
conservative treatment for discitis41
(Fig. 2). However, if the patient is
hemodynamically and neurologically
stable, all efforts should focus on deter-
mining the causative pathogen before
any treatment is initiated.
Biopsy
If the initial biopsy is nondiagnostic,
additional cultures should be performed
to exclude mycobacterial, fungal, or
brucellar infections. Friedman et al., in a
study of 21 patients with spontaneous
infectious discitis, demonstrated that
the positive yield of a second percuta-
neous biopsy increased from a range of
50% to 56% to a range of 73% to
79%42
. The authors reported that they
did not have to perform open biopsy in
anyofthepatientsinthatseries,andthey
suggested that open biopsy should be
reserved for patients with multiple neg-
ative cultures in whom an infection does
not respond to empirical antibiotic
therapy. Jiménez-Mejı́as et al. reported
on 18 cases of postoperative spondylo-
discitis in which 20 bone biopsies
(6 percutaneous and 14 open) were
performed4
. Four of the 6 patients with
Fig. 1
T1 and T2-weighted MRI scans of the
lumbarspine,demonstrating discitiswith
spreadintotheadjacentvertebralbodies.

percutaneous biopsies had positive
resultsonculture,whereasall14patients
with open biopsies had positive results
on culture.Theauthors alsonotedthat2
of the 14 patients with positive results
following open biopsy had negative
results following percutaneous biopsy.
Percutaneous endoscopic decom-
pression anddrainage (PEDD)is another
technique for obtaining a sufficient
amount of tissue directly from a disc
region with a suspected infection. Yang
et al. reported that PEDD had higher
sensitivity than image-guided biopsy
(90% compared with 47%; p 5
0.002)34
. They also found that patients
reported immediate relief of back pain
following PEDD and that a larger num-
ber of patients undergoing CT-guided
biopsy required surgery because failure to
identify the pathogen resulted in persis-
tent infection and progressive spinal
instability. Various studies have shown
diagnostic accuracy ranging from 36% to
91% for image-guided biopsy and from
45% to 87% for PEDD43-46
.
Sehn andGilula, in whatis perhaps
the most valuable study for identifying
the positive-culture rates of guided
biopsy, stratified all patients undergoing
biopsy as having a high, intermediate, or
low probability of infection, with those
in the high-probability group having
clinical and radiographic signs of infec-
tion47
. In 92 high-probability patients,
only 30% had positive cultures by
guided biopsy and in all 200 patients,
21.5% had positive guided-biopsy
cultures. That study showed a lower rate
of positive cultures compared with the
rates in previous studies, but the study
sample was more representative of what
is seen in clinical practice. Therefore, we
recommend that percutaneous biopsy
be used as the first step, followed by
repeat percutaneous biopsy if appropri-
ate; otherwise, an open biopsy should be
performed.
Antibiotics
More than half of patients with discitis
respond to nonoperative management1
.
The duration of the initial course of
antibiotic treatment has ranged from
4 to 12 weeks in most published
studies48-50
. Although there is no uni-
formly accepted duration of treatment,
most authors recommend between 6
and 10 weeks of IV antibiotics, followed
by a transition to oral antibiotics with
close monitoring of inflammatory
markers4,9,17,42,51,52
. However, a recent
study suggested that 6 weeks of antibi-
otics was sufficient to eradicate infection
in patients with pyogenic vertebral
osteomyelitis53
. During the treatment
period, bed rest or brace immobilization
should be continued for 2 to 4 weeks.
Roblot et al.,in a studyin which patients
who received intravenous antibiotics for
6 weeks were compared with those who
received antibiotics for .6 weeks, found
similar relapse and mortality rates in
both groups54
. Daver et al., in a study of
72 patients with staphylococcal osteo-
myelitis who were managed with an
early switch to oral antibiotics (12 days
ofIVadministrationfollowedby42days
of oral administration) or a prolonged
parenteral course (42 days of IV
administration followed by 21 days
of oral administration), reported a
success rate of 78% in the early-switch
group compared with 69% in the
prolonged-IV group55
.
Despite decreased vascular flow to
thevertebrae,studieshavedemonstrated
Fig. 2
Diagnostic and treatment algorithm for
the treatment of suspected discitis41
.
ROM 5 range of motion.

adequate penetration of many anti-
biotics into the vertebral body and
disc. Such drugs include clindamycin,
rifampin, metronidazole, and
fluoroquinolones. Antibiotics such as
b-lactams, glycopeptides, fosfomy-
cin, sulfonamides, and aminoglycosides
have been shown to achieve less osseous
penetration and are indicated only when
a first-line antibiotic is contra-
indicated56
. Ultimately, the choice of
antibiotic is based on the culture results;
when cultures are negative, broad-
spectrum antibiotics should be given
and laboratory values should be trended.
Empirical antimicrobial therapy is
dependent on the epidemiological risk,
clinical situation, and host immunity
(Table II). A combination regimen
including vancomycin and a third or
fourth-generation cephalosporin or an
alternative regimen combining daptomy-
cin and a quinolone should be used
empirically. For methicillin-sensitive
S. aureus (MSSA), antistaphylococcal
penicillinsorceftriaxonearethemainstays
of treatment. For MRSA, vancomycin
treatment is preferred. Streptococcal spe-
cies require treatment with ceftriaxone.
Anaerobes are treated with metronidazole
or clindamycin. Most cases of pseudo-
monal discitis require aminoglycosides
combined with ceftazidime or mer-
openem,butsomecanalsobetreatedwith
ciprofloxacin, which is effective as oral
continuation therapy2
.
Discitis caused by Brucella can be
treated with doxycycline combined with
streptomycin or rifampin2
. Tuberculous
discitis should be treated with standard
TB therapy: isoniazid, ethambutol, pyr-
azinamide, and rifampin for 2 months,
followed by isoniazid, rifampin, and
ethambutol for an additional 10
months11
. If sensitivities are known,
2-drug therapy with isoniazid and
rifampin can be used for the 10-month
period. If isoniazid and rifampin cannot
be used after the initial 2-month period,
alternative regimens must be adminis-
tered for 16 to 22 months. In the
immunocompromised patient, indinavir
and rifabutin are added to the regimen18
.
Thetreatmentforfungalinfections
is dependent on the causative agent;
therefore, microbial identification is
critical. For Candida species, flucona-
zole or amphotericin B can be used. For
Aspergillus, voriconazole or amphoteri-
cin B are effective.
Criteria for the discontinuation of
antibiotics include symptom resolution
or improvement and normalization of
ESR or CRP49,50
. It has been proposed
that a weekly decrease in CRP by 50%
represents adequate progress57
. In cases
of suspected or proven treatment failure,
care should be coordinated with the
infectious-disease team15,58
.
Operative Treatment
The clinical indications for operative
intervention are the presence of neuro-
logical compromise, substantial verte-
bral destruction with instability, large
epidural abscess, or intractable back
pain. Furthermore, when antibiotic
therapy is unsuccessful or if CRP or ESR
levels do not decrease after 1 month of
medical treatment, surgery should be
considered18
.
While debridement is the main
goal, decompression and fusion are
needed when neural compression or
spinal instability is present59
. Combin-
ing debridement with instrumentation
for stabilization has been associated with
quicker postoperative mobilization,
reduced postoperative morbidity, and
decreased risk of pseudarthrosis and
kyphosis60
.
Surgical options include the
choiceof anterior or posterior approach
with or without instrumentation in a
single setting or in a staged fashion61
.
We are not aware of any randomized
controlled trials that have evaluated
these options. McHenry et al. studied
253 patients who had an infection
around a spinal implant, 109 of whom
were managed surgically50
. The pro-
cedures were performed for drainage of
an abscess (85 patients); relief of spinal
cord compression, cauda equina, or
nerve root compression (48 patients);
and/or spinal stabilization (32
patients). The outcome was favorable
for 86 (79%) of the 109 patients.
Among the 48 patients with neuro-
logical involvement who were managed
surgically, the outcome was favorable
for 33 (69%). Valancius et al. reviewed
the records for 196 patients with dis-
citis over a 10-year period, 117 of
TABLE II General Antibiotic Recommendations for Treating Discitis Following Pathogen Identification
Pathogen First-Line Agent Alternative Agents
MSSA Antistaphylococcal penicillins or ceftriaxone Add aminoglycoside clindamycin
MRSA Vancomycin Clindamycin
Streptococcus Ceftriaxone Other third-generation cephalosporins, clindamycin
Pseudomonas Ceftazidime 1 aminoglycoside Aztreonam, carbapenem 1 aminoglycoside
Anaerobes Metronidazole or clindamycin Imipenem
Brucella Doxycycline 1 streptomycin Doxycycline 1 rifampin
M. tuberculosis Isoniazid, ethambutol, pyrazinamide, rifampin
Candida Fluconazole Amphotericin B
Aspergillus Voriconazole Amphotericin B

whom required surgical interven-
tion62
. Preoperatively, 46 of the 117
patients had neurological compromise,
of which 3 had cauda equina syndrome
and 10 were paraplegic. Seventy-five of
the 117 patients underwent posterior
debridement with instrumentation, 19
underwent debridement without
instrumentation, 7 underwent anterior
debridement alone, and 16 underwent
anterior debridement with posterior
instrumentation. Twenty-four
patientsrequiredrepeatsurgery,12had
mild neurological impairment, and 4
remained paraplegic. Twenty-seven
patients had chronic residual pain of
varying degrees.
The traditional surgical treatment
has been anterior discectomy, debride-
ment, and intervertebral disc fusion;
however, combined anterior and poste-
rior fixation can provide greater stability
and reduce the likelihood of increased
kyphosis18,60
. Involvement of the pos-
terior elements may necessitate further
debridement and stabilization. Decom-
pression and laminectomy alone may
not provide the required stability;
therefore, posterior instrumentation in
combination with thorough debride-
ment and local antibiotics are more
likely to lead to favorable outcomes60,63
.
Surgical procedures for discitis can
be accomplished in 1 or 2 stages. The
1-stage posterior approach precludes the
need for a chest tube and, when per-
formed by an experienced surgeon,
results in decreased operative time,
blood loss, length of hospital stay,
rehabilitation time, and postoperative
morbidity. However, because of limited
exposure, this procedure is more tech-
nicallychallengingandisassociatedwith
higher rates of complications, which
may include excessive bleeding, inad-
vertent neurological or parietal pleural
injury inthethoracic spine,andsequelae
arising from difficult interbody cage or
graft placement. Alternatively, in the
lumbarspine, atransforaminalapproach
can be used safely and efficaciously64
.
Ultimately, the approach and procedure
must be tailored to each specific clinical
scenario63
.
Although the use of instrumenta-
tion for the surgical treatment of an in-
fected spine has been an area of
controversy in orthopaedics, numerous
studies have indicated that the benefits
outweigh the risks. Safran et al., in a
report on 10 consecutive patients with
lumbar osteomyelitis who were man-
aged with same-day decompression and
anterior and posterior fusion, noted that
fusion and eradication of infection were
achieved in all patients65
. Przybylski and
Sharan, in a retrospective analysis of 17
patients, concluded that single-stage
debridement, arthrodesis, and internal
fixation are effective for the treatment of
pyogenic discitis66
.
The choice of implant type for
fixation is another area of recent
research. Until recently, the gold stan-
dard for fusion was autologous grafting
withlocalorharvestedboneforposterior
fusion and tricortical iliac crest bone for
anterior interbody fusion. Currently,
titanium cages are widely accepted as
being safe for use in the surgical treat-
ment of spondylodiscitis; even more
recently, polyetheretherketone (PEEK)
constructs have been introduced as a
suitable treatment67
. Walter et al., in an
initial study of PEEK cages for anterior
interbody fusion in 5 patients with
cervical spondylodiscitis, found that all
patients went on tofusion and had afull
neurological recovery at 15 months,
with no signs of treatment failure or
persistent infection68
. Pee et al., in a
study of 60 patients who were managed
with anterior debridement and fusion
with use of either autologous iliac strut
grafting or a cage (titanium, titanium
mesh, or PEEK) followed by posterior
pedicle screw fixation, reported a
higher rate of subsidence in the strut
group as compared with the cage group
(p 5 0.0041)69
. These series suggest
that titanium and PEEK, both of which
have a low propensity for biofilm for-
mation, can be used safely in cases of
spinal infection; however, given its
strength, titanium is preferred in cases
in which there is vertebral body
destruction as evidenced by end plate
erosion68-70
.
Treatment Failure
Treatment failure, defined as microbio-
logically confirmed persistent infection
despite adequate antimicrobial treat-
ment, has been reported in up to 11% of
cases48,50,54,71-74
. Persistent elevation or
poor response of inflammatory markers
to antibiotics can help identify patients
who may be at higher risk for treatment
failure. Generally, CRP improves more
rapidly than ESR and has been closely
linked to clinical status52
. In the first few
weeks, however, inflammatory markers
typically remain elevated and may even
increase72
. After 4 weeks, an appropriate
response to antibiotics would correlate
with a 25% to 33% reduction in
inflammatory marker values, and
patients with a 50% reduction in ESR
rarely develop treatment failure31,75
.
Yoon et al. found that an ESR of .50
mm/hr and a CRP of .2.75 mg/dL
predicted a significantly higher risk of
treatment failure76
. However, some
patients with persistently elevated
markers may not necessarily have treat-
ment failure because ESR and CRP have
low specificity. As a result, the entire
clinical picture should be evaluated in
conjunction with laboratory tests to
definitively diagnose treatment failure.
Many studies have evaluated the
utility of monitoring the response to
treatment with MRI. If a patient is
showing a good clinical response with
improvement of inflammatory markers,
there is no need for MRI72,75,77-80
. In
fact, MRI in the first 4 weeks following
the initiation of treatment may falsely
show signs of disease progression despite
clinical improvement. Radiographic evi-
dence of inflammation of the disc space
may persist months to years after the
infection in the absence of any clinical
signs of infection75,77-80
. In patients who
are not showing clinical improvement,
appropriately timed MRI may be war-
ranted to look for changes and potential
abscesses in the paravertebral soft tissues
and the epidural space72,75,77-80
.
As is the case when diagnosing
acute, untreated discitis, image-guided
biopsy is the gold standard for confirm-
ing treatment failure. Biopsy allows for

identification of the persistent microbi-
ological etiology. If the first biopsy has
no yield, an additional percutaneous
biopsy or an open biopsy can be per-
formed toobtainalargersampleoftissue
for culture.
Conclusion
Although discitis is not a common
diagnosis, it should be included in a
differential diagnosis for patients with
severe back pain and constitutional
symptoms of infection. MRI is the gold
standard imaging modality, and
CT-guided biopsy and culture are the
gold standards for definitive diagnosis.
Biopsy should always be performed
prior to initiating treatment if the
patient is hemodynamically and neuro-
logically stable. Antibiotic treatment is
very successful, although surgery may be
indicated in specific cases.
Kartik Shenoy, MD1,
Amit Singla, MBBS, MS2,
Jonathan D. Krystal, MD3,
Afshin E. Razi, MD1,
Yong H. Kim, MD1,
Alok D. Sharan, MD, MHCDS4
1Department of Orthopedic Surgery, NYU
Langone Health, NYU Langone
Orthopedic Hospital, New York, NY
2Department of Orthopaedics, All India
Institute of Medical Sciences, New Delhi,
India
3Orlin & Cohen Orthopedic Group,
Woodbury, New York
4WESTMED Spine Center, Yonkers,
New York
E-mail address for K. Shenoy: kartik.shenoy@
nyumc.org
ORCIDiDforK.Shenoy:0000-0002-8373-
4450
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