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Discussion Starter · #1 ·
This is the latest from the Vet on Titan ...after another exam He is getting better he was up and around yesterday anyway here it is ...kinda long

Review the clinical presentation of discospondylitis.

Summarize and discuss the current knowledge regarding diagnosis and
treatment of the condition.

Discuss management of problematic cases.

Key Points

Bacterial infection from foreign bodies or hematogenous spread is the
most common cause of discospondylitis.

Every effort should be made to isolate causative organisms prior to
antimicrobial therapy.

Many cases may require chronic treatment.

Poorly responsive cases are often the result of inappropriate
antimicrobial selection particularly when fungal organisms are present.


Etiology and Pathogenesis

1. Migrating foreign bodies (GI, lungs , paravertebral tissues)

2. Hematogenous spread

3. Local extension of paravertebral infection

4. Penetrating wounds

5. Iatrogenic (disc or vertebral surgery)

Grass seeds, fox tails are probably the most common foreign bodies
implicated, however actual seeds are rarely found. Spondylitis
involving the L2-L4 vertebrae may well be the result of seeds
migrating via the lungs/diaphragm to the crural insertions.

Hematogenous spread is probably the most common cause of
discospondylitis, however a causal relation has not been definitively
demonstrated. Urinary tract, dental and endocarditis infections are
most commonly found associated with lesions. Brucella canis infections
most likely result from spread of genital infections.

Trauma or prior disease may predispose to infection of the disc
space/vertebrae, and immunocompromised animals may be at higher risk.
Fungal discospondylitis, particularly Aspergillus, is seen in German
Shepherd dogs at an increased frequency.

Organisms most commonly isolated from blood, affected vertebrae, and
urine of dogs with discospondylitis are coagulase- positive
Staphylococcus spp (aureus, intermedius). Other organisms isolated
include Bacteroides capillosus, Brucella canis, Nocardia sp ,
Streptococcus canis, Corynebacterium sp, Escherichia coli, Proteus sp,
Pasteurella sp, Paecilomyces sp, Aspergillus sp, and Mycobacterium sp.
Coccidioides immitis may cause vertebral body osteomyelitis.
Hepatozoon canis infection has been associated with periosteal bone
proliferation of the vertebrae as well as other bones of the body.
Spirocerca lupi infection may cause productive bony changes on the
ventral aspect of thoracic vertebrae where the aorta and the esophagus
run in parallel course.

Discospondylitis occurs less commonly in cats.

Clinical Findings

Diskospondylitis may occur in dogs or cats of any age, however it is
most commonly seen in giant and large breeds of dog. Any level of the
vertebral column may be affected by discospondylitis, and multiple
lesions may be seen, in either adjacent vertebrae or nonadjacent
vertebrae. Discospondylitis occurs more commonly in thoracic and
lumbar spine than in cervical spine. The lumbosacral disk space
frequently is involved.

Clinical findings depend on the location of the affected vertebra or
vertebrae. The most common clinical signs are weight loss, anorexia,
depression, fever, reluctance to run or jump, and apparent spinal pain
(which may be severe). Hyperesthesia may be present only over the site
of the lesion or may be poorly localized, especially with involvement
of multiple sites.

Severe lesions may result in overt neurological signs due to
extradural compression of the spinal cord or cauda equina secondary to
granulation tissue, bony proliferation, fracture or luxation of
vertebrae. Occasionally, extension of the infection may result in a
meningitis or myelitis.



Signs are often non specific and may have been present for weeks or
months. The animal may have had episodes of pyrexia.

Clinical signs

Animals may have apparent spinal pain with apparently stiff gait,
shifting lameness or hunched posture. Neurological deficits, if
present, will depend on the location of the lesion(s) and may range
from mild proprioceptive deficits to para/tetra plegia if severe
spinal cord compression is present. Neurological deficits are more
common when the lumbosacral intervertebral disc space is affected.


Animals may or may not be febrile and may have a normal or elevated
peripheral white blood cell count.

Plain Spinal Radiography

Ideally images should be obtained under general anesthesia and a
complete survey of the vertebral column should be done as multiple
lesions are common. Typical radiographic findings are destruction of
the bony end-plates adjacent to an infected disc, collapse of the
intervertebral disc, and varying degrees of new bone production. Early
lesions may consist only of lytic areas in affected vertebral end-
plates. More advanced lesions show a mixture of bone lysis and
extensive new bone production, with osteophytes bridging adjacent
vertebrae containing a central destructive focus. Affected vertebral
bodies may be shortened, and bony proliferation may result in fusion
of one or more vertebrae. Fractures, luxations may be apparent in
severe cases. Care should be taken to rule out other causes of
lytic/proliferative lesions such as neoplasia, healing fracture,
unstable fracture, congenital malformation, or postoperative changes.
Discospondylitis usually can be distinguished from a n
eoplastic lesion, as neoplasms rarely cross intervertebral disc
spaces. Lesions of spondylosis deformans have intact (and more
sclerotic) vertebral end-plates. Older dogs may have a pattern of bony
destruction of end-plates that is due to a noninflammatory process
associated with degeneration of the disk. In such cases, destruction
of end-plates occurs secondary to instability of the disc.

Clinical signs usually precede radiographic signs (2-4 weeks)
therefore suspected cases with negative imaging should be re imaged in
2-4 weeks.

Alternative Imaging

Bone scintigraphy, computed tomography (CT) and magnetic resonance
imaging if available are generally more sensitive than radiography,
particularly for early lesions.

Myelography and or MRI/CT is indicated for animals with neurological
deficits, and is mandatory if decompressive surgery is contemplated.

CSF Analysis

Collection of CSF is indicated in animals with neurologic deficits.
Cerebrospinal fluid may be normal, or may have an increased protein
content in cases in which diskospondylitis lesions cause extradural
compression of spinal cord or result in meningitis and/or myelitis.
The CSF white blood cell count may be normal, or may be elevated, with
an increase in PMN neutrophils in CSF from animals with meningitis or

Microbial Culture

Aerobic, anaerobic, and fungal cultures of blood and urine should be
done prior to treatment in an attempt to isolate causative organisms.
Cultures of CSF are indicated if the WBC count is elevated. Cultures
of fluid from draining sinuses may also be done. Efforts should be
made to diagnose B. Canis infection in all dogs with diskospondylitis.
Needle aspiration of lesions is possible, however fluoroscopic
guidance is usually necessary. The LS disc space can be aspirated
safely without fluoroscopy using plain radiographic guidance. Surgical
exploration and curettage may be necessary in refractory cases.


Every effort should be made to obtain cultures and antimicrobial
sensitivities of infectious agents involved. Treatment consists of
long-term use of an antimicrobial that is effective against the
causative organism(s) If an organism is not cultured, dogs without
severe neurologic deficits may be treated empirically, assuming
infection with the most common organism isolated from animals with
diskospondylitis (coagulase-positive, beta-lactamase positive
Staphylococcus sp). Antibiotics that are most effective for this
purpose are cephalosporins, or beta-lactamase resistant penicillins
such as oxacillin and cloxacillin.

Clinical signs may recur if the infection is not completely eliminated
prior to cessation of antibiotic therapy, and repeated cultures of
blood and urine and ongoing treatment with an appropriate antibiotic
may be necessary. Treatment is continued for at least 6 weeks, and
vertebral radiographs are done every 4 to 6 weeks to monitor
progression/ regression of a lesion, and to monitor for development of
new lesions. Radiographic signs of resolution (decreased lytic lesions
and bony proliferation and fusion) may lag behind signs of clinical
resolution by 4-8 weeks, particularly in older dogs. Antibiotic
administration may be necessary for prolonged periods (> 6 months).
Some cases will relapse when antibiotics are discontinued and
prolonged (often lifelong) therapy may be necessary.

Brucella canis infections are uncommon. A combination of minocycline
or tetracycline and streptomycin is recommended for treatment of B.
canis infections. Infected dogs should be neutered to eliminate risk
of transmission. B. canis infections have public health significance,
as people may become infected.

Clinical improvement in animals with diskospondylitis (resolution of
fever, improved appetite, reduction of apparent spinal pain) should be
seen within 2 weeks of starting antibiotic therapy. Use of analgesics
and restriction of exercise during the first weeks of treatment may be

If clinical improvement is not seen, treatment should be reevaluated
and cultures repeated. Presence of fungal organisms, particularly
Aspergillus sp and Paecilomyces sp is a common reason for poor
response to broad spectrum antibacterial agents. Treatment of fungal
infections is possible using amphotericin and azole antifungals,
however response is often transient and incomplete.

Surgical exploration of a lesion should be considered in animals that
are unresponsive to treatment or have persistent draining tracts
suggestive of grass seed migration. Objectives of surgery are
curettage of lesions and harvesting of material for bacterial and
fungal culture. Decompressive surgery is indicated if evidence of
spinal cord compression is found on myelography and if animals show
severe or progressive neurologic deficits. Surgical stabilization of
the vertebrae may be necessary following decompression. Surgical
stabilization of affected sites may also aid in resolution of
infections in refractory cases where instability is a significant

Prognosis for animals with diskospondylitis depends on the ability to
eliminate the causative organism(s) and on the degree of neurologic
dysfunction. Animals with severe neurologic deficits have a guarded to
poor prognosis. Animals with fungal infections, especially if
infections are disseminated, carry a particularly poor prognosis.

Additional Detail

Antimicrobial Agents


Amphotericin B (Fungizone)
Dog/Cat 0.5-0.8mg/kg 2-3x weekly
Dilute in 0.45%NS/2.5% dextrose
(Dog-<20kg 500ml)
(Dog->20kg 1000ml)
Don't use conc. > 20mg/L

Discontinue if BUN > 50mg/dL
Treatment can resume if renal parameters normalize.

Itraconazole (Sporanox)
Dog 5-10mg/kg q24h
Cat 10mg/kg q24h
Monitor liver enzymes
Split or reduce dose if anorexia and vomiting

Fluconazole (Diflucan)
Dog 2.5-10mg/kg q12h
Cat 50mg q12h
As for Itraconazole


Trimethoprim/Sulphonamide combination
Dog/Cat 15-30mg/kg q12h
Gram neg, Staphylococcus

Dog/Cat 5mg/kg q12h
Gram neg (poor gram pos)

10-15mg/kg q8-12h
Anaerobes (watch for neurotoxicity)

Dog/Cat 25-50mg/kg q8h
Esp. Gram neg

Dog/Cat 10-30mg/kg q8h
Gram pos (beta lactamase res)

Amoxicillin clavulanic acid
Dog 10-25mg/kg q8-12h
Cat 11-62.5mg/kg q8-12h
Gram pos/neg (beta lactamase res)

Dog/Cat 22-40mg/kg q8h
Gram pos

Dog/Cat 2-5mg/kg q6-8h
Gram pos, Gram neg and anaerobes
Reserve for resistant infections


Discospondylitis is a clinical problem which can often be readily
diagnosed based on clinical signs and plain spinal radiography. The
most common etiological agents are bacterial, and response to
appropriate antimicrobial treatment is often good. Isolation and
culture of infectious agents is a major goal in management of the
disease. Long term monitoring and treatment may be necessary. Poor
response to treatment is often the result of inappropriate
antimicrobial selection or the presence of fungal organisms.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted
by this speaker)
Peter J. Dickinson, BVSc, PhD, DACVIM (Neurology)
Assistant Clinical Professor, Neurology/Neurosurgery
University of California, Davis
Davis, CA

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Discussion Starter · #3 ·
yes, he has been on antibiotics & pain meds since monday. He is doing a 100% better now, vet wants to keep him on the antibiotics for about 5 more weeks again i want to thanks everyone for the corcern & thoughts shown on here
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