Clinical signs: Spinal pain is the most common initial clinical sign in this disease, which is most frequently seen in large intact male middle-aged dogs. Although it can occur in any animal, the condition is less common in toy and chondrodystrophoid breeds of dog’, as well as in cats. Approximately 30% of dogs have signs of systemic illness such as fever and weight loss.
Pathogenesis: Discospondylitis is due to infection of the intervertebral disc and adjacent vertebrae; if the infection is confined to the vertebral body, it is called vertebral osteomyelitis or spondylitis (). Staphylococcus intermedius is the most common aetiological agent of canine discospondylitis; other less commonly identified organisms include Streptococcus spp., Escherichia coli, Actinomyces spp. and Brucella canis, as well as Aspergillus spp. Young German Shepherd bitches seem to be predisposed to aspergillosis (), whereas young Basset Hounds contract discospondylitis due to systemic tuberculosis (). Haematogenous spread from distant foci of infection, penetrating wounds, surgery, or plant material migration can cause direct infection of the disc space or vertebrae, which is usually seen at the level of L2-4. Immunosuppression due to factors such as diabetes mellitus and hyperadrenocorticism is considered a predisposing cause.
- • Haematological changes are usually not present unless there are concurrent conditions such as endocarditis
- • Urine cytology may reveal bacterial or fungal agents
- • Blood and urine cultures should be performed in all suspected cases and are positive in up to 75% and 50% of cases, respectively ()
- • Serology for brucellosis should also be performed, especially in view of its zoonotic potential; this has been reported to be positive in up to 10% of cases.
Definitive diagnosis is usually made with spinal radiographs, although radiographic change may not be evident in the first 2-4 weeks of infection. The most commonly affected site is L7-S1, but other frequently affected sites include the caudal cervical / cranial thoracic vertebrae and the thoracolumbar junction. As this can be a multifocal disease, the entire spine should be radiographed. Radiographic evidence of disease includes narrowing of the disc space, accompanied by subtle irregularity of both endplates through to gross lysis and osseous proliferation of the adjacent vertebral bone () and even fractures (). Radiography can also be used to monitor the response to treatment or the progression of the disease (), although clinical progression is equally important, as radiographic change can lag behind clinical improvement. Myelography is indicated in patients with substantial neurological deficits to rule out concurrent disc disease; however, tnis should be reserved for the cases that are refractory to antibiotic therapy, when a surgical treatment may be considered.
Computed tomography (CT) can identify subtle endplate erosion and paravertebral soft tissue swelling more readily than radiography. Post-myelogram CT clearly defines compression of the neural tissues by infected tissues, as does MRI (). MRI can also highlight the inflammation in the surrounding muscles. However, as radiographs can be diagnostic, advanced imaging studies are reserved for cases that are refractory to treatment, or for those that have normal or equivocal radiographic studies.
Another diagnostic imaging option in dogs with discospondylitis is technetium-99m bone scanning (scintigraphy), which shows an increased uptake of the radiopharmaceutical at the affected disc space and endplates (). Care must be taken when interpreting this finding, as spondylosis also causes some increase in uptake.
If urine and blood culture, and brucellosis serology, have not identified an aetiological agent in cases of discospondylitis, percutaneous needle aspiration of the disc space can be a safe procedure to obtain tissue for bacterial and fungal cultures and cytology. However, this procedure requires general anaesthesia, sterile surgical preparation and fluoroscopic or CT guidance of the needle, and is usually only performed in patients unresponsive to initial broad-spectrum antibiotics. The procedure has been documented to be up to 75% sensitive (); open biopsy of the vertebrae may be considered if needle aspiration is unrewarding. This has yielded positive cultures in approximately 80% of patients (). In all cases, diagnostic investigation of potential systemic infectious foci should be considered. This should include abdominal ultrasonography for prostatic or renal disease, thoracic radiographs for pulmonary disease, and cardiac ultrasonography for endocardial disease.
Treatment and prognosis: Once radiographic evidence of discospondylitis is present, treatment for the common potential pathogen Staphylococcus intermedius may be started. The treatment of discospondylitis consists of antibiotics, cage rest and analgesics (Drug therapy for discospondylitis / osteomyelitis). Results of cultures may require alteration of this choice.
Drug therapy for discospondylitis / osteomyelitis.
|20-30 mg / kg orally q8h
20 mg / kg i.v., i.m. or s.c. q6h
20 mg / kg orally q12h
|Beta-haemolytic Streptococcus spp.||Amoxicillin||20 mg / kg orally q12h|
|Escherichia coll||Enrofloxacin||5-11 mg / kg orally q12h|
|10-20 mg / kg orally q24h
25 mg / kg orally q24h
|Aspergillus spp.||Fluconazole||2.5-5 mg / kg orally q24h|
Intravenous antibiotics should be considered if severe neurological compromise is present; otherwise, oral antibiotics are acceptable. However quickly the patient improves, continuation of the antibiotics for 8 weeks is recommended (). Resolution of clinical signs, such as pain and fever, should be expected within 5 days of initiating therapy; however, complete neurological resolution may take 2-3 months. Residual deficits may remain, but persistent pain indicates an active disease, and these patients should be treated with an additional antibiotic and considered for further diagnostics as they may have a potential fungal infection or surgical lesion.
Surgical decompression is rarely needed, and should only be considered in refractory cases or those with severe neurological deficits that show no sign of improvement within 3-5 days.
Non-steroidal anti-inflammatory drugs should be considered in dogs for the treatment of pain while awaiting the effect of the antibiotics, but should not be necessary after 5 days and should be discontinued to allow clinical assessment of the patient. Corticosteroids are not appropriate anti-inf lammatories in this disease.
The prognosis for this disease is generally very good unless the aetiology is fungal or there is endocarditis; the potential for recurrence should be considered, especially if brucellosis has been diagnosed or an underlying immunosuppressive condition is present. Residual neurological deficits are possible, and in those cases that have severe neurological deficits associated with the infection the prognosis should initially be guarded.