Discospondylitis: Diagnostic and Therapeutic Aspects

Discospondylitis is a bacterial or fungal infection of the intervertebral disc space and contiguous vertebral endplates. When the lesion involves only the vertebral body, the terminology is spondylitis. Nestel provided the first description of discospondylitis in a dog secondary to tuberculosis in 1957 []. Since then, this disease has been reviewed multiple times [2]. The avascular nucleus pulposus is nourished by the dense capillary bed of the adjacent vertebral end plates. Commonly, the infectious agent migrates hematogenously toward the slowly flowing venous channels of the vertebral end plates, proliferates, and spreads to the disk by local diffusion. Remote infected sites, vegetal material migration, extension of paravertebral abscess, penetrating wounds, or vertebral surgeries are often implicated in bacterial or fungal discospondylitis. It is a painful condition that, later in the course of the disease, may induce neurological deficits because of extradural spinal cord or nerve root compression.

Diagnosis

The diagnosis of discospondylitis is based on clinical findings and complementary examination results.

Clinical Findings

Discospondylitis has been more often described in young adult to middle-aged dogs of large or giant breeds; males are twice more often affected than females [3,4]. Although rare, discospondylitis has also been described in cats [5,6]. The clinician should look for a history of interdigital wound or inhaled grass awn, recent use of immunomodulating drugs to treat immune-mediated diseases of young dogs (e.g., suppurative aseptic meningomyelitis, polyarthritis), or recent viral infection with immunosuppressive capacity (e.g., parvovirus). Any chronic skin, ear, bladder, prostatic, uterine, or oral infection may also be a source of bacteria.

Hyperesthesia and lameness are the most common initial clinical signs that the owner describes. The pain may stay unlocalized, and the owner will report only decreased spontaneous physical activity. Pain and lameness often decrease with administration of anti-inflammatory drugs but recur as soon as the drugs are discontinued. Depending on the immune status of the patient and the nature of the infectious agent, the disease evolves in a subacute or chronic manner. Later, pain may become so severe that the animal is reluctant to move and becomes aggressive if manipulated. Excruciating pain is usually associated with severe cord or nerve root compression, subluxation, or pathologic vertebral fracture. Systemic signs of infection are often not present initially; hyperthermia may be the only sign but it is not a constant finding. Later in the course of the disease, weight loss, anorexia, and localized pain become more obvious. Reactive inflammatory osseous or discal tissues protrude in the vertebral canal and induce spinal cord or nerve root compression, which explains signs of ataxia and paresis. The localization of the affected vertebrae along the vertebral column determines the clinical presentation. With a C1-C5 or T3-L3 compressive lesion, the clinical findings are decreased conscious proprioception and upper motor neuron signs on the four limbs or rear limbs only, respectively. With a C6-T2 compressive lesion, decreased conscious proprioception in all four limbs, lower motor neuron signs in the front, and upper motor neuron signs in the rear limbs are present. The vertebral segment most commonly involved is L4-S1, especially the lumbosacral junction. With this lesion, the patient will manifest a more or less complete "cauda equina syndrome": rear end pain, short-strided pelvic limb gait, pelvic limb lameness or root signature, and later, lower motor neuron signs, i.e., rear limb weakness, tail paralysis, and urinary and fecal incontinence. In lesions of the cervical spine, which is rarely involved, pain precedes paresis or paralysis usually weeks before the lesion protrudes enough to cause spinal cord or spinal root compression. When the diagnosis is made late in the course of the disease, lesions may be multiple with adjacent or nonadjacent vertebrae involved.

Complementary Exam Findings

Early in the course of the disease, the differential diagnosis may include many conditions. Systemic disease inducing hyperthermia and generalized weakness, orthopedic conditions such as polyarthritis or panosteitis, other neurologic diseases such as polymyositis or juvenile meningitis have the same clinical presentation as discospondylitis. When pain is localized to the vertebral column or when neurologic deficits are more obvious, plain radiographs under general anesthesia are the first diagnostic tools of choice. It is essential to radiograph the entire vertebral column because more than one space may be involved, pain may not be localized above the involved vertebrae, or the major radiographic changes may not be localized at the most painful sites. Radiographic characteristics of discospondylitis are decreased size of the intervertebral space (Fig. 47-1), lysis of the vertebral endplates, sclerosis of the adjacent vertebral bodies, and sometimes, spondylosis. The time interval between the onset of clinical signs and the first radiographic signs (i.e., irregularity or lysis of the middle endplates area) may be two to four weeks [7]. This is why radiographs must be repeated in a few weeks when initial radiographs are not diagnostic but the suspicion of discospondylitis is high. More advanced lesions may show shortening of the vertebral bodies or subluxation or collapse of the vertebral bodies. Once discospondylitis has been diagnosed, a thorough physical examination is essential to look for a primary site of infection (urinary or genital tract, ear canals, teeth, etc.).

Figure 47.1. Lateral radiograph of a midlumbar discospondylitis; notice the early signs of end plate lysis and intervertebral space collapsus.

Myelographic findings indicate extradural compression because of a protruding infected disc, swollen and displaced ligaments, or periosteal reaction. However, a myelographic study is rarely necessary unless multiple affected sites are present and the clinician wants to evaluate which one is the most compressive for surgical decompression and culture.

Computed tomography and magnetic resonance imaging are also useful tools for the diagnosis of discospondylitis (Fig. 47-2 and Fig. 47-3) [8]. Magnetic resonance imaging, especially, may detect subtle nucleus and annulus changes earlier than radiographic identification [9]. Increased T2 and decreased T1 signal intensity of intervertebral discs, end plates, and subvertebral soft tissues, as well as interface contrast enhancement are classically described [10,11]. These advanced imaging techniques do not eliminate the need for culture of the causative organism for definitive diagnosis and treatment (see below).

Figure 47.2. Sagittal computed tomographic reconstruction of a lumbosacral discospondylitis in a dog; notice the bone window setting that enlightens the lesion.

Figure 47.3. Sagittal T2-weighted magnetic resonance image of a lumbosacral discospondylitis in a dog; notice the contrast enhancement of the intervertebral space.

Bone scintigraphy with gallium-67 or technetium-99m may also detect a disc inflammation sooner than radiographs, especially if spondylosis is misleading; a hot spot will be found in the first case, not in the second. However, the sensitivity of this test is poor; on an aged dog, it does not rule out neoplasia. Discospondylitis and spondylitis may be difficult to distinguish initially from a primary vertebral neoplasm in adult dogs; except for osteoblastic sarcoma, a primary vertebral neoplasm should not cross the intervertebral space.

White blood cell count and urine analysis usually do not show a neutrophilic leukocytosis unless there is a concurrent systemic infection. Cerebrospinal fluid collection and culture are not necessary. A moderate proteinorachia and, more rarely, a mild pleocytosis may be found. Diffuse suppurative meningitis associated with an extension of an abscess to the subarachnoid space is uncommon; when it does occur, prognosis is extremely poor and generalized sepsis is highly probable.

In order to isolate the causative organism, aerobic and anaerobic bacterial culture (and fungal culture depending on the geographic region the patient has visited) should be done prior to treatment. Urinary culture may help to detect the causative agent up to 50% of the time. Blood culture is positive in up to 75% of cases [12]. When a draining tract of the paravertebral region is present, it should be cultured during the surgical exploration for a foreign body. The infectious agent may also be cultured from a spinal needle-aspiration guided by fluoroscopy. An ultrasound-guided aspirate is also technically possible on lumbar or lumbosacral sites. Finally, a surgical biopsy must be considered if the previous cultures are negative and treatment is ineffective. The most commonly encountered agents are Staphylococcus sp. coagulase positive, Streptococcus sp., Aspergillus sp., and Mycobacterium sp. More recently, discospondylitis caused by Pseudomonas aeruginosa, Enterococcus faecalis, Staphylococcus epidermidis, and Bordetella sp. have been published [9,13,14]. Before breeding dogs, an agglutination test must always be performed to confirm the absence of Brucella canis; this test has an excellent predictive value [15,16]. Infection with this organism is considered an important public health consideration in many countries, as the disease is transmissible to humans, especially those handling aborted puppy fetuses. Results of blood culture are less likely to be positive for Brucella canis than for discospondylitis caused by other organisms [17]. The fungal agents able to induce discospondylitis are Aspergillus sp., Paecilomyces sp., Coccidioides immitis, and Actinomyces sp. [18-20].

Therapeutic Aspects

Ideally, identification of the causative organism and sensitivity results help to select the antimicrobial of choice. Bactericidal antibiotics are recommended for patients that may be immunocompromized. A treatment lasting a minimum of 6 weeks is necessary. Without identification of the organism or pending the results, assuming that Staphylococcus sp. coagulase positive is the most common agent, the following are appropriate first choice antibiotics: cephalosporins (cephalexin: Rilexine, Virbac, 20-30 mg/kg b.i.d., IV, IM, or PO), beta lactamase-resistant penicillins (amoxicillin and clavulanic acid: Clavamox, Pfizer, 12.5 mg/kg b.i.d., PO), and clindamycin (Antirobe, Pharmacia, 11 mg/kg b.i.d., PO). Intravenous treatment is preferred initially if the disease is long standing. Nonsteroidal anti-inflammatory drugs or narcotic agents may be necessary for pain control. The author regularly uses steroids at an anti-inflammatory dosage (prednisolone: Megasolone, Merial, 0.2-0.3 mg/kg b.i.d., PO) to alleviate the pain when nonsteroidal drugs are not effective. They must be tapered and discontinued within a week or two. Clinical improvement must be noticed within one week; by that time, steroids, when used, are tapered. When the lysis is extensive, because pathologic fractures are possible, the patient must have only minimal physical activity for the first weeks. If the patient is responsive to therapy, radiographs should be repeated no more than every 4 weeks to assess the progression or regression of the lytic lesions. In adult dogs, the radiographic deterioration continued, despite a successful clinical response, for 3 to 9 weeks [7]. Radiographic evidence of healing may take 4 to 6 months.

In a patient that fails to improve, the clinician should consider reassessment and culture of the disc space by aspiration or open biopsy, especially if the neurologic deficit progresses. Fluoroscopy-guided percutaneous discectomy or surgical exploration must then be considered in order to fenestrate and decompress the infected site [21]. Biopsies for histopathologic analysis and culture are submitted along with urine and blood. Internal stabilization (plates, pins, screws, and methylmetacrylate) may be necessary if stability is compromised, although the risk of implant superinfection is high. A surgical technique involving distraction and stabilization of the lumbosacral vertebral segment using external skeletal fixation associated with or without cancellous bone graft has been described [22].

Dogs infected with Brucella canis should not be treated. In the countries where this disease is considered a zoonosis, the infected dogs are euthanized.

Fungal infection must be treated with ketoconazole (Nizoral, Janssen, 10 mg/kg, PO, q 24 h) or itraconazole (Sporanox, Janssen, 5 mg/kg, PO, q 24 h). Temporary remission is more common that definitive cure [13,20,23].

Prognosis

Patients with severe neurologic deficit have a poorer prognosis than those with pain only. However, in a multicenter retrospective study, neither significant correlation between the degree of compression in the affected site and the clinical outcome, nor between ambulatory status and the final outcome was found [24].