Discospondylitis

DISEASES OF THE SPINE

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DISCOSPONDYLITIS Michael P. Moore, DVM, MS

Discospondylitis is inflammation of intervertebral discs, associated end plates, and adjacent vertebral bodies causing destruction and proliferation of bone. Discospondylitis is most commonly the result of a bacterial infection. Fungal infections cause discospondylitis less commonly. Discospondylitis is most common in large and giant breeds of dog. It can occur in the cat. Any age of dog may be affected. Males may be affected more than females. Any vertebra may be affected, although thoracic and lumbar vertebra are most commonly involved. 1, 9 Clinical signs vary from subclinical to overt signs of inflammation. Clinical signs may include fever, anorexia, weight loss, lethargy, reluctance to move, and spinal pain. Neurologic abnormalities may be present if the disease process is associated with spinal cord compression. Spinal cord compression with discospondylitis may be caused by pathologic fracture of vertebral bodies or end plates or disc rupture. Discospondylitis occasionally results in meningitis, which causes clinical signs of spinal cord dysfunction. 1, 9 ETIOPATHOGENISIS Hematogenous Spread

Hematogenous spread of organisms to intervertebral discs, end plates, or vertebral bodies is thought to be the most common pathogenesis. 1, 9 Infection may originate from bacteremia associated with endocarditis, dental disease, urogenital tract infections, or other From the Department of Veterinary Clinical Medicine and Surgery, Washington State University College of Veterinary Medicine, Pullman, Washington

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 22 • NUMBER 4 • JULY 1992

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sites. With urinary tract infections, retrograde flow of blood through vertebral sinuses has been suggested as a possible mechanism for infection of vertebral structures. Cause and effect, however, have not been established in cases with both urinary tract infection and discospondylitis. 1, 9 Coagulase-positive Staphylococcus organisms (S. intermedius, S. aureus) are the most frequent organisms isolated. 1, 8, 9Other bacterial isolates include, Streptococcus canis, Pasteurella spp., Proteus spp., Corynebacterium spp., Actinomyces spp., Nocardia spp., Bacteroides spp., and Mycobacterium Spp.l, 8, 9 Brucella canis is another less common isolate. The fungi Aspergillus spp. and Paecilomyces spp. have also been cultured. 9 The Coccidioides immitis may cause vertebral body osteomyelitis. 9

Foreign Bodies

Migrating plant materials such as grass awns have been associated with a variety of inflammatory syndromes including discospondylitis. 4,9 These grass awns usually have barbed ends that allow them to advance forward but not backward. Wheat (Triticum vulgare), barley (Hordeum vulgare), cheat grass (also known called downy brome) (Bromus tectorum), and foxtails (Hordeum jubatum) are examples of grasses with awns that have this characteristic. 4 Certain geographic regions have these types of grasses. Although the exact portal of entry for the grass awn in these cases is not known, there are several proposed theories. 4 , 9 One proposed mechanism is that these grasses may migrate to paravertebral structures after penetrating skin over the paravertebral structures or abdomen. Muscular contractions may aid in migration of the grass awn to paravertebral and vertebral structures in these cases. 9 Swallowing the grass awn and penetration through the bowel wall has been suggested as another portal of entry. The awn would have to migrate along the mesentery, to the attachment of the mesenteric root on the ventral paravertebral structures, and ultimately localize to the vertebral column. 9 Convincing evidence, however, such as scarring of the bowel wall or mesentery and associated structures has not been reported. Inhalation of the grass awn, and migration through the lungs or mediastinum, then along the crura of the diaphragm, has also been suggested as a portal of entry.9 The muscular insertion of the crura of the diaphragm is the ventral lumbar bodies of L-2-L-4. Grass awnassociated discospondylitis and spondylitis occur most frequently in the L-2-L-4 vertebral bodies. Grass awn infections are associated with a variety of bacteria. One of the more common pathogenic isolates is Actinomyces Spp.2,7 Mixed infections with organisms such as Staphylococcus spp., Streptococcus spp., Bacteroides'spp., Proteus mirabilis, Pasteurella spp., and Pseudomonas spp., frequently accompany infections with Actinomyces Spp.2 Less frequently Nocardia spp. can be cultured. 7

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Other Factors2 , 8, 9

Previous trauma to the intervertebral disc, vertebral body, or end plate (e.g., intervertebral disc disease) may playa role in development of discospondylitis. Discospondylitis may occur as a complication of disc surgery. Immunosuppression has been identified and suggested as a factor in kenneled dogs with discospondylitis. Direct extension of paravertebral infections may also cause discospondylitis, spondylitis, or vertebral osteomyelitis. Cats may develop one of these syndromes as the result of fight wounds of paravertebral structures. The author knows of one case of discospondylitis complicated by meningitis in a coonhound associated with trauma from a fight with a bear. Actinomyces was cultured from the cerebrospinal fluid. CLINCOPATHOLOGIC ABNORMALITIES2, 8, 9

Clinical signs of pain, reluctance to stand or jump, anorexia, fever, or spinal cord dysfunction may be present. White blood cell counts may be increased and characterized by a neutrophilia with a left shift, or they may be normal. Any vertebral body, end plate, or disc space may be involved. The thoracic and lumbar vertebra, however, are most commonly involved. Radiographic abnormalities vary with the duration of the discospondylitis. Early in the course of disease, bony lysis of the end plates may be seen. With time, collapse of the -disc space and bony proliferation with bridging of vertebral bodies will become evident. The bony proliferation may be extensive, making it difficult to identify the bony lysis. Special imaging such as linear tomography or computed tomography may be helpful in demonstrating the bony lysis when there is extensive bony proliferation. More than one disc space may be affected. Osteomyelitis of other bones may also be present, especially when discospondylitis is due to hematogenous spread. Other organ systems may be affected. Cardiac disease (i.e., arrhythmias and murmurs), urogenital disease, and hepatic dysfunction may be associated with bacteremia. In the author's experience, one or more related problems (problems other than discospondylitis) may be present with migrating plant awns. Associated problems include draining paralumbar abdominal or thoracic wall tracts, sublumbar masses (granulomas) visualized by radiography, spondylitis, and septic pleural and mediastinal effusions. DIAGNOSIS2, 8, 9

The diagnosis is ultimately based upon demonstrating the bony lysis of the vertebral end plates (Fig. 1).2,8,9 Development of radiographic abnormalities, however, may take 2 to 4 weeks after infection. 8 Therefore early on in the disease, radiographic abnormalities may not

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Figure 1. An example of progression of bony proliferation associated with discospondylitis. The bottom radiograph was taken 4 weeks after the top radiograph. (Courtesy of Dr. Ronald D. Sande, Pullman, Washington.)

be observed. Clinical signs of spinal hyperesthesia or neurologic dysfunction are not always present with discospondylitis. Without clinical signs of spinal column disease, making a diagnosis of discospondylitis can be difficult. Fever and persistent urinary tract infection are often features of discospondylitis. In the absence of clinical signs of spinal

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disease, the clinical signs of fever of unknown origin or recurrent urinary tract infections may justify spinal radiographs to rule out discospondylitis. Culture and sensitivity should be attempted to determine the etiology. Blood should be cultured because bacteremia is often associated with discospondylitis. Because urinary tract infections may accompany discospondylitis, urine should also be cultured. A sample for culture may be obtained directly from the lesion by needle" aspiration with fluoroscopic guidance. A biopsy specimen of the lesion for culture may also be obtained by surgical exploration. Surgical biopsy should be reserved for cases with extenuating circumstances such as therapeutic failures. Cardiac, urogenital, and hepatic systems should be assessed because discospondylitis may be associated with bacteremia and urogenital infections. Skeletal survey radiographs should be evaluated for other bony involvement. Nuclear medicine imaging may be helpful in diagnosing additional bone lesions. Discospondylitis with exudative pleural or mediastinal effusions; draining thoracic, paralumbar, or abdominal wall tracts; or radiographic evidence of sublumbar masses should be taken as evidence for a possible grass awn-associated problem. In fact, clinical signs of grass awn-associated problems may not be characteristic of discospondylitis. Instead respiratory problems or persistent draining tracts of the body wall may be more prominent clinical signs. Discospondylitis, spondylitis, or vertebral body osteomyelitis of the cranial lumbar vertebra may be detected only after radiographic imaging intended for other problems (e.g., thoracic radiographs). Dogs with radiographic evidence of discospondylitis should be tested for Brucella canis. The serologic procedures such as the rapid slide agglutination test and tube agglutination test can be used for screening. 2, 8, 9 False-negative results are rare with both tests (1 0/0). Falsepositive results, however, are common with both tests. 3 The agar gel immunodiffusion test is a more sensitive and specific serodiagnostic test. 3 Demonstrating the organism by blood culture is definitive.

THERAPY After demonstrating radiographic evidence of discospondylitis, microbial blood and urine culture and sensitivity should be performed. If possible, a fluoroscopic-guided aspirate of the lesion should be obtained for culture and sensitivity. If coexisting cardiac, urogenital, and hepatic problems are present, specific therapies for these problems may be indicated. Surgical decompression, stabilization, and curettage of lesions along with medical therapy may be warranted in animals with severe neurologic abnormalities secondary to disc collapse or pathologic fractures. Such cases, however, should be given a guarded to poor prognosis.

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Antimicrobial therapy should be based on the culture results. If Brucella serodiagnost~c tests are negative, the veterinarian can be reasonably sure (1 % or less false-negative results) that Brucella is not the causative agent. If the culture results are negative and grass awnassociated discospondylitis is not suspected, treatment for coagulasepositive Staphylococcus spp. should be initiated because it is the most common isolate. Beta-Iactamase-resistant antibiotics should be used because both S. intermedius and S. aureus can produce beta-Iactamase. 6 There are many synthetic beta-Iactamase-resistant penicillins that can be selected. Among these, dicloxacillin (20 to 50 mg/kg, per os, every 8 hours), cloxacillin (10 to 15 mg/kg, per os, every 6 hours), and oxacillin (15 to 25 mg/kg, per os, every 6 to 8 hours) are recommended firstchoice antibiotics. 6, 8 First-generation cephalosporins have also been used. 8 Clindamycin (5 to 15 mg/kg, per os, every 8 hours) is also an effective antimicrobial for discospondylitis caused by coagulase-positive Staphylococcus Spp.8 Amoxicillin with clavulanic acid (a beta-Iactamase inactivater) or other beta-Iactamase inhibitors (methicillin, nafcillin) may also be considered. 3 Less effective antibiotics include lincomycin, chloramphenicol, erythromycin, trimethoprim-sulfonamides, and tetracyclines. Therapy should continue for at least 6 weeks and may need to be continued for up to 6 months in some cases. Therapy generally results in improvement within 4 to 5 days. If there is no improvement after 7 to 10 days of therapy, the case should be reevaluated. Resolution of radiographic lesions can be used as a guide to therapy but has some limitations. It may take 2 to 4 weeks after resolution of infection to visualize radiographic improvement. Perhaps what is more important when monitoring, active areas of lysis may be masked with extensive bony remodeling. In cases with extensive bony proliferation, it may be prudent to extend therapy for 4 to 6 weeks past radiographic resolution of bony lysis. Nuclear imaging, linear tomography, or computed tomography may prove to be better monitoring methods. In cases of suspected grass awn-associated discospondylitis, surgical removal of the grass awn combined with antimicrobial therapy directed against cultured organisms is ideal. Finding the grass awn in these cases, however, is similar to trying to find a needle in a haystack. Also finding one grass awn does not preclude the presence of another. Consequently the author does not recommend routine surgical exploration in these cases. Debulking may decrease the mass of affected tissue and could possibly result in inadvertent removal of the grass awn. However, the author has appreciated acceptable results with strictly a medical approach in most cases. Debulking and surgical exploration are reserved for unresponsive cases. Medical therapy for suspected grass awn-associated discospondylitis should be based on culture results. Actinomyces spp. is a frequently cultured organism in such cases by the laboratory at Washington State University. Other bacterial isolates commonly accompany Actinomyces spp. and should also be treated. In suspected grass awn-associated cases of discospondylitis with a negative culture result, treatment is started for Actinomyces spp. Penicillin (100,000 U/kg given intramuscularly or subcutaneously

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every 12 to 24 hours) is the therapy of choice. Penicillin G (65,000 U/kg given orally every 8 hours at least 1 hour before or 2 hours after eating) has been reported to be an effective treatment. 7 Amoxicillin (10 to 20 mg/kg given orally every 8 to 12 hours) has proved to be an acceptable substitute for the author. Some species of Actinomyces (A. hordeovulneris), however, may form cell wall-deficient L-phase variants and are reported to respond poorly to ampicillin type products. 7 Other antibacterials that may be used include clindamycin, chloramphenicol and erythromycin, rifampin, cephaloridine, and minocycline. 7 Antimicrobials that are not effective include aminoglycosides, metronidazole, cephalexin, oxacillin, and dicloxacillin. 7 Nocardia spp. is a less frequently isolated organism. Therapy with sulfadiazine, 80 mg/kg, or sulfisoxazole, 50 mg/kg given per os, every 8 hours appears to be effective in spite of variable in vitro sensitivity results. 7 At least 6 weeks of therapy for suspected grass awn-associated discospondylitis is usually required and may need to be continued for up to 6 months. The prognosis for successful therapy for discospondylitis caused by brucellosis is guarded. 3 There is a high rate of recurrences. Males should be neutered because there is some evidence suggesting an inability to clear the prostate gland of infection. Before attempting treatment, the client should be informed about the risk of human infection from contact with the pet. Minocycline (25 mg/kg every 24 hours or divided every 12 hours given per os) combined with dihydrostreptomycin therapy (5 mg/kg every 12 hours given intramuscularly or subcutaneously) or gentamicin therapy (2 mg/kg every 12 hours given intramuscularly or subcutaneously) has been reported to be the most successful therapy. 3 This treatment is continued for 2 to 3 weeks and may be more successful if repeated 2 or more times. Therapy with ketoconazole alone or in combination with amphotericin B may be attempted for vertebral body osteomyelitis caused by coccidioidomycosis. 5 Combined therapy with ketoconazole and amphotericin B may be attempted for discospondylitis caused by aspergillosis. 5 Azole derivatives other than ketoconazole (itraconazole, fluconazole and vinbunazole) are antifungal agents that may be considered. 5 References 1. Braund KG, Brewer BD, Mayhew IG: Inflammatory, infectious, immune, parasitic and vascular diseases. In Oliver JE, Hoerlein BF, Mayhew IG, eds: Veterinary Neurology. Philadelphia, WB Saunders, 1987, pp 231-232. 2. Brennan KE, Ihrke PJ: Grass Awn migration in dogs and cats: A retrospective study of 182 cases. J Am Vet Med Assoc 182(11):1201-1204, 1983. 3. Carmichael LE, Greene CE: Canine Brucellosis. In Greene CE, ed: Infectious Diseases of the Dog and Cat. Philadelphia, WB Saunders, 1990, pp 573-584. 4. Case A: Poisoning and injury by plants. In Kirk RW, ed: Current Veterinary Therapy VIII, Small Animal Practice. Philadelphia, WB Saunders, 1983, pp 145-152. 5. Greene CE: Antifungal chemotherapy. In Greene CE, ed: Infectious Diseases of the Dog and Cat. Philadelphia, WB Saunders, 1990, pp 649-658. 6. Greene CE, Ferguson DC: Antibacterial chemotherapy. Greene CE, ed: Infectious Diseases of the Dog and Cat. Philadelphia, WB Saunders, 1990, pp 461-493.

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7. Hardie EM: Actinomycosis and nocardiosis. In Greene eE, ed: Infectious Diseases of the Dog and Cat. Philadelphia, WB Saunders, 1990, pp 585-591. 8. Kornegay IN, Anson LW: Musculoskeletal infections. In Greene CE, ed: Infectious Diseases of the Dog and Cat. Philadelphia, WB Saunders, 1990, pp 88-91. 9. LeCouteur RA, Child G: Diseases of the spinal cord. In Ettinger SJ, ed: Textbook of Veterinary Internal Medicine, ed 3. Philadelphia, WB Saunders, 1989, pp 650-654.

Address reprint requests to Michael P. Moore, DVM, MS Department of Veterinary Clinical Medicine and Surgery Washington State University College of Veterinary Medicine Pullman, WA 99164-6610