Pathology in Practice

David M. Wong Departments of Veterinary Clinical Sciences (Wong, Hepworth, Sponseller) and Pathology (Whitley), College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

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Elizabeth M. Whitley Departments of Veterinary Clinical Sciences (Wong, Hepworth, Sponseller) and Pathology (Whitley), College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

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Kate Hepworth Departments of Veterinary Clinical Sciences (Wong, Hepworth, Sponseller) and Pathology (Whitley), College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

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Brett A. Sponseller Departments of Veterinary Clinical Sciences (Wong, Hepworth, Sponseller) and Pathology (Whitley), College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

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History

A 12-year-old 400-kg (880-lb) Pony of the Americas mare was evaluated because of a 2-week history of weight loss and a 1-week history of inappetence, lethargy, intermittent fever, and grunting coupled with generalized signs of pain when moving backward. The pony had mild lameness attributed to cellulitis of the left forelimb 1 month prior, but the condition had clinically resolved with treatment. One dose of ceftiofur was administered IM 1 day prior to the evaluation.

Clinical and Gross Findings

On initial examination (day 1), the pony was bright and responsive but had clinical signs of generalized pelvic pain evidenced as resentment to rectal palpation; the pony also grunted when made to step backward. Clinical signs of forelimb lameness were not observed, but may have been masked by an abnormal hind limb gait, characterized initially as a stiff, stilted gait suggestive of associated pain. Tachycardia (54 beats/min) was present, and pleural roughening was observed via thoracic ultrasonography. The total WBC count was within the reference limit, but a toxic left shift was present during the first 2 days of hospitalization; leukocytosis (22.59 × 103 leukocytes/μL; reference interval, 5.0 × 103 leukocytes/μL to 11.0 × 103 leukocytes/μL) characterized by neutrophilia (17.62 × 103 neutrophils/μL; reference interval, 2.1 × 103 neutrophils/μL to 6.7 × 103 neutrophils/μL) with toxic changes was detected on day 3. Other notable clinicopathologic derangements included mild anemia (Hct, 26%; reference interval, 34% to 45%), monocytosis (0.76 × 103 monocytes/μL [day 1] to 2.94 × 103 monocytes/μL [day 3]; reference interval 0 × 103 monocytes/μL to 0.5 × 103 monocytes/μL) and hyperfibrinogenemia (1,100 mg/dL [day 1] to 2,000 mg/dL [day 3]; reference interval, 100 to 400 mg/dL). Results of cytologic examination of an abdominal fluid sample collected on day 1 were considered normal.

Despite administration of antimicrobials and flunixin meglumine, the pony had intermittent fever and was reluctant to ambulate; prolonged recumbency and difficulty rising progressed to inability to rise on day 3. Deep pain reflexes of the hind limbs were still present on day 4, but owing to continued deterioration in its condition, the pony was euthanized by IV administration of pentobarbital sodium and phenytoin sodium.

Gross findings at necropsy included a soft, 10 × 8 × 25-cm, red-brown mass that had expanded the retropleural and retroperitoneal space ventral to the T13 through T18 vertebrae and had caused necrosis of the origins of the psoas major muscles. On sectioning, the vertebral bodies were mottled red-tan-brown, and the periosteum was firm and thickened uniformly along the length of the affected vertebrae (Figure 1). The dura of the spinal cord in the T5-S2 region was covered by red-tan material that expanded the extradural fat and was most abundant in the caudal thoracic region (T14 through T18). Friable, red-tan material expanded the sheaths of the superficial and deep digital flexor tendons of the left forelimb at the level of the carpus, extending approximately 10 cm proximally and distally. The synovium of the left carpal joint was thickened and red, and joint spaces contained friable, red-tan material.

Figure 1—
Figure 1—

Photographs of a transverse section of the T18 vertebral body (A) with a magnified image of that vertebral body (B) and a sagittal section of the left forelimb (C) of a 12-year-old Pony of the Americas mare that was evaluated because of a 2-week history of weight loss and a 1-week history of inappetence, lethargy, intermittent fever, and grunting coupled with generalized signs of pain when moving backward. One month prior, the pony had mild lameness of the left forelimb (attributable to cellulitis), which resolved with treatment. Three days after the initial evaluation, the pony was euthanized because of its deteriorating condition. In panel A, there is mottled red-tan-brown discoloration of the vertebral body (arrowhead) and hypaxial musculature and red-tan discoloration of the extradural adipose tissue (arrow). The spinal canal is labeled (asterisk). In panel B, bony tissue (arrowhead) is visible radiating from the cortex of the vertebral body (arrow). In panel C, there is abundant, red-tan, friable material within the tendon sheaths and in the radiocarpal and intercarpal joint spaces of the left forelimb. In all panels, bar = 1 cm.

Citation: Journal of the American Veterinary Medical Association 247, 1; 10.2460/javma.247.1.55

Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →

Histopathologic and Microbiological Findings

Tissue samples from numerous tissues including the carpal joint, thoracic vertebrae, brain, spinal cord, sciatic nerve, heart, lungs, liver, kidneys, spleen, adrenal glands, skin, uterus, lymph nodes, and large and small intestines were routinely processed for microscopic examination. The vertebral periosteum was expanded by radiating trabeculae of woven bone extending at right angles from the vertebral body, consistent with the formation of reactive periosteal bone (Figure 2). Variably mature fibroplasia was present between trabeculae of the exostotic bone, admixed with large groups of degenerating neutrophils, which occasionally surrounded colonies of gram-negative, rod-shaped bacteria. Trabeculae of exostotic bone closest to the vertebral cortex were undergoing remodeling by osteoclasts, indicative of a long-term process. In many areas, the fibroplasia ran parallel to the trabeculae, suggesting that those areas were a component of the inflammatory process, not just residual periosteum. Multifocal to coalescing marrow spaces in the vertebral body contained many viable and degenerating neutrophils and colonies of similar bacteria. Vertebral myeloid hyperplasia was also observed in lesser affected regions. The dura of the thoracic spinal cord was covered by a dense plaque of fibrin with myriad degenerating neutrophils and mild, multifocal hemorrhage. In the spinal cord, some axonal spaces in the dorsal, lateral, and ventral funiculi were empty and rare myelin degeneration and phagocytosis (digestion chambers) was present; rare swollen axons (spheroids) were also evident. Spinal nerves of affected cord segments were surrounded by inflammation and fibroplasia, with small numbers of digestion chambers. Abundant fibrin, hemorrhage, and viable and degenerating leukocytes (neutrophils and macrophages) were present in the carpal joint space.

Figure 2—
Figure 2—

Photomicrographs of sections of a thoracic vertebra (A) and vertebral canal in the thoracic portion of the vertebral column (B) of the mare in Figure 1. A—In this vertebral body, there is proliferation of new bone in the periosteum and abundant suppurative inflammation. Thin trabeculae of reactive bone (thin arrow) radiate from the cortical bone of the vertebral body (thick arrow). H&E stain; bar = 100 μm. B—Extradural tissues (arrow), including epidural adipose tissue, of the vertebral canal are expanded by hemorrhage, fibrin, and inflammatory infiltrate (epidural steatitis). The spinal cord is labeled (asterisk). H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 247, 1; 10.2460/javma.247.1.55

The synovial membranes of the radiocarpal and intercarpal joints were hypertrophic and hyperplastic, forming papillary projections into the joint space; many lymphocytes, plasma cells, macrophages, neovascularization, and immature fibroplasia were detected in the subintima. Mild, acute, interstitial pneumonia, severe splenic and lymph node lymphoid depletion, and systemic congestion also were present. Other microscopic findings included congestion of intertubular renal and cardiac blood vessels and scattered foci of mild, acute myocardial and cerebral leptomeningeal hemorrhage. No relevant microscopic findings were observed in tissues samples from the uterus, intestines, liver, adrenal glands, sciatic nerve, or skin. Bacterial culture of a sample of the red-brown mass ventral to the T13 through T18 vertebrae yielded heavy, pure growth of Klebsiella pneumoniae.

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: chronic, suppurative, thoracic vertebral osteomyelitis and periostitis; suppurative spinal pachymeningitis and epidural steatitis, with axonal degeneration; and chronic carpal tenosynovitis and arthritis in the left forelimb.

Case summary: vertebral osteomyelitis and paravertebral abscess (K pneumonia infection), carpal tenosynovitis, and arthritis in a pony.

Comments

Osteomyelitis is defined as an inflammatory process of the bone and bone marrow that results in bone destruction and is caused by infectious microorganisms.1 In the veterinary medical literature, vertebral osteomyelitis has been described in various species, including dogs, cats, calves, lambs, and foals,2–10 but is less frequent in adult horses.11–14 Vertebral osteomyelitis most often results from hematogenous seeding from a primary site of infection, traumatic injury, or contiguous spread from an infection in adjacent soft tissue; however, iatrogenic inoculation during spinal surgery can also serve as a source of infection in applicable species.15

A small number of reports11–14 of vertebral osteomyelitis or paravertebral abscesses in adult horses have described clinical signs including fever, signs of neck or back pain, muscle twitching, generalized stiffness, shuffling gait, progressive ataxia, limb weakness, muscle atrophy, and intermittent fever. Many affected horses have been described as having difficulty rising from recumbency and a history of prolonged or persistent recumbency.11–14 An inflammatory leukogram along with hyperfibrinogenemia was detected in the pony described in the present report as well as previously reported cases.11–14 Moderate to severe elevations in serum fibrinogen concentrations (≥ 900 mg/dL) have been used as a diagnostic indicator of physeal or epiphyseal osteomyelitis in foals.18 Evaluation of CSF samples from horses with vertebral osteomyelitis may reveal no abnormal characteristics; however, a small number of affected horses have had high total protein concentration and WBC count.11,12 Although bacteriologic culture of blood is highly recommended for people suspected of having vertebral osteomyelitis, in a study12 of 5 horses with vertebral osteomyelitis, 2 underwent bacteriologic culture of blood, which yielded no growth.

Plain radiography can be used as an initial diagnostic screening method in humans with vertebral osteomyelitis and may help rule out other causes of clinical signs.16 However, radiographic changes can take weeks to months to become detectable, thereby delaying diagnosis.17 Although not routinely feasible in adult horses, MRI and CT is used in people and small animals to help differentiate causes of neurologic deficits and identify evidence of vertebral osteomyelitis.2,3,16 Ultrasonography may serve as an adjunctive imaging technique in horses with vertebral osteomyelitis.

Treatment for vertebral osteomyelitis includes long-term administration of broad-spectrum antimicrobial and anti-inflammatory medications, surgical exploration and debridement of affected bone, or drainage of accessible abscesses (eg, cervical vertebral body).12,13 Penicillin and trimethoprim-sulfamethoxazole have been used in horses with vertebral osteomyelitis, but other antimicrobials, selected ideally on the basis of bacterial culture and antimicrobial susceptibility results, may be viable options.12,13 Of 10 adult horses described previously (including the case described in the present report),11–14 3 survived after medical or surgical treatment and had no reported long-term neurologic deficits.

The exact pathogenesis of the vertebral osteomyelitis in the pony described in the present report was unknown, but bacteremia originating from the chronic forelimb infection initially observed 1 month prior was suspected. Interestingly, the median time between onset of symptoms to diagnosis was 1.8 months in a retrospective study15 of vertebral osteomyelitis in 253 humans, and that interval can range from 6 weeks to 7 months, exemplifying the subacute nature of the illness, the insidious progression of disease, and the fact that clinicians are unaccustomed to consider vertebral osteomyelitis as a differential diagnosis because of the rarity of this disease process.15,17 The presence of bacteremia in the pony of the present report was supported by the suppurative interstitial pneumonia, lymphoid depletion, and systemic congestion. However, in horses, hematogenous spread of bacteria is typically limited to foals with septicemia. Thus, although not confirmed, immunosuppression with lymphoid depletion was possible in this case. In addition, multiple joints were affected grossly, to varying degrees, which may have been secondary to bacteremia. No evidence of traumatic injury to the vertebrae, hypaxial musculature, or regional subcutis was evident, ruling out traumatic injury as a source of vertebral infection. In previously described equine cases, the suspected nidus of infection included infection and abscesses in the perivertebral area, lungs, or mediastinum.12

In the case described in the present report, clinical signs likely resulted from the proliferative bone along the ventral surface of the vertebral bodies and development of a large diffuse abscess that expanded the underlying retroperitoneal and retropleural soft tissues, resulting in compression of the associated spinal cord. Further damage to the thoracic portion of the spinal cord resulted from a combination of compression from the space-occupying inflammatory exudate in the spinal canal and injury associated with the cytokine and vascular components of inflammation.15 Vertebral osteomyelitis should be considered as a differential diagnosis in horses with signs of back pain, fever, abnormal gait, and evidence of a systemic inflammatory process.

References

  • 1. Goodrich LR. Osteomyelitis in horses. Vet Clin North Am Equine Pract 2006; 22: 389417.

  • 2. Bové CM, Roberts BK. What is your diagnosis? Abscess. J Am Vet Med Assoc 2010; 236: 3334.

  • 3. Maeta N, Kanda T, Sasaki T, et al. Spinal epidural empyema in a cat. J Feline Med Surg 2010; 12: 494497.

  • 4. Zani DD, Romano L, Scandella M, et al. Spinal epidural abscess in two calves. Vet Surg 2008; 37: 801808.

  • 5. Sherman DM, Ames TR. Vertebral body abscesses in cattle: a review of five cases. J Am Vet Med Assoc 1986; 188: 608611.

  • 6. Scott PR, Penny CD, Murray LD. A field study of eight ovine vertebral body abscess cases. N Z Vet J 1991; 39: 105107.

  • 7. Scott PR, Will RG. A report of Froin's syndrome in five ovine thoracolumbar epidural abscess cases. Br Vet J 1991; 147: 582584.

  • 8. Chaffin MK, Honnas CM, Crabil MR, et al. Cauda equine syndrome, diskospondylitis, and a paravertebral abscess caused by Rhodococcus equi in a foal. J Am Vet Med Assoc 1995; 206: 215220.

    • Search Google Scholar
    • Export Citation
  • 9. Olchowy TW. Vertebral body osteomyelitis due to Rhodococcus equi in two Arabian foals. Equine Vet J 1994; 26: 7982.

  • 10. Giguère S, Lavoie JP. Rhodococcus equi vertebral osteomyelitis in 3 Quarter Horse colts. Equine Vet J 1994; 26: 7477.

  • 11. Sweers L, Carstens A. Imaging features of discospondylitis in two horses. Vet Radiol Ultrasound 2006; 47: 159164.

  • 12. Markel MD, Madigan JE, Lichtensteiger CA, et al. Vertebral body osteomyelitis in the horse. J Am Vet Med Assoc 1986; 188: 632634.

    • Search Google Scholar
    • Export Citation
  • 13. Chladek DW, Ruth GR. Isolation of Actinobacillus lignieresi from an epidural abscess in a horse with progressive paralysis. J Am Vet Med Assoc 1976; 168: 6466.

    • Search Google Scholar
    • Export Citation
  • 14. Kelly WR, Collins JD, Farrely BT, et al. Vertebral osteomyelitis in a horse associated with Mycobacterium tuberculosis var bovis (M. bovis) infection. Am Vet Radiol Soc 1972; 13: 5969.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15. McHenry MC, Easley KA, Locker GA. Vertebral osteomyelitis: long-term outcome for 253 patients from 7 Cleveland-area hospitals. Clin Infect Dis 2002; 34: 13421350.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16. Zimmerli W. Vertebral osteomyelitis. N Engl J Med 2010; 362: 10221029.

  • 17. Mylona E, Samarkos M, Kakalou E, et al. Pyogenic vertebral osteomyelitis: a systemic review of clinical characteristics. Semin Arthritis Rheum 2009; 39: 1017.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18. Newquist JM, Baxter GM. Evaluation of plasma fibrinogen concentration as an indicator of physeal or epiphyseal osteomyelitis in foals: 17 cases (2002–2007). J Am Vet Med Assoc 2009; 235: 415419.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Photographs of a transverse section of the T18 vertebral body (A) with a magnified image of that vertebral body (B) and a sagittal section of the left forelimb (C) of a 12-year-old Pony of the Americas mare that was evaluated because of a 2-week history of weight loss and a 1-week history of inappetence, lethargy, intermittent fever, and grunting coupled with generalized signs of pain when moving backward. One month prior, the pony had mild lameness of the left forelimb (attributable to cellulitis), which resolved with treatment. Three days after the initial evaluation, the pony was euthanized because of its deteriorating condition. In panel A, there is mottled red-tan-brown discoloration of the vertebral body (arrowhead) and hypaxial musculature and red-tan discoloration of the extradural adipose tissue (arrow). The spinal canal is labeled (asterisk). In panel B, bony tissue (arrowhead) is visible radiating from the cortex of the vertebral body (arrow). In panel C, there is abundant, red-tan, friable material within the tendon sheaths and in the radiocarpal and intercarpal joint spaces of the left forelimb. In all panels, bar = 1 cm.

  • Figure 2—

    Photomicrographs of sections of a thoracic vertebra (A) and vertebral canal in the thoracic portion of the vertebral column (B) of the mare in Figure 1. A—In this vertebral body, there is proliferation of new bone in the periosteum and abundant suppurative inflammation. Thin trabeculae of reactive bone (thin arrow) radiate from the cortical bone of the vertebral body (thick arrow). H&E stain; bar = 100 μm. B—Extradural tissues (arrow), including epidural adipose tissue, of the vertebral canal are expanded by hemorrhage, fibrin, and inflammatory infiltrate (epidural steatitis). The spinal cord is labeled (asterisk). H&E stain; bar = 100 μm.

  • 1. Goodrich LR. Osteomyelitis in horses. Vet Clin North Am Equine Pract 2006; 22: 389417.

  • 2. Bové CM, Roberts BK. What is your diagnosis? Abscess. J Am Vet Med Assoc 2010; 236: 3334.

  • 3. Maeta N, Kanda T, Sasaki T, et al. Spinal epidural empyema in a cat. J Feline Med Surg 2010; 12: 494497.

  • 4. Zani DD, Romano L, Scandella M, et al. Spinal epidural abscess in two calves. Vet Surg 2008; 37: 801808.

  • 5. Sherman DM, Ames TR. Vertebral body abscesses in cattle: a review of five cases. J Am Vet Med Assoc 1986; 188: 608611.

  • 6. Scott PR, Penny CD, Murray LD. A field study of eight ovine vertebral body abscess cases. N Z Vet J 1991; 39: 105107.

  • 7. Scott PR, Will RG. A report of Froin's syndrome in five ovine thoracolumbar epidural abscess cases. Br Vet J 1991; 147: 582584.

  • 8. Chaffin MK, Honnas CM, Crabil MR, et al. Cauda equine syndrome, diskospondylitis, and a paravertebral abscess caused by Rhodococcus equi in a foal. J Am Vet Med Assoc 1995; 206: 215220.

    • Search Google Scholar
    • Export Citation
  • 9. Olchowy TW. Vertebral body osteomyelitis due to Rhodococcus equi in two Arabian foals. Equine Vet J 1994; 26: 7982.

  • 10. Giguère S, Lavoie JP. Rhodococcus equi vertebral osteomyelitis in 3 Quarter Horse colts. Equine Vet J 1994; 26: 7477.

  • 11. Sweers L, Carstens A. Imaging features of discospondylitis in two horses. Vet Radiol Ultrasound 2006; 47: 159164.

  • 12. Markel MD, Madigan JE, Lichtensteiger CA, et al. Vertebral body osteomyelitis in the horse. J Am Vet Med Assoc 1986; 188: 632634.

    • Search Google Scholar
    • Export Citation
  • 13. Chladek DW, Ruth GR. Isolation of Actinobacillus lignieresi from an epidural abscess in a horse with progressive paralysis. J Am Vet Med Assoc 1976; 168: 6466.

    • Search Google Scholar
    • Export Citation
  • 14. Kelly WR, Collins JD, Farrely BT, et al. Vertebral osteomyelitis in a horse associated with Mycobacterium tuberculosis var bovis (M. bovis) infection. Am Vet Radiol Soc 1972; 13: 5969.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15. McHenry MC, Easley KA, Locker GA. Vertebral osteomyelitis: long-term outcome for 253 patients from 7 Cleveland-area hospitals. Clin Infect Dis 2002; 34: 13421350.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 16. Zimmerli W. Vertebral osteomyelitis. N Engl J Med 2010; 362: 10221029.

  • 17. Mylona E, Samarkos M, Kakalou E, et al. Pyogenic vertebral osteomyelitis: a systemic review of clinical characteristics. Semin Arthritis Rheum 2009; 39: 1017.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 18. Newquist JM, Baxter GM. Evaluation of plasma fibrinogen concentration as an indicator of physeal or epiphyseal osteomyelitis in foals: 17 cases (2002–2007). J Am Vet Med Assoc 2009; 235: 415419.

    • Crossref
    • Search Google Scholar
    • Export Citation

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