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A 4 week old filly presented for a 1 week history of failure to thrive, weakness, and progressive neurologic deficits including spinal ataxia. Bloodwork was performed by the rDVM one day prior to presentation and was within normal limits. A dose of Excede (Ceftiofur crystalline free acid) was administered at that time. At the time of birth, the foal was diagnosed with partial failure of passive transfer and plasma was administered. There was no known history of trauma and the mare had no significant medical history.

On presentation, the filly was mentally appropriate, but weak, unable to ambulate on her own, and only able to stand with support. On physical exam, there was a right-sided, palpable soft tissue swelling lateral to the cranial cervical spine. The filly also had a right-sided head tilt and was reluctant to extend her neck. Vitals were normal and the remainder of the physical exam was within normal limits.

Cervical radiographs were made under light sedation.


Radiographic Images

C-spine lateral

C-spine lateral collimated

C-spine VD

C-spine VD collimated

  • The osseous structures of the caudal skull and cervical spine are unremarkable.
  • There is a focal increase in soft tissue in the retropharyngeal region causing compression of the caudal aspect of the guttural pouch. A 2.6cm round soft tissue structure is superimposed on the caudal aspect of the guttural pouches. This is outlined dorsally by a thin line of gas. There are numerous small gas bubbles within the soft tissues dorsal to the 3rd/4th cervical vertebral bodies.
  • The next day a CT was pursued under general anesthesia.

Computed Tomography Images

Transverse images are displayed with a soft tissue window on the left and a bone window on the right.


There is a 6x4x2.5cm lobular, soft tissue attenuating (HU: 30) mass containing multiple gas foci right and ventral to the atlantoocciptal junction. A hypoattenuating soft tissue tract extends from the caudal margin of the mass tracking through the right lateral physis of C1, which is irregular and wide with patchy lysis and sclerosis of the surrounding bone. The tract communicates with similarly hypoattenuating soft tissue containing gas foci that extends along the ventrolateral aspect of the spinal canal from the foramen magnum to the cranial aspect of C2. There is moderate compression and dorsal displacement of the spinal cord in this region, worse on the right side.  There is additional right-sided bony lysis of cranial C1.

Hypoattenuating soft tissue containing gas foci and wispy to linear hyperattenuating material also dissects along the muscular and fascial planes of the right neck, dorsal to the cervical spine and ventral to the right splenius m, extending from the level of C3 to C6. Although the tract becomes indistinct cranial to C3, the fascial planes of the right neck are wider compared to the left.

The bilateral parotid and medial retropharyngeal lymph nodes are homogeneously soft tissue attenuating (HU: 30) and are moderately enlarged, worse on the right, causing rostrolateral displacement and partial collapse of the guttural pouches.

Radiographic Imaging Diagnosis:

  1. Retropharyngeal reactive lymphadenopathy and abscess or hematoma.
  2. Dorsal cervical abscessation or iatrogenic gas from injection.


CT Imaging Diagnosis:

  1. Cranial cervical paraspinal abscess with invasion into the spinal canal causing moderate extradural spinal cord compression and C1 osteomyelitis.
  2. Right dorsal mid to caudal cervical abscessation and cellulitis, likely an extension from the more cranial abscess.  This may also be secondary to regional injection. Hyperattenuating material likely represents inspissated pus or alternatively, medication such as verbally reported antibiotic.
  3. Regional reactive lymphadenopathy.


Osteomyelitis of the foal most commonly occurs secondary to pneumonia, omphalophlebitis, or gastrointestinal disease and is most common in the femur, tibia, and distal phalanx. Vertebral osteomyelitis is rare in horses, but has been reported in the cervical and lumbar regions secondary to hematogeneous dissemination in foals associated with gram negative organisms, Rhodococcus equi, and  Streptococcus spp.

Radiographic evidence of osteomyelitis may not be detected until there is 30-50% reduction in bone density with up to a 3 week delay from the onset of clinical symptoms. In several cases of R. equi vertebral osteomyelitis, radiographs were normal despite extensive bone destruction on post-mortem examination. Computed tomography is an excellent diagnostic tool for evaluation of the vertebral column of the foal, offering increased sensitivity for both soft tissue abscessation and bony lysis. In this case, CT was pursued following initial radiographs due to the severity of neurologic deficits and lack of osseous pathology. CT allowed definitive diagnosis of vertebral compression and characterization of previously unseen osseous abnormalities, which markedly change the prognosis for future performance.

An atlanto-occiptal tap was performed at the time of CT and cerebrospinal fluid showed marked septic neutrophilic inflammation with coccobacilli bacteria. At this time, the foal also had a marked leukocytosis of 19.7*109 WBCs/L characterized by 84% segmented neutrophils. Ultrasound guidance was used to lance the paraspinal abscess, but was of limited utility for evaluating the extent of involvement within the spinal canal. Culture results were positive for S. zooepidemicus. Blood culture results were negative.

Treatment for vertebral osteomyelitis may involve long-term antibiotics, NSAIDs, surgical debridement, and wound care. However, the prognosis is generally guarded to poor due to the presence of extensive bony destruction and concurrent extradural spinal compression. In this case, the owners in this case elected to take the foal home and the foal was lost to follow-up. At the time of discharge, the foal was responding well to medical management with broad spectrum antibiotics, anti-inflammatory medications, gastroprotectants, and supportive care. The filly was able to stand on her own intermittently, but unable to walk and needed assistance to nurse.



  1. Stewart AJ, Salazar P, Waldridge BM, Hathcock J, Whitley EM, Welles EG. Computed tomographic diagnosis of a pathological fracture due to rhodococcal osteomyelitis and spinal abscess in a foal. Equine Vet Educ. 2007;19(5):231-235. doi:10.2746/095777307X207024.
  2. GIGUÈRE S, LAVOIE JP. Rhodococcus equi vertebral osteomyelitis in 3 Quarter Horse colts. Equine Vet J. 1994;26(1):74-77. doi:10.1111/j.2042-3306.1994.tb04336.
  3. Hu AJ, Grant B, Cannon J. Cervical vertebral osteomyelitis in a 4-month-old foal. Equine Vet Educ. 2009;21(2):71-75. doi:10.2746/095777309X397897.
  4. Toribio RE, Mudge MC. Diseases of the foal. Equine Med Surg Reprod Second Ed. 2013;(January):20-450. doi:10.1016/B978-0-7020-2801-4.00020-1.
  5. Koch C, Witte S. Septic osteitis and osteomyelitis in foals – are antimicrobials alone enough? Equine Vet Educ. 2013;25(2):67-73. doi:10.1111/j.2042-3292.2012.00409.x.
  6. Crabtree JR, Jorgensen A. Cervical Vertebral Osteomyelitis With Secondary Septic Arthritis of the Atlantoaxial Joint in a Foal: A Case Report. J Equine Vet Sci. 2012;32(9):599-606. doi:10.1016/j.jevs.2011.12.007.
  7. Neil KM, Axon JE, Begg AP, et al. Retrospective study of 108 foals with septic osteomyelitis. Aust Vet J. 2010;88(1-2):4-12. doi:10.1111/j.1751-0813.2009.00539.x.