Cervical vertebral osteomyelitis in a 4‐month‐old foal

Vertebral body osteomyelitis in the cervical spine secondary to Rhodococcus equi has been treated both medically and surgically. This Case Report describes a 4‐month‐old foal exhibiting severe neurological signs from R. equi vertebral body osteomyelitis. Rapid, significant resolvement of neurological signs was noted in this case with surgical debridement and use of synthetic bone filler. The outcome suggests that aggressive surgical therapy in conjunction with synthetic allograft may be indicated in treatment of cervical vertebral body osteomyelitis.     

Bacteremia and septic arthritis in a West African dwarf crocodile

An anorectic, adult West African dwarf crocodile was examined because of bilateral hind limb paresis. Clinical findings included multiple skin wounds, osteomyelitis of the distal portions of the right radius and ulna, severe anemia, and Serratia marcescens bacteremia. The crocodile died after a blood transfusion. At necropsy, hemorrhage in the subarachnoid space, suppurative polyarthritis, and gastric ulceration were found. Serratia marcescens and Morganella morganii were isolated from multiple tissues and body fluids. It was concluded that the bilateral paresis was caused by severe septic arthritis secondary to bacteremia, and that the crocodile died from spinal injury caused by the blood transfusion into the supravertebral vein.     

Morphometric dimensions of the caudal cervical vertebral column in clinically normal Doberman Pinschers, English Foxhounds and Doberman Pinschers with clinical signs of disk-associated cervical spondylomyelopathy

Client-owned, clinically normal Doberman Pinschers (n=20), English Foxhounds (n=17), and Doberman Pinschers with clinical signs of disk-associated cervical spondylomyelopathy (DA-CSM) (n=17) were prospectively studied. All dogs underwent magnetic resonance imaging (MRI) of the cervical vertebral column. To evaluate vertebral canal stenosis, the canal occupying ratios of the spinal cord and cerebrospinal fluid (CSF)-column were calculated from C5 to C7. To evaluate the degree of spinal cord compression and the amount of canal compromise, the compression ratio, remaining spinal cord and CSF-column area, and vertebral canal and dorsoventral vertebral canal compromise ratios were calculated at the site of most severe compression. For each canal occupying ratio, there was a significant higher value (implicating less space available for the spinal cord in the vertebral canal) at the level of C7 for clinically affected Doberman Pinschers compared with clinically normal English Foxhounds. The remaining spinal cord area was significantly smaller in dogs with clinically relevant spinal cord compression compared to dogs with clinically irrelevant spinal cord compression. Relative stenosis of the caudal cervical vertebral canal occurred more often in Doberman Pinschers with DA-CSM compared to English Foxhounds and a critical degree of spinal cord compression should be reached to result in clinical signs.     

Spinal dural ossification causing neurological signs in a cat

A six-year-old Ragdoll cat underwent examination due to a six-month history of slowly progressive gait abnormalities. The cat presented with an ambulatory tetraparesis with a neurological examination indicating a C1-T2 myelopathy. Radiographs of the spine showed a radiopaque irregular line ventrally in the vertebral canal dorsal to vertebral bodies C3-C5. In this area, magnetic resonance imaging revealed an intradural extramedullary/extradural lesion compressing the spinal cord. The spinal cord was surgically decompressed. The cause of the spinal cord compression was dural ossification, a diagnosis confirmed by histopathological examination of the surgically dissected sample of dura mater. The cat gradually improved after the procedure and was ambulating better than prior to the surgery. The cat’s locomotion later worsened again due to ossified plaques in the dura causing spinal cord compression on the same cervical area as before. Oral prednisolone treatment provided temporary remission. Ten months after surgery, the cat was euthanized due to severe worsening of gait abnormalities, non-ambulatory tetraparesis. Necropsy confirmed spinal cord compression and secondary degenerative changes in the spinal cord on cervical and lumbar areas caused by dural ossification. To our knowledge, this is the first report of spinal dural ossification in a cat. The reported cat showed neurological signs associated with these dural changes. Dural ossification should be considered in the differential diagnosis of compressive spinal cord disorders in cats.     

Blastomycotic osteomyelitis associated with severe lameness in a horse

A 12-year-old Quarter horse gelding was presented for evaluation of severe right forelimb lameness, 2 draining tracts over the lateral aspect of the right proximal antebrachium, and weight loss. A presumptive diagnosis of blastomycotic osteomyelitis was established based on radiographs and cytology of the exudate. This diagnosis was confirmed at necropsy.     

Diffuse osteomyelitis of the fourth metacarpal bone in a horse caused by Clostridium perfringens

Osteomyelitis in adult horses, often associated with trauma or iatrogenic infection following surgery, usually presents as a focal area of infected bone. Diffuse osteomyelitis, affecting both the cortex and medulla, along the full length of a bone is encountered less frequently and treatment of such infections is not well reported in horses. The 2-year-old Warmblood mare in this case was diagnosed with diffuse osteomyelitis affecting the 4th metacarpal bone with concurrent unicortical fracture of the third metacarpal bone following traumatic injury. Computed tomography (CT) aided diagnosis in this case, providing critical additional detail to that obtained with radiography and ultrasound. This case highlights the value of CT in the diagnosis of diffuse osteomyelitis. This is the first reported case of diffuse osteomyelitis caused by Clostridium perfringens in horses. Successful treatment in this case consisted of surgical debridement of the associated abscess, followed by systemic and locoregional antimicrobial therapies.     

A field study of eight ovine vertebral body abscess cases

A vertebral body abscess extending into the epidural space causing spinal cord compression was diagnosed in the cervical spinal cord in four lambs and the thoracic spinal cord in four lambs. The affected lambs were aged between 4 and 10 weeks and clinical signs had been present for 7-21 days before veterinary examination. Treatment with high doses of penicillin did not result in an improvement of the neurological signs and all lambs were destroyed on humane grounds. Collection and analysis of cerebrospinal fluid (CSF) revealed a significant increase in the protein concentration in lumbar compared to cisternal CSF samples. There was a neutrophilic pleocytosis in two lumbar CSF samples. In lambs aged between 4 and 10 weeks with no history of previous locomotor dysfunction, paresis of more than 1 week duration may be suggestive of a vertebral body abscess which has extended into the epidural space causing spinal cord compression. Stagnation of CSF caudal to the lesion results in an increased protein concentration in the lumbar sample.     

Cervical vertebral canal endoscopy in the horse: intra- and post operative observations

Reasons for performing study: Despite modern medical diagnostic imaging, it is not possible to identify reliably the exact location of spinal cord compression in horses with cervical vertebral stenotic myelopathy (CVSM). Vertebral canal endoscopy has been successfully used in man and a technique for cervical vertebral canal endoscopy (CVCE) has been described in equine cadavers. Objective: To determine the feasibility and safety of CVCE in healthy mature horses. Methods: Six healthy mature horses were anaesthetised. A flexible videoendoscope was subsequently introduced via the atlanto‐occipital space into the epidural space (epiduroscopy, Horses 1–3) or the subarachnoid space (myeloscopy, Horses 4–6) and advanced to the 8th cervical nerve. Neurological examinations were performed after surgery and lumbosacral cerebrospinal fluid (CSF) analysed in horses that had undergone myeloscopy. Results: All procedures were completed successfully and all horses recovered from anaesthesia. Anatomical structures in the epidural space (including the dura mater, nerve roots, fat and blood vessels) and subarachnoid space (including the spinal cord, blood vessels, arachnoid trabeculations, nerve roots and the external branch of the accessory nerve) were identified. During epiduroscopy, a significant increase in mean arterial pressure was recognised, when repeated injections of electrolyte solution into the epidural space were performed. In one horse of the myeloscopy group, subarachnoid haemorrhage and air occurred, resulting in transient post operative ataxia and muscle fasciculations. No complications during or after myeloscopy were observed in the other horses. CSF analysis indicated mild inflammation on Day 7 with values approaching normal 21 days after surgery. Conclusions: Endoscopic examination of the epidural and subarachnoid space from the atlanto‐occipital space to the 8th cervical nerve is possible and can be safely performed in healthy horses. Potential relevance: Cervical vertebral canal endoscopy might allow accurate identification of the compression site in horses with CVSM and aid diagnosis of other lesions within the cervical vertebral canal.     

Spinal Epidural Abscess in Two Calves

Objective— To report clinical signs, diagnostic and surgical or necropsy findings, and outcome in 2 calves with spinal epidural abscess (SEA). Study Design— Clinical report. Animals— Calves (n=2). Methods— Calves had neurologic examination, analysis and antimicrobial culture of cerebrospinal fluid (CSF), vertebral column radiographs, myelography, and in 1 calf, magnetic resonance imaging (MRI). A definitive diagnosis of SEA was confirmed by necropsy in 1 calf and during surgery and histologic examination of vertebral canal tissue in 1 calf. Results— Clinical signs were difficulty in rising, ataxia, fever, apparent spinal pain, hypoesthesia, and paresis/plegia which appeared 15 days before admission. Calf 1 had pelvic limb weakness and difficulty standing and calf 2 had severe ataxia involving both thoracic and pelvic limbs. Extradural spinal cord compression was identified by myelography. SEA suspected in calf 1 with discospondylitis was confirmed at necropsy whereas calf 2 had MRI identification of the lesion and was successfully decompressed by laminectomy and SEA excision. Both calves had peripheral neutrophilia and calf 2 had neutrophilic pleocytosis in CSF. Bacteria were not isolated from CSF, from the surgical site or during necropsy. Calf 2 improved neurologically and had a good long‐term outcome. Conclusion— Good outcome in a calf with SEA was obtained after adequate surgical decompression and antibiotic administration. Clinical Relevance— SEA should be included in the list of possible causes of fever, apparent spinal pain, and signs of myelopathy in calves.     

Spinal epidural empyema in seven dogs

OBJECTIVE: To characterize the clinical signs, diagnostic and surgical findings, and outcome in dogs with spinal epidural empyema (SEE). STUDY DESIGN: Retrospective study. ANIMALS: Seven dogs. METHODS: Dogs with SEE between 1992 and 2001 were identified from a computerized medical record system. Inclusion criteria were: neurologic examination, vertebral column radiographs, myelography, antimicrobial culture and susceptibility of material collected surgically from the vertebral canal, a definitive diagnosis of SEE confirmed by surgery, and microscopic examination of tissue from the vertebral canal. RESULTS: Common signs were lethargy, fever, anorexia, apparent spinal pain, and paraparesis/plegia. Common laboratory abnormalities were peripheral neutrophilia, and neutrophilic pleocytosis in cerebrospinal fluid (CSF). Three dogs had concurrent discospondylitis and 1 of these had vertebral luxation. On myelography, extradural spinal cord compression was focal (2 dogs), multifocal (3), or diffuse (2). Bacteria were isolated not from CSF but from blood, surgical site, pleural fluid, or urine in 6 dogs. Dogs were administered antibiotics and had surgical decompression by hemilaminectomy. Five dogs improved neurologically and had a good long-term outcome. Two dogs were euthanatized, 1 because of worsening of neurologic signs and pneumonia, and the other because of herniation of a cervical intervertebral disc 1 month postoperatively, unrelated to the SEE. CONCLUSION: Dogs with SEE may have a good outcome when treated by surgical decompression and antibiotic administration. CLINICAL RELEVANCE: SEE should be included in a list of possible causes for dogs with fever, apparent spinal pain, and myelopathy.     

Nematode eggs observed in cytology of cerebrospinal fluid diagnostic for intramedullary Spirocerca lupi spinal cord migration

Spinal spirocercosis due to aberrant Spirocerca lupi nematode migration is an emerging etiology for acute myelitis in dogs in Israel, causing severe, mostly nonsymmetrical hind limb paresis or paralysis, and sometimes tetraparesis or tetraparalysis. So far, incidental identification of parasites during spinal surgery or at necropsy provides the only definite diagnosis, while antemortem diagnosis of this condition has been uncertain. Specifically, antemortem diagnosis is based on the typical clinical presentation of acute, progressive, asymmetrical hind limb paresis or paralysis, with moderate to severe eosinophilic to mixed cerebrospinal fluid (CSF) pleocytosis and increased CSF protein concentration. Exclusion of other differential diagnoses also requires using spinal cord imaging. In this novel report, we document a case of an intradural spinal spirocercosis in a dog, diagnosed antemortem, by detecting S lupi eggs in the CSF, and subsequent treatment, resulting in the resolution of the clinical signs.     

Presumptive organophosphate-induced delayed neurotoxicity in a paralyzed bull

A case of presumptive organophosphate-induced delayed neurotoxicity in a bull is described. All signs were referable to a focal cervical or diffuse spinal cord lesion. These included recumbency with severe symmetrical paresis of all 4 limbs, the hind limb involvement being greater than the forelimbs. CSF analysis was normal. The bull was killed and necropsied. There were no gross CNS lesions. Histopathologic finds are characterized and their resemblance to lesions observed in delayed neurotoxicity caused by organophosphate compounds is discussed. The bull had been treated with organophosphate insecticide (famphur) 43 days prior to the onset of signs.     

Bone marrow contamination of canine cerebrospinal fluid

Bone marrow cells were identified in cytocentrifuge preparations of cerebrospinal fluid (CSF) obtained by lumbar punctures from two dogs. CSF analyses were characterized by normal or increased total cell counts, normal or increased total protein concentration and the presence of erythrocytes. Hematopoietic cells present included both erythroid and myeloid precursors and, in one case, an erythroblastic island was seen. Peripheral blood smear examination confirmed that the hematopoietic cells observed were not the result of blood contamination. Neither case was associated with a difficult tap procedure, nor with a specific disease process. Contamination may have resulted from actual marrow penetration or from extramedullary hematopoiesis in the dura mater. Accurate interpretation of CSF cytology requires the consideration of possible bone marrow contamination when hematopoietic cells are observed.     

Diffuse leptomeningeal histiocytic sarcoma in the cerebrospinal fluid of 2 dogs

Two adult male castrated dogs were evaluated for progressive paraparesis and ataxia. Neurologic examination showed severe ataxia, delayed proprioceptive placement in the pelvic limbs, pain upon palpation of the lumbar spine as well as facial paresis in one dog, and decreased withdrawal reflex of the pelvic limbs in the other dog. Magnetic resonance imaging (MRI) in both dogs showed diffuse meningeal and intramedullary lesions. However, no evidence of a mass was found. Biopsies could not be performed safely due to the location of the lesions. Cerebrospinal fluid (CSF) examination revealed an inflammatory pleocytosis associated with increased protein concentration and numerous large atypical round cells, often multinucleated. Nuclear fragmentation, micronuclei, and rare atypical mitoses were observed. Immunocytochemistry revealed CD1⁺ and CD11c⁺ staining, which, in concert with the morphology confirmed the diagnosis of histiocytic sarcoma (HS). Euthanasia was elected due to poor prognosis. Histopathologic examination showed diffuse spinal and meningeal infiltration with CD18⁺ neoplastic cells, without any evidence of mass formation, which completed the diagnosis of diffuse leptomeningeal HS involving the brain and the spinal cord. Canine central nervous system (CNS) HS has been seldom reported in the literature, with only isolated cases identified on CSF cytology. The cases reported here are remarkable in describing a diffuse CNS leptomeningeal HS associated with neoplastic cells in the CSF of dogs without a tumor mass. These cases emphasize the potential critical importance of CSF analysis in providing an antemortem diagnosis of neoplasia in neurologic patients.     

Large anaplastic spinal B‐cell lymphoma in a cat

Abstract: A 5‐year‐old female spayed domestic shorthair cat was presented for evaluation of tetraparesis. The neurologic lesion was localized to the cervical spinal segment (C1–C6). A left axillary mass was identified, and the results of fine needle aspiration cytology indicated malignant round cell neoplasia of possible histiocytic origin. The cells were large, had marked anisocytosis and anisokaryosis, occasional bi‐ and multinucleation, and cytoplasmic vacuolation. Euthanasia was performed due to the poor prognosis associated with severe, progressive neurologic signs and a malignant neoplasm. Postmortem examination revealed spinal cord compression and an extradural mass at the C1–C2 spinal segment, with neoplastic cells in the adjacent vertebral bodies, surrounding skeletal muscle, left axillary lymph node, and bone marrow from the right femur. The initial histologic diagnosis was anaplastic sarcoma, but immunohistochemical results indicated the cells were CD20+ and CD45R+ and CD3?, compatible with a diagnosis of B‐cell lymphoma. CD79a staining was nonspecific and uninterpretable. Weak to moderate CD18 positivity and E‐cadherin positivity were also observed. Clonality of the B‐cell population could not be demonstrated using PCR testing for antigen receptor gene rearrangement. To the authors' knowledge, this is the first reported case of a feline spinal anaplastic B‐cell lymphoma exhibiting bi‐ and multinucleated cells. The prognostic significance of this cell morphology and immunophenotype is unknown.     

Cerebrospinal fluid analysis and magnetic resonance imaging in the diagnosis of neurologic disease in dogs: a retrospective study

BACKGROUND: Diagnosis of central nervous system (CNS) abnormalities in dogs can be challenging antemortem. Historically, cerebrospinal fluid (CSF) analysis has been used for routine diagnostic evaluation of animals with suspected neurologic disease; however, with increasing availability of magnetic resonance (MR) imaging, the need for concurrent CSF analysis may be questioned. OBJECTIVE: The purpose of this study was to retrospectively assess and compare the diagnostic information contributed from MR imaging and CSF analysis in a population of dogs presenting with neurologic disease. METHODS: Results of concurrent MR imaging and CSF analysis were evaluated in dogs presented for neurologic diseases. Based on clinical diagnosis, the sensitivity of CSF analysis and MR imaging for detecting a nervous system abnormality was calculated. Dogs with diagnoses confirmed by other diagnostic modalities were also evaluated separately. RESULTS: A total of 256 dogs were included in the study. For clinical diagnoses in which abnormalities were expected, MR imaging abnormalities were found in 89% and CSF abnormalities in 75% of dogs; CSF abnormalities were more common than MR imaging abnormalities only in inflammatory CNS disease. The majority of CSF abnormalities were nonspecific; an etiologic diagnosis was determined in only 2% of CSF samples. MR imaging excelled in detecting structural disorders, revealing 98% of vertebral abnormalities. In confirmed cases (n = 55), 76% of MR images and 9% of CSF samples were diagnostic. When intervertebral disk disease (IVDD) and vertebral malformation were excluded from analysis (n = 16 remaining), 25% of MR images and 6% of CSF cytology results were highly indicative of the confirmed diagnoses; CSF titer results provided the diagnosis in 25% of these cases. CONCLUSION: CSF analysis may not be necessary when MR findings of IVDD or vertebral malformation/instability are obvious; however, when the cause of neurologic disorder is uncertain, concurrent MR imaging and CSF analysis provides the greatest assistance in establishing a clinical diagnosis.     

Fibrocartilaginous embolic myelopathy in a horse

Fibrocartilaginous embolic myelopathy was diagnosed in a 11-year-old, male, Tennessee Walking Horse by histopathological examination of the spinal cord after the horse was killed because of severe neurological dysfunction. Both ventral funiculi of C6 and C7 cervical spinal cord had extensive necrosis with blood vessels containing fibrocartilaginous emboli. A similar fibrocartilaginous embolus was observed in a single large spinal artery adjoining the vertebral leptomeninges.     

Association of Enterococcus cecorum with vertebral osteomyelitis and spondylolisthesis in broiler parent chicks

Enterococcus cecorum is the most frequently occurring enterococcal species in the intestine of chickens of over 12 weeks of age, and there are few reports on its isolation from the skeleton of broiler parent chicks. In the present study, observations on vertebral osteomyelitis and spondylolisthesis ('kinky back syndrome') showing high incidence in 8 broiler parent flocks in different parts of Hungary are summarised. Clinical signs were seen only in roosters between 5 and 13 weeks of age. Diseased birds were alert and remained sitting on their hocks with their feet slightly raised off the ground. Incidence of the disease among male birds ranged from 8% to 30% depending on flocks. Enlargement and distortion of the body of the 6th vertebra were seen as the main pathological lesions. The cavity of the spinal canal was constricted by the distorted vertebral bodies. Resorption of bone tissue and sequestrum formation, signs of increased osteoclast activity, proliferation of fibrotic tissues, infiltration with heterophils and formation of sclerotic layers were detected in the vertebral bodies. From all 24 samples collected from the vertebral lesions, Enterococcus cecorum was isolated and identified using metabolic fingerprinting as well as 16S rRNA gene sequencing. Demonstration of E. cecorum from the vertebral lesions in all examined broiler breeder roosters showing the same clinical and pathological findings in different flocks suggested the pathogenic role of this microorganism for the first time in Hungary.     

Pyogranulomatous meningoencephalitis due to Actinomyces sp. in a dog

Actinomyces sp. are commensal, filamentous, gram-positive, acid-fast-negative bacteria that can cause pyogranulomatous inflammation in animals and humans. Central nervous system (CNS) disease is a rare presentation of actinomycosis and is usually due to extension from infected wounds or seeding from distant sites. A dog with progressive, poorly localized neurologic signs had primary CNS actinomycosis without history or evidence of previous trauma or other organ involvement. Histologically, there was a severe pyogranulomatous meningoencephalitis with intralesional filamentous bacteria that were also visible on cytology of the cerebral spinal fluid (CSF) postmortem. Actinomyces sp. was cultured postmortem from the CSF, confirming the diagnosis. This case demonstrates that Actinomyces sp. can be a causative agent of primary CNS disease in dogs.     

Thoracolumbar spinal cord compression due to vertebral process degenerative joint disease in a family of Shiloh Shepherd dogs

Five young Shiloh Shepherd Dogs (4 males and 1 female) related by a common sire were studied because of progressive pelvic limb weakness and incoordination. All dogs had a spastic paraparesis and pelvic limb ataxia consistent with an upper motor neuron and general proprioceptive lesion between spinal cord segments T3 and L3. Proliferative lesions involving one or more of the articular processes from the 11th thoracic vertebrae to the 2nd lumbar vertebra were observed on radiographs of the thoracolumbar vertebrae. Dorsal compression of the spinal cord was identified during imaging studies at these sites. Abnormalities of the synovial joints and bony proliferation of the involved articular processes were identified at postmortem examination in 2 dogs. The articular processes and associated vertebral arches protruded into the vertebral canal, indenting the dorsal surface of the spinalcord. Degenerative joint disease (DJD) was identified histologically. A compressive myelopathy was diagnosed in the spinal cord. These dogs were affected by a compressive myelopathy as a consequence of vertebral process DJD that likely has a geneticcomponent. The DJD could have been caused by a primary vertebral malformation or an injury to the processes at a young age causing malarticulation.