Hind Limb Paresis Research Articles

A clinical case of B-cell lymphoma in a Japanese Black cow with monoclonal proliferation of B-cells as revealed by polymerase chain reaction based on the immunoglobulin light chain gene.

A 35-month-old Japanese Black cow was presented to a local veterinarian with a main complaint of premature labor. There was no swelling of lymph nodes on the body surface and no palpable mass on rectal examination. Although atypical lymphocytes were observed in the peripheral blood, no lymphocytosis was recorded. On Day 12, the cow developed hindlimb paresis and was euthanized. Necropsy revealed swelling of some lymph nodes, and white nodules in uterus and right atrial appendage. Histopathological examination revealed B-cell lymphoma. In clonality analysis of peripheral blood and tumor tissue, monoclonal proliferation was detected by PCR for immunoglobulin light chain (IgL) λ, suggesting neoplastic proliferation of B-cell. IgL-PCR is thought to be a possible tool for diagnosis of B-cell lymphoma.

Ovalbumin-specific CD4+ and CD8+ T cells contribute to different susceptibility for Theiler's murine encephalomyelitis virus persistence.

Theiler's murine encephalomyelitis virus (TMEV) is the causative agent of TMEV-induced demyelinating disease (TMEV-IDD); a well-established animal model for the chronic progressive form of human multiple sclerosis (MS). In susceptible mice with an inadequate immune response, TMEV-IDD is triggered by virus persistence and maintained by a T cell mediated immunopathology. OT-mice are bred on a TMEV-resistant C57BL/6 background and own predominantly chicken ovalbumin (OVA)-specific populations of CD8+ T cells (OT-I) or CD4+ T cells (OT-II), respectively. It is hypothesized that the lack of antigen specific T cell populations increases susceptibility for a TMEV-infection in OT-mice on a TMEV-resistant C57BL/6 background. OT-I, OT-II, and C57BL/6 control mice were infected intracerebrally with the TMEV-BeAn strain. Mice were scored weekly for clinical disease and after necropsy, histological and immunohistochemical evaluation was performed. OT-I mice started to develop progressive motor dysfunction between 7 and 21 days post infection (dpi), leading up to hind limb paresis and critical weight loss, which resulted in euthanasia for humane reasons between 14 and 35 dpi. OT-I mice displayed a high cerebral virus load, an almost complete absence of CD8+ T cells from the central nervous system (CNS) and a significantly diminished CD4+ T cell response. Contrarily, only 60% (12 of 20) of infected OT-II mice developed clinical disease characterized by mild ataxia. 25% of clinically affected OT-II mice (3 of 12) made a full recovery. 5 of 12 OT-II mice with clinical disease developed severe motor dysfunction similar to OT-I mice and were euthanized for humane reasons between 13 and 37 dpi. OT-II mice displayed only low virus-immunoreactivity, but clinical disease correlated well with severely reduced infiltration of CD8+ T cells and the increased presence of CD4+ T cells in the brains of OT-II mice. Though further studies are needed to reveal the underlying pathomechanisms following TMEV infection in OT mice, findings indicate an immunopathological process as a main contributor to clinical disease in OT-II mice, while a direct virus-associated pathology may be the main contributor to clinical disease in TMEV-infected OT-I mice.

Computed Tomography Neurography for Visualization of the In Vivo Nervous System: A Proof of Concept.

The human peripheral nervous system embodies anatomical, physiologic, and diagnostic perplexities that remain unexplained. Yet in the course of human history, there are no mechanisms, such as computed tomography (CT) or radiography, by which to image the peripheral nervous system in vivo using a contrast agent that is identified by ionizing radiation, which would aid in surgical navigation, diagnostic radiology, and basic science thereof. A novel class of contrast was created by linking iodine to lidocaine. The radiodensity of 0.5% experimental contrast molecule was compared with a control of 1% lidocaine by placing 1.5-mL aliquots of each liquid into centrifuge tubes and performing micro-computed tomography (micro-CT) synchronously under identical settings. Physiologic binding to the sciatic nerve was evaluated by injecting 10 mg of the experimental contrast and 10 mg of the control into the contralateral sciatic nerve, and documenting loss of hindlimb function and recovery. In vivo visualization of the sciatic nerve was evaluated by injecting 10 mg of experimental contrast or control into either sciatic nerve and imaging the hindlimbs under identical conditions using micro-CT. The mean Hounsfield unit of the contrast was 56.09 compared with -0.48 for control (116-fold increase, P = .0001). Hindlimb paresis revealed similar degree of paresis, baseline recovery, and time to recovery. In vivo enhancement between the contralateral sciatic nerves was similar. Iodinated lidocaine offers a viable mechanism for in vivo peripheral nerve imaging using CT; however, it requires modification to improve in vivo radiodensity.

Dual transgene amelioration of Lama2-null muscular dystrophy.

Null mutations of the Lama2-gene cause a severe congenital muscular dystrophy and associated neuropathy. In the absence of laminin-α2 (Lmα2) there is a compensatory replacement by Lmα4, a subunit that lacks the polymerization and α-dystroglycan (αDG)-binding properties of Lmα2. The dystrophic phenotype in the dy3K/dy3K Lama2-/- mouse were evaluated with transgenes driving expression of two synthetic laminin-binding linker proteins. Transgenic muscle-specific expression of αLNNd, a chimeric protein that enables α4-laminin polymerization, and miniagrin (mag), a protein that increases laminin binding to the receptor αDG, separately improved median mouse survival two-fold. The double transgenes (DT) improved mean survival three-fold with increases in overall body weight, muscle size, and grip strength, but, given absence of neuronal expression, did not prevent hindlimb paresis. Muscle improvements included increased myofiber size and number and reduced fibrosis. Myofiber hypertrophy with increased mTOR and Akt phosphorylation were characteristics of mag-dy3K/dy3K and DT-dy3K/dy3K muscle. Elevations of matrix-bound α4-, β1 and γ1 laminin subunits were detected in muscle extracts and immunostained sections in response to DT expression. Collectively, these findings reveal a complimentary polymerization and αDG-binding benefit to Lama2-/- mouse muscle largely mediated through modified laminin-411.

Suspected ischaemic myelopathy following lumbosacral epidural steroid injection in a dog

AbstractAn 11‐year‐old, female, spayed crossbreed with an 18‐month history of degenerative lumbosacral stenosis presented for routine epidural steroid injection 4 months after previous injection. Following epidural steroid injection, the dog developed severe left hindlimb paresis with reduced to absent sciatic reflexes, delayed conscious proprioception in the limb, absence of anal tone and lower motor neuron urinary incontinence. Magnetic resonance imaging was performed, which demonstrated findings consistent with an ischaemic myelopathy. The dog's left hindlimb paresis improved on cage rest; however, urinary incontinence remained. The dog was subsequently euthanased due to quality‐of‐life concerns. This is the first published report of suspected ischaemic myelopathy developing in a dog after epidural steroid injection.

Botryomycosis‐like discospondylitis of the thoracic spine in a Friesian horse with severe bilateral pelvic limb ataxia and paresis

SummaryBotryomycosis is an uncommon chronic bacterial pyogranulomatous infection of cutaneous and, rarely of visceral origin, that can rarely invade the osseous tissues. An 8‐year‐old Friesian gelding was presented with severe bilateral hindlimb ataxia and paresis of 2‐weeks' duration. Radiographic examination revealed a large osteolytic lesion at the T10‐T11 intervertebral disc space. Post‐mortem examination revealed discospondylitis with abscess formation and histological presence of pyogranulomatous inflammation with coccoform bacteria rimmed by Splendore‐Hoeppli material. Staphylococcus aureus was identified by bacteriological examination. This case report describes the clinical presentation, imaging features and post‐mortem findings of a Friesian gelding presenting with severe bilateral hindlimb ataxia and paresis caused by compression and degeneration of the spinal cord due to a botryomycosis‐like thoracic discospondylitis. Botryomycosis‐like infection should be considered in the differential diagnosis of focal expansile bone lesions demonstrating diffuse osteolysis, sclerosis and interrupted bone margins.

Disfunção da pars intermedia da hipófise em equinos associado a adenoma pituitário

ABSTRACT: The clinical syndrome of the pituitary pars intermedia dysfunction (PPID) is the most common endocrinopathy of older horses. This syndrome is characterized by several clinical and pathological changes, which are usually associated with adenomas of the pars intermedia (PI) of the pituitary gland. The aim of this work is to describe five cases of pituitary adenoma of the PI associated with PPID in horses, addressing its clinical and pathological aspects. The horses had a mean of 22 years of age. The main clinical signs were hirsutism and paresis of hind limbs, and at post mortem examination all horses had hirsutism, and a nodule in the pituitary gland, which was histologically characterized as an adenoma of PI (5/5). Furthermore, two horses had gross lesions suggestive of chronic laminitis. Moreover, there was intense parasitism of Sarcocystis neurona (2/5), Strongylus vulgaris (1/5), Parascaris equorum (1/5), Draschia megastoma (1/5), and Klossiella equi (1/5).

Tmprss6 Depletion-Mediated Iron Deficiency Attenuates the Clinical Course of Plasmodium Berghei Infection in Mice

Background Anaemia and malaria cause a great burden of disease and commonly co-exist. Field studies have linked iron deficiency with decreased malaria risk but may be confounded. We aimed to define the association between iron status and malaria risk in an in vivo experimental system. Using the P. berghei mouse malaria model, we assessed the impact of both severe iron overload and iron deficiency using inducible hepcidin (Hamp) knockout (iHamp-KO), Tmprss6 knockout (Tmprss6-KO) and Tmprss6 knockdown (Tmprss6-KD) mouse models. Homozygous mutations of HAMP (encoding hepcidin) cause severe iron overload, while homozygous inactivation of TMPRSS6 leads to hepcidin overexpression and iron deficiency. MethodsP. berghei infection of C57BL/6 mice is an experimental model of cerebral and severe malaria. The majority of mice develop neurological symptoms between day 6-10 post infection, surviving mice usually develop hyperparasitaemia and symptoms of severe anaemia by day 20. Mice were infected with PbmCherryLuci sporozoites by intravenous injection. Luciferase activity was used to assess liver infection and egress. Mice were analysed by IVIS at 24, 36, 52 and 55/56 hours post infection. From day 3 post infection peripheral parasitaemia was assessed daily. Mice were euthanised if they showed signs of cerebral malaria (such as loss of self-righting reflex and hind-limb paresis), severe anaemia, or if parasitaemia reached >20% (iHamp-KO and Tmprss6-KO) or >30% (Tmprss6-KD) in line with animal ethics requirements. iHamp-KO mice received tamoxifen intraperitoneally daily for 5 days 3 months prior to infection to induce Hamp deletion. Controls were iHamp-KO littermates that received vehicle alone. Tmprss6-KO mice were infected at about 24 weeks of age and compared to littermate heterozygote controls which are known to have a negligible phenotype. Tmprss6-KD was achieved through treatment of WT mice with siTMP, a GalNAc siRNA conjugate targeting Tmprss6. Mice received siTMP 5mg/kg s.c. 3 weekly starting 8 weeks prior to P. berghei infection, or a single treatment on day 3 (expected onset of blood stage infection) or day 6 (expected onset of high risk period for cerebral malaria), while controls received PBS. Results iHamp-KO mice had lower peak liver infection (p=0.0097), but egress was not affected, and there was no effect on overall survival or survival from cerebral malaria. Tmprss6-KO mice showed higher liver infection compared with heterozygous littermate controls at all timepoints, but egress was not different. Tmprss6-KO mice had improved overall survival compared with heterozygous controls (p=0.0004) and improved survival from cerebral malaria (p=0.0004). All 7 heterozygous controls succumbed to cerebral malaria by day 10, compared to 1 of 6 Tmprss6-KO animals (Figure 1). We further investigated effects of iron deficiency on malaria severity using Tmprss6 knockdown. Mice treated with siTMP for 8-10 weeks had markedly reduced Tmprss6 and elevated Hamp expression in the liver, and lower haemoglobin, MCV, and plasma iron. Tmprss6-KD mice, treated 8 weeks prior to P. berghei infection exhibited reduced parasitaemia, and took longer to reach 10%, 20% and 30% parasitaemia (Figure 2). There was no change in survival from cerebral malaria. Tmprss6-KD after infection did not change parasitaemia or survival. Conclusion Experimental iron deficiency via Tmprss6 downregulation attenuated malaria disease phenotype in mice. These data provide experimental evidence to support observational data that iron deficiency provides protection against malaria infection. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Amelioration of muscle and nerve pathology of Lama2-related dystrophy by AAV9-laminin-αLN linker protein.

LAMA2 deficiency, resulting from a defective or absent laminin α2 subunit, is a common cause of congenital muscular dystrophy. It is characterized by muscle weakness from myofiber degeneration and neuropathy from Schwann cell amyelination. Previously it was shown that transgenic muscle-specific expression of αLNNd, a laminin γ1–binding linker protein that enables polymerization in defective laminins, selectively ameliorates the muscle abnormality in mouse disease models. Here, adeno-associated virus was used to deliver linker mini-genes to dystrophic dy2J/dy2J mice for expression of αLNNd in muscle, or αLNNdΔG2′, a shortened linker, in muscle, nerve, and other tissues. Linker and laminin α2 levels were higher in αLNNdΔG2′-treated mice. Both αLNNd- and αLNNdΔG2′-treated mice exhibited increased forelimb grip strength. Further, αLNNdΔG2′-treated mice achieved hind limb and all-limb grip strength levels approaching those of WT mice as well as ablation of hind limb paresis and contractures. This was accompanied by restoration of sciatic nerve axonal envelopment and myelination. Improvement of muscle histology was evident in the muscle-specific αLNNd-expressing mice but more extensive in the αLNNdΔG2′-expressing mice. The results reveal that an αLN linker mini-gene, driven by a ubiquitous promoter, is superior to muscle-specific delivery because of its higher expression that extends to the peripheral nerve. These studies support a potentially novel approach of somatic gene therapy.

A rare lysosomal storage disorder: Feline mucopolysaccharidosis VII

AbstractA 9‐week‐old, male domestic shorthair presented with a 2‐week history of progressive hindlimb weakness and reduction in normal play behaviour. At 17 weeks of age, the patient exhibited progressive hindlimb paresis and ataxia and had developed facial dysmorphia and bilateral corneal clouding, prompting investigation into a mucopolysaccharidosis disorder. Peripheral blood cytology, increased urinary glycosaminoglycan excretion and radiographic findings (generalised epiphyseal dysplasia, coxofemoral luxation and vertebral fusion) suggested mucopolysaccharidosis. Definitive diagnosis was obtained through serum enzymatic testing, which yielded a complete deficiency in β‐glucuronidase and increased compensatory activity in α‐L‐iduronidase and B‐arylsulfatase. This pattern was consistent with a diagnosis of feline mucopolysaccharidosis VII, and palliative therapy was initially implemented. The patient ultimately died at 21 months of age.

Degenerative Myelopathy and Neuropathy in NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) Mice Caused by Lactate Dehydrogenase-Elevating Virus (LDV).

Following implantation of patient-derived xenograft (PDX) breast carcinomas from three separate individuals, 33/51 female NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice presented with progressive, unilateral to bilateral, ascending hindlimb paresis to paralysis. Mice were mildly dehydrated, in thin to poor body condition, with reduced to absent hindlimb withdrawal reflex and deep pain sensation. Microscopically, there was variable axonal swelling, vacuolation, and dilation of myelin sheaths within the ventral spinal cord and spinal nerve roots of the thoracolumbar and sacral spinal cord, as well as within corresponding sciatic nerves. Results of PCR screening of PDX samples obtained at necropsy and pooled environmental swabs from the racks housing affected animals were positive for lactate dehydrogenase-elevating virus (LDV). LDV is transmitted through animal-animal contact or commonly as a contaminant of biologic materials of mouse origin. Infection is associated with progressive degenerative myelopathy and neuropathy in strains of mice harboring endogenous retrovirus (AKR, C58), or in immunosuppressed strains (NOD-SCID, Foxn1nu), and can interfere with normal immune responses and alter engraftment and growth of xenograft tumors in immunosuppressed mice. This is the first reported series of LDV-induced poliomyelitis in NSG mice and should be recognized as a potentially significant confounder to biomedical studies utilizing immunodeficient xenograft models.

Osteoporose em suínos

ABSTRACT: Forty-six pigs presented muscle weakness, hind limb paresis and paralysis, weight loss, lateral recumbency, and death in a clinical course of 7 to 10 days. Two pigs were necropsied and exhibited bone fragility, bone callus formation, and multiple fractures in the limbs, ribs, and vertebrae. Microscopically, there was a diffuse and marked decrease in thickness and number of trabeculae. These were disconnected, with a “free-floating” appearance, while the cortex of the long bones was thinned, with an increase of the cortical porosity by enlargement of Haversian canals and endosteal erosion and decreased osteoblastic activity. Flame atomic absorption spectrometry in liver samples revealed significant zinc overload (>2300ppm) and copper deficiency (<33.1ppm). In this communication, we present the first pathologic description of an outbreak of osteoporosis in pigs, and we also provide a brief review of metabolic bone diseases in pigs.

Parotid Salivary Gland Extramedullary Plasmacytoma with Local Lymph Node Metastasis in a Dog

ABSTRACTA 12 yr old spayed female mixed-breed dog presented for evaluation of a recurrent soft-tissue sarcoma. On physical examination, a firm mass was palpated ventral to the left ramus of the mandible. A fine-needle aspirate of the mass was suggestive of a round-cell neoplasm. A complete blood count, serum biochemical profile, and an abdominal ultrasound with liver and splenic aspirates were performed, and no clinically relevant abnormalities were identified. Advanced imaging of the skull identified an enlarged parotid salivary gland and an enlarged ipsilateral medial retropharyngeal lymph node. The medial retropharyngeal lymph node was sampled via fine-needle aspiration, and a round-cell population similar to what was present in the mass was identified. An incisional biopsy was performed under general anesthesia, which yielded a diagnosis of salivary gland extramedullary plasmacytoma, confirmed with immunohistochemistry (MUM-1). The parotid salivary gland and medial retropharyngeal lymph node were then surgically excised, and metastasis to the lymph node was confirmed by histopathology. The dog remained alive for 685 days after surgery until she was euthanized for hindlimb paresis of undetermined cause.

Evaluation of some blood parameters in the experimental autoimmune encephalomyelitis mouse model

Multiple sclerosis (MS) is a chronic neuroinflammatory demyelinating disorder of the central nervous system with unclear exact etiology. The experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice is the most common animal model for MS sharing many clinical and pathophysiological features to expand our knowledge on the pathophysiology of the disease and to develop novel treatment strategies. The current study was planned to evaluate the effect of EAE on hematologic and plasma total protein and albumin levels in C57BL/6 mice.
 EAE was induced with myelin oligodendrocyte glycoprotein (MOG35-55) peptide in the female C57BL/6 mice. The EAE clinically caused paralyzed tail, hind limb paresis, and uncoordinated movement in the mice. The EAE-induced mice hematologically had a mild increase in white blood cell count without altering neutrophil-lymphocyte ratio but no change in vital hematological parameters such as red blood cell count, packed cell volume, and hemoglobin level. Moreover, the EAE produced a rise in the plasma total protein level and an attenuation in plasma albumin level in the mice.
 In conclusion, our findings show that the EAE model in mice might not cause any significant change hematologically, except a slight increase in the white blood cell count, and might produce changes in the plasma protein level. The EAE-induced blood parameter effects, as the findings of the current study, could take consideration in terms of understanding the pathophysiology of the disease and developing a novel therapeutic approach for the disease.

Incidence, survival time, and surgical treatment of parathyroid carcinomas in dogs: 100 cases (2010-2019).

To evaluate outcomes of dogs with parathyroid carcinoma (PTC) treated by surgical excision and to describe the incidence of postoperative hypocalcemia, degree of hypocalcemia, duration of hospitalization, duration of calcium supplementation, and survival time. 100 client-owned dogs with PTC admitted to academic, referral veterinary institutions. In a retrospective multi-institutional study, medical records of dogs undergoing surgical excision of PTC between 2010 to 2019 were reviewed. Signalment, relevant medical history, clinical signs, clinicopathologic testing, imaging, surgical findings, intraoperative complications, histologic examination, and survival time were recorded. 100 dogs with PTC were included, and 96 dogs had clinical or incidental hypercalcemia. Common clinical signs included polyuria (44%), polydipsia (43%), hind limb paresis (22%), lethargy (21%), and hyporexia (20%). Cervical ultrasonography detected a parathyroid nodule in 91 of 91 dogs, with a single nodule in 70.3% (64/91), 2 nodules in 25.3% (23/91), and ≥ 3 nodules in 4 (4/91)% of dogs. Hypercalcemia resolved in 89 of 96 dogs within 7 days after surgery. Thirty-four percent of dogs developed hypocalcemia, on the basis of individual analyzer ranges, within 1 week after surgery. One dog had metastatic PTC to the prescapular lymph node, and 3 dogs were euthanized for refractory postoperative hypocalcemia. Estimated 1-, 2-, and 3-year survival rates were 84%, 65%, and 51% respectively, with a median survival time of 2 years. Excision of PTC results in resolution of hypercalcemia and excellent long-term tumor control. Surgical excision of PTC is recommended because of resolution of hypercalcemia and a good long-term prognosis. Future prospective studies and long-term follow-up are needed to further assess primary tumor recurrence, metastasis, and incidence of postoperative hypocalcemia.

Trpm5 channels encode bistability of spinal motoneurons and ensure motor control of hindlimbs in mice

Bistable motoneurons of the spinal cord exhibit warmth-activated plateau potential driven by Na+ and triggered by a brief excitation. The thermoregulating molecular mechanisms of bistability and their role in motor functions remain unknown. Here, we identify thermosensitive Na+-permeable Trpm5 channels as the main molecular players for bistability in mouse motoneurons. Pharmacological, genetic or computational inhibition of Trpm5 occlude bistable-related properties (slow afterdepolarization, windup, plateau potentials) and reduce spinal locomotor outputs while central pattern generators for locomotion operate normally. At cellular level, Trpm5 is activated by a ryanodine-mediated Ca2+ release and turned off by Ca2+ reuptake through the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump. Mice in which Trpm5 is genetically silenced in most lumbar motoneurons develop hindlimb paresis and show difficulties in executing high-demanding locomotor tasks. Overall, by encoding bistability in motoneurons, Trpm5 appears indispensable for producing a postural tone in hindlimbs and amplifying the locomotor output.

Case Report: Successful Therapy of Spontaneously Occurring Canine Degenerative Lumbosacral Stenosis Using Autologous Adipose Tissue-Derived Mesenchymal Stem Cells

The management of degenerative lumbosacral stenosis (DLSS) in dogs usually requires aggressive, costly surgical treatments that may themselves present complications, while do not fully resolve the symptoms of the disease. In this study, the dog diagnosed with severe DLSS, with hind limb paresis, was treated using a new and least invasive treatment. Cultured autologous adipose tissue-derived mesenchymal stem cells (AT-MSCs) were injected bilaterally at the level of L7-S1, in the vicinity of the external aperture of the intervertebral foramen of DLSS patient. In the previously described treatments of spontaneous intervertebral disc degeneration in dogs, intradiscal injections of MSCs did not lead to positive effects. Here, we report a marked improvement in clinical outcome measures related to the ability of a dog to walk and trot, which were expressed by a numeric rating scale based on a veterinary assessment questionnaire. The improved status persisted throughout the observed time course of 4.5 years after the AT-MSC transplantation. To the best of our knowledge, this is the first case of successful therapy, with long-term positive effect, of spontaneously occurring canine DLSS using presented treatment that, we believe, represents a contribution to current knowledge in this field and may shape both animal and human DLSS treatment options.

Acute hindlimb paresis caused by extension of a peripheral nerve sheath tumour into the spinal canal of a horse

SummaryA 10‐year‐old Quarter Horse gelding presented for a large, slowly growing mass in the right thoracic region caudal to the withers (approximately at the level of thoracic vertebrae 10 to 16). The mass was surgically removed, the horse returned to normal riding activity, and no external regrowth was observed. Two years after surgery, the horse developed progressive signs of hindlimb weakness, ataxia and adopting a dog‐sitting stance. Post‐mortem examination confirmed spinal canal infiltration and spinal cord compression (at the level of the 12th thoracic vertebra) by a similar soft tissue sarcoma as diagnosed previously. Immunohistochemistry confirmed the tumour as a peripheral nerve sheath tumour (PNST) likely originating from the twelfth thoracic spinal nerve. This report demonstrates that with incomplete tumour resection, local recurrence and extension of a PNST into the central nervous system can occur even years after initial tumour removal. Immunohistochemistry to differentiate the type of soft tissue sarcoma in cases with close association to the nervous system may prove beneficial to anticipate this uncommon complication. Early surgical resection with adjunctive therapies should be considered in these cases.

Consequences of Canine Ehrlichiosis: Clinical Case Successfully Resolved

This work aims to report the case of a canine that survived erlichiosis with severe consequences of the disease, such as meningitis, hind limb paresis, circle walking, cerebrovascular accident. The onset of paresis was sudden, soon after a hygienic grooming. X-ray examinations ruled out suspected trauma. A cerebrovascular accident is suspected due to vasculitis found by electrocardiogram examination. Traditional treatment for doxycycline-based erlichiosis (200 mg) 1 comp. 2 x day for 24 days was recommended; anti-inflammatory drug Prednisone - IDB for 15 days, antianemic Erythros - 1 comp./day, Leucogen (H) 5 mL (2 x day) immunomodulator for platelet elevation and a peripheral and cerebral vasodilator Revimax - 1 comp./ day were the drugs of choice. The case seems to suggest that the bacterium, through the hematogenous route, reaches the intervetbral discs, paralyzing the pelvic limbs, bladder, anal sphincter and tail, and may even cause neurological disorders and even lead to death of the animal. Since paresis and stroke, as well as hydrocephalus and meningitis, clinical signs were much more atypical and are currently becoming more frequent.

Ovarian Carcinoma with Skeletal Metastasis in a Yacare Caiman (Caiman yacare)

Abstract A 39-yr-old intact adult female Yacare caiman (Caiman yacare) presented with hindlimb paresis. Magnetic resonance imaging and computed tomography studies revealed a compressive vertebral m...