Pulmonary basaloid squamous cell carcinoma in a dog

A 9-year-old neutered male crossbred dog with a 4-week history of progressive vestibulocerebellar signs was presented for necropsy examination. Gross examination revealed neoplastic growth in the lungs, thoracic lymph nodes, the left kidney and the cerebellum. Microscopically, the tumour consisted of an infiltrative, densely cellular, basaloid epithelial neoplastic growth with extensive areas of abrupt keratinization. Immunohistochemically, neoplastic cells expressed p63 and partially expressed cytokeratins 5/6. Based on these findings, the tumour was diagnosed as a primary pulmonary basaloid squamous cell carcinoma (BSSC) with metastasis to regional lymph nodes, kidney and brain. As far as the authors are aware, this is the first description of BSCC in an animal species

Clinical and genetic characterisation of dystrophin-deficient muscular dystrophy in a family of Miniature Poodle dogs

Four full-sibling intact male Miniature Poodles were evaluated at 4–19 months of age. One was clinically normal and three were affected. All affected dogs were reluctant to exercise and had generalised muscle atrophy, a stiff gait and a markedly elevated serum creatine kinase activity. Two affected dogs also showed poor development, learning difficulties and episodes of abnormal behaviour. In these two dogs, investigations into forebrain structural and metabolic diseases were unremarkable; electromyography demonstrated fibrillation potentials and complex repetitive discharges in the infraspinatus, supraspinatus and epaxial muscles. Histopathological, immunohistochemical and immunoblotting analyses of muscle biopsies were consistent with dystrophin-deficient muscular dystrophy. DNA samples were obtained from all four full-sibling male Poodles, a healthy female littermate and the dam, which was clinically normal. Whole genome sequencing of one affected dog revealed a >5 Mb deletion on the X chromosome, encompassing the entire DMD gene. The exact deletion breakpoints could not be experimentally ascertained, but we confirmed that this region was deleted in all affected males, but not in the unaffected dogs. Quantitative polymerase chain reaction confirmed all three affected males were hemizygous for the mutant X chromosome, while the wildtype chromosome was observed in the unaffected male littermate. The female littermate and the dam were both heterozygous for the mutant chromosome. Forty-four Miniature Poodles from the general population were screened for the mutation and were homozygous for the wildtype chromosome. The finding represents a naturally-occurring mutation causing dystrophin-deficient muscular dystrophy in the dog

Delayed Forebrain Syndrome Due to Traumatic Frontoethmoidal Meningoencephalocele in a Cat

Meningoencephalocele is a protrusion of meninges and brain through an opening in the cranium; in humans it may be congenital, traumatic, neoplastic or idiopathic, whilst in small animals only congenital form has been reported. A 3-year-old, client-owned, neutered male DSH cat was referred with one-month history of three generalized tonic-clonic seizures and intermittent left thoracic limb spontaneous knuckling. Nine months ago, the animal had been bitten on the head by a wild carnivore. Prior to the traumatic event the cat was reported to be neurologically normal. On admission, physical examination was unremarkable. Neurological examination revealed left hemi-neglect syndrome, characterised by decreased postural reactions on the left thoracic and pelvic limb, and absent menace bilaterally, most likely post-ictal. Neuroanatomical localisation was right forebrain. Haematology, biochemistry and bile acid stimulation test were unremarkable. Blood serology for Toxoplasma gondii, FIV, FeLV and FCoV were all negative. MRI of the head revealed protrusion of brain and meninges into the right frontal sinus, mild meningeal contrast uptake of the protruding tissue and the adjacent brain in the calvarium. CSF analysis was unremarkable. Final diagnosis was traumatic frontoethmoidal meningoencephalocele with late-onset forebrain syndrome due to presumptive post-traumatic encephalomalacia. The cat remained seizure-free on the four-month follow-up. This is the first report of traumatic meningoencephalocele in small animals. The finding in this case emphasizes the importance of a complete neurological investigation in patients with history of head trauma despite the absence of initial neurological signs. Differentials for delayed neurological signs after traumatic meningoencephalocele include encephalomalacia, recurrent meningitis with/without CSF rhinorrhea or cerebral ischaemic infarction

Delayed forebrain syndrome due to presumptive traumatic intranasal meningoencephalocele in a cat

A 3-year-old male neutered domestic shorthair cat was referred with 1-month history of three generalised tonic-clonic epileptic seizures and left-sided thoracic limb knuckling. Nine months previously, the cat was bitten on the right upper palpebral region without manifesting neurological signs. On admission, physical and neurological examination revealed left-sided postural reaction deficits and absent menace response. Thus, a right-forebrain neurolocalisation was reached. Haematology, biochemistry, bile acid stimulation test, infectious diseases serology and cerebrospinal fluid analysis were unremarkable. Cerebral MRI revealed extension of brain and meninges into the right frontal sinus. Final diagnosis of a right-sided traumatic frontoethmoidal meningoencephalocele was made. The cat remained seizure free under phenobarbital treatment with residual left-sided postural reaction deficits at 9 months follow-up. This is the first report of presumptive traumatic meningoencephalocele in a cat, which emphasises the importance of complete neurological investigation and regular long-term follow-up checks in patients with historical head trauma despite the absence of initial neurological signs

Delayed Forebrain Syndrome Due to Traumatic Frontoethmoidal Meningoencephalocele in a Cat

Meningoencephalocele is a protrusion of meninges and brain through an opening in the cranium; in humans it may be congenital, traumatic, neoplastic or idiopathic, whilst in small animals only congenital form has been reported. A 3-year-old, client-owned, neutered male DSH cat was referred with one-month history of three generalized tonic-clonic seizures and intermittent left thoracic limb spontaneous knuckling. Nine months ago, the animal had been bitten on the head by a wild carnivore. Prior to the traumatic event the cat was reported to be neurologically normal. On admission, physical examination was unremarkable. Neurological examination revealed left hemi-neglect syndrome, characterised by decreased postural reactions on the left thoracic and pelvic limb, and absent menace bilaterally, most likely post-ictal. Neuroanatomical localisation was right forebrain. Haematology, biochemistry and bile acid stimulation test were unremarkable. Blood serology for Toxoplasma gondii, FIV, FeLV and FCoV were all negative. MRI of the head revealed protrusion of brain and meninges into the right frontal sinus, mild meningeal contrast uptake of the protruding tissue and the adjacent brain in the calvarium. CSF analysis was unremarkable. Final diagnosis was traumatic frontoethmoidal meningoencephalocele with late-onset forebrain syndrome due to presumptive post-traumatic encephalomalacia. The cat remained seizure-free on the four-month follow-up. This is the first report of traumatic meningoencephalocele in small animals. The finding in this case emphasizes the importance of a complete neurological investigation in patients with history of head trauma despite the absence of initial neurological signs. Differentials for delayed neurological signs after traumatic meningoencephalocele include encephalomalacia, recurrent meningitis with/without CSF rhinorrhea or cerebral ischaemic infarction

Risk factors associated with short-term mortality and recurrence of status epilepticus in dogs

Background: Status epilepticus (SE) is an emergency associated with serious consequences for both patient and owner. Data regarding risk factors for short-term mortality or recurrence in dogs with SE is limited. Objective: Identify risk factors associated with short-term mortality (euthanasia or spontaneous death) and recurrence of SE in dogs. Animals: One hundred twenty-four client-owned dogs that sustained an episode of SE. Methods: Retrospective multicenter study using data collected from medical records of dogs presented in SE to the contributing institutions. Multivariable logistic regression analysis was performed using a manual backwards stepwise approach to identify risk factors associated with short-term mortality and recurrence of SE after discharge. Results: Short-term mortality for affected dogs was 29.8%. Factors significantly associated with short-term mortality included increased patient age, shorter duration of hospitalization, development of SE before arrival, and SE caused by a potentially fatal etiology. Status epilepticus recurred in 27% of dogs that survived to discharge. Factors significantly associated with recurrence of SE included prior history of pharmacoresistant epilepsy and predominance of a focal seizure phenotype. Conclusions and Clinical Importance: Our results may be used to inform clinicians and dog owners regarding risk factors for both short-term mortality and recurrence in dogs with SE

Immunofluorescent analysis of muscle biopsies for localisation of dystrophy associated proteins.

<p>Immunofluorescent staining of cryosections from dog 1 (dystrophic) and a control dog using antibodies to laminin α2, the rod domain and carboxy terminus (C-terminus) of dystrophin, dysferlin, α- and β-sarcoglycans (αSG and βSG respectively) and utrophin (DRP2). An antibody against spectrin was used as a control for membrane integrity. Staining was absent for the rod domain and carboxy terminus of dystrophin, decreased for β-sarcoglycans and similar for laminin α2, dysferlin, α-sarcoglycans and spectrin. Utrophin was visualized along the sarcolemma in the dystrophic dog but not on the sarcolemma of the control muscle. Regeneration was robust as shown by the antibody against developmental myosin heavy chain (dMHC).</p

Representative histopathology of muscle cryosections from the infraspinatus muscle of dog 1.

<p>Multifocal areas of myofibre degeneration are characterised by scattered and groups of necrotic fibres undergoing phagocytosis (a) and large clusters of basophilic regenerating fibres (b) consistent with a dystrophic phenotype (H&E stain).</p

Western blotting of skeletal muscle from dystrophic dogs (dogs 1 and 2).

<p>Shown are stainings for the rod (DYS1) and carboxy terminus (DYS2) of dystrophin in the affected and control dogs. Bands are visible at approximately 395 kDA for the control muscle, but are not detectable in the dystrophic dogs. β-actin was used as a loading control and bands staining at a molecular weight of approximately 43 kDa confirm similar amounts of loaded protein in dystrophic and control dogs.</p