Nasal and ocular amyloidosis in a 15-year-old horse

Localized nasal, conjunctival and corneal amyloidosis was diagnosed in a 15-year-old pony with nasal and conjunctival masses and severe dyspnoea. Multiple swellings had been evident in the nostrils for at least two years and had gradually increased in size before presentation due to dyspnoea and exercise intolerance. Surgical debulking of the masses was performed and histological examination revealed large amounts of extracellular, hyaline, eosinophilic, Congo red positive material in the lamina propria of the nasal mucosa. A tentative diagnosis of localized nasal amyloidosis was made. The treatment relieved the clinical signs, however, the nasal masses recurred and bilateral conjunctival, papillary masses developed. The horse was euthanized. Nodular nasal and papillary conjunctival masses consisting of rubbery, grey to yellow tissue were found at necropsy. At the limbus this tissue infiltrated and expanded the cornea. The masses consisted of amyloid and moderate infiltrates of T lymphocytes and B lymphocytes were present in the tissue. No predominance of either cell type was observed and no distinct neoplastic mass could be identified. Ultrastructural examination of the nasal mucosa and cornea confirmed the presence of abundant extracellular deposits of non-branching fibrils ranging from 9–11 nm in diameter consistent with amyloid. Immunohistochemistry of amyloid revealed no labelling for AA amyloid, and no peptides representing serum amyloid A (SAA) were detected by microscopic laser dissection and subsequent mass spectrometry. Peptides from immunoglobulin kappa-like light chains were detected and are suggestive of AL amyloidosis, however the results were inconclusive and a final identification of the amyloid protein could not be made.Nasal amyloidosis is a clinical entity of localized amyloid deposits in the horse. Localized amyloidosis involving the conjunctiva of the horse is previously described in only seven cases and the present case is the first case of combined, localized nasal and corneal amyloidosis in the horse. In several reported cases surgical excision has provided clinical improvement and return to normal levels of exercise, while medical treatment has had no effect. The present case however, shows that rapid recurrence and progression of nasal amyloidosis to involve ocular tissues can occur and lead to recurrent respiratory obstruction.

Electronic supplementary material

The online version of this article (doi:10.1186/s13028-014-0050-6) contains supplementary material, which is available to authorized users.     

Equine herpesvirus myeloencephalopathy in a 14-year-old quarter horse stallion

A 14-year-old, quarter horse stallion was presented in lateral recumbency, unable to rise. Equine herpesvirus myeloencephalopathy was diagnosed, based on presentation, clinical signs, and the ruling out of other possibilities. After initial rapid improvements, ataxia remained, as did chronic cystitis secondary to bladder paralysis. He was euthanized after 2 months.     

Glanzmann thrombasthenia in a 17-year-old Peruvian Paso mare

A 17-year-old Peruvian Paso mare was evaluated for bilateral epistaxis that had been present for at least 3 years. The mare had mild anemia, platelet count within the reference interval, unremarkable coagulation times, and a negative Coggins test. On endoscopic examination, structural abnormalities were not observed in the nasal cavities, pharynx, larynx, trachea, or either guttural pouch, but petechiation was noted in the nasal mucosa. Additional tests revealed prolonged cutaneous bleeding time, normal concentration of von Willebrand factor antigen, an abnormal clot retraction test, and failure of plalelet aggregation in response to agonists, suggesting a functional disorder of platelets. Genetic analysis indicated the horse was homozygous for a 10-base-pair deletion that included the last 3 base pairs of exon 11 and the first 7 base pairs of intron 11 of the gene encoding glycoprotein IIb. The diagnosis was Glanzmann thrombasthenia (GT) caused by a structural defect in glycoprotein IIb. GT is an autosomal recessive disorder caused by a defect in the glycoprotein IIb-IIIa complex on platelet surfaces. Separate genes encode each glycoprotein, and mutations in either gene can result in GT. This case of GT is unique given the age of the mare at the time of diagnosis. We conclude that GT, although an inherited disorder, should be considered in horses with suspected dysfunctional platelets, regardless of age.     

Bacterial meningitis and encephalitis in ruminants.

The clinical aspects of bacterial meningitis in neonates are described in this article. Specific types of meningitis affecting adult cattle are also described. Other conditions occurring less frequently,such as frontal sinusitis and brain abscess, are discussed.     

Reactive mesothelial hyperplasia associated with chronic peritonitis in a 20-year-old Quarter horse

A 20-year-old gelding was diagnosed with peritonitis and severe reactive mesothelial hyperplasia. Exploratory laparotomy findings were suggestive of a neoplastic etiology; however, additional diagnostics ruled this out and the horse made a full recovery. This report demonstrates the difficulty and value of differentiating between reactive and neoplastic mesothelial processes.     

Morphine-associated pruritus after single extradural administration in a horse

Pruritus following a single administration of 100 microg kg(-1) of preservative-free morphine sulphate given via an extradural catheter was seen in a 580 kg horse. The catheter was placed in the first intercoccygeal space. Focal irritation, represented by both local alopecia over the left gluteal muscles and serum exudation, occurred 4-8 hours after injection. This was attributed to the extradural morphine administration.     

Squamous cell carcinoma and suspect peripheral nerve sheath tumor in a 10-year-old Paint horse

A round mass 4 cm in diameter was present on the proximal rostro-lateral border of the right pinna of a 10-year-old, gelded, Paint horse. A preliminary histopathological diagnosis of a potential squamous cell carcinoma and peripheral nerve sheath tumor was made, and the lesion was resected at the base of the lateral edge of the ear.     

Otitis media‐interna and secondary meningitis associated with Corynebacterium pseudotuberculosis infection in a horse

A one‐year‐old Thoroughbred colt was evaluated because of facial nerve paralysis, ataxia and fever. Neurological evaluation found the colt to be obtunded and grade 3/5 ataxic in all 4 limbs. Right‐sided facial nerve paralysis was present and a large, deep corneal ulcer noted in the right eye. Signs of vestibular disease were also present, including circling towards the right and horizontal nystagmus. A complete blood count showed mild leucocytosis, neutrophilia and hyperfibrinogenaemia. A computed tomography (CT) examination of the skull was performed under general anaesthesia and a diagnosis of right sided otitis media‐interna was made. Culture of fluid taken from the middle ear and cerebrospinal fluid collected from the atlanto‐occipital site yielded pure growth of Corynebacterium pseudotuberculosis. Initial therapy consisted of antimicrobial treatment with cefotaxime and anti‐inflammatory treatment with flunixin meglumine. Six days after initiating treatment, the colt developed Clostridium difficile associated colitis. The colitis resolved with supportive care and the colt was discharged from the hospital receiving chloramphenicol. Eight months later, the colt continued to be mildly ataxic (grade 1/5), with a slight head tilt and facial nerve paralysis. To the authors' knowledge, this is the first reported case of otitis media‐interna due to C. pseudotuberculosis in the horse.     

Bilateral arytenoid cartilage paralysis after inhalation anesthesia in a horse

An 8-year-old Quarter Horse gelding was anesthetized for surgical exploration and debridement of a chronic draining wound in the intermandibular space. Anesthesia was without complication other than persistently low PaO2. Severe airway obstruction was evident immediately after extubation, requiring tracheostomy. Endoscopic diagnosis was bilateral arytenoid paralysis, which gradually resolved over the next 7 days. Compression, trauma, or tension of the recurrent laryngeal nerves are the postulated causes of idiopathic laryngeal hemiplegia in horses. The extremely extended position of the head and neck during anesthesia, perhaps compounded by low arterial oxygen content, may have resulted in a hypoxemic insult to the recurrent laryngeal nerves and caused bilateral arytenoid paralysis in this horse.     

Urticaria in the horse after anaesthesia

Extract

Sir:- I read with interest the case report, “An unusual reaction in a horse during anesthesia” by I.L. Anderson, N.Z. vet. J. 31:85 (1983), describing the development of generalized urticaria in a horse after induction of anesthesia with guaiphenesin and thiopentone.