Congenital internal hydrocephalus in a quarter horse foal

Since the normal absorption of CSF occurs in the cerebral veins and venous sinuses, any obstruction to the normal flow and absorption of CSF will result in accumulation of CSF central to the site of obstruction. Such accumulation within the cranium is defined as hydrocephalus.A foal was presented with an enlarged and an abnormally-shaped skull, but with normal behavior. The filly's condition deteriorated. Radiographs showed a domeshaped cranial vault with compression of the frontal sinus region. Massive hydrocephalus with little normal cerebral tissue left was diagnosed with ultrasound.Surgery was attempted to relieve the pressure. Eventually the foal was euthanized. Post-mortem confirmed the radiographic and ultrasound diagnosis. Since there was a lack of demonstrable obstruction, the authors suspected the foal had suffered from the Arnold-Chiari syndrome.     

Corneal stromal abscess in a horse

A thoroughbred yearling presented with a focal, yellow, midstromal corneal opacity with concurrent iridocyclitis which was consistent with a corneal stromal abscess. When continued, appropriate, medical therapy failed to improve the patient's condition, penetrating keratoplasty was performed for diagnosis and therapy. Histopathology showed that the deep corneal stroma and Descemet's membrane were severely infiltrated with necrotic neutrophils and numerous, intralesional fungal hyphae. Culture was negative. Bacteria were not isolated, consistent with a fungal corneal stromal abscess. The resultant corneal scar did not interfere with the horse's racing career.     

Sclerosing odontogenic carcinoma in the mandible of a horse

A 15-year-old Cob mare was presented for investigation of a mandibular mass. Radiography identified an oval-shaped mass occupying the intramandibular space, with a heterogeneous osseous opacity throughout the left hemimandible. Histopathology combined with immunohistochemistry was consistent with a diagnosis of sclerosing odontogenic carcinoma, which to date has only been described, rarely, in human patients. The mass was removed using a mandibular-sparing surgical technique allowing preservation of the dental arcade. Follow-up 5 years after surgery confirmed no signs of regrowth. This case report describes the successful treatment of a previously unreported mandibular neoplasm in the horse.     

Actinomycosis of the mandible, mimicking a malignancy in a horse

Osteomyelitis of the mandible with Actinomyces species was diagnosed in a 4-year-old sports horse with radiographic changes suggestive of neoplasia. Surgical debridement, intravenous and local iodine solution treatment were administered. Mandibular Actinomyces infections are reported in humans and ruminants; they have not been previously reported in the horse.     

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.     

Suspected transient pseudohypoaldosteronism in a 10-day-old quarter horse foal

A 10-day-old quarter horse colt was presented for signs of disorientation and inability to nurse. Hydronephrosis/hydroureters, with concomitant pyelonephritis and a severe electrolytes disturbance, were diagnosed. The clinical findings closely resembled those described for a syndrome of transient pseudohypoaldosteronism in human neonates.     

Intracranial medulloblastoma as the cause of progressive ataxia in a 6-month-old draft horse cross gelding

We describe the unique clinical presentation of a central nervous system neoplasm in a 6-month-old draft horse cross gelding. Based on the neurologic examination at admission, neurolocalization was most consistent with a mildly asymmetric cervical, multifocal, or diffuse myelopathy. Mild vestibular involvement also was considered, but no cranial nerve deficits were observed. The gelding was negative for Sarcocystis neurona or Neospora hughesi based on paired serum and cerebrospinal fluid (CSF) samples analyzed, with no evidence of cervical compression based on contrast myelography. The horse was euthanized because of progression of clinical signs. At necropsy, a mass was identified associated with the cerebellum, and histopathology was consistent with medulloblastoma, which has not been reported previously in the horse.     

Unilateral orbital lacrimal gland abscess in a horse

A 20-year-old Thoroughbred gelding presented for evaluation of a periorbital dorsal swelling of the left eye that had been intermittently present for 3 months. Upon ocular examination, a firm, non-painful swelling was identified under the upper eyelid in the region of the orbital lacrimal gland, and was noted to extend anteriorly from underneath the dorsal orbital rim. Ultrasonographic examination revealed a mixed echogenic mass along the dorsal orbital rim that followed the contour of the globe. CT scan showed a moderately contrast enhancing mass that was contiguous with the eyelid. Differential diagnoses included neoplasia, inflammatory lesions such as a granuloma, foreign body or abscess. Surgical exploration and excision of the mass revealed a lobular structure with a purulent center. Histopathology identified the mass as the orbital lacrimal gland with concurrent severe dacryoadenitis. Culture of the purulent center of the mass revealed beta-hemolytic Staphylococcus aureus. The patient was maintained on supportive care and antibiotic treatment based on sensitivity postoperatively. No recurrence was reported 40 months later. This paper aims to identify bacterial dacryoadenitis as a cause for unilateral periorbital swelling in the horse. Differential diagnoses for this presentation, as well as successful surgical management are discussed. To the author's knowledge, this is the first case of bacterial dacryoadenitis and subsequent abscessation of the orbital lacrimal gland in the horse.     

Lameness diagnosis and treatment in the quarter horse racehorse

Lameness problems constitute a major part of racing Quarter Horse practice. This article considers the diagnosis, prognosis, and treatment of the frequently encountered lamenesses. The main conditions included are synovitis, intra-articular fractures, osteochondritis dissecans, and degenerative joint disease as they relate to the coffin, fetlock, carpal, and tarsal joints. Intra-articular injection techniques and medications are discussed because of the frequency of joint disease. Bucked shins and stress fractures are also reviewed.     

Unilateral white line disease and laminitis in a quarter horse mare

A 5-year-old quarter horse mare presented with unilateral, severe, chronic forelimb lameness. Radiographs revealed extensive hoof wall separation and capsular rotation of the distal phalanx. Treatment included dorsal hoof wall resection, phenylbutazone, a bar shoe, and stall rest. Whether white line disease or laminitis was the primary lesion remains unclear.     

Bleeding disorder (von Willebrand disease) in a quarter horse

Bleeding diathesis in a Quarter Horse filly was caused by von Willebrand disease. Hemorrhage occurred mainly from mucosal surfaces and after trauma. Quantitative and qualitative measurements of plasma von Willebrand factor (vWF) documented a specific deficiency of vWF high molecular weight multimers, and concurrently greater than expected deficiency of vWF activity relative to vWF concentration. These findings are characteristic of type-II von Willebrand disease in human beings. Application of vWF assays used in human and small animal medicine now permits evaluation of vWF and diagnosis of von Willebrand disease in horses with bleeding disorders.     

Hemophilia A in two related quarter horse colts

Severe hemorrhagic diathesis caused by hemophilia A (factor VIII:C deficiency) was diagnosed in 2 related Quarter Horse colts. Clinical signs consisted of dyspnea and dysphagia attributable to cranial cervical hematoma in one colt and to intra-abdominal hemorrhage resulting in death of the second colt. Factor VIII:C deficiency, a defect of the intrinsic coagulation pathway, is suggested by results of coagulation studies--prolonged activated partial thromboplastin time, normal prothrombin time, and normal primary bleeding time. The diagnosis was confirmed by results of factor VIII:C assays. Hemophilia A is inherited as an X chromosome-linked trait.     

Glycogen branching enzyme deficiency in quarter horse foals

Seven related Quarter Horse foals that died by 7 weeks of age were examined for glycogen branching enzyme (GBE) deficiency. Clinical signs varied from stillbirth, transient flexural limb deformities, seizures, and respiratory or cardiac failure to persistent recumbency. Leukopenia (5 of 5 foals) as well as high serum creatine kinase (CK; 5 of 5), aspartate transaminase (AST; 4 of 4), and gamma glutamyl transferase (GGT; 5 of 5) activities were present in most foals, and intermittent hypoglycemia was present in 2 foals. Gross postmortem lesions were minor, except for pulmonary edema in 2 foals. Muscle, heart, or liver samples from the foals contained abnormal periodic acid Schiff's (PAS)-positive globular or crystalline intracellular inclusions in amounts proportional to the foal's age at death. Accumulation of an unbranched polysaccharide in tissues was suggested by a shift in the iodine absorption spectra of polysaccharide isolated from the liver and muscle of affected foals. Skeletal muscle total polysaccharide concentrations were reduced by 30%, but liver and cardiac muscle glycogen concentrations were normal. Several glycolytic enzyme activities were normal, whereas GBE activity was virtually absent in cardiac and skeletal muscle, as well as in liver and peripheral blood cells of affected foals. GBE activities in peripheral blood cells of dams of affected foals and several of their half-siblings or full siblings were approximately 50% of controls. GBE protein in liver determined by Western blot was markedly reduced to absent in affected foals, and in a half-sibling of an affected foal, it was approximately one-half the amount of normal controls. Pedigree analysis also supported an autosomal recessive mode of inheritance. The affected foals have at least 2,600 half-siblings. Consequently, GBE deficiency may be a common cause of neonatal mortality in Quarter Horses that is obscured by the variety of clinical signs that resemble other equine neonatal diseases.     

Identification of degenerative germ cells in semen from a quarter horse stallion

A 3-year-old Quarter Horse stallion was presented for evaluation of potential fertility. An impairment in spermatogenesis was suspected as the stallion produced semen with reduced percentages of progressively motile and morphologically normal spermatozoa. In addition, when semen was collected daily from the stallion, daily spermatozoal output (DSO) was found to be below normal. Semen from this stallion also contained spherical cells of unknown origin. The following report describes the identification of these cells as degenerating spermatids by the use of light and electron microscopy.