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.     

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.     

Hepatoencephalopathy and hypocalcemia in a miniature horse mare.

A pregnant, miniature horse mare had clinical signs of hepatoencephalopathy and concurrent hypocalcemia. The signs included dullness, inappetence, blindness, head pressing, weakness, muscle fasiculations, uveitis, and urinary incontinence. Hepatic dysfunction and hypocalcemia were confirmed by serum biochemical analysis. The mare was treated successfully with a continuous infusion of Ringer solution, calcium gluconate, dextrose, B-complex vitamins, sodium ampicillin, and flunixin meglumine; topical administration of ophthalmic ointments; and decompression of the urinary bladder. Histologic examination of a liver biopsy specimen revealed acute hepatic necrosis, which likely was associated with administration of a vaccine of equine origin 2 months earlier.     

Postanesthetic recumbency associated with hyperkalemic periodic paralysis in a quarter horse.

Anesthesia and surgery in a Quarter Horse affected with hyperkalemic periodic paralysis resulted in euthanasia after 7 days of postoperative recumbency. Initial recovery was uneventful after extensive sinus surgery, but within 2 hours, the horse had severe muscle weakness. Plasma electrolyte concentrations were within the normal range during the period of recumbency. There was no clinical or laboratory evidence of severe muscle damage. Despite treatment with acetazolamide, isoproterenol, and intensive nursing, the horse was unable to stand for more than a few seconds and developed severe decubital ulcers. Ultrastructural examination revealed nemaline rods and swollen mitochondria in disrupted myofibers.     

Episodic muscle tremors in a quarter horse: resemblance to hyperkalemic periodic paralysis

A three year old Quarter Horse stallion was presented with a one year history of episodes of generalized muscle tremors and stiffness, and spasm of the muscles of facial expression, lasting 10-15 minutes. Between attacks, the horse was either normal or had a localized muscle tremor in the flank region. Episodes appeared unrelated to exercise. The major abnormal findings included 1) a rise in plasma potassium from a resting level of 4.4 to 7.9 mmol/L during an attack and 2) electromyographic findings of generalized increased insertion activity and myotonic discharges. The horse was treated with hydrochlorothiazide tablets for nine months, during which time no further attacks were noted. However, four months after the drug was stopped, sporadic focal muscle tremors reappeared; two months later, generalized attacks were seen. Despite reinstitution of the diuretic, a focal flank tremor persisted. Two related horses in the same stable also were reported by the owner to exhibit sporadic generalized muscle twitching. The abnormal findings of the present case differ from clinical syndromes previously reported in horses. Some similarities to hyperkalemic periodic paralysis in humans are noted.     

Bone abscess in the mandible of a quarter horse gelding

A 4-year-old Quarter horse gelding presented with a swelling in the soft tissues over the junction of the body and ramus of the left mandible. Radiography showed a well circumscribed lytic area within the mandible surrounded by sclerosis unassociated with any tooth. Aspiration of the lesion yielded pus. The abscess cavity was opened, curetted and lavaged. A Penrose drain was placed in the abscess cavity for 10 days. Bacteriological culture of the exudate and soft tissues from the abscess produced a few colonies of Staphylococcus intermedius. Histopathology showed chronic pyogenic infection. The horse recovered well and was normal 1 year after treatment.     

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.     

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.     

Genetic mapping of dominant white (W), a homozygous lethal condition in the horse (Equus caballus)

Dominant white coat colour (W) is a depigmentation syndrome, known in miscellaneous species. When homozygous in the horse (similar in mice), the mutation responsible for the white phenotype is lethal in a very early stage of gestation. It seems, that the action of the dominant white allele is not always fully penetrant, resulting occasionally in spotted look alike offspring. These horses resemble a coat colour pattern known as sabino spotting. So far, it is not known whether dominant white (W) and sabino spotting (S) share a common genetic background. In this study, a pedigree consisting of 87 horses segregating for dominant white (W) was used to genetically localize the horse (W)‐locus. Microsatellite ASB23 was found linked to (W), which allowed us to map dominant white to a region on horse chromosome 3q22. Tyrosine kinase receptor (KIT) was previously mapped to this same chromosome region (3q21–22). KIT and its ligand (KITLG) are responsible for the normal function of melanogenesis, haematopoiesis and gametogenesis. So far, sequence analysis of different KIT gene fragments did not lead to new polymorphisms, except for a SNP detected in KIT intron 3 (KITSNPIn3). Additional microsatellites from ECA3q (TKY353 and LEX7), together with KITSNPIn3 allowed us to state more precisely the (W)‐mutation. The positional results and comparative functional data strongly suggest that KIT encodes for the horse (W)‐locus.     

Cerebral haemorrhage in a pregnant Standardbred mare with Evan's syndrome

A 3‐year‐old pregnant Standardbred mare was treated at the University of Helsinki Equine Teaching Hospital for severe idiopathic immune‐mediated thrombocytopenia and haemolytic anaemia (Evan's syndrome). Despite initial improvement with supportive care and immunosuppressive doses of corticosteroids and azathioprine, the mare died from a fatal cerebral haemorrhage on Day 21 of treatment.     

Testicular feminization syndrome in a mare.

Testicular feminization syndrome was diagnosed in a mare with aggressive, stallion like behavior and a history of infertility. She was found to have a high baseline testosterone concentration suggesting that testicular tissue was present, and ovarian-like structures examined by use of transrectal ultrasonography had the appearance typical of testicular tissue. Although her external female genitalia appeared normal, her vagina ended in a blind sac, and no cervix or uterus were identified. Surgery was performed, and structures removed from the abdominal cavity were determined to be hypoplastic testicles. Removal of the testicular tissue resulted in complete resolution of her aggressive behavior. Chromosomal evaluation revealed that the mare had 64X,Y (normal male) karyotype. Testicular feminization syndrome is a condition characterized by insensitivity of reproductive tissues to androgens during development because of an abnormality in androgen receptors. This androgen insensitivity results in development of normal external female genitalia, with high testosterone concentrations being released from developing testicles. Testicular feminization syndrome has not been commonly diagnosed in horses, but should be considered as a differential diagnosis for overly aggressive mares with a history of infertility.