Clinical, cytologic and histopathologic manifestations of protothecosis in two dogs

Two cases of sudden onset of blindness associated with ocular protothecosis in dogs are reported. Both were adult, spayed female, mixed-breed dogs that lacked the usual clinical signs of systemic infection with Prototheca species. Physical abnormalities at the time of presentation were limited to the affected eyes which had serous discharge, hyperemic conjunctiva, and aqueous flare. The pupillary light reflexes were slow, and the menace reflexes were absent. Both dogs had glaucoma. Results of complete blood counts and serologic titres for antibodies to Blastomyces dermatitidis and Histoplasma capsulatum were within reference intervals. Protothecosis was diagnosed by cytologic analysis of vitreous humor and was confirmed at necropsy. These two cases were unusual because of their presenting signs and prolonged course of disease progression.     

Blindness, optic atrophy and sinusitis in the horse

Objective  The case histories described each presented with a visual deficit, varying from permanent total blindness with ophthalmoscopic evidence of optic atrophy to variable and transient visual disturbances, including occasional blindness, but with absence of ophthalmoscopic or any other ocular abnormality.
Animals studied  Three horses of widely different age and type, but all with an original history of upper respiratory tract infection.
Procedure  All three cases were examined by a specialist veterinary ophthalmologist. In addition, magnetic resonance imaging (MRI) and, where possible, postmortem and histopathological examinations were performed.
Results  The common factor to all three cases proved to be infection of the spheno-palatine sinuses with subsequent distension and compression of adjacent optic nerve(s) and optic chiasm.
Conclusions  Specialist veterinary ophthalmological examination proved of extremely limited value. The importance of MRI (and CT) scans for accurate diagnosis, and therefore possible successful treatment, is emphasized. Our cases were compared with similar cases in man, where visual disturbances due to spheno-palatine sinus involvement are recognized, but rare, in similar situation.     

Acute vision loss after general anesthesia in a cat

A 6‐year‐old, male castrated, domestic shorthair cat presented with a 2‐week history of blindness following general anesthesia. Behavioral changes, lethargy, inappetence and neurological deficits were also noted. Ophthalmic evaluation revealed blindness, normal pupillary light response and dazzle response, but no other abnormalities. Serodiagnostic testing for common infectious agents was negative and a cerebrospinal fluid analysis was normal. History and postmortem examination following euthanasia revealed cerebrocortical necrosis most consistent with anesthesia related hypoxia.     

Episodic blindness and ataxia in a horse with cholesterinic granulomas

An 11‐year‐old Oldenburg mare presented following three episodes of acute, transient blindness, ataxia, and disorientation within the preceding 7 months. Clinical improvement, including return of vision, occurred within 1 week of initiating corticosteroid therapy for each of the three episodes. However, mild right‐sided miosis was a consistent finding on ophthalmic examinations. Routine clinicopathologic testing revealed no significant abnormalities, and testing of cerebral spinal fluid for selected infectious diseases was unrewarding. Computed tomography of the brain demonstrated a hyperattenuating mass with peripheral mineralization in the rostroventral aspect of each lateral ventricle. The mare was euthanized due to a guarded to poor prognosis. On histopathology, the masses consisted of clusters of cholesterol clefts admixed with leukocytes, mineral deposits, and connective tissue. Cholesterinic granulomas of the lateral ventricles and hydrocephaly were diagnosed. Cholesterinic granulomas should be considered a differential diagnosis in horses presenting for intermittent blindness.     

Sudden acquired retinal degeneration syndrome (SARDS) – a review and proposed strategies toward a better understanding of pathogenesis,early diagnosis,and therapy

Sudden acquired retinal degeneration syndrome (SARDS) is one of the leading causes of currently incurable canine vision loss diagnosed by veterinary ophthalmologists. The disease is characterized by acute onset of blindness due to loss of photoreceptor function, extinguished electroretinogram with an initially normal appearing ocular fundus, and mydriatic pupils which are slowly responsive to bright white light, unresponsive to red, but responsive to blue light stimulation. In addition to blindness, the majority of affected dogs also show systemic abnormalities suggestive of hyperadrenocorticism, such as polyphagia with resulting obesity, polyuria, polydipsia, and a subclinical hepatopathy. The pathogenesis of SARDS is unknown, but neuroendocrine and autoimmune mechanisms have been suggested. Therapies that target these disease pathways have been proposed to reverse or prevent further vision loss in SARDS‐affected dogs, but these treatments are controversial. In November 2014, the American College of Veterinary Ophthalmologists' Vision for Animals Foundation organized and funded a Think Tank to review the current knowledge and recently proposed ideas about disease mechanisms and treatment of SARDS. These panel discussions resulted in recommendations for future research strategies toward a better understanding of pathogenesis, early diagnosis, and potential therapy for this condition.     

Congenital stationary night blindness in a Thoroughbred and a Paso Fino

This report documents congenital stationary night blindness (CSNB) in two non-Appaloosa horse breeds (Thoroughbred and Paso Fino). History of vision impairment since birth, normal ocular structures on ophthalmic examination, and electroretinographic findings were consistent with CSNB. In one horse (Thoroughbred), a 9-year follow-up was carried out. In the Paso Fino, severe vision impairment from birth to approximately 1 year of age in both dim and bright light situations led to humane euthanasia and histopathologic confirmation of the disorder.     

Surgical management of an extrahepatic portosystemic shunt in a foal: A multidisciplinary problem

A 5‐week‐old American Miniature filly was referred due to intermittent neurological signs of 4 weeks' duration. Clinicopathological findings showed increased ammonia and bile acids in venous blood samples. Abdominal ultrasonography detailed a portosystemic shunt (PSS). The foal underwent laparotomy and operative mesenteric portovenography, which further defined the PSS as extrahepatic portocaval in configuration. The PSS was occluded and intraoperative portovenography confirmed successful shunt occlusion. The foal made a good recovery from surgery and had a successful showing career until she succumbed to colic just over 3 years after surgery.     

Early retinopathy in the Bernese Mountain Dog in France: preliminary observations

The objective of the study was to describe a form of early retinopathy in the Bernese Mountain Dog in France. Sixty-two Bernese Mountain Dogs (38 males and 24 females), whose ages ranged from 2 months to 9 years, were examined over a period of 3 years. Visual behavior, pupillary light reflexes, menace responses and ocular fundi were evaluated in all animals. Electroretinography (ERG) was performed on six of the affected dogs after dark adaptation. Fluorescein angiography (FA) was performed on one affected dog. Whenever possible, the pedigrees of the affected dogs were evaluated. A histological examination of the retina was performed on one of the affected dogs. Eight dogs (seven males and one female) were diagnosed with retinopathy with an early onset of clinical signs. (Four dogs were aged between 3 months and 1 year, two dogs were aged 2 and 3.5 years, and one dog was 7 years old.) Night vision was impaired in most of the dogs. Retinopathy was characterized ophthalmoscopically by a bilateral, symmetrical horizontal zone of tapetal hyper-reflectivity adjacent to and above the optic disc, and sometimes by peri-papillary hyper-reflectivity. ERG changes included a reduction in b-wave amplitude varying from one case to another. Fluoroscein angiography demonstrated an ischemic-type alteration with epitheliopathy opposite the hyper-reflective zone. Pedigree examinations suggested a familial predisposition. The histological examination indicated photoreceptor degeneration that was more pronounced in the central tapetal zone. In France, retinopathy in the Bernese Mountain Dog involves an early retinal degeneration that produces specific manifestations of the ocular fundus, night visual impairment or blindness, and has familial transmission.     

Suspected ivermectin toxicosis in a miniature mule foal causing blindness

A 9-week-old miniature mule foal presented to the Veterinary Medical Teaching Hospital for acute blindness, ataxia, and depression following an overdose of an over-the-counter ivermectin-based de-worming medication. Ophthalmic examination and electrodiagnostic evaluation eliminated outer retinal abnormalities as the primary cause of the bilateral blindness, implicating instead a central neurologic effect of the drug. With symptomatic and supportive care, the foal recovered fully and regained its vision.     

Suspected venous air embolism in three horses

Venous air embolism was suspected in 3 hospitalised horses on the basis of an inadvertently open jugular venous line. Subsequently the 3 horses developed clinical signs including cardiovascular collapse, cardiac dysrhythmia, pulmonary oedema, behavioural abnormalities and neurological signs consistent with central nervous system injury. Treatment included intranasal oxygen therapy, i.v. fluid administration and anti‐inflammatory therapy. Specific therapy aimed at treating air embolism in man is reviewed, with pertinent therapy potentially applicable to horses emphasised.     

Analysis of a deletion in the nephronophthisis 4 gene in different dog breeds

Cone‐rod dystrophy is a progressive inherited retinal degenerative disorder that occurs in humans and dogs. The deletion in the nephronophthisis 4 (NPHP4) gene was established as a causative mutation in standard wire‐haired Dachshunds. We analyzed all varieties of Dachshunds from the Czech Republic and five other dog breeds and found that the deletion in the NPHP4 (in heterozygous state) is present not only in standard‐, but also in miniature wire‐haired Dachshunds, but not in other varieties of Dachshunds or in other breeds.     

STRUCTURAL AND FUNCTIONAL CHANGES RELEVANT TO MAXILLARY ARTERIAL FLOW OBSERVED DURING COMPUTED TOMOGRAPHY AND NONSELECTIVE DIGITAL SUBTRACTION ANGIOGRAPHY IN CATS WITH THE MOUTH CLOSED AND OPENED

Some cats develop blindness during procedures with mouth gags, which possibly relates to maxillary arterial occlusion by opening the mouth. Our first aim was to use computed tomography (CT) to describe how vascular compression is possible based on morphologic differences between mouth positions. Our second aim was to use nonselective digital subtraction angiography to assess whether opening the mouth induces collateral circulation. Six healthy cats were examined. During CT, the maxillary artery coursed between the angular process of the mandible and the rostrolateral wall of the tympanic bulla. The median distance between these structures was shorter when the mouth was opened (left, 4.3 mm; right, 3.6 mm) vs. closed (left, 6.9 mm; right, 7.1 mm). Additionally, the distance was shorter on the side ipsilateral to the gag (P = 0.03). During nonselective angiography, with the mouth closed, there was strong sequential opacification of the external carotid arteries, maxillary arteries, maxillary retia mirabilia, cerebral arterial circle, and basilar artery. Additionally, there was uniform opacification of the cerebrum and cerebellum. With the mouth opened, opacification of the maxillary arteries (rostral to the angular processes) was reduced in all cats, the cerebral arterial circle and basilar artery had simultaneous opacification in four of six (67%) cats, and the cerebrum had reduced opacification compared to the cerebellum in four of six (67%). In conclusion, the maxillary arteries are situated such that they can be compressed when opening the mouth. Opening the mouth did not consistently induce collateral circulation sufficient to produce comparable cerebral opacification as when the mouth was closed.     

Intracranial meningioma causing partial amaurosis in a cat

Objective To describe a case of intracranial meningioma causing visual impairment in a cat, successfully treated by surgery. Procedures An adult neutered male domestic cat was referred with a 10‐month history of progressive visual impairment and altered behavior. Investigations included physical, ophthalmologic and neurological examinations as well as hematology, serum biochemistry and CT scan of the head. Results The menace response was absent in the left eye and decreased in the right eye. Electroretinograms were normal on both eyes, as was ophthalmic examination, ruling out an ocular cause and allowing a presumptive diagnosis of partial amaurosis due to a post‐retinal lesion. CT scan demonstrated a large sessile extra axial mass along the right parietal bone and thickening of the adjacent bone. Cerebrospinal fluid was not collected because high intracranial pressure represented a risk for brain herniation. A right rostrotentorial craniectomy was performed to remove the tumor. Ten days after surgery, vision was improved, neurological examination was normal and normal behavior was restored. Ten months after surgery, ophthalmological examination showed no visual deficit and CT scan did not reveal any sign of recurrence. Conclusion Advanced imaging techniques allow veterinarians to detect early cerebral diseases and to provide specific treatment when it is possible. In cases of feline amaurosis due to intracranial meningioma, the vital prognosis is good while the visual prognosis is more uncertain, but recovery of normal vision and normal behavior is possible as demonstrated in the present case.