Neuronal ceroid lipofuscinosis in Merino sheep

OBJECTIVE: To characterise neuronal ceroid lipofuscinosis (NCL) in Merino sheep. DESIGN: A prospective clinical, pathological, biochemical and genetic study. PROCEDURE: NCL cases were studied from a medium-wool Merino flock, the stud of origin of its replacement rams, and an experimental flock established at the University of Sydney. RESULTS: Behavioural changes and visual impairment were first detected at 7 to 12 months of age and progressed, with associated motor disturbances and at later stages seizures, to premature death by 27 months of age. At necropsy there was severe cerebrocortical atrophy associated with neuronal loss, astrocytosis and the presence in neurons of eosinophilic intracytoplasmic storage bodies with the characteristics of a lipopigment. In the retina there was progressive loss of photoreceptor cells. Storage bodies isolated from fresh brain, liver and pancreas formed electron-dense aggregates and coarse multilamellar and fine fingerprint profiles ultrastructurally, and consisted mainly of the hydrophobic protein, subunit c of mitochondrial ATP synthase. A homozygosity mapping approach localised the gene causing the disease in Merino sheep to the chromosomal region (OAR7q13-15) associated with NCL in South Hampshire sheep. CONCLUSION: NCL in Merino sheep is a subunit c-storing disease, clinically and pathologically similar to NCL in South Hampshire sheep. We propose that the disease in both breeds represents mutation at the same gene locus in chromosomal region OAR7q13-15.     

Assessment of retinal function and characterization of lysosomal storage body accumulation in the retinas and brains of Tibetan Terriers with ceroid-lipofuscinosis

OBJECTIVE: To characterize lysosomal storage body accumulation in the retina and brain of Tibetan Terriers with ceroid-lipofuscinosis and determine whether the disease in these dogs is accompanied by impaired retinal function and retinal degeneration. ANIMALS: Three 7- to 10-year-old Tibetan Terriers with ceroid-lipofuscinosis and 1 healthy 5-year-old Tibetan Terrier. PROCEDURE: Owners completed a questionnaire to identify behavioral and physical signs indicative of ceroid-lipofuscinosis. Neurologic, behavioral, and ophthalmologic evaluations, including full-field electroretinograms, were performed on each dog. Fluorescence, light, and electron microscopy were performed on specimens of retina, cerebral cortex, and cerebellum of all dogs postmortem. RESULTS: Behavioral assessments of the affected dogs revealed moderate visual impairment in low-light conditions but good vision in bright light. On funduscopic evaluation of these dogs, abnormalities detected ranged from none to signs of moderately advanced retinal degeneration. Compared with findings in the control dog, electroretinography revealed depressed rod cell function with some impairment of cone cell function in the affected dogs. Morphologically, disease-specific storage bodies were detected in retinal Müller cells and neurons, particularly in ganglion cells, and in cells of the cerebral cortex and cerebellum in affected dogs. Substantial photoreceptor cell loss and disruption of photoreceptor outer segment morphology appeared to develop late in the disease. IMPLICATIONS FOR HUMAN MEDICINE: The similarities between ceroid-lipofuscinosis in Tibetan Terriers and some forms of ceroid-lipofuscinosis in humans suggest that the canine disease may have a genetic and biochemical basis similar to that of one of the ceroid-lipofuscinosis disorders in humans.     

Pathology and Neurotoxicity in Dogs after Repeat Dose Exposure to a Serotonin 5-HT1B Inhibitor

AZD3783, a cationic amphiphilic drug and a potent inhibitor of the 5-hydroxytryptamine (5-HT_1B) receptor, was explored as a potential treatment for depression. To support clinical trials, repeat dose toxicity studies in rats and dogs were conducted. Here we report toxicity findings in dogs after dosing from 1 to 3 months. In the 1-month study, there were minimal neuronal vacuolation in the brain, a marked increase in liver enzymes accompanied by hepatocellular degeneration/necrosis and phospholipidosis (PLD), and PLD/cholecystitis in the gallbladder of animals dosed at 47 mg/kg/day. In the 3-month study, neurotoxicity resulted in euthanasia of one animal dosed at 30 mg/kg/day after 86 days. Extensive pathologic changes were seen in all animals in retina epithelium (inclusion bodies), brain (neuronal vacuolation, degeneration, or necrosis and nerve fiber degeneration), spinal ganglia (vacuolation, degeneration, or necrosis), as well as sciatic and optic nerves (degeneration). Pigment-laden macrophages were observed in the lung, kidney, liver, gallbladder, bone marrow, gastrointestinal tract, and lymphoid tissues. Also seen were vitrel and retinal hemorrhage in the eyes. A brain concentration and pathology study showed that the concentration of AZD3783 in the brain was approximately 4 times higher than in the plasma after 4 weeks of dosing, however, they were similar in all regions examined, and did not correlate with areas with pathologic findings. Our findings with AZD3783 in dogs have not been reported previously with other CNS compounds that effect through serotonergic pharmacology.     

Electroretinography recordings using a light emitting diode active corneal electrode in healthy beagle dogs

Electroretinography (ERG) is a well-established diagnostic procedure for objectively evaluating retinal function. In this study, ERG in beagle dogs, which are a popular experimental animal, was performed to determine the normal range of ERG variables and assess differences between the left and right eyes. ERG findings including rod, combined rod-cone, single-flash cone, and 30-Hz flicker responses were recorded with an LED-electrode in 43 sedated beagle dogs. The subjects were divided into young (< 1 year old), adult (1~5 years old), and senile animals (≥ 6 years old). Normal ERG ranges were obtained. Significant differences in b-wave amplitude along with b/a ratio of the combined rod-cone response were found between the young and adult animals as well as young and senile dogs. No significant differences were observed between the left and right eyes. ERG variables in beagle dogs differed by age due to age-related retinal changes. Thus, we propose that normal ERG ranges should be determined according to age in each clinic and laboratory using its own equipment because each institution usually has different systems or protocols for ERG testing.     

Loss of glutamine synthetase immunoreactivity from the retina in canine primary glaucoma

Purpose Changes in retinal glutamate distribution occur in primary glaucoma (PG) in dogs. Although the redistribution resembles that induced by ischemia, decreases in glutamine synthetase (GS) activity may also induce a similar glutamate redistribution. We examined the distribution of GS, glutamate, and glial fibrillary acidic protein (GFAP), a marker for reactive glia, in PG retinas by immunohistochemistry to determine whether decreases in GS and formation of reactive glia are associated with glutamate redistribution and neuronal damage. Animals Sections from 14 control dog eyes and 22 eyes from dogs with PG. Methods Sections from 14 control and 22 glaucomatous globes were immunohistochemically stained for GS, glial fibrillary acidic protein or glutamate. Results In semiquantitative immunogold studies, decreases in GS staining density were strongly correlated with glutamate redistribution and neuronal damage. In less quantitative immunoperoxidase staining of acute (≤ 5 days after clinical signs) and chronic PG retinas, GS immunoreactivity was decreased in focal regions of some acute PG retinas, and there were widespread decreases in chronic PG retinas. GFAP immunoreactivity was increased in Müller cells primarily in severely damaged regions of chronic PG retinas. Conclusions Decreases in GS immunoreactivity were associated with glutamate redistribution. These decreases in GS occurred even in mildly damaged regions of retina before retinal thinning. Reactive Müller cells were seen primarily in chronic PG in severely damaged regions. Decreases in GS may potentiate ischemia‐induced early glutamate redistribution and neuronal damage in canine PG.     

The effects of cataract stage, lens-induced uveitis and cataract removal on ERG in dogs with cataract

OBJECTIVE: The purpose of this study was to determine the effects of cataract stage, lens-induced uveitis and cataract removal on the electroretinogram (ERG) of dogs with cataract. ANIMALS STUDIED: Fifty-seven dogs diagnosed with unilateral or bilateral cataract whose ERG was recorded at Rakuno Gakuen University Teaching Animal Hospital from 2001 to 2004. PROCEDURES: Four responses were recorded during the ERG: rod ERG, standard combined ERG, single-flash cone ERG and 30-Hz flicker ERG. Cataracts were divided into four stages: incipient, immature, mature and hypermature, and with or without lens induced uveitis (LIU). Noncataractous eyes of dogs with unilateral cataract were used as the control. We compared ERG amplitude, implicit time, and the b- to a-wave amplitude ratio of cataractous vs. noncataractous eyes, preoperative vs. postoperative cataractous eyes, and cataractous eyes with and without LIU. RESULTS: No significant difference was found in ERG amplitude between incipient, immature and hypermature cataractous eyes, while in mature cataractous eyes decreased amplitude was confirmed in all responses compared with control eyes. However, no significant difference in b/a ratio was found at any stage of cataract. In postoperative eyes, increased amplitude was recorded in all responses compared to preoperative values. In eyes with LIU a decreased amplitude in the rod ERG and b-wave of standard combined ERG was recorded and, furthermore, a significant decline was confirmed in b/a ratio. CONCLUSION: ERG values were influenced by cataract stage and LIU. LIU was associated with a reduction in the b/a ratio.     

A review of electroretinography waveforms and models and their application in the dog

Electroretinography (ERG) is a commonly used technique to study retinal function in both clinical and research ophthalmology. ERG responses can be divided into component waveforms, analysis of which can provide insight into the health and function of different types and populations of retinal cells. In dogs, ERG has been used in the characterization of normal retinal function, as well as the diagnosis of retinal diseases and measuring effects of treatment. While many components of the recorded waveform are similar across species, dogs have several notable features that should be differentiated from the responses in humans and other animals. Additionally, modifications of standard protocols, such as changing flash frequency and stimulus color, and mathematical models of ERG waveforms have been used in studies of human retinal function but have been infrequently applied to visual electrophysiology in dogs. This review provides an overview of the origins and applications of ERG in addition to potential avenues for further characterization of responses in the dog.     

Psittacine beak and feather disease in three captive sulphur-crested cockatoos (Cacatua galerita) in Thailand

Three sulphur-crested cockatoos (Cacatua galerita) were diagnosed as psittacine beak and feather disease (PBFD). Histopathology of the feather pulp and follicles showed intracytoplasmic botryoid clusters or granular inclusion bodies in epithelial cells and macrophages. Electron microscopy revealed multiple cytoplasmic clusters of electron dense viral particles corresponding to the inclusions. PBFD virus (circovirus) DNA-specific product was detected from formalin-fixed paraffin-embedded feathers by nested polymerase chain reaction (PCR) method.     

Chronic ocular lesions associated with bi-directional microbeam radiation therapy in an experimental rat study for therapy of C6 and F98 gliomas

Objectives  To describe the chronic ocular lesions associated with microbeam radiation therapy (MRT) in an experimental rat study.
Procedures  MRT was administered bi-directionally with a skin entry dose of 350 Gy. During laterally directed irradiation, the beam entered the head on the right with the center of the beam array 3 mm posterior to the center of the right eye. During irradiation in anterior-posterior direction, the right eye was almost completely in the path of the beam array. Twelve months after MRT ophthalmic examinations were completed on 37 treated (MRT+) and 16 control (MRT–) rats. Electroretinography (ERG) was completed in two MRT+ and one MRT– rat. Histopathology was performed on eyes of 16 MRT+ and 9 MRT– rats, and retinal and choroidal thicknesses were measured.
Results  Biomicroscopic and indirect ophthalmoscopic examinations revealed fundus pallor and retinal vascular attenuation in 33 of 37 right and 2 of 37 left eyes of MRT+ rats. Cataracts were present in the right eyes of 12 of 37 MRT+ rats. ERG amplitudes were reduced in the eyes of MRT+ rats. Light microscopy revealed retinal lesions ranging in severity with loss of outer to inner retinal cell layers, in 16 of 16 right and of 8 of 16 left eyes MRT+ rats. The mean right retinal thickness of MRT+ rats was reduced.
Conclusions  Eyes within the field treated with MRT at a dose of 350 Gy develop retinal degeneration and occasionally, cataract.     

Neuronal ceroid-lipofuscinosis in longhaired Chihuahuas: clinical, pathologic, and MRI findings

Neuronal ceroid-lipofuscinosis (NCL) is a rare group of inherited neurodegenerative lysosomal storage diseases characterized histopathologically by the abnormal accumulation of ceroid- or lipofuscin-like lipopigments in neurons and other cells throughout the body. The present article describes the clinical, pathologic, and magnetic resonance imaging (MRI) findings of the NCL in three longhaired Chihuahuas between 16 mo and 24 mo of age. Clinical signs, including visual defects and behavioral abnormalities, started between 16 mo and 18 mo of age. Cranial MRI findings in all the dogs were characterized by diffuse severe dilation of the cerebral sulci, dilated fissures of diencephalons, midbrain, and cerebellum, and lateral ventricular enlargement, suggesting atrophy of the forebrain. As the most unusual feature, diffuse meningeal thickening was observed over the entire cerebrum, which was strongly enhanced on contrast T1-weighted images. The dogs' conditions progressed until they each died subsequent to continued neurologic deterioration between 23 mo and 24 mo of age. Histopathologically, there was severe to moderate neuronal cell loss with diffuse astrogliosis throughout the brain. The remaining neuronal cells showed intracytoplasmic accumulation of pale to slightly yellow lipopigments mimicking ceroid or lipofuscin. The thickened meninges consisted of the proliferation of connective tissues with abundant collagen fibers and mild infiltration of inflammatory cells suggesting neuroimmune hyperactivity. Although the etiology of this neuroimmune hyperactivity is not currently known, MRI findings such as meningeal thickening may be a useful diagnostic marker of this variant form of canine NCL.     

GM2 Gangliosidosis in Shiba Inu Dogs with an In‐Frame Deletion in HEXB

Consistent with a tentative diagnosis of neuronal ceroid lipofuscinosis (NCL), autofluorescent cytoplasmic storage bodies were found in neurons from the brains of 2 related Shiba Inu dogs with a young‐adult onset, progressive neurodegenerative disease. Unexpectedly, no potentially causal NCL‐related variants were identified in a whole‐genome sequence generated with DNA from 1 of the affected dogs. Instead, the whole‐genome sequence contained a homozygous 3 base pair (bp) deletion in a coding region of HEXB. The other affected dog also was homozygous for this 3‐bp deletion. Mutations in the human HEXB ortholog cause Sandhoff disease, a type of GM2 gangliosidosis. Thin‐layer chromatography confirmed that GM2 ganglioside had accumulated in an affected Shiba Inu brain. Enzymatic analysis confirmed that the GM2 gangliosidosis resulted from a deficiency in the HEXB encoded protein and not from a deficiency in products from HEXA or GM2A, which are known alternative causes of GM2 gangliosidosis. We conclude that the homozygous 3‐bp deletion in HEXB is the likely cause of the Shiba Inu neurodegenerative disease and that whole‐genome sequencing can lead to the early identification of potentially disease‐causing DNA variants thereby refocusing subsequent diagnostic analyses toward confirming or refuting candidate variant causality.     

Neuronal ceroid lipofuscinosis in a Vietnamese pot-bellied pig (Sus scrofa)

The neuronal ceroid ipofuscinoses (NCL) are a group of heritable, neurodegenerative, storage diseases, typically with an autosomal recessive mode of inheritance. Cytoplasmic accumulation of storage material in cells of the nervous system and, variably in other tissues, characterizes NCL. NCL has been reported in many animal species, but to the authors' knowledge, this is the first report of the disease in a pig. Blindness and seizures are common clinical signs of disease, neither of which was a feature in this pig. The lesions were restricted to the central nervous system, which was diffusely affected, with the most severe lesions in the hippocampus, cerebral cortex, and cerebellum. The histologic lesions included neuronal loss and gliosis, which contributed to mild cerebrocortical and cerebellar atrophy and accumulation of autofluorescent storage material in neurons and glial cells. The storage material had morphologic, histologic, and ultrastructural properties typical of NCL.     

Treatment of serous retinal detachments associated with optic disk pits in dogs

Serous retinal detachment, associated with optic disk pit, was diagnosed in 28 eyes of 24 dogs. Xenon arc photocoagulation was used in treatment of the detachment. Of 24 dogs, 21 were Collies. In 23 eyes, retinal detachments affected temporal and/or inferior portions of the retina. In 5 eyes, detachments were predominantly superior and/or nasal. A single photocoagulation treatment resulted in reattachments in 25 eyes. Of the 3 remaining detachments, 2 eyes improved with additional photocoagulation, and 1 eye, which was not treated further, had a complete retinal detachment.     

Acute blindness in dogs: Sudden acquired retinal degeneration syndrome versus neurological disease (140 cases, 2000–2006)

Objective  To evaluate dogs with amaurosis and compare signalment, history, ophthalmic examination and neurologic abnormalities between dogs diagnosed with sudden acquired retinal degeneration syndrome (SARDS) versus neurological disease (ND). Animals Studied-140 dogs with acute vision loss and ocular abnormalities insufficient to account for visual deficits. An electroretinogram (ERG) was performed on each dog.
Procedures  Medical records were reviewed and information was collected for all dogs meeting the inclusion criteria. Dogs diagnosed with SARDS were compared to those with ND based on signalment, duration of clinical signs, past medical problems, clinicopathologic findings, and ophthalmic and physical examination abnormalities.
Results  120 dogs were diagnosed with SARDS and 20 dogs with ND based on ERG results. Mixed-breed dogs were most commonly diagnosed with SARDS as well as ND. Pure breed dogs frequently diagnosed with SARDS included the Miniature Schnauzer and Dachshund. Dogs with SARDS did not differ significantly from those with ND based on age or sex distribution. Cushing's-like symptoms were reported more frequently in SARDS dogs as well as conjunctival hyperemia and retinal vascular attenuation. Papilledema and asymmetric visual deficits were observed more frequently in dogs with ND. Dogs with ND were no more likely than SARDS dogs to have additional neurological deficits.
Conclusions  Appreciable overlap of clinical signs exists between dogs with SARDS and dogs with ND resulting in acute vision loss. As a significant portion of dogs (14%) in the present study were diagnosed with ND, an ERG to rule out ND is indicated in dogs with amaurosis.     

Morphometric analysis of the retina from horses infected with the Borna disease virus

Borna disease (BD) is a fatal disorder of horses, often characterized by blindness. Although degeneration of retinal neurons has been demonstrated in a rat model, there are controversial data concerning whether a similar degeneration occurs in the retina of infected horses. To investigate whether BD may cause degeneration of photoreceptors and possibly of other neuronal cells at least at later stages of the disease, we performed a detailed quantitative morphologic study of retinal tissue from Borna-diseased horses. BD was diagnosed by detection of pathognomonic Joest-Degen inclusion bodies in the postmortem brains. Paraffin sections of paraformaldehyde-fixed retinae were used for histologic and immunohistochemical stainings. Numbers of neurons and Müller glial cells were counted, and neuron-to-Müller cell ratios were calculated. Among tissues from 9 horses with BD, we found retinae with strongly altered histologic appearance as well as retinae with only minor changes. The neuron-to-Müller cell ratio for the whole retina was significantly smaller in diseased animals (8.5 +/- 0.4; P < .01) as compared with controls (17.6 +/- 0.8). It can be concluded that BD in horses causes alterations of the retinal histology of a variable degree. The study provides new data about the pathogenesis of BD concerning the retina and demonstrates that a loss of photoreceptors may explain the observed blindness in infected horses.     

Electroretinography using contact lens electrode with built-in light source in dogs

Electroretinography (ERG) is an effective method for the diagnosis of retinal disease. In the dog, dependable ERG recording is difficult without the use of an expensive device like a Ganzfeld full-field stimulator. The International Society for Clinical Electrophysiology of Vision has defined the standard flash stimulus condition (SF) and evaluation of the retina using the b/a ratio in humans. In dogs, evaluation using the b/a ratio has not been reported, whereas the intensity of SF has been defined. In this study, we performed a convenient ERG recording method using a contact lens electrode with a built-in light source (LED-electrode), and confirmed SF as reported previously. ERG recordings were performed on 15 healthy beagle dogs under sedation. We performed bilateral ERG at 12 different intensities after 30 min dark adaptation. After 10 min light adaptation, we recorded single flash cone and flicker cone response using the SF determined in this study. In this study, SF of 3.0 cd/m(2)/sec (6,000 cd/m(2), 0.5 msec) resulted in b/a=2. The intensity for rod response that recorded only the b-wave was 0.0096 cd/m(2)/sec (80 cd/m(2), 0.12 msec). We could achieve ERG for each response easily and smoothly under sedation, and without general anesthesia. Using an LED-electrode, we could perform more quantitative and reproducible ERG examinations than with traditional methods. We propose that the b/a ratio is the most useful parameter in ERG reporting for evaluating retinal function.     

Ocular and systemic manifestations after oral administration of a high dose of enrofloxacin in cats

OBJECTIVE: To characterize the effects of oral administration of a high dose of enrofloxacin to cats. ANIMALS: 24 (12 male and 12 female) young healthy cats. PROCEDURES: Cats were allocated on the basis of sex into 2 groups (4 males and 4 females/ group) from which 3 subgroups for 3 durations (3, 5, or 7 days) of enrofloxacin (50 mg/kg, PO, q 24 h) or control solution (1 mL of water, PO, q 24 h) administration that began on day -1 were created. Funduscopic examinations were performed daily. Electroretinography (ERG) was performed before and every 2 to 3 days after the start of oral administration. Four cats/study group were euthanized on days 3, 5, and 7, and eyes were collected for light and electron microscopic evaluations. RESULTS: Neurologic, funduscopic, and ERG abnormalities were evident only in cats administered enrofloxacin. Funduscopic changes (granular appearance or graying of the area centralis) were noticed on or before day 3 (after only 3 days of enrofloxacin administration), with subsequent similar changes along the visual streak. Vascular attenuation (between days 2 and 4) and generalized tapetal hyperreflectivity (between days 5 and 7) followed. Reduction in b-wave ERG amplitude preceded funduscopic changes. Morphologic changes in the photoreceptor layers correlated with duration of enrofloxacin administration, with generalized degenerative changes evident after 3 doses. CONCLUSIONS AND CLINICAL RELEVANCE: The study indicated that a high dose of enrofloxacin (50 mg/kg/d, PO) induced retinal and systemic changes. Enrofloxacin at 10 times the recommended dosage is acutely toxic to the outer retina of clinically normal cats.     

Homozygous PPT1 Splice Donor Mutation in a Cane Corso Dog With Neuronal Ceroid Lipofuscinosis

A 10‐month‐old spayed female Cane Corso dog was evaluated after a 2‐month history of progressive blindness, ataxia, and lethargy. Neurologic examination abnormalities indicated a multifocal lesion with primarily cerebral and cerebellar signs. Clinical worsening resulted in humane euthanasia. On necropsy, there was marked astrogliosis throughout white matter tracts of the cerebrum, most prominently in the corpus callosum. In the cerebral cortex and midbrain, most neurons contained large amounts of autofluorescent storage material in the perinuclear area of the cells. Cerebellar storage material was present in the Purkinje cells, granular cell layer, and perinuclear regions of neurons in the deep nuclei. Neuronal ceroid lipofuscinosis (NCL) was diagnosed. Whole genome sequencing identified a PPT1c.124 + 1G>A splice donor mutation. This nonreference assembly allele was homozygous in the affected dog, has not previously been reported in dbSNP, and was absent from the whole genome sequences of 45 control dogs and 31 unaffected Cane Corsos. Our findings indicate a novel mutation causing the CLN1 form of NCL in a previously unreported dog breed. A canine model for CLN1 disease could provide an opportunity for therapeutic advancement, benefiting both humans and dogs with this disorder.     

Evaluation of short-term increased intraocular pressure on flash- and pattern-generated electroretinograms of dogs

OBJECTIVE: To determine the electrodiagnostic and histologic response of short-term increases of intraocular pressure (IOP) on transient pattern electroretinograms (PERG) and flash electroretinograms (FERG) in the eyes of dogs. ANIMALS: 8 healthy mixed-breed dogs. PROCEDURE: Transient PERG and FERG waveforms were recorded from dogs (while anesthetized) as IOP was increased from baseline (7 to 19 mm Hg) to 90 mm Hg. One hundred mean PERG responses and a single FERG response were recorded at each step during 3 recording sessions. Globes of each dog were enucleated after euthanasia on posttreatment day 7 and evaluated by a pathologist. RESULTS: Increases in spatial frequency resulted in decreased amplitudes of N2 (second negative PERG peak). Increases in IOP resulted in decreases in all 3 PERG waveforms and the FERG waveform. All values began to return to baseline after short-term increases in IOP on day 0, and waveforms were not significantly different on posttreatment days 3 and 7 CONCLUSIONS: Data suggest that short-term increases in IOP affect PERG and FERG waveforms, and PERG waveforms are more sensitive to increases in IOP Differences were not detected between treated and control eyes on histologic examination. Further studies are necessary to determine at what IOP permanent damage to ganglion and photoreceptor cells will develop and whether PERG is a reliable clinical diagnostic technique for use in dogs to reveal retinal damage that is secondary to increased IOP prior to changes in waveforms generated by FERG in dogs.     

Multifocal retinitis in New Zealand sheep dogs

Thirty-nine percent of 1,448 working sheep dogs were affected with varying degrees of multifocal retinal disease on ophthalmoscopic examination. Lesions consisted of localized areas of hyperreflexia in the tapetal fundus, often associated with hyperpigmentation. Severely affected animals had widespread hyperreflexia with retinal vascular attenuation. Only 6% of 125 New Zealand dogs raised in urban environment were similarly affected. Both eyes of 70 dogs from New Zealand were examined histologically. Forty-seven of 70 dogs had ocular inflammatory disease. Ten other dogs had noninflammatory eye disease, and 13 dogs had normal eyes. Histologically, eyes with inflammatory disease were divided into three categories: Dogs 3 years of age or less with active inflammatory disease of the retina, uvea, and vitreous. Four dogs in this group had migrating nematode larvae identified morphologically as genus Toxocara. Diffuse retinitis and retinal atrophy in conjunction with localized retinal necrosis and choroidal fibrosis. Dogs in this category were severely, clinically affected. Chronic, low-grade retinitis with variable retinal atrophy. Most dogs in this category were over 3 years of age, and many were visually functional. The existence of a definable spectrum of morphological changes associated with inflammation, suggests that Toxocara sp. ocular larva migrans may be the cause of a highly prevalent, potentially blinding syndrome of working sheep dogs in New Zealand.