Previously described in humans and domestic animals, retinal dysplasia has three clinical forms: focal/multifocal, geographic and total. A young orphan crab-eating fox (Cerdocyon thous) from wildlife, male, approximately 45 days old referred to the Wildlife Medicine and Ophthalmology Services of the “Governador Laudo Natel” Veterinary Hospital of the Universidade Estadual Paulista, Jaboticabal Campus, SP, Brazil, where it received primary outpatient care. The patient was in good general health condition, without hematological, biochemistry or serological alterations and no signs of visual impairment. Indirect binocular ophthalmoscopy showed retinal changes in the left eye, distributed over the tapetal area in the form of grayish folds and rosettes. In the affected areas, tapetal reflectivity was reduced. No other ophthalmic abnormalities were observed. This is the first report of retinal dysplasia in the crab-eating fox (Cerdocyon thous) from wildlife.

Objective-To determine the usefulness of retina samples for detection of disease-associated prion protein by use of a commercially available enzyme immunoassay (EIA) intended for rapid identification of sheep and cattle with transmissible spongiform encephalopathies (TSEs). Samples-Retina, brainstem at the level of the obex, and retropharyngeal lymph node samples obtained from 15 TSE-inoculated sheep (scrapie [n = 13] or transmissible mink encephalopathy passaged through a bovid [2]); retina and brainstem samples obtained from 11 TSE-inoculated cattle (transmissible mink encephalopathy passaged through a bovid [7] or classical BSE [4]); and negative control tissue samples obtained from 2 sheep and 2 cattle that were not inoculated with TSEs. Procedures-Tissue samples were homogenized and analyzed for detection of abnormally folded disease-associated prion protein with a commercially available EIA and 2 confirmatory assays (western blot analysis or immunohistochemical analysis). Results-Retina sample EIA results were in agreement with results of brainstem sample EIA or confirmatory assay results for negative control animals and TSE-inoculated animals with clinical signs of disease. However, TSE-inoculated animals with positive confirmatory assay results that did not have clinical signs of disease had negative retina sample EIA results. Retina sample EIA results were in agreement with brainstem sample immunohistochemical results for 4 TSE-inoculated sheep with negative retropharyngeal lymph node EIA results. Conclusions and Clinical Relevance-Results of this study suggested that retina samples may be useful for rapid EIA screening of animals with neurologic signs to detect TSEs.

Akabane virus (AKV) strain OBE-1 was inoculated IV into 17 pregnant sheep. Ten fetuses infected at 29 to 45 days of gestation and examined 29 to 30 days later had AKV antigen in the following groups of cells: neuroglial cells in the brain and spinal cord, ganglion cells in the cranial and abdominal ganglia, layer of ganglion cells in the retina, ganglion cells (Auerbach's plexus) in small intestine, hepatocytes, cells in the arterial wall of mesenteric membrane, and trophoblast cells in the placenta. Prior to detection of circulating virus-neutralizing antibody, immunoglobulin-containing cells were found initially at 59 days of gestation in the peripheral portion of white pulp tissue in the spleen. After that, numbers of immunoglobulin-containing cells gradually increased. These results indicated that AKV may have strong affinity for neuronal and ganglional cells in infected fetuses and immunoglobulin-containing cells might be considered the earliest immunologic response to AKV replication in the fetus.

Electroretinogram (ERG) and visual-evoked potential (VEP) recordings were taken from ten Suffolk-cross sheep. Stimuli for VEP were 1.5 flashes of white light/s; ERG stimuli were single flashes. The ERG measurements of the a and b wave latencies and a-to-b amplitude were measured between the lower eyelid and the vertex, with ground on the nuchal crest. The VEP after monocular stimulation were measured between the nuchal crest and the interorbital line, with ground on the vertex. Measurements consisted of the latencies to seven alternating positive and negative peaks P1, N1 P2, N2, P3, N3 and P4, and six amplitudes, P1-N1, N1-P2, P2-N2, N2-P3, P3-N3 and N3-P4. Average latencies for the a and b waves were 13.6 and 28.2 ms; the mean ab amplitude was 131.68 micromole. Average latencies for the seven VEP peaks were 35.0, 43.1, 52.8, 64.1, 74.5, 90.4 and 112.2 ms. Mean amplitudes ranged from 3.90 to 8.29 microV.

The lateral distribution and temporal changes in the eye standing potential of 15 dogs with normal eyes (as determined by use of an ophthalmoscope and electroretinography) were measured by use of noninvasive methods. The standing potential was converted to an alternating potential by controlled eye movement. The light peak occurred 6 minutes after a stimulus intensity increase of 4 log units. The ratios of the highest measured voltage after the light step divided by the voltage measured immediately before the light step ranged from 1.27 to 2.07 (mean 1.74 +/- SEM, 0.064). The responses typically decayed slowly after the light peak. The potential after the light peak did not return to prelight step values during the observation period. The field potential of the standing potential decreased nonlinearly in temporal direction from the outer canthus.

The vascular permeability of the ocular fundus, alterations in the coagulation system, and plasma concentrations of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were studied in dogs following intradermal inoculation with 5 x 10(5) TCID50 of Rickettsia rickettsii. Twenty-four to 48 hours after the onset of fever and rickettsemia, multifocal areas of retinal vasculitis were evident, which corresponded to areas of altered vascular permeability demonstrated by fluorescein angiography. The number and intensity of retinal vessels with sodium fluorescein leakage peaked during the second week after inoculation, and retinal vascular permeability remained altered during the third week of infection, well past the phase of clinical and clinicopathologic recovery. Development of retinal vasculitic foci was associated with thrombocytopenia, increased concentrations of circulating fibrinogen, and slight prolongation of activated partial thromboplastin time. Increased concentrations of fibrin/fibrinogen degradation products were detected in 4 of 9 dogs. Despite the degree of vascular endothelial damage evident on fluorescein angiographic and histologic studies in these dogs, plasma TXB2 and 6-keto-PGF1 alpha concentrations were not increased.

A transretinal method for recording the summed potentials generated by photoreceptors of the isolated canine retina in vitro is reported. Pieces from 10 retinas of 5 clinically and visually normal dogs were maintained in a recording chamber and superperfused with a modified cell culture medium. Sodium glutamate added to the medium eliminated electrical responses from retinal glia and allowed the summed receptor potentials to be recorded. The response to flashes of light consisted of a negative potential, which increased in amplitude in a graded manner and in complexity with increased stimulus intensity. The response was similar in waveform to that reported in other vertebrate species, using intracellular and extracellular techniques. This method of recording the mass transretinal receptor potentials in vitro will be of value for investigating abnormal photoreceptor functions in dogs in the early stages of inherited retinal degeneration.

The microanatomy of the donkey eye is important to understand because pathological disorders affecting them are relatively common. The current study aimed to document the cellular components of donkey's retinae using light and electron microscopic studies. Ten donkey retinae were dissected and processed for semi-thin sections and electron microscopic studies. The photoreceptor layer was made up of the outer and inner segments of rods and cones. The outer segments were filled with invaginations of cell membranes that form stacks of membranous disks. Shed discs of photoreceptor outer segments could be seen in the photoreceptor layer as well as near the Müller cells. The inner segments of cones were conical in shape, while those of rods were slim rod-shaped. Both were filled with long thin mitochondria and free ribosomes. Three rows of photoreceptor cell nuclei made up the outer nuclear layer. The rod nuclei had more electron-dense chromatin than those of the cones. There were two rows of cell nuclei in the inner nuclear layer that represent the following four cell classes: horizontal cells, bipolar cells, amacrine cells, and Müller cells. Bipolar cells constitute the bulk of the inner nuclear layer. They were elongated in shape and had thick branched dendrites. Amacrine cells were in the inner face of the INL. It could be observed within IPL and known as displaced amacrine cells. Muller glial cells were irregular elongated in shape with many cytoplasmic processes. They were distributed in the INL among the bipolar cells. Müller cells were observed in the inner plexiform layer, the ganglion cell layer, and the nerve fiber layer.  In conclusion, this study characterized the detailed cytological organization and ultrastructure of the healthy donkey retina. which maintains the fundamental laminar architecture characteristic of other mammalian retinas, and consists of 10 distinguishable layers. When compared to previously described retinal morphologies in domestic species, some distinctive characters were observed in donkey retinal cells.

Mitochondrial transcription factor A (Tfam) has been implicated in the pathogenesis of retinal dysplasia in miniature schnauzer dogs and it has been proposed that affected dogs have altered mitochondrial numbers, size, and morphology. To test these hypotheses the Tfam gene of affected and normal miniature schnauzer dogs with retinal dysplasia was sequenced and lymphocyte mitochondria were quantified, measured, and the morphology was compared in normal and affected dogs using transmission electron microscopy. For Tfam sequencing, retina, retinal pigment epithelium (RPE), and whole blood samples were collected. Total RNA was isolated from the retina and RPE and reverse transcribed to make cDNA. Genomic DNA was extracted from white blood cell pellets obtained from the whole blood samples. The Tfam coding sequence, 5' promoter region, intron1 and the 3' non-coding sequence of normal and affected dogs were amplified using polymerase chain reaction (PCR), cloned and sequenced. For electron microscopy, lymphocytes from affected and normal dogs were photographed and the mitochondria within each cross-section were identified, quantified, and the mitochondrial area (μm2) per lymphocyte cross-section was calculated. Lastly, using a masked technique, mitochondrial morphology was compared between the 2 groups. Sequencing of the miniature schnauzer Tfam gene revealed no functional sequence variation between affected and normal dogs. Lymphocyte and mitochondrial area, mitochondrial quantification, and morphology assessment also revealed no significant difference between the 2 groups. Further investigation into other candidate genes or factors causing retinal dysplasia in the miniature schnauzer is warranted.

In dogs, the retina develops during the postnatal period in a manner similar to that in other animals born with closed eyelids. Photoreceptor inner segments are initially observed as a cytoplasmic bulge protruding sclerad through the external limiting membrane. Outer segment formation begins when a centriole within the inner segment attaches to the distal inner segment cell membrane. A few round mitochondria are observed within the early inner segments. As maturation proceeds, the number of mitochondria within the inner segments increases and the mitochondria elongate, orienting parallel to the long axis of the inner segment.