Ocular anatomy and correlation with histopathologic findings in two common octopuses (Octopus vulgaris) and one giant Pacific octopus (Enteroctopus dofleini) diagnosed with inflammatory phakitis and retinitis.

PURPOSE: Review octopus ocular anatomy and describe the histopathologic findings in three octopuses diagnosed with phakitis and retinitis. ANIMALS: Two common octopuses (Octopus vulgaris) and one giant Pacific octopus (Enteroctopus dofleini) with a history of ophthalmic disease. METHODS: A literature search was performed for the ocular anatomy section. Both eyes from all three octopuses, and two control eyes, were submitted for histopathologic evaluation. Hematoxylin and eosin stain was used for standard histopathologic evaluation; GMS stain was used to screen for fungi, gram stain for bacteria; and Fite's acid fast stain for acid fast bacteria. RESULTS: Anatomically, the anterior chamber of the octopus has direct contact with ambient water due to an opening in the dorsal aspect of a pseudocornea. The octopus lens is divided into anterior and posterior segments. The anterior half is exposed to the environment through the opening into the anterior chamber. Neither part of the lens has a lens capsule. The retina is everted, unlike the inverted vertebrate retina, and consists of just two layers. Histopathology revealed inflammatory phakitis and retinitis of varying severity in all six eyes of the study animals. No intraocular infectious organisms were recognized but one common octopus eye had clusters of coccidian parasites, identified as Aggregata sp., in extraocular tissues and blood vessels. CONCLUSION: We describe inflammatory phakitis and retinitis in two species of octopuses. The underlying cause for the severe intraocular response may be direct intraocular infection, water quality, an ocular manifestation of a systemic disease, or natural senescence.

Feline Infectious Peritonitis: Immunohistochemical Features of Ocular Inflammation and the Distribution of Viral Antigens in Structures of the Eye.

Feline infectious peritonitis (FIP) is a serious, widely distributed systemic disease caused by feline coronavirus (FCoV), in which ocular disease is common. However, questions remain about the patterns of ocular inflammation and the distribution of viral antigen in the eyes of cats with FIP. This study characterized the ocular lesions of FIP including the expression of glial fibrillary acidic protein and proliferating cell nuclear antigen by Müller cells in the retina in cases of FIP and to what extent macrophages are involved in ocular inflammation in FIP. Immunohistochemistry for FCoV, CD3, CD79a, glial fibrillary acidic protein, calprotectin, and proliferating cell nuclear antigen was performed on paraffin sections from 15 naturally occurring cases of FIP and from controls. Glial fibrillary acidic protein expression was increased in the retina in cases of FIP. Müller cell proliferation was present within lesions of retinal detachment. Macrophages were present in FIP-associated ocular lesions, but they were the most numerous inflammatory cells only within granulomas (2/15 cats, 13%). In cases of severe inflammation of the ciliary body with damage to blood vessel walls and ciliary epithelium (3/15, 20%), some macrophages expressed FCoV antigens, and immunolabeling for calprotectin on consecutive sections suggested that these FCoV-positive macrophages were likely to be recently derived from blood. In cases of severe and massive inflammation of most ocular structures (4/15, 26%), B cells and plasma cells predominated over T cells and macrophages. These results indicate that gliosis can be present in FIP-affected retinas and suggest that breakdown of the blood-ocular barrier can allow FCoV-bearing macrophages to access the eye.

Evaluation of adverse effects in tamoxifen exposed healthy female dogs.

BACKGROUND: Mammary tumors are among the most frequent neoplasms in female dogs, but the strategies employed in animal treatment are limited. In human medicine, hormone manipulation is used in cancer therapy. Tamoxifen citrate is a selective inhibitor of oestrogen receptors and exerts a potent anti-oestrogen effect on the mammary gland. The aim of this study was to evaluate the adverse effects when exposing healthy female dogs to tamoxifen. METHODS: Tamoxifen was administered for 120 days at a dose of 0.5 or 0.8 mg/kg/day to either intact or spayed female dogs. The effects were assessed through clinical examination, haematology, serum biochemistry, ophthalmology and bone marrow aspirate examination. Ovariohysterectomy was performed and the uterus examined by histopathology. RESULTS: Vulva oedema and purulent vaginal discharge developed with 10 days of tamoxifen exposure in all groups. Pyometra was diagnosed after around 90 days of exposure in intact females with frequencies increasing during the following 30 days of exposure. Up to 50% of dogs within the groups developed retinitis but none of the dogs had signs of reduced visual acuity. The prevalence of retinitis in each group was similar after 120 days of exposure. Haematological, biochemical and bone marrow changes were not observed. Due to the high risk of developing pyometra after prolonged exposure to tamoxifen, only spayed animals should be given this medication. CONCLUSIONS: A dose of 0.8 mg tamoxifen/kg body weight/day is recommended when treating tamoxifen-responsive canine mammary tumors. Due to the high risk of developing pyometra, ovariohysterectomy is recommended.

Viral encephalopathy and retinopathy of Dicentrarchus labrax and Sparus aurata farmed in Tunisia.

Viruses belonging to the Nodaviridae family cause disease worldwide among a large number of species of marine fish, and have been described in all continents. In the present study, a total of 69 farmed Tunisian sea bass (Dicentrarchus labrax) and 24 sea bream (Sparus aurata) samples were tested monthly for the detection of betanodavirus. The virus was identified in both species using indirect immunofluorescence assays (IFAT) and RT-PCR. In addition sequence analysis of part of the coat protein gene indicated that both species were infected by highly related, but distinct, strains belonging to the RGNNV genotype. The sequence of the coat protein gene of several strains was identical but up to 9 different sequences were detected in a single farm. In addition, viral sequences obtained from fish that were held at lower temperature (<20 degrees C) were distinct from the rest of the sequences.

Antibody-mediated retinopathies in canine patients: mechanism, diagnosis, and treatment modalities.

Antibody-mediated retinopathies may be widely present among the canine population. Early diagnosis and appropriate treatment are essential for visual preservation and reversal of blindness in these patients. The principal purpose of this review is to describe the mechanistic basis, clinical signs, diagnostic methods, and treatment options for retinal diseases causing sudden onset of blindness with absence of typical signs of intraocular inflammation or retinal degeneration-sudden acquired retinal degeneration syndrome and immune-mediated retinitis.

Halicephalobus gingivalis (H. deletrix) infection in two horses in southern California.

Two horses, a 16-year-old male Holsteiner and a 5-year-old male miniature horse, were diagnosed with halicephalobiasis at the California Veterinary Diagnostic Laboratory System, San Bernardino Branch, in April and June of 1998. Over a period of 4 weeks, the Holsteiner horse developed renal dysfunction, blepharospasm, and blindness in the right eye. A 15-cm-diameter mass was detected on ultrasound examination in the right kidney. Terminally, the animal developed seizures and was euthanized. The miniature horse had a 6-week-long illness characterized by testicular enlargement and uveitis. This animal developed ataxia and died. Necropsy examination revealed bilateral enlargement of the kidneys in both horses, petechial hemorrhages of the optic nerve (Holsteiner), and a diffusely firm and enlarged left testicle (miniature horse). Microscopic evaluation of tissues revealed granulomatous nephritis, optic neuritis, retinitis, and encephalitis in both horses and orchitis in only the miniature horse with intralesional rhabditiform nematodes. Halicephalobus gingivalis was found in the urine sediment of both animals and in semen of the Holsteiner horse.

Transmission of viral encephalopathy and retinopathy (VER) to yolk-sac larvae of the Atlantic halibut Hippoglossus hippoglossus: occurrence of nodavirus in various organs and a possible route of infection.

The susceptibility of the Atlantic halibut Hippoglossus hippoglossus yolk-sac larvae to viral encephalopathy and retinopathy (VER) was investigated by waterborne challenge experiments with nodavirus. Transfer of VER was indicated by several lines of evidence. A significantly higher cumulative mortality was observed after challenge with virus compared to mock challenge, and increasing doses of virus resulted in shorter incubation periods. When the challenge was performed on the day after hatching, the time from inoculation to the time when 50% of the larvae were dead (LT50) ranged from 26 to 32 d. Postponement of challenge for 13 d reduced the LT50 to 14 d, indicating that the susceptibility of the larvae to the present nodavirus strain was low during the first 2 wk after hatching. The progression of the infection was monitored by sequential immunohistochemistry and electron microscopy. On Day 18 after hatching the initial signs of infection were observed as a prominent focus of immunolabelling in the caudal part of the brain stem. In the same larvae immunolabelled single cell lesions were observed in the stratified epithelium of the cranial part of the intestine. The portal of entry into the larvae may thus have been the intestinal epithelium, while the route of infection to the CNS may have been axonal transport to the brain stem through cranial nerves such as the vagus nerves. Later in the infection, lesions became more severe and widespread and were also found throughout the brain and spinal cord and in the retina, cranial ganglia, intestine, liver, olfactory epithelium, yolk-sac epithelium, gills and pectoral fins. The mortality in all virus-challenged groups was 100%. This study thus demonstrates that the present nodavirus strain is able to replicate and cause VER in Atlantic halibut yolk-sac larvae at temperatures as low as 6 degrees C.

Retinal immunopathology in horses with uveitis.

BACKGROUND: Equine uveitis is a spontaneous disorder of horses that can serve as a model for the study of human uveitis. Although the initial presentation is that of an anterior uveitis, retinal involvement has been noted in some cases. We report here the immunohistopathology of retinas from horses with uveitis. METHODS: Sections of eyes recovered from horses with naturally occurring uveitis and from Shetland ponies with experimental leptospira-induced uveitis were stained by hematoxylin and eosin for histopathological evaluation. Immunohistochemistry was used to evaluate retinas for MHC Class II antigen expression and infiltration of T and B lymphocytes. RESULTS: Histopathological abnormalities in retinas from horses with uveitis ranged from minimal to total loss of retinal tissue. MHC Class II antigen-positive round and dendritiform cells were seen in these retinas, but were not seen in retinas from horses without uveitis. There was no significant reactivity noted in the retinal pigment epithelial cells or Muller cells. Numbers of MHC Class II antigen-expressing cells and T lymphocytes correlated with the extent of retinal histopathology. B lymphocytes were seen primarily in retinas from horses that were seroreactive for Leptospira interrogans serovar pomona. Retinas from ponies with experimental uveitis had changes similar to those from horses with spontaneous uveitis. CONCLUSIONS: These results suggest that retinal pathology may be a primary immunological event in equine uveitis, provide evidence that leptospira-associated uveitis may be a distinct subset of equine uveitides, underscore the relevance of the study of equine uveitis to human uveitis, and support the plausibility of a post-infectious immunopathogenesis of some naturally occurring uveitides in both humans and horses.

[Pathology of the retina]. / Pathologie der Netzhaut.

Degenerations (atrophies) of the retina are divided into primary (hereditary) and secondary forms including glaucomatous retinopathy of retinal atrophy. The pathogenesis of inflammation of the retina is considered. This condition generally appears in association with inflammation of the choroid (chorioretinitis), but can also occur as an isolated inflammatory condition during infectious disease (distemper). The functional conditions for retinal detachment, its rhegmatogenous and nonrhegmatogenous types, as well as the consequences of retinal detachment are described. Comparison of the pathology of retinal tumors shows that retinoblastoma is not known in animals. However, neuroepithelial tumors like the so-called acquired adenoma and adenocarcinoma of the mature ciliary epithelium as well as the rare congenital tumors of the embryonic neuroepithelium i.e. the medulloepithelioma and the ganglioneuroma are seen in animals. Finally, the rare but not unusual parasitic retinopathies are mentioned.

Microscopic lesions of spontaneous ocular blastomycosis in dogs.

Ocular tissues from 13 dogs with naturally-occurring blastomycosis were examined histologically. Choroiditis and separation of the sensory retina from its epithelium were the most prominent lesions, although all three coats of the eye were always involved. Severe panophthalmitis was associated with a marked exudative reaction within the ocular tissues. Whereas inflammation of the anterior ocular tissues was often intense, it was rarely associated with the presence of B. dermatitidis. Sequelae to the ocular inflammation included cataract, synechiae, rubeosis iridis, and closure of the drainage angle. The last of these resulted in glaucoma and resulting degeneration of the optic nerve.

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.

Sulfadiazine-induced allergy in six Doberman pinschers.

Treatment with sulfadiazine-trimethoprim caused serious, but reversible, allergic drug reactions in 6 Doberman Pinschers 10 to 21 days after the first drug exposure and/or within 1 hour to 10 days after reexposure. Nonseptic polyarthritis was found in all dogs. Glomerulonephropathy, focal retinitis, polymyositis, skin rash, fever, anemia, leukopenia, and thrombocytopenia were found in some dogs. These clinical abnormalities were typical of an immune-mediated vasculitis and mimicked other immune-mediated disorders. In a drug challenge study, 1 dog was given sulfadiazine and trimethoprim separately. Administration of trimethoprim alone did not result in any abnormalities; however, exposure to sulfadiazine caused recurrence of the polyarthritis, glomerulonephropathy, and focal retinitis within 5 days, suggesting that sulfadiazine likely was the offending agent in all cases. In addition, during the sulfadiazine reexposure, marked complement activation was documented at the time clinical signs were apparent, supporting the suggestion that sulfadiazine caused an immune complex disease (type-III hypersensitivity reaction). Since all dogs were of the same breed, a genetic predisposition of some Doberman Pinschers to react adversely to sulfadiazine was suspected.

Metastatic protothecal retinitis in a dog. Electron microscopic observations.

Disseminated protothecosis, due to Prototheca wickerhamii, was present in a two-year-old female dog with a nine-month history of hemorrhagic colitis and diarrhea. Shortly thereafter, the dog developed "acute blindness" of the left eye. Euthanasia was done after medical therapy failed to control the disease. Histologically, the eye had multiple microabscesses and necrotic foci containing myriad protothecal organisms under the detached retina. Numerous organisms also were present in the mucosa and walls of the colon. The identification of P. wickerhamii was confirmed by the histologic appearance and immunofluorescent studies. The ultrastructural features of P. wickerhamii also were studied.

Fluorescein angiography of the normal and diseased ocular fundi of the laboratory dog.

A method was determined for fluorescein angiography of the ocular fundus of the laboratory Beagle, using a portable fluorescein fundus camera. A 10% solution of sodium fluorescein was injected by a syringe pump in the right cephalic vein of each dog. Acepromazine maleate (0.5 mg/kg, IV) with ketamine hydrochloride (10 mg/kg, IM) provided chemical restraint. Of the 10-, 25-, and 50-mg/kg dosages of fluorescein, 25 mg/kg permitted satisfactory fluorescence of the choroidal and retinal vasculature and the recirculation phase. High-speed color film permitted good quality photography of the tapetal and nontapetal retinal vessels. Reduced retinal blood vessel and pigment epithelium permeability was demonstrated by fluorescein angiography in dogs with chorioretinitis associated with systemic blastomycosis, retinitis associated with distemper, serous retinal detachment, and preretinal hemorrhage.

Pathogenetic studies of infection of the bovine fetus with bovine viral diarrhea virus. II. Ocular lesions.

Twenty-three susceptible pregnant heifers were inoculated with bovine viral diarrhea virus at 150 +/- 1 days of gestation. Seven additional heifers were inoculated between 65 and 115 days of gestation. Acute ocular lesions were seen in fetuses taken 17-21 days after inoculation of the dams at 150 days. By the fourth week, the acute lesions were beginning to resolve, and in newborn animals focal to total retinal atrophy was seen. The acute lesions were characterized by a mild to moderate retinitis that resulted in various degrees of destruction of the different layers, mononuclear cuffing of inner retinal vessels, proliferation of pigment epithelium, and choroiditis. Residually there was an absence of cellular elements in the atrophied areas of the retina, frequently a loss of layering and various numbers of pigment-containing cells. Moderately severe acute inflammation was seen in the retina of the fetus taken at 22 days after inoculation of its dam at 95 days. Ocular lesions did not occur in the other fetuses taken from heifers inoculated at earlier stages of gestation.