Nodavirus provokes subclinical encephalitis and retinochoroiditis in adult farmed Atlantic cod, Gadus morhua L.

Viral nervous necrosis (VNN) caused by beta-nodavirus affects many species of farmed marine fish, in particular juveniles. Apparently healthy, normally feeding, adult farmed Atlantic cod, Gadus morhua, were sampled in a farm 14 months after an outbreak of VNN with clinical signs. Following necropsy, brain and eye tissues were examined by histology, immunohistochemistry and polymerase chain reaction (PCR). Nodavirus-provoked cell death and inflammation was detected in eye and brain, particularly in the retina and cerebellum and differed from that previously described in Atlantic cod during clinical stages of VNN. Virus was detected both by PCR and immunohistochemistry. This is, to the best of our knowledge, the first description of pathological changes associated with chronic subclinical nodavirus infection in Atlantic cod. Our observations suggest that severe infection and pathological changes may go undetected if investigations are restricted to clinical examination and macroscopic evaluation at necropsy.

Bartonella vinsonii subspecies berkhoffi as a possible cause of anterior uveitis and choroiditis in a dog.

A 2-year old, neutered, female spaniel mixed breed was referred to the North Carolina State University Veterinary Teaching Hospital for evaluation of bilateral anterior uveitis. The dog was febrile and, in addition to anterior uveitis, multifocal hyporeflective lesions were present in the tapetal fundus of both eyes. The antibody titer for Bartonella vinsonii subspecies berkhoffi was positive (1 : 512). Aqueous paracentesis was performed for PCR in an attempt to detect B. vinsonii in the eye but was unsuccessful. The ocular manifestations of Bartonella infection in humans are currently expanding as more sensitive serologic and PCR techniques are being developed to identify Bartonella spp. In addition to optic neuritis and neuroretinitis, retinochoroidal lesions are one of the most common manifestations of B. henselae infection, and are frequently accompanied by vitreous or anterior segment inflammation. Diagnosis of a Bartonella infection in humans can be made on serology alone, in conjunction with ocular examination findings. The ultimate proof of B. vinsonii (berkhoffi) as a direct cause of ocular disease would be detection of the infectious agent in the eye. However, it is unknown at this time whether Bartonella causes ocular disease primarily, secondarily via an autoimmune reaction, or both. Due to the difficulties associated with culture of Bartonella spp. and the limitations of PCR, serology is currently the most useful tool for screening dogs for possible Bartonella spp. infection. In the case presented here, even though the PCR was negative, the clinical signs of anterior uveitis and choroiditis might reasonably be associated with B. vinsonii (berkhoffi) seroreactivity, which was repeatable on three separate occasions. Clinical improvement was also accompanied by a post-treatment decrease in B. vinsonii (berkhoffi) seroreactivity, potentially supporting resolution of Bartonella infection in this dog. This is the first reported case of a possible association between uveitis, choroiditis and Bartonella infection in the dog, without clinical manifestations of other organ or tissue involvement. Future studies based on PCR analysis of intraocular fluids may clarify the involvement of B. vinsonii (berkhoffi) in dogs with intraocular inflammatory disease. Furthermore, performing fluorescein angiography in dogs with elevated Bartonella titers may also prove useful in the identification and characterization of lesions.

Management of intraocular inflammatory disease.

The uvea of the eye is divided into the anterior uvea (iris and ciliary body) and posterior uvea (choroid). Clinical signs of anterior uveitis include conjunctival hyperemia, corneal edema, aqueous flare, miosis, and a decrease in intraocular pressure. Inflammation of the posterior uvea often involves the retina as well resulting in a chorioretinitis. Clinical signs of chorioretinitis may include multifocal lesions in tapetal or nontapetal fundus, retinal detachment, and a decrease in vision. The etiology of uveitis is complex and includes numerous infectious, neoplastic, immune-mediated, and other diseases. Treatment is directed at the underlying systemic disease, if present, as well as symptomatic treatment for the eye. The diagnostic and therapeutic approach to a patient with uveitis is discussed.

Effect of Newcastle disease virus on ocular and paraocular tissues in experimentally inoculated chickens.

The effects of a mesogenic strain of Newcastle disease virus on ocular and paraocular structures were studied in 10-to-12-week-old chickens inoculated conjunctivally, intraocularly, intracerebrally, or intravenously. Paraffin-embedded tissues were examined by light and fluorescent microscopy using conventional staining and immunohistochemistry. Lesions were most severe in intraocularly inoculated chickens, where a marked iridocyclochoroiditis was evident from 8-12 hours up to 21 days postinfection. Viral antigens were detected in the iris, ciliary body, Schlemm's canal, and occasionally the lens, choroid, and base of the pecten. Although optic neuritis and iridocyclochoroiditis were found in intracerebrally inoculated birds, no viral antigens were detected in the optic nerve.

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.

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.