Feline immunodeficiency virus (FIV) infection in the cat is a well-evaluated model of human immunodeficiency virus (HIV)-1 infection in man with both viruses associated with significant neuropathology. Although studies in both HIV and FIV infections have shown that virus enters the brain in the acute stages of disease, little is known of the mechanisms of viral entry. The dissection of this stage is fundamental to the development of therapies that may prevent or modulate central nervous system (CNS) infection. The present study was designed to characterize the early sequential neuropathological changes following infection with FIV(GL8), a strain known to enter the CNS in acute infection. Cats were infected either by the intraperitoneal (n = 13) or intravenous (n = 12) route with 2000 cat infectious units of virus. Histopathological assessments following intraperitoneal infections were at 4 (n = 2), 5 (n = 1), 8 (n = 3), 10 (n = 1), 16 (n = 1), 32 (n = 2), 52 (n = 2), and 104 (n = 1) weeks post infection whereas animals infected intravenously were examined (n = 3) at 1, 4, 10, and 23 weeks post infection. The most significant lesions following both routes of infection were lymphocyte-rich perivascular infiltrates within cerebral and cerebellar meninges, in choroid plexus and spinal cord dura mater and within epineurium of the sciatic nerve. In addition, following intravenous infection perivascular infiltrations were noted in parenchymal blood vessels primarily of cerebral white matter. Infiltrates were composed of CD79+ B cells and CD3+ T cells. The latter population contained a mixture of CD4+ and CD8+ cells. The severity of lesions increased in intensity in the 8-to 16-week period following infection and then began to wane. The evaluation of this large group of cats at multiple time points revealed pathology comparable with that of early stage HIV-1-associated encephalitis. Moreover, in contrast to previous FIV neuropathology studies, transient meningeal, choroid plexus, and parenchymal vascular pathology were consistent significant findings suggesting that, as in HIV-1 infection, blood-brain barrier and choroid plexus brain barrier integrity are both compromised in early infection.

Animal models of human immunodeficiency virus 1, such as feline immunodeficiency virus (FIV), provide the opportunities to dissect the mechanisms of early interactions of the virus with the central nervous system (CNS). The aims of the present study were to evaluate viral loads within CNS, cerebrospinal fluid (CSF), ocular fluid, and the plasma of cats in the first 23 weeks after intravenous inoculation with FIV GL8 . Proviral loads were also determined within peripheral blood mononuclear cells (PBMCs) and brain tissue. In this acute phase of infection, virus entered the brain in the majority of animals. Virus distribution was initially in a random fashion, with more diffuse brain involvement as infection progressed. Virus in the CSF was predictive of brain parenchymal infection. While the peak of virus production in blood coincided with proliferation within brain, more sustained production appeared to continue in brain tissue. In contrast, proviral loads in the brain decreased to undetectable levels in the presence of a strengthening PBMC load. A final observation in this study was that there was no direct correlation between viral loads in regions of brain or ocular tissue and the presence of histopathology.

An Ayrshire dairy herd was investigated for occurrence of ocular abnormalities in new-born calves. Ophthalmic examinations were performed on all the animals in the herd and 26% of them were diagnosed with bilateral cataracts. Cataracts varied in extent and severity but the majority were restricted to the lens nucleus. Epidemiological analysis showed the prevalence was higher in male animals and lower in animals born to heifers. A family tree was designed but no genetic impact of dam lines was evident. Sire data was incomplete and could therefore not be included. Based on the information provided by the farmer there was no obvious environmental or nutritional cause of these cataracts. However, data records were incomplete and further investigation/monitoring of the herd would be needed to establish a cause and enable a better insight into the aetiology of this disease in cattle.

A retrobulbar glioma, causing retinal detachment, is described in an 8‐year‐old Labrador bitch. Contrast radiography was used as an aid to diagnosis. Résumé. Description d'un gliome rétrobulbaire, ayant provoqué un décollement de la rétine, apparu chez une chienne Labrador de 8 ans. On a eu recours à la radiographie de contraste pour étayer le diagnostic. Zusammenfassung. Ein retrobulbäres Gliom, das Netzhautablösung verursachte, wird bei einer 8 Jahre alten Labrador‐Hündin beschrieben. Für die Diagnose wurde Kontrastradio‐graphie benutzt.