Neurosyphilis with unilateral optic tract lesion causing homonymous hemianopia.

INTRODUCTION: Homonymous hemianopia is not a rare symptom. Many causative lesions and pathologies are known, although a unilateral optic tract lesion caused by syphilis is rare. CASE REPORT: A 56-year-old woman developed a congruous right homonymous hemianopia and bilateral tonic pupils with irregular shape. Brain T2-weighted and fluid attenuated inversion recovery magnetic resonance imaging (MRI) revealed a spindle-like high-intensity lesion in her left postchiasmal optic tract. The rim of this lesion enhanced with gadolinium without meningeal enhancement. Serum and cerebrospinal fluid venereal disease research laboratory tests were positive. Cerebrospinal fluid contained 71 white blood cells/microL (mononuclear cells = 97%) and 48 mg/dL of protein. The hemianopia disappeared after administration of benzylpenicillin. CONCLUSIONS: Neurosyphilis should be added to the list of differential diagnoses for an isolated optic tract lesion.

Specific pseudorabies virus infection of the rat visual system requires both gI and gp63 glycoproteins.

Transneuronal transport of pseudorabies virus (PRV) from the retina to visual centers that mediate visual discrimination and reflexes requires specific genes in the unique short region of the PRV genome. In contrast, these same viral genes are not required to infect retinorecipient areas of the brain involved in circadian rhythm regulation. In this report, we demonstrate that viral mutants carrying defined deletions of the genes encoding glycoprotein gI or gp63, or both, result in the same dramatic transport defect. Efficient export of either gI or gp63 from the endoplasmic reticulum to the Golgi apparatus in a fibroblast cell line requires the presence of both proteins. We also show that gI and gp63 physically interact, as demonstrated by pulse-chase and sucrose gradient sedimentation experiments. Complex formation is rapid compared with homodimerization of PRV glycoprotein gII. We suggest that gI and gp63 function in concert to affect neurotropism in the rat visual circuitry and that a heterodimer is likely to be the unit of function.

Anterograde transport of HSV-1 and HSV-2 in the visual system.

The anterograde spread of herpesvirus in the visual system subsequent to retinitis has been observed clinically. We compared the ability of two well-studied Herpes simplex virus (HSV) strains to be transported in the anterograde direction in the hamster visual system: strain McIntyre, representing HSV-1, and strain 186, representing HSV-2. Intravitreal injection of HSV-2 labeled more retinorecipient neurons than did HSV-1, suggesting important type differences in the ability of HSV to infect retinorecipient neurons after intravitreal injection. The most likely explanation for our results is that HSV-2 is more efficiently adsorbed than HSV-1 in the retinal ganglion cells. Our results also suggest that HSV may be useful as an anterograde transneuronal tracer for neuroanatomical studies of the visual system.

Two alpha-herpesvirus strains are transported differentially in the rodent visual system.

Uptake and transneuronal passage of wild-type and attenuated strains of a swine alpha-herpesvirus (pseudorabies [PRV]) were examined in rat visual projections. Both strains of virus infected subpopulations of retinal ganglion cells and passed transneuronally to infect retino-recipient neurons in the forebrain. However, the location of infected forebrain neurons varied with the strain of virus. Intravitreal injection of wild-type virus produced two temporally separated waves of infection that eventually reached all known retino-recipient regions of the central neuraxis. By contrast, the attenuated strain of PRV selectively infected a functionally distinct subset of retinal ganglion cells with restricted central projections. The data indicate that projection-specific groups of ganglion cells are differentially susceptible to the two strains of virus and suggest that this sensitivity may be receptor mediated.

Spread of Creutzfeldt-Jakob disease virus along visual pathways after intraocular inoculation.

We studied the targeting of spongiform lesions within the visual pathways after intraocular injection with the Fujisaki strain of Creutzfeldt-Jakob disease (CJD) virus. The first lesions were observed 18 weeks postinoculation in the most superficial layer of the superior colliculus and in the lateral geniculate body contralateral to the side of the inoculation. Asymmetrical lesions in the superior colliculus were found also in mice sacrificed at 19, 22, and 27 weeks postinoculation. These results demonstrate that CJD virus spreads within the CNS via central axons of the visual pathways following intraocular inoculation.

Spread of vesicular stomatitis virus along the visual pathways after retinal infection in the mouse.

Vesicular stomatitis virus (VSV) was injected into the left eyeball of 3-week-old mice and it infected the retinal ganglion cells. The infection spread rapidly along the visual pathways to the postsynaptic neurons in the contralateral superior collicle (SC) and lateral geniculate body (LGB). The distributional pattern of the viral immunoreactivity indicated an anterograde axonal transport of the infectious material. A subsequent spread to the ganglion cells of the right retina further indicated retrograde axonal VSV transport. Within the retina the infection spread from the ganglion cells to the pigment epithelium. Although a transneuronal spread of the VSV infection was observed, no VSV budding from or uptake in synaptic membranes was demonstrated ultrastructurally in the retina or the superior collicle. In the retina virions budded from the perikaryal and dendritic plasma membranes of the ganglion cells as well as from the nerve cell bodies of the inner and outer nuclear layers, but not from the receptor segments. In the superior collicle budding was also observed from the plasma membranes of nerve cell bodies and dendrites. In contrast, the intraocular injection of Sendai virus caused a limited retinal ganglion cell infection, with no further propagation in the retina or to the SC or LGB.

Transsynaptic spread of varicella zoster virus through the visual system: a mechanism of viral dissemination in the central nervous system.

We report a patient with pathologic evidence of anterograde spread of varicella zoster virus (VZV) through the visual system. A 29-year-old homosexual man developed the acquired immunodeficiency syndrome (AIDS) 2 months before the onset of left herpes zoster ophthalmicus. During the next 11 months, the zoster infection progressed to involve the left eye, with resultant keratitis, iritis, retinitis, and eventual blindness. Later, the patient developed bilateral blindness, left hemiparesis, and fatal pneumonia. At autopsy, the brain revealed destruction of the visual system and adjacent structures, with sparing of the remainder of the brain. Glial cells near the areas of necrosis showed Cowdry type A intranuclear inclusions. In situ hybridization with probes to VZV nucleic acid sequences were positive in the necrotic brain and retinal areas. Hybridization with probes to cytomegalovirus, herpes simplex virus type II, human immunodeficiency virus, and Epstein-Barr virus were negative. Electron microscopy revealed characteristic herpes group nucleocapsids. This case provides insight into the mechanisms of virus dissemination and the production of encephalitis.

Targeting of scrapie lesions and spread of agent via the retino-tectal projection.

Scrapie infectivity and degenerative vacuolation was initially localized within the contralateral superior colliculus following intraocular injection. The time course of these events was prolonged. With the ME7 strain of scrapie in Sincs7 genotype mice, infectivity began to rise in the superior colliculus from about 70 days, followed by the earliest asymmetrical lesions there from 120 days, with death occurring at about 250 days, at which time vacuolar degeneration was widespread in the brain. With other mouse Sinc genotype mouse/agent strain combinations the process was even further prolonged. With 87V scrapie strain in Sincp7 genotype mice the first lesions to appear were in the contralateral tectum at 300 days. It is concluded that scrapie agent can spread within ganglion cell axons.