Complete ophthalmoplegia after zoster ophthalmicus.

Complete ophthalmoplegia following herpes zoster ophthalmicus (HZO) is rare. We report three cases of HZO-associated complete ophthalmoplegia and review thirteen additional cases reported in the English language medical literature over the past 30 years. HZO-associated complete ophthalmoplegia occurs mostly in individuals over the age of 50 years and usually occurs within one to two weeks of the development of cutaneous HZO. The prognosis for recovery is good, with-significant improvement typically seen within 2 months and complete or near resolution within 18 months time.

Detection of varicella-zoster virus DNA in conjunctivas of patients with herpes zoster.

Detection of varicella-zoster virus (VZV) DNA was carried out in the conjunctivas of 18 patients with herpes zoster by polymerase chain reaction. The rate of VZV DNA detection in conjunctivas was 3/4 in herpes zoster ophthalmicus associated with eruption on the dorsum nasi, 2/5 in herpes zoster ophthalmicus without eruption on the dorsum nasi, 1/2 in herpes zoster with eruption on the cheek and lower jaw, 1/2 in generalized herpes zoster and 0/5 in herpes zoster associated with eruption on the trunk or extremities, respectively. The reason for the detection of VZV DNA in conjunctivas is discussed.

Herpes zoster ophthalmicus: the virus strikes back.

The objective of this article is (1) to review the range of anterior segment ocular disease caused by varicella-zoster virus (VZV), (2) to discuss the pathophysiology of the mechanisms involved in the ensuing tissue damage, and (3) to bring the reader up to date on the current management and therapy of herpes zoster ophthalmicus (HZO). The design of this article is a review of the literature with special emphasis on the ocular manifestations of HZO. The conclusions reached by this review include that HZO is a common form of the recurrent form of HZ infection caused by VZV. Although HZO is generally benign in most nonimmunocompromised patients, the incidence of ocular complications is high. Immunocompromised hosts manifest HZ (and HZO) in much higher frequencies and develop more severe sequelas, which may lead to loss of vision, dissemination of the virus, or death. An increased incidence of acquired and iatrogenic immunodeficiency states has given rise to a greater occurrence of recurrent VZV infection. Thus, there is a greater need for earlier diagnosis and appropriate management of the protean manifestations of this potentially disastrous disease.

Detection of varicella zoster virus DNA and viral antigen in human cornea after herpes zoster ophthalmicus.

This article describes the histopathology, immunohistochemistry, and varicella zoster virus DNA in situ hybridization of 14 corneal buttons obtained from 14 patients (average age 69.0 years) after perforating keratoplasty (four patients) or surgical enucleation (10 patients) at different times after the clinical onset of herpes zoster ophthalmicus (average 58.7 months). The main histopathologic features were intense stromal vascular scarring (12 patients) and granulomatous reaction to Descemet's membrane (nine patients). Using the peroxidase-antiperoxidase method, varicella zoster virus (VZV) antigen could be detected by immunohistochemistry in two patients within epithelial cells of the cornea and in the limbal episclera during the active phase of herpes zoster ophthalmicus. For in situ hybridization we used the 35S-labeled HindIII A and C fragment of VZV and identified viral DNA in five corneal buttons obtained 1 day to 8 years after the clinical onset of infection. Viral DNA was mainly found in mononuclear cells with eosinophilic intracytoplasmic inclusions within vascular stromal scars, in keratocytes, and in epithelial cells of the cornea. Our results show that VZV DNA is detectable in human cornea even 8 years after the clinical onset of herpes zoster ophthalmicus and may indicate VZV persistence in a latent form in corneal tissue or reactivation of the virus from an endogenous or exogenous source causing a severe and often recurrent keratitis in the progress of herpes zoster ophthalmicus.

Ophthalmic herpes zoster.

A current review of ophthalmic zoster is presented including its virology, immunology, epidemiology and pathogenesis. We give our findings in 1356 patients referred to the Zoster Clinic at Moorfields Eye Hospital, London. The treatment of the disease and its ocular complications is discussed.

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.

Secondary bacterial keratitis in herpes zoster ophthalmicus.

We report a case of an unusual complication of herpes zoster ophthalmicus, secondary bacterial keratitis. Compared with previously reported cases, ours is unique in its early occurrence in the course of zoster and the lack of predisposing factors such as steroid use, contact lens use, or prior corneal disease or surgery. The opportunistic pathogen Branhamella cattarhalis responded well to medical therapy. We feel that bacterial superinfection must always be a concern in patients with herpes zoster keratitis, even early in their often prolonged chronic disease.

Binding and internalization of herpes simplex virus-antibody complexes by polymorphonuclear leukocytes.

We studied the interactions between rabbit polymorphonuclear leukocytes (PMN) and the RE strain of herpes simplex virus type 1 (HSV-1) to determine better the role of inflammatory cells in herpetic stromal keratitis. PMN were found to be nonpermissive for HSV replication and were unable to bind virus in the absence of antibody. However, PMN did bind and internalize HSV-antibody complexes in vitro as was demonstrated visually by electron microscopic studies and quantitatively by measurement of activity associated with radiolabeled HSV-antibody complexes. Virus used for immune complex formation was labeled with either 125Iodine or 35S-methionine. In some experiments, anti-HSV IgG used for immune complex formation was labeled with 125Iodine before incubation with virus. Use of all three radiolabeling approaches resulted in the same general pattern of binding, indicating a requirement for both antibody and virus for interaction with PMN. The activity associated with PMN was increased by preincubation with complement. The results suggest an active role for PMN in controlling HSV infection through their ability to bind and ingest virus-antibody complexes.

Oral acyclovir in the treatment of acute herpes zoster ophthalmicus.

Seventy-one nonimmunocompromised patients with herpes zoster ophthalmicus, presenting within seven days of onset of characteristic skin eruption, were enrolled in a prospective, longitudinal, randomized, double-masked, placebo-controlled trial with oral acyclovir. In a previous interim report we noted more prompt resolution of dermatomal signs and symptoms with acyclovir treatment. There was also a reduction of viral shedding in acyclovir-treated patients coupled with a trend to greater rate of microdissemination of the virus in placebo-treated patients (Cobo LM, et al. Ophthalmology 1985; 92:1574-83). While further substantiating these findings, we report that a ten-day course of treatment with oral acyclovir (600 mg, five times a day) is well-tolerated and significantly reduces the incidence and severity of the most common complications of herpes zoster ophthalmicus: dendritiform keratopathy, stromal keratitis, and uveitis. While this acyclovir treatment regimen reduces the zoster-related pain during the acute phase of the disease, especially in patients treated within 72 hours of onset of skin lesions, it has no evident effect on either incidence, severity, or duration of post-herpetic neuralgia in the patients studied.

Delayed contralateral hemiplegia following herpes zoster ophthalmicus: should antiviral therapy be used?

We review clinical virological studies in the syndrome of delayed contralateral hemiplegia following herpes zoster ophthalmicus. Virus could not be isolated from the cerebrospinal fluid (CSF) of the present case, nor was antiviral antibody found in the CSF. There appear to have been no reports of successful virus isolation from the CSF although there are reports of antibody in the spinal fluid. Thus the evidence for ongoing viral replication in the central nervous system is marginal. It is suggested that the sensitive antibody assay against membrane antigens (FAMA) be used in the future as a guide to antiviral therapy.

Necrotizing retinopathy with herpes zoster ophthalmicus: a light and electron microscopical study.

A necrotizing retinopathy following a vesicular cutaneous eruption in the distribution of the right trigeminal nerve developed in a patient who had been receiving systemic corticosteroid therapy one week prior to the onset of herpes zoster ophthalmicus. Seven weeks after the herpetic symptoms began, the patient died of pneumonia following an intracerebral hematoma. At postmortem examination, unexpected multiple focal and confluent lesions, which corresponded to areas of extensive retinal necrosis, were observed in the fundus of the right eye. Intranuclear inclusions with a perinuclear halo were identified within the affected sensory retina. Electron microscopy of the retinal lesions disclosed round to oval enveloped viral particles that were characteristic of the herpes viruses. A mild lymphocytic infiltrate was evident in a demyelinated right Gasserian ganglion. Demyelination and necrosis of the right trigeminal sensory tract and adjacent areas were evident within the brain stem.