Onset Of Herpes Zoster Ophthalmicus Research Articles

Delayed Superior Orbital Fissure Syndrome Arising More than One Month after Herpes Zoster Ophthalmicus and Meningitis.

A 79-year-old woman developed herpes zoster ophthalmicus (HZO) with a vesicular rash on the nasal root, which developed soon after intravenous acyclovir therapy. Although varicella zoster virus DNA was undetectable in the cerebrospinal fluid, she presented with ophthalmoplegia without optic nerve dysfunction 32 days after the onset of HZO. We diagnosed the patient with superior orbital fissure syndrome and administered intravenous immunoglobulin and systemic corticosteroids. Ophthalmoplegia did not immediately respond to these therapies but resolved 4 months later. We should be aware that ophthalmoplegia can occur, even after HZO and meningitis are completely treated.

Prompt Antiviral Therapy Is Associated With Lower Risk of Cerebrovascular Accident Following Herpes Zoster Ophthalmicus

To examine risk factors associated with cerebrovascular accident (CVA) following herpes zoster ophthalmicus (HZO). Retrospective cohort study. Review of medical records of all patients with HZO seen at the department of Ophthalmology, Auckland District Health Board, New Zealand, between January 1, 2006, and December 31, 2016. The main outcome measure was cerebrovascular accident within 12 months of diagnosis. A total of 869 patients diagnosed with HZO were included in the study. The median age at onset of HZO was 65.5 years (interquartile range [IQR] 52.9-75.4), and 52.5% (n=456) were male. Antiviral therapy was started in 765 participants (88.0%), not used in 95 (10.9%), and not documented in 9 participants (1.0%). Four hundred sixty-eight participants (54.9%) received prompt oral antiviral therapy (≤72 hours of rash onset). A CVA occurred in the 12 months following HZO in 14 patients (1.6%) and was most common in older patients, occurring in 2.5% aged ≥65 years, 0.7% aged 40-65 years, and 0.9% aged <40 years. Hazard of CVA was highest immediately following HZO, with median time to CVA of 2.3 months (IQR 0.8-5.9 months). Patients who received prompt acyclovir had a 76.2% lower hazard of CVA (0.9% vs 2.6%, P=.022) on multivariate analysis. Cerebrovascular accident occurs in a low proportion of individuals within 1 year following HZO. Antiviral treatment for HZO may reduce the risk of subsequent CVA when given within 72 hours of rash onset.

Neurotrophic Keratopathy After Herpes Zoster Ophthalmicus.

The aim of this study was to describe risk factors for neurotrophic keratopathy (NK) after herpes zoster ophthalmicus (HZO). This study was a retrospective review of all patients seen at the Auckland District Health Board with HZO from 2006 through 2016. Cox proportional hazards analysis was performed to examine time to development of neurotrophic keratitis. Eight hundred sixty-nine patients were included in the study with a median follow-up of 6.3 years (5504.4 patient-years). The median age was 65.5 years (interquartile range 52.9-75.4), and 456 subjects (52.5%) were male. NK developed in 58 patients (6.7%), with the highest hazard 1 to 2 years after onset of HZO. On univariate analysis, age, White ethnicity, best-corrected visual acuity (BCVA) at presentation, intraocular pressure, corneal involvement, uveitis, and number of recurrences were associated with increased risk of NK. On multivariate analysis, the following factors were significant: age (hazard ratio [HR] = 1.03; P = 0.021), White ethnicity (HR = 3.18; P = 0.015), BCVA (HR = 1.81; P = 0.026), uveitis (HR = 3.77; P = 0.001), and recurrence (HR = 1.34; P < 0.001). Vision loss (BCVA ≤6/15) was more frequent in subjects with NK (65.5% vs. 16.3%, P < 0.001). NK is a relatively common and serious complication of HZO and occurs more frequently in older White individuals, those with poor visual acuity at presentation, and those with uveitis. Vision loss occurs in approximately two-thirds of patients.

Factors associated with age of onset of herpes zoster ophthalmicus.

The aim of this study was to evaluate factors associated with the age of onset of herpes zoster ophthalmicus (HZO) in the era of varicella vaccination. A retrospective series of 400 subjects with a diagnosis of HZO, and an analysis of public health databases. Variables studied included the age at onset, period of disease onset (1996-2004 and 2005-2012), sex, smoking habits, diabetes status, autoimmunity, and immunosuppressed status. Community data were gathered from the Oklahoma Outpatient Surgery Discharge Public Use Data File and the United States Census' American Community Survey data set. The mean onset age was significantly lower for 2005 to 2012 as compared with 1996 to 2004 among females (mean decrease, 9.3 years; 95% confidence interval, 4.6-13.9 years; P < 0.0001), but the mean onset age was similar between the 2 periods among males (P = 0.640). Whereas 32.3% of the patients with zoster were <60 years old in 1996 to 2004, compared with 44.8% in the 2005 to 2012 period (χ test: P = 0.017). In the multivariate model, smokers were found to have disease onset 11.5 (95% confidence interval, 6.9-16.1) years younger than nonsmokers. The proportion of younger patients with HZO increased, whereas the institutional and community data sets demonstrate a downward shift of the average age of onset of HZO among females. This may be an effect of widespread childhood varicella vaccination. Immunosuppression and smoking were also associated with a younger age of onset of HZO. This has implications for clinical care of patients at risk for developing HZO, as well as public health and vaccination policies.

Role of Magnetic Resonance Imaging in Herpes Zoster Ophthalmicus Ophthalmoplegia

Aims: To hypothesize the mechanisms of herpes zoster ophthalmicus (HZO) related ophthalmoplegia by magnetic resonance imaging (MRI). Case Presentation: A 61-year-old Chinese man diagnosed with right sided HZO and a positive Hutchinson’s sign, subsequently developed right eye complete ptosis, mydriasis and limitation of elevation 1 month after the onset of HZO. MRI showed thickening and enhancement of right oculomotor nerve and enhancement of right extraocular muscles. CSF revealed leukocytosis and positive varicella zoster virus (VZV) DNA without any clinical signs of meningitis. The diagnosis HZO-related ophthalmoplegia and asymptomatic VZV meningitis was made based on the clinical and laboratory findings. The external ocular muscle palsies of this patient were due to both oculomotor nerve palsy and orbital myositis demonstrated by MRI. Conclusion: The pathogenesis of HZO associated ophthalmoplegia is attributed to multiple factors such as neuritis of the cranial nerve and orbital myositis which can be diagnosed with MRI.

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

Objective The purpose of the study was to identify varicella zoster virus (VZV) DNA and viral antigen in human eyes at various intervals after clinical onset of herpes zoster ophthalmicus (HZO). Design A retrospective case series. Participants There were 9 eyes and 4 corneal buttons surgically obtained from 13 patients with HZO at the University Eye Hospital of Erlangen-Nürnberg between 1984 and 1994. Specimens were examined at different timepoints after clinical onset of HZO (range, 1 day-19 years; median, 36 months). Methods Histopathologic evaluation was performed on formalin-fixed and paraffin-embedded tissue by routine histology, immunohistochemistry (5-B-7 murine monoclonal antibody to VZV; peroxidase-antiperoxidase method), and DNA-in situ hybridization ( 35S deoxyadenosine triphosphate-labeled HindIII fragments [A and C] of VZV). Results Typical histopathologic changes associated with HZO were identified: vascularization of the corneal stroma (11 of 13), granulomatous reaction to Descemet’s membrane (8 of 13), fusiform-shaped ciliary scarring (5 of 9), optic neuritis (4 of 9), and perineuritis (8 of 9) and perivasculitis (8 of 9) of the long posterior ciliary nerves and arteries. VZV antigen was detected in two patients with acute infection 1 and 7 days after onset of HZO, respectively. VZV-DNA was identified in seven patients up to 10 years after onset of HZO in corneal epithelial cells (2 of 13), corneal stroma (5 of 13), inflammatory infiltrate of the anterior chamber (1 of 9), episclera (2 of 9), posterior ciliary nerves (1 of 9) and arteries (5 of 9), optic nerve (5 of 9), and adjacent leptomeninges (2 of 9). Conclusion Persistence of viral genomes, most likely accompanied by gene expression or slow viral replication, appears to be responsible for the often smoldering panophthalmitis and the chronic recurrent keratouveitis in patients with HZO. Localization of viral DNA in vascular structures suggests a role for vasculitis in the pathogenesis of some ocular findings associated with HZO.

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.