Acute retinal necrosis secondary to Varicella Zoster Virus
Authors: Vasudevan, Archana; Rojas-Moreno, Christian; Tarun, Tushar
A 54 year old female presented to the ophthalmology clinic with pain and decreased vision in her left eye. No past medical history other than primary varicella zoster infection, in her childhood. The eye exam revealed a macular region with scattered areas of retinal opacity along with patches of necrosis on the periphery. She was started on valganciclovir and referred to the infectious disease clinic. Cell Count, blood chemistry and HIV were negative. Serum was sent for polymerase chain reaction (PCR) for Varicella Zoster Virus (VZV), Herpes Simplex Virus (HSV) and Cytomegalovirus (CMV). The VZV PCR was positive. She had decreased vision on the right eye two days later, and exam revealed peripheral retinal whitening. She was admitted and started on intravenous acyclovir. VZV is one of the most common causes of ARN and has been described in both immunocompetent and immunocompromised persons. Visual changes are usually noted weeks to months after the antecedent herpes zoster. Retinal involvement is bilateral in over half of cases, suggesting that VZV reaches the central nervous system hematogenously. The retinal exam reveals multifocal necrotizing lesions, often initially involving the peripheral retina. Therapy includes intravenous acyclovir with consideration of intravitreal foscarnet and other antivirals for progressing disease. (C) 2019 Published by Elsevier Ltd.
Humoral immunity to varicella zoster virus is altered in patients with rheumatoid arthritis
Authors: Krasselt, Marco; Baerwald, Christoph; Liebert, Uwe G.; Seifert, Olga
Introduction The prevalence of herpes zoster (HZ) is high in patients with rheumatologic diseases. The incidence in patients with rheumatoid arthritis (RA) is at least twice as high as in healthy people. Nevertheless, little is known about humoral immunity against varicella zoster virus (VZV), in particular in patients with RA. We, therefore, aimed to retrospectively compare VZV antibody concentrations in a collective of patients with RA in a German outpatient clinic with age- and sex-matched controls without RA. Methods We included n = 247 patients with RA from one single university centre as well as n = 250 age- and sex-matched controls from the in-house routine in this retrospective analysis. The concentration of VZV IgG antibody concentration was either available from the records or was measured using an enzyme-linked immunosorbent assay (ELISA). Additionally, avidity for specific IgG was analysed for some of the samples. The antibody concentrations have been compared between the two groups. Moreover, a consecutive subgroup analysis after stratification by age was performed. Results A total of 68.4% (n = 169) of the included patients were treated with conventional synthetic DMARDs, either as monotherapy or in combination. Biological originator DMARDs were used in 45.8% (n = 113) of the patients, with the majority (85%, n = 96) of them being on tumour necrosis factor (TNF)-inhibiting agents. As the main result of this study, antibody titres for VZV were found to be significantly lower in RA patients compared with healthy controls (p < 0.0001). The observed difference was most pronounced for the older patients being in the sixth and seventh decade. Antibody avidity was high in both groups with a significantly higher avidity among the controls (p = 0.0006). Conclusions A possible explanation for the low VZV antibody concentration in RA patients might be premature immunosenescence, which most likely also effects the B cell compartment and humoral immunity. This thesis is emphasised by the significantly higher antibody avidity among the controls. The data also suggest that the increased HZ risk is a consequence of a poor humoral immunity. The available HZ vaccinations should contribute to decreasing the elevated HZ risk in RA patients.