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Varicella zoster virus infection
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Don Gilden, Randall J. Cohrs, Dallas Jones, Maria A. Nagel
The concept of zoster sine herpete (shingles without rash) is nearly 100 years old, a notion that received further credence when Lewis [88] described numerous zoster patients who, days later, also developed pain without rash in a different dermatome distribution, often on the opposite side. The first serologic evidence of zoster sine herpete came from a physician who developed acute trigeminal distribution pain associated with a 4-fold rise in complement-fixing antibody to VZV but not to HSV [89]. Virologic confirmation of zoster sine herpete was established after analysis of two men with thoracic-distribution radicular pain lasting for months to years revealed PCR-amplifiable VZV DNA, but not HSV DNA, in their CSF and blood MNCs [90]. After diagnosis, both men were treated successfully with intravenous acyclovir.
Herpes Simplex Virus and Bell’s Palsy
Published in Marie Studahl, Paola Cinque, Tomas Bergström, Herpes Simplex Viruses, 2017
Adour et al. (80) conducted a double-blind, controlled study to test the hypothesis that reactivation of HSV-1 is the major cause of Bell’s palsy. Their aim was to evaluate the effectiveness of treatment with an antiviral agent in combination with conventional steroids. Acyclovir in 2000 mg tablets/day for 10 days in combination with prednisolone in 1 mg/kg/day for 5 days was administered within 3 days of the onset of paralysis. They reported that the cure rate of the group receiving acyclovir–prednisone therapy (92%) was significantly higher than that of the group receiving placebo plus prednisone (76%). Interestingly, De Diego et al. (74) reported that acyclovir therapy alone resulted in a worse recovery than prednisone therapy alone. These reports, however, did not determine whether or not the patients actually had HSV-1 reactivation. Furthermore, it is not clear whether patients with zoster sine herpete were excluded from the studies following identification by appropriate virological assays. The possibility exists that HSV-1 does initiate nerve damage, but reactivation is already over by the time facial paralysis begins. The use of antiviral agents is of no benefit in such cases. Further clinical trials involving a larger patient population, and employing virological assays to distinguish zoster sine herpete from Bell’s palsy, would establish more clearly the efficacy of combination therapy with steroids and antiviral agents for the treatment of Bell’s palsy. Large, multi-institutional, randomized studies are presently ongoing in Scandinavia and Japan to address this issue.
Herpes Zoster
Published in Thomas T. Yoshikawa, Shobita Rajagopalan, Antibiotic Therapy for Geriatric Patients, 2005
Laboratory diagnostic testing is useful for differentiating herpes HZ from HSV, for suspected organ involvement, and for atypical presentations. The best specimen is vesicle fluid which contains abundant VZV. Tzanck smears may suggest VZV infection if multinucleated giant cells and intranuclear inclusions are demonstrated in stained vesicle scrapings but the technique cannot differentiate VZV from HSV infections. Available diagnostic tests include immunofluorescence antigen (IFA) or enzyme immunoassay (EIA) antigen detection, viral culture, polymerase chain reaction (PCR), and serology. IFA or EIA detection of VZV antigens in vesicle scrapings, crusts, tissue biopsy, or cerebrospinal fluid (CSF) is rapid (hours), specific, and sensitive (about 90%) when performed by technicians experienced laboratory. VZV culture from vesicle fluid, blood, CSF, or infected tissue specimens (but not crusts) is slower and less sensitive (»40%) than IFA. However, culture is the standard for the definitive diagnosis and the only method that yields infectious VZV for further analysis, such as determination of resistance to antiviral drugs. VZV DNA detection using the PCR of vesicle fluid, cells scraped or swabbed from skin lesions, crusts, respiratory secretions, CSF, or tissue obtained by biopsy is very sensitive (nearly 100%) and specific. IFA and/or culture are the primary diagnostic tests because they are more available and less expensive than PCR. However, PCR is extremely valuable in diagnosing VZV infections, particularly in unusual specimens or when the clinician suspects that IFA or culture has yielded false-negative test results. Serology can be used to diagnose zoster sine herpete or HZ retrospectively using acute and convalescent VZV IgG titers. Enzyme-linked immunosorbent assay (ELISA) is commonly used to measure antibodies to VZV because it is simple to perform and available commercially. However, commercial ELISA assays may lack sensitivity and specificity. Experts often recommend more sensitive and specific tests such as an immunofluorescence assay for antibody to VZV-induced membrane antigens (FAMA) or a VZV latex agglutination test.
Frequency of putative enteric zoster diagnosed using saliva samples in patients with abdominal pain: a prospective study
Published in Infectious Diseases, 2021
Sang Hyun Ra, Ji-Soo Kwon, Ji Yeun Kim, Hye-Hee Cha, Hyun-Jung Lee, Jiwon Jung, Min Jae Kim, Yong Pil Chong, Sang-Oh Lee, Sang-Ho Choi, Yang Soo Kim, Won Young Kim, Sung-Han Kim
Varicella-zoster virus (VZV) is a human alpha-herpesvirus, and it primarily causes varicella (chickenpox), which is initiated by an inoculation in the respiratory mucosa. After primary infection, VZV reaches in the primary afferent neurons of the dorsal root ganglia and cranial nerve ganglia, where it establishes latency [1,2]. Reactivation of latent VZV causes a painful skin rash with vesicles called herpes zoster. The diagnosis of herpes zoster is based on clinical findings because of the distinctive skin rash. However, in some cases, a definite diagnosis is needed by laboratory methods [3]. First, atypical cutaneous manifestations may occur in immunocompromised hosts. Second, some patients may experience an unexplained pain in the skin without any cutaneous lesions; this is called zoster sine herpete, which is difficult to diagnose [4]. Moreover, when VZV reactivates in the autonomic ganglia, such as those in the enteric nervous system (ENS), that do not project to the skin, dermatomal lesions may not be observed [5]. Therefore, diagnostic tools for VZV detection are needed in these ambiguous cases.
Varicella-zoster virus causing a ring-like cerebral lesion in AIDS
Published in Baylor University Medical Center Proceedings, 2020
Jennifer Nielsen Fan, Robyn R. Fader, MaryAnn P. Tran, Christie Ann Shen
Varicella-zoster virus causes chickenpox as a primary infection, subsequently becomes latent in the dorsal root ganglia for up to decades, and may reactivate and cause a painful vesicular rash in a classic dermatomal distribution. Reactivation often follows a stressful trigger or immunocompromised state. Well-known complications of varicella-zoster virus reactivation include encephalitis, motor weakness or myelopathies, cranial nerve neuropathies, zoster sine herpete, Guillain-Barre syndrome, and, most significantly, vasculitis.1 It has been estimated that only 0.4% of identified viral encephalopathies are due to varicella zoster in the United States, and 7.7% of patients hospitalized for an encephalitis presented with comorbid human immunodeficiency virus (HIV) infection.2 We report a unique case of an encephalopathic patient undergoing workup for a stroke, whose repeat brain magnetic resonance imaging (MRI) showed a ring-enhancing lesion determined to be caused by varicella-zoster virus vasculitis in the setting of a newly acquired immune deficiency syndrome.
Clinical Manifestations and Characteristics of In Vivo Confocal Microscopy in Varicella Zoster Virus-Related Corneal Endotheliitis
Published in Ocular Immunology and Inflammation, 2019
Rong-mei Peng, Yu-xin Guo, Ge-ge Xiao, Qing Lu, Bin-jia Sun, Jing Hong
In our study, only one patient had typical dermal manifestations at the onset of corneal disease. Five patients had bilateral decompensated endothelial disease. As in previous reports, the typical manifestations of VZV infection included a single involved dermatome and did not cross the midline. However, herpes zoster can also present with unique or atypical clinical manifestations, such as glioma, zoster sine herpete and bilateral herpes zoster.23 According to the literature, only 25% of VZV anterior uveitis has dermal manifestations.24 Zoster sine herpete is usually reported in the literature as case reports, and tends to be ignored by patients or physicians, with the diagnosis relying on laboratory results. In our study, all patients were atypical presentations, with the exception of one patient, and the diagnosis was supported by real-time PCR. The nasociliary branch of the ophthalmic nerve, the primary sensory nerve to the eyeball, innervates the skin of the tip of the nose and divides further into the long ciliary nerves, which provide sensory innervation to the globe, including the sclera, cornea, and uvea. 18 For this reason, the typical classic presentation of nasociliary branch infection is Hutchinson’s sign.25 However, in our study, no Hutchinson’s sign was present. The reason may simply be due to long ciliary nerve infection. In addition, infection with the VZV during pregnancy can produce an embryopathy characterized by limb hypoplasia, eye and cerebral damage, and skin lesions.26 In our study, two patients with CHED may have been infected at the fetal stage.