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Skin Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Christopher Bunker, Richard Watchorn
Varicella zoster virus (VZV) is discussed in Chapter 3, Infectious disease (Figure 18.39; Figure 18.40).
Skin, soft tissue and bone infections
Published in Miriam Orcutt, Clare Shortall, Sarah Walpole, Aula Abbara, Sylvia Garry, Rita Issa, Alimuddin Zumla, Ibrahim Abubakar, Handbook of Refugee Health, 2021
Mucocutaneous forms of HSV 1 and 2 include herpes labalis (cold sore), genital herpes and pharyngitis. A severe form (eczema herpeticum) can occur in patients with atopic eczema. Herpes simplex virus may also cause encephalitis and meningitis. Varicella zoster virus causes chickenpox as a primary infection; this lies dormant in the sensory ganglia, and reactivation causes shingles in a dermatomal distribution.
Varicella-Zoster Virus Pneumonitis *
Published in Lourdes R. Laraya-Cuasay, Walter T. Hughes, Interstitial Lung Diseases in Children, 2019
Sandor Feldman, Dennis C. Stokes
Varicella-zoster virus produces two distinct clinical syndromes: varicella in children and herpes zoster in adults. The diffuse papulovesicular rash characteristic of varicella appears in crops over a 3- to 5-day period and is the initial manifestation of VZV infection. The virus eventually becomes latent in sensory root ganglia and with certain types of stimulation reappears as herpes zoster — a cluster of papulovesicular lesions conforming to the cutaneous distribution of the affected nerve. The lesions of VZV usually remain confined to the skin, however, in high-risk patients (see Section II) the virus enters the bloodstream from where it can disseminate to one or more organ systems. Viremia in patients with severe pneumonia may persist for as long as 9 days.14
Efficacy and safety of rituximab in autoimmune pancreatitis type 1: our experiences and systematic review of the literature
Published in Scandinavian Journal of Gastroenterology, 2021
Sara Nikolic, Nikola Panic, Elina Sofia Hintikka, Lara Dani, Wiktor Rutkowski, Aleksandra Hedström, Corinna Steiner, J.-Matthias Löhr, Miroslav Vujasinovic
Concerning adverse events in the eight selected studies, the above-mentioned infusion reactions and infections were the main adverse events. The prevalence of infections was from 0–33% in selected studies [3,10,19,20,24]. Common infections were pneumonia, urinary tract sepsis, clostridium difficile colitis, dental abscess and sinusitis [24]. Of severe infections, one patient each suffered from recurrent urinary and biliary sepsis with Gram-negative and Staphylococcus aureus bacteremia, recurrent anal abscesses, Staphylococcus hominis mitral endocarditis and recurrent angiocholitis with Gram-negative bacteremia during biliary relapses [20], diverticulitis and severe neutropenia needing treatment with granulocyte colony-stimulating factor [24]. Concerning infections, varicella-zoster virus was observed in two patients [19,21]. One patient with highly aggressive IgG4-RD was given RTX and high-dose steroid pulse as a last resort and later died due to acute cholangiosepsis and pneumonia with multi-organ failure [19,21]. Other side effects described were hemolytic anemia, amaurosis fugax, leading to carotid endarterectomy, unstable angina and surgery for an IgG4-related orbital pseudotumor [23].
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.
Understanding the role of exogenous boosting in modeling varicella vaccination
Published in Expert Review of Vaccines, 2018
Sandra E. Talbird, Elizabeth M. La, Josephine Mauskopf, Alexandra Altland, Vince Daniels, Lara J. Wolfson
Varicella is an infection characterized by an itchy, blister-like rash caused by exposure to the varicella-zoster virus (VZV). Reactivation of VZV from its latent state results in herpes zoster (HZ), or shingles (Figure 1), causing a localized painful rash with blisters. HZ will affect an estimated one in three people in the United States during their lifetime [1]. VZV reactivation is assumed to result from a decline of cell-mediated immunity (CMI), an immune response that yields protective effects following infection or exposure. The mechanisms by which CMI decline are poorly understood but are thought to occur as individuals age and in individuals with immunocompromising health conditions [2]. Immunosenescence, the gradual age-related decline in both CMI (related to T cell function) and humoral immunity (related to B cell and plasma cell function), also is a factor in the risk of VZV reactivation [3]. In addition to age-related immunosenescence, latent persistent human cytomegalovirus has also been associated with age-related immune disfunction [4], and therefore may also play a role in VZV reactivation.