New Trends in Antiviral Therapy of CNS Infections
Sunit K. Singh, Daniel Růžek in Neuroviral Infections, 2013
The treatment of viral encephalitis has evolved tremendously in recent years. Acyclovir treatment has decreased mortality from 70% to 28% and morbidity from 97% to 62% in patients with herpes simplex encephalitis (HSE) (Sköldenberg 1984; Whitley 1986). This same drug has been used to treat patients with Varicella zoster virus encephalitis (Mathis et al. 2006; McKelvie et al. 2002). Cytomegalovirus (CMV) CNS infections have better prognosis when they are treated with ganciclovir, foscarnet, or valganciclovir (Anduze-Faris et al. 2000; Julin et al. 2002; Vancikova and Dvorak 2001). However, despite these and some other advances, there is still a huge need for progress in this field. Even in those situations where we now have effective drugs, the treatment results are still far from being considered completely satisfactory. Not to mention that there are still many viral infections of the CNS for which there is no treatment, like rabies and arthropod-borne viral encephalitis. Prevention of epidemic encephalitis is another concern in many regions of the world. For these reasons, great effort has been made to develop better treatments and better strategies to prevent these diseases.
Integumentary system
Aida Lai in Essential Concepts in Anatomy and Pathology for Undergraduate Revision, 2018
Herpes zoster Infection caused by varicella zoster virusMost commonly occurs in thoracic regionRisk factors: – immunosuppression– ageSymptoms: – pain– fever– vesiclesSigns: vesicular rash along dermatome distributionManagement: – analgesics– acyclovir
Determination of Antiviral Activity
Adorjan Aszalos in Modern Analysis of Antibiotics, 2020
The varicella zoster virus causes two clinical types of disease: varicella, or chicken pox; and herpes zoster, or shingles [89]. Varicella, a common and widespread disease of children, is characterized by a papular rash that usually runs a 1–2 week course. Occasionally, however, pneumonitis, which can be fatal, may occur; another uncommon complication is encephalitis. Zoster, which is characterized by varicellalike skin lesions, is quite a painful condition of adults; it is thought to be a latent infection, often activated by various stimuli, such as immunosuppressive therapy, and is a serious complication of such therapy. In such cases the disease is often manifested as a generalized infection with involvement of the lungs and encephalitis. The virus has been isolated from the dorsal route ganglia of humans formerly infected with varicella [90]. The zoster disease particularly has been a target of chemotherapeutic agents, with moderate success seen [91,92]. Animals other than humans do not seem to be susceptible to the varicella zoster virus, although Soike et al. [86,87] have reported that intratracheal and subcutaneous administration of the virus to African green monkeys will cause a disease resembling varicella in humans and have effectively used this model in studying several antiviral drugs. Until the work of the latter investigators, the cutaneous lesions induced by type 1 herpesvirus (Table 5) have generally been used as models for evaluating the potential varicella zoster inhibitory efficacy of antiviral drugs.
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.
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.
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].