scholarly journals Bullous fixed drug eruption following administration of the recombinant adjuvant Shingrix vaccine

2021 ◽  
Vol 14 (8) ◽  
pp. e241293
Author(s):  
Hallie Thompson ◽  
Laura Nichols ◽  
Tania Gonzalez Santiago

A 51-year-old woman with Crohn’s disease presented with a bullous rash on her left arm and axilla 2 days after receiving her second dose of the recombinant adjuvant Shingrix vaccine. PCR for herpes simplex virus (HSV) 1, HSV 2 and varicella zoster virus was negative. Punch biopsy revealed changes that were consistent with a bullous fixed drug eruption. She was successfully treated oral prednisone and topical triamcinolone cream. This is the first known case of a bullous fixed drug eruption due to the recombinant adjuvant Shingrix vaccine.

2015 ◽  
Vol 28 (6) ◽  
pp. 589-595 ◽  
Author(s):  
Surjo K. De ◽  
Jennifer C.L. Hart ◽  
Judith Breuer

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e22527 ◽  
Author(s):  
Peter Norberg ◽  
Shaun Tyler ◽  
Alberto Severini ◽  
Rich Whitley ◽  
Jan-Åke Liljeqvist ◽  
...  

2013 ◽  
Vol 85 (5) ◽  
pp. 833-838 ◽  
Author(s):  
Hisako Saitoh ◽  
Yuko Momma ◽  
Hiroyuki Inoue ◽  
Daisuke Yajima ◽  
Hirotaro Iwase

2018 ◽  
Author(s):  
Martin S. Hirsch

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.


2014 ◽  
Author(s):  
Martin S. Hirsch

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.


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