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Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus

BACKGROUND: We report a case of necrotizing keratitis caused by acyclovir (ACV)-resistant herpes simplex virus (HSV) with a clinical appearance similar to a previous fungal keratitis infection. METHODS: Observational case report. RESULTS: Penetrating keratoplasty was performed in the left eye with a...

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Autores principales: Toriyama, Koji, Inoue, Tomoyuki, Suzuki, Takashi, Kobayashi, Takeshi, Ohashi, Yuichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: S. Karger AG 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241636/
https://www.ncbi.nlm.nih.gov/pubmed/25473399
http://dx.doi.org/10.1159/000368297
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author Toriyama, Koji
Inoue, Tomoyuki
Suzuki, Takashi
Kobayashi, Takeshi
Ohashi, Yuichi
author_facet Toriyama, Koji
Inoue, Tomoyuki
Suzuki, Takashi
Kobayashi, Takeshi
Ohashi, Yuichi
author_sort Toriyama, Koji
collection PubMed
description BACKGROUND: We report a case of necrotizing keratitis caused by acyclovir (ACV)-resistant herpes simplex virus (HSV) with a clinical appearance similar to a previous fungal keratitis infection. METHODS: Observational case report. RESULTS: Penetrating keratoplasty was performed in the left eye with a history of herpetic keratitis that resolved with periodic treatment with ACV ointment and a topical steroid. The left eye was painful and red with an abscess and corneal erosion in the peripheral donor cornea. Examination of the scraped corneal epithelium by light microscopy and culturing identified Candida albicans; polymerase chain reaction (PCR) was negative for human herpes viruses. After antifungal treatment, the ocular pain gradually decreased and the lesions slowly improved but recurred with a similar clinical appearance. A second light microscopy examination and cultures were negative for pathogens including C. albicans. PCR was positive for HSV-1 DNA; treatment with 3% topical ACV ointment was unsuccessful. A third examination showed only HSV-1 DNA. Despite antiviral ACV ointment, no clinical improvement occurred based on the HSV DNA copy numbers, which were the same before and after treatment, indicating a possible ACV-resistant strain. When topical trifluorothymidine was substituted for ACV, clinical improvement occurred and the HSV DNA copy numbers decreased. CONCLUSION: Necrotizing keratitis induced by ACV-resistant HSV occurred independently after fungal keratitis, with a similar clinical appearance in this case, making diagnosis and treatment difficult. Monitoring the HSV DNA load by real-time PCR could be useful for refractory cases even with atypical clinical appearances.
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spelling pubmed-42416362014-12-03 Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus Toriyama, Koji Inoue, Tomoyuki Suzuki, Takashi Kobayashi, Takeshi Ohashi, Yuichi Case Rep Ophthalmol Published online: October, 2014 BACKGROUND: We report a case of necrotizing keratitis caused by acyclovir (ACV)-resistant herpes simplex virus (HSV) with a clinical appearance similar to a previous fungal keratitis infection. METHODS: Observational case report. RESULTS: Penetrating keratoplasty was performed in the left eye with a history of herpetic keratitis that resolved with periodic treatment with ACV ointment and a topical steroid. The left eye was painful and red with an abscess and corneal erosion in the peripheral donor cornea. Examination of the scraped corneal epithelium by light microscopy and culturing identified Candida albicans; polymerase chain reaction (PCR) was negative for human herpes viruses. After antifungal treatment, the ocular pain gradually decreased and the lesions slowly improved but recurred with a similar clinical appearance. A second light microscopy examination and cultures were negative for pathogens including C. albicans. PCR was positive for HSV-1 DNA; treatment with 3% topical ACV ointment was unsuccessful. A third examination showed only HSV-1 DNA. Despite antiviral ACV ointment, no clinical improvement occurred based on the HSV DNA copy numbers, which were the same before and after treatment, indicating a possible ACV-resistant strain. When topical trifluorothymidine was substituted for ACV, clinical improvement occurred and the HSV DNA copy numbers decreased. CONCLUSION: Necrotizing keratitis induced by ACV-resistant HSV occurred independently after fungal keratitis, with a similar clinical appearance in this case, making diagnosis and treatment difficult. Monitoring the HSV DNA load by real-time PCR could be useful for refractory cases even with atypical clinical appearances. S. Karger AG 2014-10-10 /pmc/articles/PMC4241636/ /pubmed/25473399 http://dx.doi.org/10.1159/000368297 Text en Copyright © 2014 by S. Karger AG, Basel http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) (www.karger.com/OA-license), applicable to the online version of the article only. Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on http://www.karger.com and the terms of this license are included in any shared versions.
spellingShingle Published online: October, 2014
Toriyama, Koji
Inoue, Tomoyuki
Suzuki, Takashi
Kobayashi, Takeshi
Ohashi, Yuichi
Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus
title Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus
title_full Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus
title_fullStr Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus
title_full_unstemmed Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus
title_short Necrotizing Keratitis Caused by Acyclovir-Resistant Herpes Simplex Virus
title_sort necrotizing keratitis caused by acyclovir-resistant herpes simplex virus
topic Published online: October, 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4241636/
https://www.ncbi.nlm.nih.gov/pubmed/25473399
http://dx.doi.org/10.1159/000368297
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