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Postoperative Candida Infection following Complex Periocular Reconstruction

ABSTRACT: Summary: Postoperative candida infection is a rarely reported complication in cutaneous surgery, although it may develop more often in particular clinical settings. We present a 59-year-old woman with a well-controlled human immunodeficiency virus infection. She developed a bright red eruption with satellite pustules 2 weeks after excision of recurrent lentigo maligna melanoma of the left lower eyelid and periocular region. Due to defect size and complexity of the reconstruction (glabellar transposition flap, Hughes flap, composite graft from upper contralateral eyelid, and full-thickness skin graft from ipsilateral retroauricular region), she was placed on prophylactic oral amoxicillin-clavulanic acid and topical bacitracin and polymyxin. Immediate postoperative course was unremarkable, and sutures were removed after 7 days. Three days later, she developed bright red erythema and pustules within the surgical site and complained of burning. Empirically she was switched to topical gentamicin and oral ciprofloxacin, and later to linezolid, due to inadequate response. Wound culture grew Candida albicans sensitive to fluconazole and voriconazole. After oral fluconazole and topical clotrimazole initiation, the patient rapidly improved. The graft remained viable and apart from small partial dehiscence on the cheek, the healing was unremarkable. Apart from the case presentation, we also discuss different factors associated with postoperative candida infection, including immunocompromised status, surgical procedure location, and postoperative antibiotic use. Early recognition and treatment of postoperative candida infections are crucial to prevent delayed healing and associated morbidity.

SUBMITTER: Wallis L

PROVIDER: S-EPMC8563074 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Herpes simplex virus 1 (HSV-1) cycles between phases of latency in sensory neurons and replication in mucosal sites. HSV-1 encodes two key proteins that antagonize the shutdown of host translation, US11 through preventing PKR activation and ICP34.5 through mediating dephosphorylation of the ? subunit of eukaryotic initiation factor 2 (eIF2?). While profound attenuation of ICP34.5 deletion mutants has been repeatedly demonstrated, a role for US11 in HSV-1 pathogenesis remains unclear. We therefore generated an HSV-1 strain 17 US11-null virus and examined its properties in vitro and in vivo In U373 glioblastoma cells, US11 cooperated with ICP34.5 to prevent eIF2? phosphorylation late in infection. However, the effect was muted in human corneal epithelial cells (HCLEs), which did not accumulate phosphorylated eIF2? unless both US11 and ICP34.5 were absent. Low levels of phosphorylated eIF2? correlated with continued protein synthesis and with the ability of virus lacking US11 to overcome antiviral immunity in HCLE and U373 cells. Neurovirulence following intracerebral inoculation of mice was not affected by the deletion of US11. In contrast, the time to endpoint criteria following corneal infection was greater for the US11-null virus than for the wild-type virus. Replication in trigeminal ganglia and periocular tissue was promoted by US11, as was periocular disease. The establishment of latency and the frequency of virus reactivation from trigeminal ganglia were unaffected by US11 deletion, although emergence of the US11-null virus occurred with slowed kinetics. Considered together, the data indicate that US11 facilitates the countering of antiviral response of infected cells and promotes the efficient emergence of virus following reactivation.IMPORTANCE Alphaherpesviruses are ubiquitous DNA viruses and include the human pathogens herpes simplex virus 1 (HSV-1) and HSV-2 and are significant causes of ulcerative mucosal sores, infectious blindness, encephalitis, and devastating neonatal disease. Successful primary infection and persistent coexistence with host immune defenses are dependent on the ability of these viruses to counter the antiviral response. HSV-1 and HSV-2 and other primate viruses within the Simplexvirus genus encode US11, an immune antagonist that promotes virus production by preventing shutdown of protein translation. Here we investigated the impact of US11 deletion on HSV-1 growth in vitro and pathogenesis in vivo This work supports a role for US11 in pathogenesis and emergence from latency, elucidating immunomodulation by this medically important cohort of viruses.

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Postoperative Candida Infection following Complex Periocular Reconstruction

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