We report on a case of HSV-1 necrotizing stromal keratitis arising from femtosecond laser arcuate keratotomy wounds after femtosecond laser-assisted cataract surgery (FLACS) in a patient without known prior ocular herpes. An 80-year-old woman underwent uncomplicated FLACS with paired arcuate keratotomies and was discharged on topical dexamethasone and ofloxacin. Fifteen days later, examination showed dendritic lesions aligned with the keratotomy incisions, stromal infiltrates/necrosis, diffuse endotheliitis, and mild anterior uveitis. Oral valacyclovir and topical antiviral therapy were started with corticosteroids, but rapid progression occurred with hypopyon, worsening stromal necrosis, and hemorrhagic hyphema. Anterior chamber tap PCR confirmed HSV-1. Treatment escalated to fortified antibiotics during workup, intravitreal ganciclovir (with intravitreal antibiotics), anterior chamber washout, hospitalization for intravenous acyclovir, and later surgical management of secondary inflammation (pupillary membrane with iris bombé) with membrane removal and peripheral iridectomies. Inflammation gradually resolved and final best-corrected visual acuity improved to 0.4 logMAR. HSV reactivation may present as severe necrotizing stromal keratitis originating at femtosecond arcuate keratotomy sites even without a known herpetic history; early recognition and aggressive antiviral therapy with careful steroid use are crucial after FLACS.

Acute retinal necrosis (ARN) usually begins in the peripheral retina, but atypical cases may initially involve the posterior pole. A 63-year-old man with no evidence of immunodeficiency presented with decreased vision and ocular hypertension in the left eye. The earliest optical coherence tomography (OCT) image showed a lesion centered on the fovea. At a subsequent examination, a whitish foveal lesion was associated with marked hyperreflectivity involving nearly the entire inner retina, posterior shadowing, and ellipsoid zone disruption. Dilated peripheral retinal examination and widefield fundus photography at the referring hospital showed no visible peripheral necrotizing retinitis; scleral depression was not performed. OCT angiography showed no detectable perfusion abnormality within the acquired 6 x 6-mm macular scan in either the superficial or deep retinal slab. Fine keratic precipitates, increased aqueous flare, and ocular hypertension raised concern for herpetic retinitis, and oral valacyclovir was started. At the first visit to our hospital, aqueous humor was collected while no peripheral lesion was visible. Four days later, an approximately four-disc-diameter inferotemporal lesion with vascular sheathing, punctate hemorrhages, and vitreous opacity appeared. On the same day, the 24-target multiplex PCR result from the aqueous sample collected at the first visit became available and was positive only for Varicella-zoster virus (VZV) DNA. Antiviral therapy with systemic corticosteroids led to regression of the retinal lesions. At 42 weeks, best-corrected visual acuity had improved to 0.6, with no retinal detachment or recurrence. This case suggests that VZV-associated ARN may initially present as an isolated foveal lesion. The OCT morphology was not typical of paracentral acute middle maculopathy because the hyperreflectivity was not confined to the middle retinal layers.

Disseminated herpes simplex virus type 2 (HSV-2) infection in adults is rare but can result in severe complications including hepatitis, encephalitis, and sepsis-like illness. Early symptoms are often nonspecific and may mimic common conditions, leading to delayed diagnosis and treatment. We present the case of a 74-year-old woman with Sjögren's syndrome who initially developed left upper eyelid erythema and swelling, followed by a viral-like prodrome with fever and myalgia, and subsequent urinary symptoms prior to traveling abroad. She was hospitalized in Spain with fever, dysuria, and transaminitis. Abdominal ultrasound demonstrated gallbladder wall thickening and free fluid without biliary obstruction, and she was empirically treated with broad-spectrum antibiotics and corticosteroids for presumed urinary tract infection and biliary disease. A language barrier complicated communication and clinical evaluation. After approximately one week of persistent symptoms, she returned to the United States and was admitted to our institution, where she was found to have culture-negative sepsis, hyponatremia, encephalopathy, anasarca, and persistent transaminitis. Extensive bacterial and fungal infectious workup was negative. HSV-2 polymerase chain reaction (PCR) was positive, confirming disseminated HSV-2 infection. During the latter part of hospitalization, she developed a small cluster of vesicular lesions. The patient improved with intravenous acyclovir followed by oral valacyclovir. Diagnostic complexity was compounded by care across different healthcare systems and a language barrier. This case highlights the staged progression of disseminated HSV-2 infection, from localized mucocutaneous involvement through a systemic viral prodrome to organ-threatening disease, and underscores the importance of considering disseminated HSV-2 in patients presenting with culture-negative sepsis and transaminitis. Early recognition and prompt antiviral therapy are essential to reduce morbidity and mortality.

Herpes zoster, also called shingles, is caused by the varicella zoster virus (VZV), which can become active again after lying dormant in nerve cells following chickenpox. Cases of herpes zoster affecting the buttocks in children that lead to urinary retention are rare. This report details a notable case of a 10-year-old girl who experienced urinary retention for nine days before she was hospitalized. Her medical history included chickenpox at approximately one year of age. Five days before the presentation, she visited a clinic where she was advised to undergo urinalysis and was prescribed antibiotics, but her condition did not improve. Around that time, the patient developed a rash on her buttocks and decided to monitor it without further treatment. As her symptoms worsened, she returned for a second urinalysis and was administered antibiotics again without relief. Upon admission, she developed a flat rash near her right buttock, raising suspicion of herpes zoster. Along with urinary issues, she complained of lower abdominal pain, and ultrasonography showed that approximately 800 mL of urine was retained in her bladder. A urinary catheter was inserted, and the patient was treated with valacyclovir. By day 4, the catheter was removed, and the shingles lesions began to crust. The patient was discharged on day 7 with no recurrence. Shingles-related urinary retention in children is extremely rare, making diagnosis challenging owing to the diverse symptoms and rash locations. This case highlights the importance of awareness of such presentations.

First-trimester (T1) cytomegalovirus (CMV) screening relies on IgG, IgM, and IgG avidity testing, but assay performance may vary according to the infection timing. To evaluate the ability of two IgM and three IgG avidity assays to detect maternal primary CMV infection (MPI) occurring in T1 or the periconceptional period. We analyzed 176 serum samples from 94 pregnant women with precisely dated MPI based on seroconversion. Samples were tested using two IgM assays (LIAISON CMV IgM II, Alinity i CMV IgM) and three IgG avidity assays (VIDAS CMV IgG Avidity II, LIAISON CMV IgG Avidity II, Alinity i CMV IgG avidity). For detection of MPI within 4 months, the IgM sensitivity was 99% (122/123) with LIAISON and 92% (94/102) with Alinity i. IgG avidity sensitivity for excluding MPI <4 months was 99% (124/125) with LIAISON, 98% (121/123) with VIDAS, and 92% (111/120) with Alinity i. The positive predictive value of low avidity was highest with VIDAS, followed by LIAISON and Alinity i. Retesting intermediate-avidity results with a second assay improved the estimation of MPI timing. All three avidity assays reliably excluded T1 MPI. Alinity i showed reduced sensitivity for ruling out periconceptional infection, supporting confirmatory testing in equivocal cases.

Viral infections are common in pregnancy and contribute significantly to maternal and fetal/neonatal morbidity and mortality. Certain viruses cause congenital infection with potentially devastating fetal/neonatal consequences, ranging from structural anomalies (birth defects), fetal growth restriction, and stillbirth to congenital viral syndromes with long-term end-organ damage and neurodevelopmental disorders. While a comprehensive review of all viral infections in pregnancy is beyond the scope of this article, this review focuses on the management of herpes simplex virus and cytomegalovirus.

Herpes simplex virus (HSV) infections are widespread and cause a significant global health burden. Clinical manifestations range from herpes labialis and genital herpes to life-threatening herpes simplex encephalitis or neonatal herpes. Current treatment relies on nucleoside analogs such as acyclovir, valacyclovir or famciclovir. The emergence of resistance to these drugs is of concern in transplant recipients and immunocompromised patients. Next-generation helicase-primase inhibitors are under clinical development to provide more efficacious treatments and address resistance to current therapies. Adibelivir (IM-250) is a potent HSV helicase-primase inhibitor (HPI) with nanomolar activity against both HSV1 and HSV2. In the present study, we assessed the susceptibility of more than 50 clinical isolates and laboratory strains against adibelivir. Across all strains tested, adibelivir inhibited HSV replication in cell culture with mean EC50 values of 21 nM (HSV1) and 35 nM (HSV2), compared to up to 42-fold higher EC50 values for acyclovir (883 nM for HSV1 and 1456 nM for HSV2). No preexisting variants with a lack of susceptibility were identified. Furthermore, no cross-resistance was observed between nucleoside analogs and HPIs and finally, the antiviral activity depended on serum concentration and infectious dose. Collectively, these data establish the baseline susceptibility profile of HSV clinical isolates to adibelivir prior to its broader clinical introduction. Adibelivir retains activity against nucleoside-resistant HSV strains and exhibits synergistic antiviral effects when combined with acyclovir, penciclovir and foscarnet in vitro. These results support clinical evaluation of adibelivir as a therapeutic option for HSV infections and as a candidate for combination therapy.

Genital herpes is a common sexually transmitted infection, yet its clinical presentation can be highly variable, particularly in immunocompetent individuals. Atypical manifestations often lead to misdiagnosis and delayed treatment. We report a case of a 59‑year‑old female who presented with a six‑month history of vulvar erythema, exudation, increased discharge, pruritus, and pain. She had been repeatedly diagnosed with vulvitis and contact dermatitis, receiving multiple courses of antibiotics, corticosteroids, and antihistamines without sustained improvement. Two vulvar biopsies revealed non‑specific dermatitis with eosinophilic infiltration, and extensive microbiological workup was negative for common pathogens. After hospitalization, localized saline cleansing helped reveal pinpoint erosions on the labia, prompting HSV‑2 DNA testing by polymerase chain reaction (PCR), which confirmed the diagnosis. Serological testing suggested a previous HSV‑2 exposure rather than a primary infection. The patient was treated with valacyclovir, resulting in complete resolution within eight days. This case underscores the importance of considering HSV infection in patients with chronic or recurrent vulvitis, especially when conventional treatments fail. In this instance, saline cleansing served as a simple bedside observation to unmask subtle lesions, though it should not be regarded as a validated diagnostic maneuver without further evidence. Early recognition and targeted antiviral therapy remain essential to prevent prolonged morbidity.