The neurologic manifestations of anti-GQ1b antibody syndrome continue to expand and include a spectrum of immune-mediated neuropathies such as Miller Fisher syndrome, Bickerstaff brainstem encephalitis, and optic neuropathy. Asialo-GM1 antibodies are associated with motor or sensorimotor neuropathies, particularly multifocal motor neuropathy. Reports describing concurrent seropositivity for anti-GQ1b and asialo-GM1 antibodies presenting with unilateral facial weakness and limb symptoms remain scarce. A 55-year-old woman with chronic back pain initially presented to an outside facility with new-onset left lower motor neuron facial palsy accompanied by paresthesia and extremity weakness. Neuro-axis MRI demonstrated moderate-to-severe multilevel spinal and neuroforaminal stenosis. She was discharged with prednisone and acyclovir for presumed idiopathic Bell's palsy. Shortly thereafter, she presented to our institution with worsening symptoms. Examination revealed diminished strength, hypoesthesia, and decreased reflexes with a persistent left lower motor neuron cranial nerve VII palsy. The remainder of the cranial nerve examination was normal, and there was no ophthalmoplegia or ataxia. Lumbar puncture demonstrated albuminocytologic dissociation. A ganglioside antibody panel was positive for anti-GQ1b and asialo-GM1 antibodies. This case highlights an unusual presentation of concurrent anti-GQ1b and asialo-GM1 antibody positivity manifesting as unilateral facial palsy and limb weakness initially attributed to Bell's Palsy. Recognition of ganglioside antibody syndromes as potential mimickers of Bell's palsy is essential to ensure prompt diagnosis and treatment, thereby reducing the risk of neurological morbidity.

Many cases of encephalitis are caused by an autoimmune response, and some are associated with underlying malignancies. Here we present the case of a 17-year-old female patient who was admitted to the pediatric ward with acute gastroenteritis, seizures, and behavioral changes. A brain computed tomography (CT) scan ruled out acute infarction, haemorrhage, mass lesions, and other intracranial injuries, while the initial EEG showed no epileptic discharges. In the absence of a definitive diagnosis, midazolam was administered to treat tonic-clonic seizures, while ceftriaxone and acyclovir were started for suspected infection. However, her condition deteriorated further and she was transferred to the ICU, where she was intubated. A Cell-Based Assay (CBA) revealed the presence of anti-NMDAR antibodies and a contrast-enhanced brain MRI showed leptomeningeal enhancement without limbic involvement. She was subsequently treated with intravenous immunoglobulins and high-dose corticosteroids. A subsequent transabdominal ultrasound scan revealed an oval, fluid-filled ovarian cyst. Based on these findings, her right ovary was removed, resulting in a gradual improvement in her condition. This case highlights that paraneoplastic autoimmune encephalitis may be misclassified due to persistent psychiatric symptoms with negative EEG and CSF findings. When clinical suspicion remains high despite negative initial instrumental and laboratory findings, it is essential to repeat these investigations. In such cases, neuroantibody testing may play a crucial role in establishing the diagnosis.

A 63-year-old male with type 2 diabetes developed herpes zoster ophthalmicus (HZO), initially presenting with a left-sided headache and eyelid itching. He was misdiagnosed with cluster headache but later returned with a vesicular rash, prompting treatment with IV acyclovir. He later exhibited ptosis, diplopia, and vision loss in the left eye. Examination revealed proptosis, ophthalmoplegia, RAPD, and corneal anesthesia. MRI revealed enhancement of the left extraocular muscles and optic nerve sheath, consistent with orbital apex syndrome (OAS). Lumbar puncture confirmed varicella zoster virus involvement, and repeat imaging revealed CNS vasculitis and a subacute thalamic infarct. The patient was treated with antivirals, IV steroids, and antiplatelet therapy. Visual acuity and motility improved significantly post-treatment. This case highlights the rare but serious complication of OAS secondary to HZO. OAS involves dysfunction of multiple cranial nerves and may mimic other orbital syndromes but is distinguished by optic nerve involvement. Prompt recognition and aggressive treatment are critical to prevent permanent visual and neurological deficits in HZO-associated OAS.

Varicella zoster virus (VZV) is an exclusively human alphaherpesvirus that infects >90% of the global population. Primary infection typically causes varicella (chickenpox), after which VZV establishes lifelong latency in ganglionic neurons along the entire neuroaxis. Virus reactivation, typically triggered by age-associated immune dysfunction or immune suppressive conditions, produces herpes zoster (shingles) that can be complicated by post-herpetic neuralgia. In limited instances, VZV reactivation (and rarely primary infection) also produces multisystem disease including vasculopathy, cranial neuropathies, myelopathy and cardiovascular or gastrointestinal complications; these complications can occur without, or temporally dissociated from, rash. Diagnosis of varicella or herpes zoster relies on clinical presentation of a disseminated or dermatomal-distribution rash, respectively; diagnosis of VZV infection (owing to replicating virus) is more challenging when cases are atypical and/or occur without rash. Prevention strategies include administration of live attenuated varicella vaccine and recombinant zoster vaccine. VZV infection is treated with antiviral drugs including oral valacyclovir (drug of choice), famciclovir, acyclovir or amenamevir; for severe or disseminated disease, intravenous acyclovir or foscarnet (when other drugs fail) are used. Critical challenges remain in recognizing and diagnosing atypical presentations, developing novel therapeutics, establishing the causal role of VZV in vascular and neurodegenerative disease, and achieving broader vaccine implementation worldwide.

Genital herpes is one of the most common sexually transmitted infections worldwide, primarily driven by herpes simplex virus type 2 (HSV-2). In immunocompetent individuals, the disease typically manifests as self-limiting vesicular lesions that progress to painful ulcerations. However, in patients living with human immunodeficiency virus (HIV), the clinical presentation can be remarkably atypical, chronic, and severe due to impaired cell-mediated immunity. In this specific population, hypertrophic or extensive vegetative ulcerations frequently mimic other infectious diseases and malignancy, creating a complex diagnostic dilemma for clinicians. This case report describes a 41-year-old woman who presented with persistent, chronic ulcerated vulvar lesions. Due to the aggressive and granulomatous clinical appearance of the lesions, the initial differential diagnoses focused heavily on donovanosis (granuloma inguinale) and vulvar malignancy. To establish an accurate diagnosis, an extensive clinical investigation was performed. Polymerase chain reaction (PCR) testing definitively confirmed HSV-2 infection. Upon initial evaluation, the patient was found to have a newly diagnosed HIV infection during the current admission; however, she later disclosed a prior diagnosis of HIV dating back to 2005, which she had not previously reported. The patient was managed with targeted intravenous acyclovir therapy, which resulted in significant and complete clinical improvement of the vulvar lesions. This case emphasizes the high variability of opportunist-associated cutaneous presentations in the context of advanced immunosuppression. It underscores the vital role of molecular diagnostics and tissue biopsies in distinguishing atypical herpes simplex virus presentations from other sexually transmitted infections and malignancies, ensuring timely antiviral intervention.

Pritelivir, a novel helicase-primase inhibitor, has successfully completed a global Phase 3 trial for refractory herpes simplex virus (HSV) infections in immunocompromised patients. This case report is the first clinical use of pritelivir in Herpes simplex encephalitis (HSE). An allogeneic hematopoietic cell transplant recipient developed HSE and was treated with acyclovir. After 1.5 months, while still on valacyclovir prophylaxis, HSE relapsed, confirmed by Magnetic Resonance Imaging (MRI) and HSV1 DNA detection in cerebrospinal fluid (CSF). Following transient response to acyclovir and foscarnet, combined pritelivir/acyclovir treatment was initiated in this comatose patient with cerebral edema and necrosis. Clinical improvement occurred with increased alertness and motor activity, enabling discharge to rehabilitation. MRI showed no further progression, and CSF HSV DNA load became undetectable. No relevant adverse effects were observed. Pritelivir plasma and CSF concentrations exceeded the 50% effective concentration for HSV1. This case highlights the potential of pritelivir for treating HSE.

Acyclovir is the first-line treatment for neonatal herpes simplex virus infection; however, safety evidence in neonates remains limited. This study aimed to evaluate the safety profile of acyclovir in neonates using real-world pharmacovigilance data from the Food and Drug Administration Adverse Event Reporting System. This retrospective observational study analyzed adverse event (AE) reports in neonates (≤28 days) in which acyclovir was identified as the primary suspected drug in the Food and Drug Administration Adverse Event Reporting System from 2004 to Q3 2024. Disproportionality analyses were performed using the reporting odds ratio (ROR), proportional reporting ratio (PRR), Bayesian confidence propagation neural network, and empirical Bayesian geometric mean (EBGM). Positive risk signals were defined as those meeting the statistical significance criteria across all 4 methods. A total of 130 reports comprising 409 AEs were identified. Four system organ classes showed positive risk signals: skin and subcutaneous tissue disorders (ROR = 6.22, PRR = 5.88, lower limit of 95% confidence interval [CI] of the information component [IC025] = 1.98, lower limit of 95% CI of EBGM [EBGM05] = 4.16), general disorders and administration site conditions (ROR = 4.27, PRR = 3.47, IC025 = 1.47, EBGM05 = 2.85), hepatobiliary disorders (ROR = 3.85, PRR = 3.74, IC025 = 1.19, EBGM05 = 2.43), and renal and urinary disorders (ROR = 3.84, PRR = 3.70, IC025 = 1.24, EBGM05 = 2.51). At the preferred term level, 12 positive signals were detected, with the strongest signals observed for infusion site necrosis/edema (ROR = 939.92, 95% CI: 97.56-9055.25), arthritis (ROR = 179.47, 95% CI: 52.33-615.44), skin exfoliation/necrosis (ROR = 131.18, 95% CI: 46.00-374.06), and Kawasaki disease (ROR = 114.20, 95% CI: 36.21-360.15). Notably, Kawasaki disease, rectal hemorrhage, and necrotizing colitis were not described in existing product labeling. Acyclovir use in neonates may be associated with immune, gastrointestinal, hepatic, and renal AEs, underscoring the need for careful clinical monitoring. Further prospective studies are warranted to validate these associations.

Varicella-zoster virus (VZV) reactivation is a recognized complication in patients with multiple myeloma, particularly during treatment-associated immunosuppression. Although disseminated VZV infection is uncommon, delayed diagnosis may result in life-threatening disease. We report a Japanese woman in her 70s with relapsed and refractory multiple myeloma who developed anorexia, vomiting, and fever before the appearance of disseminated vesicular eruptions during daratumumab-based therapy. Laboratory findings showed cytopenia, marked liver dysfunction, and hypogammaglobulinemia. Disseminated VZV infection was confirmed by antigen testing, and prompt intravenous acyclovir resulted in clinical recovery. This case highlights that disseminated VZV infection may initially present with gastrointestinal symptoms before characteristic skin lesions during anti-CD38-based therapy, representing an important diagnostic pitfall. Early recognition, prompt antiviral therapy, and consideration of antiviral prophylaxis may help reduce the risk of severe disease.

Disseminated herpes zoster (DHZ) in immunocompromised patients is uncommon but potentially life-threatening. Pulmonary involvement is particularly rare and can mimic miliary tuberculosis, complicating the diagnosis. We report herein a 51-year-old, male, Japanese patient with a human immunodeficiency virus (HIV) infection, uncontrolled diabetes mellitus, and hidradenitis suppurativa in whom DHZ developed five months after he discontinued adalimumab therapy. He presented with a five-day history of fever, abdominal pain, and generalized vesicular eruptions. Chest computed tomography revealed small, diffusely distributed, bilateral nodules suggestive of miliary tuberculosis. However, acid-fast bacillus tests repeatedly returned negative. Endoscopic evaluation revealed multiple, gastric ulcerations, and immunohistochemical staining of gastric ulcer biopsy specimens confirmed a varicella-zoster virus infection. Intravenous acyclovir rapidly improved the cutaneous lesions, and the pulmonary nodules resolved almost entirely within 18 days. The gastrointestinal ulcers also healed with the antiviral therapy. The present case highlights the importance of considering DHZ in the differential diagnosis of diffuse, pulmonary nodules in immunocompromised patients, especially those with an HIV infection and a history of biologic therapy. Prompt diagnosis, appropriate, radiological follow-up, and early administration of antiviral therapy are crucial to ensuring a favorable clinical outcome.

Bilateral facial nerve palsy is a rare neurological condition in children and is infrequently associated with primary Varicella (chickenpox) infection. We report the case of a 10-year-old previously healthy girl who developed simultaneous bilateral lower motor neuron facial weakness 3 weeks after a self-limiting varicella infection. The patient presented with acute onset inability to close both eyes, difficulty smiling, drooling of saliva, and impaired oral competence. At presentation, the characteristic vesicular rash had completely resolved. Neurological examination demonstrated bilateral lower motor neuron facial nerve palsy with loss of forehead creases, lagophthalmos, flattening of the nasolabial folds, inability to puff the cheeks, and bilateral Bell's phenomenon, without additional neurological deficits. Laboratory investigations and brain magnetic resonance imaging (MRI) were unremarkable. Based on the temporal relationship with recent varicella infection and exclusion of alternative etiologies, a diagnosis of bilateral facial nerve palsy secondary to varicella-zoster virus infection was established. The patient was treated with intravenous aciclovir, corticosteroids, supportive eye care, and facial physiotherapy. Follow-up after 6 weeks demonstrated marked clinical improvement, including restoration of facial symmetry, improved eye closure, recovery of smiling ability, and resolution of drooling. This case highlights a rare neurological complication of primary varicella infection and emphasizes the importance of early recognition and multidisciplinary management to achieve favorable neurological outcomes.