Acute nonsexually acquired genital ulceration (NSAGU) is uncommon in young children and presents a substantial diagnostic challenge because of its broad differential diagnosis. A 2-year-old girl presented with extensive bilateral vulvar ulceration and edema without systemic symptoms. Comprehensive evaluation excluded several infectious etiologies, sexually transmitted infections, and other major causes, although lesion-based herpes simplex virus testing was unavailable. The ulcers gradually resolved over 38 days following oral acyclovir, a single dose of ceftriaxone, and supportive care. Based on the clinical course and exclusion of alternative diagnoses, the presentation was considered most compatible with NSAGU, although a definitive infectious trigger could not be identified. This case highlights the importance of a broad diagnostic evaluation and cautious interpretation when definitive virologic testing is unavailable.

Herpes zoster (shingles) is the clinical manifestation of the reactivation of latent varicella-zoster virus from the dorsal root and cranial nerve ganglia. Approximately one-third of the population will develop herpes zoster, which most commonly results in a self-limited, painful, vesicular, dermatomal rash that resolves within 2 to 4 weeks. Complications of herpes zoster can result in chronic debility. Postherpetic neuralgia, a persistent dermatomal pain syndrome lasting longer than 90 days after symptom onset, is the most common complication, occurring in 10% to 18% of people who have herpes zoster. Older adults and immunocompromised individuals are at higher risk of developing herpes zoster and its associated complications. Treatment for herpes zoster involves antiviral medications (eg, acyclovir, valacyclovir, famciclovir) with or without adjunctive pain management. First-line treatment of postherpetic neuralgia includes gabapentinoids, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants. Topical drugs are an adjunctive treatment. Herpes zoster and its complications are largely preventable with vaccination (recombinant zoster vaccine), which is covered by Medicare and commercial insurances. Two doses of recombinant zoster vaccine are recommended for adults 50 years and older and those 19 years and older with immunocompromise. Obstacles to receiving vaccination include low awareness, administration errors, necessity of receiving multiple doses, and vaccine adverse effects.

Herpes simplex keratitis (HSK) caused by herpes simplex virus type 1 (HSV-1) is a major cause of infectious corneal blindness in developed countries. The disease reflects a variable combination of viral replication, immune-mediated inflammation and neurotrophic dysfunction, whose respective contributions determine both the clinical presentation and therapeutic strategy. Standard management relies on antiviral agents to suppress viral replication, corticosteroids to control immune stromal involvement and ocular surface optimisation to address chronic inflammation and neurotrophic impairment. Refractory forms, defined by a lack of clinical improvement despite appropriate treatment, require reassessment of adherence, pharmacokinetic exposureand underlying pathophysiology. In such cases, antiviral dose adjustment, the use of steroid-sparing immunomodulators and rigorous control of ocular surface inflammation are essential. Neurotrophic keratopathy may benefit from growth factor-based therapies, autologous serum, recombinant nerve growth factor or scleral lenses. The emergence of acyclovir-resistant HSV-1 strains, particularly in immunocompromised or long-term treated patients, represents an increasing concern. In these situations, alternative agents such as trifluridine, foscarnet or more recently, helicase-primase inhibitors, including amenamevir, have demonstrated clinical efficacy. The new strategies outlined here will all provide benefit in treating the drivers of refractory HSK, to quickly resolve and reduce risk of recurrence, providing new opportunities to prevent vision loss in refractory and antiviral-resistant cases.

Herpes zoster involving transferred free-flap skin is rare, particularly during the immediate postoperative period. A 49-year-old man underwent release of severe post-burn contracture of the left hand and wrist and reconstruction with a lateral thoracic perforator free flap. Pruritus and erythema developed on the contralateral upper back on postoperative day (POD) 0, followed by a thoracic dermatomal vesicular eruption on POD 3 that was clinically diagnosed as herpes zoster. Intravenous acyclovir was initiated. On POD 6, morphologically similar vesicles appeared on the transferred flap, and distal partial flap necrosis subsequently demarcated. Herpes simplex virus testing was negative, but varicella-zoster virus testing was unavailable; therefore, involvement of the flap could not be virologically confirmed. This unusual temporal sequence highlights viral reactivation as a differential consideration when vesicular lesions appear during early free-flap monitoring, while standard assessment for vascular compromise must continue.

Seasonal influenza vaccination is widely implemented and generally safe; however, rare immunological adverse events have been reported. We describe a case of multifocal mucocutaneous Herpes simplex virus type 1 (HSV-1) infection temporally associated with seasonal influenza vaccination in a 28-year-old man without a known immunocompromising condition. Seven days after vaccination, he developed oral ulcerative lesions and multiple vesicular eruptions involving the anterior chest wall, pubic region, and penile shaft. A multiplex polymerase chain reaction assay performed on specimens obtained from clinically apparent lesions detected HSV-1 DNA, whereas HSV-2 and other sexually transmitted pathogens included in the assay were not detected. Intravenous acyclovir was administered, resulting in complete clinical resolution. Although causality cannot be established, the close temporal relationship between influenza vaccination and the onset of HSV-1 infection is noteworthy, while alternative explanations cannot be excluded. This case highlights the importance of considering HSV infection in the differential diagnosis of multifocal mucocutaneous lesions occurring after influenza vaccination without implying a causal relationship.

Background: Herpes simplex encephalitis (HSE) is a rare but life-threatening infection of the central nervous system associated with high mortality and severe neurological sequelae. The diagnosis may be particularly challenging in patients presenting with atypical clinical or laboratory findings. Case presentation: An 85-year-old woman presented with progressive impairment of consciousness and generalized neurological deterioration. Initial neuroimaging suggested an acute ischemic stroke, whereas subsequent brain magnetic resonance imaging (MRI) demonstrated bilateral temporal and insular cortical abnormalities suggestive of encephalitis. Cerebrospinal fluid (CSF) analysis revealed no pleocytosis, and blood tests showed no markers of systemic inflammation during admission, which initially lowered the suspicion of infectious encephalitis. Although no inflammatory cells were detected in the routine CSF examination, polymerase chain reaction (PCR) testing confirmed infection with herpes simplex virus type 1 (HSV-1). Despite the prompt initiation of acyclovir after suspicion of encephalitis with MRI, together with corticosteroid therapy, anticonvulsants, and supportive treatment, the clinical course was fatal. Conclusions: This case highlights the diagnostic challenges associated with HSE, particularly in patients with normocellular CSF and radiological findings that may mimic other neurological conditions, including ischemic stroke. The absence of CSF pleocytosis does not exclude HSE, although the timing of CSF sampling should be considered when interpreting this finding. Early MRI and molecular CSF diagnostics remain essential for establishing an accurate diagnosis and ensuring timely treatment.

Varicella-zoster virus (VZV) and Epstein-Barr virus (EBV) are uncommon causes of aseptic meningitis in immunocompetent individuals. We report two cases of polymerase chain reaction (PCR)-confirmed viral meningitis caused by VZV and EBV in previously healthy young adults and compare their clinical presentation, cerebrospinal fluid (CSF) findings, neuroimaging, treatment response, and outcomes with previously reported cases. Both patients presented with lymphocytic meningitis and normal neuroimaging findings. The patient with VZV meningitis experienced rapid clinical improvement following acyclovir therapy and developed a vesicular rash two days after symptom onset, whereas the patient with EBV meningitis presented with a broader range of systemic and neurological symptoms and showed a more gradual recovery. Despite a shared lymphocytic CSF pattern, the two cases demonstrated distinct clinical and laboratory profiles. These findings highlight the importance of molecular testing for definitive diagnosis and support consideration of both viruses in the differential diagnosis of aseptic meningitis in immunocompetent patients.

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.