Varicella Zoster Virus Polymerase Chain Research Articles

D-Penicillamine Induced Myelotoxicity: A Unique Case.

Purpose: A case of D-penicillamine-related myelotoxicity in a patient with Wilson's disease is reported. Summary: There is a paucity of literature regarding D-penicillamine (DPA) induced myelotoxicity in the setting of Wilson's disease (WD). A 22-year-old male presented with a 1-week history of bleeding gums and dizziness. Four months prior, he had been diagnosed with Wilson's disease and started on a regimen of DPA. His blood counts demonstrated profound pancytopenia. Due to concern for suspected drug-induced myelotoxicity, DPA was discontinued. Parvovirus B19, Epstein-Barr virus, cytomegalovirus, and varicella zoster virus polymerase chain reaction studies were negative and there was no evidence of hematological malignancy. Bone marrow biopsy demonstrated hypocellularity and trilineage hypoplasia with corresponding aspirate flow cytometry confirming the absence of acute leukemia. The patient was started on subcutaneous granulocyte-colony stimulating factor, provided transfusion support with packed red blood cells and platelets. Despite these measures, his blood count failed to recover, and he was discharged on eltrombopag 150mg daily with plans for outpatient transfusion support. DPA was permanently discontinued, and he was prescribed trientine 750mg daily. Unfortunately, his myelotoxicity remained consistent, requiring regular transfusions. He is currently undergoing evaluation for bone marrow transplant. Conclusion: DPA-induced myelotoxicity is a rare clinical entity. Our case demonstrates a unique clinical presentation of this phenomenon. Guidelines to mitigate the risk of and treat this toxicity remain to be determined.

Bullous Tinea Pedis

A woman in her 70s presented with a skin eruption on the left dorsal foot that had developed spontaneously 2 weeks before. The rash initially appeared with pruritic papules that evolved to fluid-filled blisters and persisted despite self-treatment with topical hydrocortisone 1% cream and antibiotic ointment. Examination revealed an erythematous plaque with tense and denuded bullae (Figure 1). She received oral cephalexin for presumed bullous impetigo. Bacterial culture and herpes simplex virus and varicella zoster virus polymerase chain reaction (PCR) swab results were negative.

Case 302: Supratentorial Lymphocytic Inflammation with Parenchymal Perivascular Enhancement Responsive to Steroids.

Part one of this case appeared 4 months previously and may contain larger images. A 21-year-old immunocompetent man who was a long-term resident of Qatar presented to the emergency department with recurrent episodes of unprovoked generalized tonic-clonic seizures lasting 2-3 minutes that spontaneously resolved and were associated with postictal confusion. The patient also had progressive mild diplopia, intermittent dizziness, and numbness in the left arm over the course of 3 months. The patient did not have any other systemic symptoms or chronic medical diseases. He did not have any history of intake of illicit drugs, supplements, or regular medications; he had not received any recent vaccinations; and he had not undergone any surgical procedures. He had no history of travel. At presentation, vital signs were normal. Neurologic examination showed mild left homonymous hemianopia, normal gait with no cerebellar signs, and preserved sensations, power, tone, and reflexes in all four limbs. An electroencephalogram showed no epileptiform discharges. Chest CT and extensive laboratory work-up, including viral, fungal, bacterial, and parasite work-up, thyroid function tests, and immunologic blood tests yielded normal results. Those included normal complete and differential blood counts and normal serum chemistry. Serum analysis was negative for antinuclear antibody, Sjögren syndrome antigens A and B, cytoplasmic antineutrophil cvtoplasmic antibody, and paraneoplastic profile. Serum evaluation was also negative for human immunodeficiency virus type 1 and type 2 RNA, and Brucella, Schistosoma, and toxoplasma antibodies. Venereal Disease Research Laboratory (VDRL) and rapid plasma regain (RPR) test results were negative. Cerebrospinal fluid (CSF) analysis revealed clear fluid and normal pressure and biochemistry, except for elevated protein concentration (0.48 g/L) (normal range, 0.15-0.45 g/L). There were 43 leukocytes/µL (99% lymphocytes) (normal range, 0-5 leukocytes/µL; lymphocytes range, 40%-80%), with no atypical or malignant cells. CSF Gram staining, acid-fast staining, cryptococcal antigen, varicella-zoster virus polymerase chain reaction (PCR), herpes simplex virus PCR, VDRL, and RPR test results were negative. CSF cultures did not show any evidence of growth of bacteria, fungi, or acid-fast bacillus. CSF flow cytometry did not show a monoclonal lymphoid population. No CSF oligoclonal bands were detected. Conventional brain MRI with intravenous administration of contrast material and perfusion study were performed and included different sequences (Figs 1-3).

Acyclovir-induced neurotoxicity with a positive cerebrospinal fluid varicella zoster PCR result creating a management dilemma: a case report

BackgroundVaricella zoster virus central nervous system infections can present as aseptic meningitis, encephalitis, myelitis, and vasculopathy. Diagnosis is based on identification of varicella zoster virus deoxyribonucleic acid (DNA) in the cerebrospinal fluid by polymerase chain reaction. Therapy for these infections is acyclovir or valacyclovir. However, acyclovir can have neurotoxic effects that can mimic the presentation of varicella zoster virus central nervous system disease. We present a rare presentation of a patient who had acyclovir-induced neurotoxicity who also had a false-positive cerebrospinal fluid varicella zoster virus polymerase chain reaction result, creating a management dilemma. We review the clinical characteristics of acyclovir-induced neurotoxicity. In addition, we present the diagnostic characteristics of the cerebrospinal fluid viral polymerase chain reaction and alternative methods to diagnose central nervous system varicella zoster virus disease.Case presentationA 68-year-old Hispanic man with end-stage renal disease was diagnosed with cutaneous zoster at an outside facility and was started on acyclovir 4 days prior to admission. His family noted worsening confusion, agitation, speech difficulty, and hallucinations, leading them to bring him to the emergency department. His cerebrospinal fluid varicella zoster virus polymerase chain reaction result was positive, indicating the presence of varicella zoster virus deoxyribonucleic acid in the cerebrospinal fluid; however, he did not have cerebrospinal fluid pleocytosis typical of varicella zoster virus meningoencephalitis. Pharmacy records from the outside hospital revealed supratherapeutic acyclovir dosing. This led to a diagnostic dilemma over whether this patient had varicella zoster virus encephalitis or acyclovir-induced neurotoxicity. Acyclovir was discontinued, and the patient underwent two sessions of hemodialysis to remove acyclovir, which led to a full neurologic recovery.ConclusionsVaricella zoster virus encephalitis and acyclovir-induced neurotoxicity can have similar presentations. Varicella zoster virus deoxyribonucleic acid can be present in the cerebrospinal fluid during active cutaneous zoster in the absence of central nervous system disease. If concern for central nervous system varicella zoster virus disease remains high, additional testing with cerebrospinal fluid serology can be performed. Compared with central nervous system varicella zoster virus disease, acyclovir-induced neurotoxicity has a more predictable clinical resolution once drug therapy is discontinued or the patient undergoes hemodialysis, which can aid in making the diagnosis. Clinicians should be aware of this rare and dangerous complication of acyclovir. In addition, clinicians should have an understanding of the diagnostic limitations of cerebrospinal fluid viral polymerase chain reaction and have alternative approaches available to diagnose central nervous system varicella zoster virus disease when it is suspected.

Abducens Nerve Palsy Associated with Ramsay-Hunt Syndrome

Ramsay-Hunt syndrome is an infectious disease caused by the varicella zoster virus. It is usually associated with facial and vestibulocochlear nerve palsy, but other cranial nerve dysfunction can be accompanied. We present a 68-year-old woman with abducens nerve palsy associated with Ramsay-Hunt syndrome. She showed abduction limitation of left eye with peripheral facial palsy and vestibulopathy of the left side. Varicella zoster virus polymerase chain reaction of cerebrospinal fluid was positive and internal auditory canal magnetic resonance imaging was revealed enhancement of labyrinthine segment of left facial nerve. Although abducens nerve palsy is uncommon feature of Ramsay-Hunt syndrome, but it can be developed by several different mechanisms. Keywords: Abducens nerve palsy; Ramsay-Hunt syndrome 중심 단어: ì™¸ì „ ì‹ ê²½ë§ˆë¹„, Ramsay-Hunt 증후군

Ramsay Hunt Syndrome associated with central nervous system involvement in an adult: a case report

Background: Ramsay Hunt Syndrome with cerebellar encephalitis is rare in adult. Case Report: We describe a 55-year-old diabetic female who presented with truncal ataxia, right peripheral facial palsy and right ear pain associated with erythematous vesicular lesions in her external auditory canal. Later, she developed dysmetria, fluctuating diplopia and dysarthria. No facial lesions were identified and lesions were limited to the external auditory canal. Cerebral spinal fluid tested positive for varicella zoster virus polymerase chain reaction. She was diagnosed with Ramsay Hunt Syndrome with spread to the central nervous system and treated with acyclovir intravenous therapy (10 mg/kg every 8 hours). Her facial palsy completely resolved within 48 hours of acyclovir treatment, however, vesicular lesions, imbalance and cerebellar symptoms remained; a tapering course of high dose prednisone was then added.Discussion: Prognosis for facial palsy is poor in Ramsay Hunt Syndrome: Only 10% of patients will have complete resolution of their facial palsy. Improvement of facial palsy may be a good marker for response to treatment. Conclusion: Varicella zoster virus reactivation affecting the central nervous system in adults is rare. Knowledge of Ramsay Hunt syndrome with brainstem and/or cerebellar involvement is important for diagnosis and for consideration of antiviral and prednisone treatment.

Herpes Zoster Duplex Bilateralis in an Immunocompetent Adolescent Boy: A Case Report and Literature Review

Simultaneous involvement of herpes zoster in multiple dermatomes is uncommon, and even more so in immunocompetent individuals. We report a case wherein a healthy adolescent boy presented with herpes zoster in two distinct dermatomes, raising concern for immunodeficiency, but he was found to be immunocompetent on further testing. A 14-year-old boy with no significant past medical history developed painless vesicular eruptions in two distinct distributions. Varicella zoster virus polymerase chain reaction was positive from unroofed vesicles in both regions. Initial laboratory studies disclosed abnormalities of unknown significance in natural killer (NK) cell percentage and function. The patient was treated with appropriate antiviral therapy. Repeat studies while healthy were not suggestive of an underlying NK cell defect. There are few case reports describing herpes zoster in two or more dermatomes in children. Previously described presentations most commonly occurred in the context of primary immunodeficiency, acquired immunodeficiency, or immunosuppressive medications. Because of the rarity of this presentation in immunocompetent patients, the authors recommend a thorough immune evaluation of all children presenting with isolated multidermatomal zoster.