Cases reported "Chickenpox"

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1/11. central nervous system and renal vasculitis associated with primary varicella infection in a child.

    A 7-year-old girl with primary varicella presented with encephalopathy and focal neurologic deficits 10 days after her first skin lesions appeared. She was discovered to have bilateral wedge-shaped renal infarctions, and ischemic lesions in the conus medullaris, cerebral cortex, and deep gray matter consistent with a medium and large vessel arteritis on magnetic resonance imaging. This complication has never before been reported in an immunocompetent child with primary varicella infection, and it represents a rare but serious complication of childhood chickenpox.
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2/11. Postvaricella angiopathy: report of a case with pathologic correlation.

    Varicella is a common childhood illness, and central nervous system complications occur frequently. Delayed angiopathy has been described, although there are few reports of clinicopathologic correlation. A previously well 4-year-old male is presented. He suffered varicella 2 months before presentation with extensive right middle cerebral artery (MCA) territory infarction. cerebral angiography demonstrated an isolated 89% stenosis of the right proximal MCA. He developed cerebral edema refractory to medical treatment and progressed to transtentorial herniation. Right frontal temporoparietal craniotomies were performed with evacuation of infarcted brain tissue. Pathologic studies revealed small vessel vasculitis with lymphocytic infiltration of the vessel wall. Areas of demyelination were present within the white matter. polymerase chain reaction for varicella was negative on brain tissue. Postvaricella angiopathy, although an uncommon complication, may affect both small and large blood vessels, with catastrophic results.
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3/11. retinal vasculitis associated with chickenpox.

    PURPOSE: To report retinal vasculitis in a young, immunocompetent Asian female adult with chickenpox. methods: Interventional case report. A 32-year-old woman had chickenpox 2 weeks before blurred vision in the left eye. The visual acuity was 20/20 for the right eye and 30/50 for the left eye. The left eye presented keratic precipitates, moderate (2 ) cells in the anterior chamber and numerous cells (3 ) in the vitreous. The disk was normal. Perivenous exudation was noted mainly in the inferior retina. The sheathed retinal vessels showed late staining but no remarkable leakage on fluorescein angiography. The right eye was normal. RESULTS: After treatment with acyclovir for 10 days, the visual acuity in the left eye improved to 20/20, and the vasculitis resolved. CONCLUSION: retinal vasculitis may present as a complication of primary varicella infection in an immunocompetent adult.
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4/11. cerebral infarction in an adult with disseminated varicella.

    A 26-year-old patient with disseminated varicella developed a cerebral infarction 11 days into the illness. cerebral infarction, typically delayed, is primarily reported in association with zoster with only one previous report in primary varicella. The mechanism is speculative and thrombosed vessels with and without vasculitis have been demonstrated. Our patient showed mild evidence of systemic alteration in immune function, suggesting the possibility of vasculitis.
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5/11. immunization, abrasion, and sunburn as localizing factors in chicken pox.

    Three children had striking localization of varicella lesions to skin overlying a diphtheria-pertussis-tetanus toxoid (DPT) immunization injection site, a facial abrasion, and a sunburn of the trunk, respectively. Presumably, during the viremic stage of varicella, the virus passed from damaged blood vessels into the skin. A disabling myalgia in the thigh at the DPT site in one child may also have been the result of localization of the varicella virus in the muscle during the inapparent viremic stage. This suggests that an injection given during an occult viremia could trigger an unexpected reaction at the site.
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6/11. chickenpox with delayed contralateral hemiparesis caused by cerebral angiitis.

    chickenpox and herpes zoster ophthalmicus are caused by the same virus. herpes zoster ophthalmicus can be followed by contralateral hemiparesis, which is thought to be caused by spread of varicella-zoster virus to blood vessels contiguous to the trigeminal nerve and its branches. We report what we believe to be the first case of a patient with chickenpox followed by hemiparesis in whom there was angiographic evidence of an associated vasculitis similar to that found with herpes zoster ophthalmicus.
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7/11. Pathogenesis of varicella-zoster angiitis in the CNS.

    A 20-year-old man with Hodgkin's disease experienced ophthalmic zoster with dissemination and CNS involvement. At autopsy, he was found to have granulomatous angiitis involving the basilar artery, and electron microscopy revealed virus-like particles in the outer layers of the vessel walls, but not the endothelium. This suggests that granulomatous angiitis of the CNS in varicella-zoster infections results from direct viral invasion of blood vessels, perhaps by contiguous spread from cranial nerves.
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8/11. adult-type systemic varicella in a female patient in course of treatment of her so-called reactive lymphocytic (T-cell) hyperplasia.

    A 31-year-old woman was examined in this case. biopsy revealed an abnormal nontumorous proliferation of T-cells in the lymph node. Clinically, the patient was treated by C-MOPP and steroid under clinical suspicion of T-cell lymphoma. In the period of observation of the course of illness, the patient contracted varicella from her real child and died on the 8th day of illness. She was examined pathologically, electron microscopically, and by the fluorescent antibody technique. Virus infections foci, which were mostly necrotic ones, were found in the parenchymatous and interstitial cells of skin, lung, adrenal gland, digestive organs, liver, lymph nodes, and genital organs. In the circulatory system, proliferative foci with degeneration of endothelial and adventitial cells were noticed in small veins or venules, but little change was found in the arterial system. Electron microscopic observation suggested a destruction of the so-called limiting basement membrane around blood vessels. This was an important finding indicative of a mechanism of viral transmission to the interstitial cell system.
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9/11. Postinfectious purpura fulminans caused by an autoantibody directed against protein S.

    OBJECTIVE: To determine the mechanism responsible for idiopathic purpura fulminans, we investigated the procoagulant and anticoagulant pathways in five consecutive patients, four after varicella, and the fifth after a nonspecific infection. methods: Procoagulant and anticoagulant factors, including protein c, protein S, and antithrombin iii, were measured by quantitative or functional assays. Anti-protein S autoantibodies were identified by dot blotting and Western blotting, and quantified serially by enzyme-linked immunosorbent assay. Clinical and laboratory data were collated retrospectively. RESULTS: In each case the disease began 7 to 10 days after the onset of the precipitating infection, with rapidly progressive purpura leading to extensive areas of skin necrosis. The illness was complicated by impaired perfusion of limbs or digits (two patients), peripheral gangrene resulting in an above-knee amputation (one patient), and major organ dysfunction caused by thromboembolic phenomena involving the lungs (two patients), the heart (one patient), or the kidneys (one patient). Protein S levels were virtually undetectable at the time of admission and failed to respond to infusions of fresh frozen plasma, despite correction of other procoagulant and anticoagulant factors. All five children had anti-protein S IgM and IgG autoantibodies, which persisted for less than 3 months after admission. Decline in the anti-protein S IgG antibody concentration was associated with normalization of the plasma protein S levels. CONCLUSIONS: Autoimmune protein s deficiency may be a common mechanism causing postinfectious idiopathic purpura fulminans. Recognition of the pathophysiologic mechanism may provide a rational basis for treatment. Immediate heparinization, infusions of fresh frozen plasma, and, in cases complicated by major vessel thrombosis, the use of tissue-type plasminogen activator may limit thromboembolic complications.
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10/11. Pre-eruptive neurologic manifestations associated with multiple cerebral infarcts in varicella.

    A boy, 4 years, 9 months of age, presented with acute hemiplegia, lethargy, ataxia, and dysarthria 24 hours prior to the eruption of typical varicella exanthem. magnetic resonance imaging findings were typical of multiple cerebral ischemic infarcts. It is suggested that during the period of secondary viremia varicella zoster virus invaded the cerebral blood vessels causing vasculopathy and cerebrovascular infarcts.
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