Cases reported "Herpes Zoster"

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1/21. MRI in human immunodeficiency virus-associated cerebral vasculitis.

    Cerebral ischaemia caused by inflammatory vasculopathies has been described as complication of human immunodeficiency virus (hiv) infection. Imaging studies have shown ischaemic lesions and changes of the vascular lumen, but did not allow demonstration of abnormalities within the vessel wall itself. Two hiv-infected men presented with symptoms of a transient ischaemic attack. Initial MRI of the first showed no infarct; in the second two small lacunar lesions were detected. In both cases, multiplanar 3-mm slice contrast-enhanced T1-weighted images showed aneurysmal dilatation, with thickening and contrast enhancement of the wall of the internal carotid and middle cerebral (MCA) arteries. These findings were interpreted as indicating cerebral vasculitis. In the first patient the vasculopathy progressed to carotid artery occlusion, and he developed an infarct in the MCA territory, but then remained neurologically stable. In the second patient varicella zoster virus (VZV) infection was the probable cause of vasculitis. The clinical deficits and vasculitic MRI changes regressed with antiviral and immunosuppressive therapy.
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2/21. Zosteriform and epidermotropic metastatic primary cutaneous squamous cell carcinoma.

    The first case of primary cutaneous squamous cell carcinoma (SCC) to cause zosteriform and epidermotropic metastasis to skin is reported. The patient is a 72-year-old Japanese woman. A cutaneous SCC appeared on the lateral side of her right knee and was removed. After dissection of the right inguinal lymph nodes, which revealed metastases, and irradiation of the right inguinal region, the patient presented with slightly pruritic and painful erythematous papules on the right hip and small brownish papules and vesicles with crusts on the anterior side of the right thigh. The eruptions were in a zosteriform distribution along the right L1 to L3 dermatomes. Histologically neoplastic squamous cell nests were observed in the epidermis, below the epidermal-dermal junction, and within lymphatic vessels in the deeper reticular dermis. We postulate that neoplastic cells with the ability to fuse with adjacent squamous epithelium may have been carried beneath the basal lamina or to the epidermis via dermal lymphatic backflow, resulting in epidermotropic metastasis.
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3/21. Palpable purpura at the site of previous herpes zoster in association with mixed cryoglobulinemia and hepatitis c virus infection.

    A 70-year-old woman affected with chronic active hepatitis c and mixed cryoglobulinemia presented a palpable purpura on her abdominal skin in a metameric configuration, fourteen months after a herpes zoster in the same site. Histopathology showed a small vessel leukocytoclastic vasculitis in the superficial dermis. Post-zoster eruptions are variable, and their spectrum is still expanding, although the pathogenesis remains to be elucidated. Perhaps our case represents an isomorphic reaction, because this palpable purpura, probably related to HCV infection, occurred several months after herpes zoster.
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4/21. Unilateral occlusion of the middle cerebral artery after varicella-zoster virus infection.

    We report a 4-year-old child who developed hemiplegia 6 months after varicella-zoster virus (VZV) infection. cerebral angiography showed complete occlusion of the right middle cerebral artery with basal moyamoya vessels. Elevation of anti-VZV antibody in the cerebrospinal fluid indicated central nervous system involvement. The association between VZV cerebral angitis and unilateral occlusion of right middle cerebral artery is discussed.
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5/21. Meningoencephalomyelitis with vasculitis due to varicella zoster virus: a case report and review of the literature.

    Varicella zoster virus (VZV) encephalitis is associated with large or small vessel vasculopathy. We report the case of a 67-year-old woman with a history of non-Hodgkin's lymphoma and cancers of the breast and colon, who presented with a zosteriform rash and brown-sequard syndrome. Despite 10 days therapy with intravenous acyclovir, meningoencephalitis developed and the patient died 15 days after onset of neurological symptoms. autopsy showed meningoencephalomyelitis with necrotising vasculitis of leptomeningeal vessels, which is a rare complication of VZV, and we review the literature of the nine similar published cases. polymerase chain reaction of cerebrospinal fluid for VZV was negative 6 days after onset of neurological symptoms, but became positive by day 10. Only one multinucleated giant cell with intranuclear Cowdry type A inclusions was seen within an endothelial cell in a leptomeningeal vessel involved by vasculitis.
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6/21. Varicella-zoster vasculitis presenting with intracranial hemorrhage.

    Cerebral vasculitis presenting with intracranial hemorrhage is a rare but known entity. We discuss here the case of a 61-year-old woman presenting with subarachnoid hemorrhage. cerebral angiography showed vasculitic changes involving the small and medium-sized vessels. She also had a concomitant herpes zoster rash on her back. A 3-month follow-up angiogram revealed partial resolution of the vasculitic changes.
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7/21. Multiple cerebral infarcts due to varicella-zoster virus large-vessel vasculopathy in an immunocompetent adult without skin involvement.

    We report the case of a 52-year-old immunocompetent man with varicella-zoster virus large-vessel vasculopathy and multiple bilateral cerebral infarcts who had no history of skin involvement. Etiologic diagnosis was made by isolation of varicella-zoster virus from a cerebrospinal fluid specimen. The patient had marked improvement in mental status after acyclovir therapy was initiated.
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8/21. Presence, distribution and spread of productive varicella zoster virus infection in nervous tissues.

    Nervous tissue lesions were retrospectively studied for detection of productive varicella zoster virus (VZV) infection in 33 autopsied cases, including 19 herpes zoster (HZ) (10 trigeminal, nine spinal) and 14 cases of nodular brainstem encephalitis without HZ. Immunocytochemistry for VZV antigens and in situ hybridization with a biotinylated VZV DNA probe were used on formol-fixed paraffin sections. Peripheral and central nervous system, skin and striated muscle were investigated in serial sections; available tissue blocks, however, varied between cases. Varicella zoster virus production (both antigen and DNA) in nervous tissue was found in HZ cases but only of short survival after a rash of up to 7 wks (eight out of 12 patients). Varicella zoster virus was visualized in nerve cells, glial cells, schwann cells and blood vessels. In the central nervous system (CNS), VZV was detected in trigeminal nuclei (one out of 10 brains) or disseminated nodular brainstem lesions (one out of 10 brains), in subependymal microvessels (one out of 10 brains) or vasculitic arteries (two out of 19 brains or spinal cords). In the peripheral nervous system (PNS), VZV (DNA and antigen) was found in neurons and satellite cells of sensory ganglia (four out of seven cases with sampling of ganglia), and in damaged nerve fibres including a muscle nerve in one case; myositis with VZV in affected muscle fibres was found in the latter case. In nodular brainstem encephalitis, one case contained VZV within nodular lesions. We conclude that (i) VZV neural spread is suggested by detectable virus in ganglia, nerve fibres and CNS target nuclei; (ii) haematogenous spread of VZV is suggested by detection of virus in CNS microvessels and in disseminated brainstem encephalitis; (iii) VZV myositis may occur in zosteric myotomes; and (iv) VZV is a possible agent in nodular brainstem encephalitis.
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9/21. Varicella-zoster virus encephalitis in acquired immunodeficiency syndrome: report of four cases.

    Four patients with acquired immunodeficiency syndrome, a 27-year-old female intravenous drug abuser and three males (two drug addicts aged 27 and 33 years and a 40-year-old homosexual) presented with a rapidly progressive encephalopathy. Two had generalized varicella-zoster virus skin infection, one had had a regressive thoracic zoster rash 7 months previously and one had no history of cutaneous eruption. Neuropathological examination revealed, in each case, multifocal necrotic changes with numerous, intranuclear Cowdry type A inclusion bodies in glial cells, endothelial cells, macrophages and neurons, within and around the lesions. These inclusion bodies were stained positively for varicella-zoster virus by immunocytochemistry and contained herpes virus nucleocapsids by electron microscopy. molecular biology using the polymerase-chain-reaction method demonstrated viral genome. In one case, zoster-induced non-inflammatory vasculopathy involved medium sized leptomeningeal vessels and was associated with circumscribed areas of cortico-subcortical infarction. In another case, varicella-zoster virus encephalitis was associated with human immunodeficiency virus encephalitis and a secondary cerebral lymphoma. Multinucleated giant cells expressing human immunodeficiency virus proteins in their cytoplasm, were found in the lymphomatous deposits and in the varicella-zoster virus necrotic lesions. In these latter lesions, Cowdry type A inclusion bodies could be seen in the nuclei of some multinucleated giant cells confirming previous observations of MGCs co-infected by hiv and CMV, and supporting the hypothesis that dna viruses interact with hiv, thus increasing its effect.
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10/21. Varicella-zoster-virus folliculitis promoted clonal cutaneous lymphoid hyperplasia.

    Post herpes zoster (HZ) reactions have been associated with panoply of neoplastic, inflammatory, and fibro-inflammatory cutaneous disorders. Varicella zoster virus (VZV) DNA has not been identified in most of these reports. After an episode of HZ, a healthy, active 90-year-old female developed ulcerative nodules in the affected trigeminal V1 dermatome and the contra-lateral trigeminal region over a 1-year period. Excision and/or biopsy of all these lesions showed similar pathologic changes that consisted of herpetic folliculitis, adjacent dense mixed nodular lymphocytic infiltrates with germinal centers (cutaneous lymphoid hyperplasia (CLH)), and in the deeper excision specimens, an obliterative vasculitis of a vessel with smooth muscle in its wall. Immunophenotype analysis revealed a mixed, predominate T- and B-cell population without loss of pan-T cell antigens or aberrant expression by B cells of T-cell antigens. polymerase chain reaction for herpetic DNA was positive for VZV DNA. Lymphocyte gene rearrangement analysis revealed 2 distinct, anatomically and chronologically, monoclonal B-cell populations and a monoclonal T-cell population in one nodule. Treatment with valacyclovir has lead to almost complete resolution of her cutaneous nodules after 6 months of therapy. In this case, it can be surmised that persistence of VZV infection and lack of effective cell-mediated immunity lead to development of both immunopathology (vasculitis) and excessive lymphoid cell proliferation (CLH).
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