Cases reported "Herpes Zoster"

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1/32. Paroxysmal cold haemoglobinuria in an adult with chicken pox.

    Paroxysmal cold haemoglobinuria (PCH) is an autoimmune disorder characterized by intravascular haemolysis causing haemoglobinuria. It is due to a biphasic haemolysin known as the Donath-Landsteiner antibody, which binds specifically to the P antigen of red blood cells at low temperatures, leading to complement activation and red cell lysis at 37 degrees C. PCH is a rare disease which predominantly affects the paediatric population, occurring mostly during viral infections. We report on what is possibly the first case of PCH in an adult to be precipitated by chicken pox infection.
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2/32. herpes zoster of the maxillary branch of the trigeminus nerve. Virological and serological studies.

    A 70-year-old male had erythematous and vesiculous lesions in the area of the right maxillary branch of the trigeminus nerve and was clinically diagnosed as having herpes zoster; virological and serological investigations of this case were carried out. Consequently, an electron microscopic observation revealed a great number of virus particles of herpes type in the vesiculous lesion and in baby hamster kidney BHK21/WI-21 cells, cultured after inoculating the fluid from the vesicle formed on the patient's upper lip or from serum harvested during the viremia. When BHK21/WI-21 cells infected with this virus were tested for antigenicity by an indirect immunofluorescent staining technique, they showed a positive staining to antivaricella-zoster virus. When serum of this patient was assayed fof the antibody level against varicella-zoster virus by the complement fixation test at various time intervals during the therapeutic period, this antibody titer on recovery period showed a threefold increase in comparison to that at onset. From these findings, this infectious disease was precisely diagnosed as herpes zoster.
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3/32. 10: herpes simplex and varicella-zoster virus infections.

    Any new patient with suspected genital herpes should have diagnostic testing with virus identification. Type-specific serological tests that distinguish between antibodies for type 1 and type 2 herpes simplex virus (HSV) may be useful to determine previous exposure but cannot be used to diagnose recurrences of genital herpes. Initial episodes of genital herpes usually require antiviral therapy, while recurrences may be treated with continuous antiviral suppression (if frequent) or episodic therapy; patient counselling and education (including how to recognise lesions) are essential. Topical or systemic therapy is available for initial and recurrent non-genital herpes simplex. Primary varicella infection (chickenpox) and herpes zoster (shingles) are usually diagnosed clinically, but can be confirmed by detection of varicella-zoster virus antigens or nucleic acid from swabs of lesions or by antibody tests. Antiviral therapy should be considered in chickenpox if disease is complicated or the patient is immunocompromised. In herpes zoster, antiviral therapy should be given within 72 hours of onset to patients aged over 50 years or with severe pain or neurological abnormalities to reduce the likelihood and duration of postherpetic neuralgia. The availability of effective antiviral therapy makes early diagnosis vital
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4/32. 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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5/32. Unique angiopathy after herpes virus infection.

    OBJECTIVE: We describe 3 Japanese patients with peculiar renal and/or coronary arterial stenosis and/or multiple aneurysms after herpes virus infection, following ischemic symptoms. We investigated for viral antigens and viral dna in situ, and for shared abnormalities of cellular immunity. methods: Panarteriography was performed diagnostically, and patients were grouped as follows: 3 patients with peculiar renal and/or coronary artery narrowing and/or multiple aneurysms; another 3 patients with renal fibromuscular dysplasia; and other young adults with effort angina, with no history of herpes virus infection, as controls. Detection of viral antigens and viral dna in situ was done by polymerase chain reaction method and immunohistochemical staining. Cellular immunity was examined at the time of ischemic symptoms. RESULTS: Viral antigens and dna were scarcely detected, except in herpes zoster skin lesion with leukocytoclastic vasculitis. However, shared abnormalities of cellular immunity, such as a decreased CD4 T cell number and reduced natural killer cell activity, were more prominent in the 3 patients with unique vasculopathy after herpes virus infection. CONCLUSION: Unique vasculopathy following herpes virus infection might be a more severe and extensive disease. We speculate that sustained viral infection, repetitive activation of virus related antigens, and suppressed immune state might contribute to formation of peculiar vascular alterations.
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6/32. Early-second-trimester use of acyclovir in treating herpes zoster in a bone marrow transplant patient. A case report.

    bone marrow transplantation from a human leukocyte antigen (HLA)-identical sibling for treatment of severe aplastic anemia among women of reproductive age is becoming more common. Successful pregnancy has been reported to occur in several such patients. A woman delivered a healthy, term, female infant 18 months after a transplant from her HLA-identical sister. Her pregnancy was complicated by disseminated herpes zoster, treated with intravenous acyclovir at 14 weeks' gestation, before the diagnosis of pregnancy. While there have been several case reports involving the use of acyclovir in the third trimester, primarily in the treatment of varicella infections, there have been no previous reports of such an early utilization of this antiviral drug.
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7/32. 'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection.

    Background: Specific cutaneous infiltrates in patients with leukemia generally carry a grim prognosis. However, non-neoplastic skin diseases may be associated with recruitment of normal and neoplastic leukocytes circulating in the peripheral blood. In those instances, neoplastic cells may be detected in skin lesions without an adverse effect on prognosis. methods: In a patient with B-cell chronic lymphocytic leukemia, a specific infiltrate developed at the site of a florid herpes simplex infection. Clinically, the lesion presented itself as an ulcerated tumor. Results: Histopathologically, the lesion was characterized by a dense, diffuse infiltrate of small hyperchromatic lymphocytes throughout the entire dermis. lymphocytes showed an aberrant CD20( )/CD43( )/CD5( ) phenotype of neoplastic B cells, and monoclonal rearrangement of immunoglobulin gamma genes could be demonstrated by polymerase chain reaction. Although criteria for leukemia cutis were fulfilled, the patient did well. Conclusions: The cutaneous infiltrate of neoplastic cells seemed to be part of a physiologic response to the antigenic stimulus, rather than indicating an exacerbation of leukemia. Ziemer M, Bornkessel A, Hahnfeld S, Weyers W. 'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection.
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8/32. 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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9/32. Coexistence of psoriasis and linear IgA disease in a patient with recent herpes zoster infection.

    We report the case of a 29-year-old man with chronic plaque psoriasis who developed linear IgA disease following herpes zoster infection. There has only been one previous report describing the coexistence of psoriasis and linear IgA disease, which was confirmed by immunopathological studies. In our patient, immunoblotting studies identified IgA antibodies binding to BP180 and BP230 antigens, and IgG autoantibodies binding weakly to the BP180 antigen. This is an interesting case that we believe is an example of epitope spreading in the development of autoimmune subepidermal bullous diseases.
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10/32. Varicella-zoster virus retinitis in patients with the acquired immunodeficiency syndrome.

    We examined five patients infected with the human immunodeficiency virus who developed a rapidly progressive necrotizing retinitis characterized by early patchy choroidal and deep retinal lesions and late diffuse thickening of the retina. In all but one case, the retinitis began in the posterior pole with little or no clinical evidence of vasculitis. All five patients had relentless progression of disease and were left with atrophic and necrotic retinae, pale optic-nerve heads, and narrowed vasculature. None of the patients developed aqueous or vitreal inflammation or retinal detachment. Clinical and laboratory evidence suggested that varicella-zoster virus was the causal agent in all five cases. First, the onset of retinitis in four cases either succeeded or was coincident with an eruption of dermatomal zoster. Second, varicella-zoster virus was cultured from the two chorioretinal specimens and varicella-zoster virus antigen was detected in the vitreal aspirate from one case. Third, by means of immunocytochemistry, varicella-zoster virus antigen was found in the outer retinae of both enucleation specimens. Fourth, viral capsids with the size and shape of herpesviridae were found in the outer retinae of both enucleation specimens. The clinical features observed in this study are distinct from those described for the acute retinal necrosis syndrome and appear to constitute a new and highly characteristic pattern of varicella-zoster virus-induced disease.
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