Cases reported "Herpes Zoster"

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1/26. Herpes incognito.

    Can a microscopist suspect that telltale histopathologic changes of infection by herpesvirus (varicella, zoster, or simplex) are nearby even when no diagnostic epithelial changes are present in the sections being studied? Punch-biopsy specimens from three patients are presented; in two of those cases herpesvirus infection was not even a clinical consideration. The initial histopathologic sections from these patients did not show changes of herpesvirus infection, but step sections revealed focal diagnostic changes. Atypical lymphocytes were present in each of these cases. When atypical lymphocytes are found in concert with a pattern of an inflammatory-cell infiltrate that does not conform precisely to any well-defined entity, a microscopist should consider that the findings may represent changes near infection by herpesvirus. In addition, we reviewed every case we diagnosed as herpesvirus infection over an 18-month period and found that in just over two thirds of those specimens (32 out of 45 cases), atypical lymphocytes accompanied the characteristic epithelial changes induced by herpesvirus.
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2/26. Monitoring four herpesviruses in unrelated cord blood transplantation.

    Cord blood transplantation, which has lower risk of graft-versus-host disease than bone marrow transplantation, might have higher risk of infections. A system to quantify four herpesviruses, CMV, human herpesvirus 6 (HHV6), EBV, varicella-zoster virus using the real-time PCR assay was established and applied for prospective viral load monitoring in three recipients undergoing cord blood transplantation. CMV and HHV6 were detected in peripheral blood from all three recipients, while EBV was detected in two. Varicella-zoster virus was not detected at all. At the peak of HHV6 or CMV, each patient showed virus-related symptoms. During the pre-transplant period, CMV dna was detected in two recipients who later developed CMV-related diseases. These observations indicate that our system is not only useful for managing herpesviruses infections in transplant recipients, but also a powerful method for clarifying the relationships between the viral load and clinical symptoms.
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3/26. Herpesvirus infection of seborrheic keratoses.

    We present three examples of patients with seborrheic keratoses complicated by necrotizing herpesvirus infection. Two patients had localized cutaneous herpetic infections, and the third patient had a generalized cutaneous herpesvirus infection. Two of the lesions were thought to be squamous cell carcinoma. The third was clinically identified as inflamed seborrheic keratosis. Herpesvirus infection was not clinically suspected in two of the patients. The histologic changes were similar in all cases. Epidermal proliferation was accompanied by hyperkeratosis and pseudo horn cyst formation. Extensive keratinocyte necrosis was present along with balloon degeneration of keratinocytes, herpetic viral inclusions, and multinucleated giant cells. Viral lesions of molluscum contagiosum and human papillomavirus have been observed in benign skin proliferations. Nevertheless, we were unable to find descriptions of herpesvirus involvement in seborrheic keratosis in a medline search. Necrotic seborrheic keratoses should be carefully examined for the possibility of herpesvirus infection, a condition that may be improved by prompt medical intervention as demonstrated in one of our cases.
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4/26. Concurrent herpes simplex type 1 and varicella-zoster in the V2 dermatome in an immunocompetent patient.

    A unique feature of herpesviruses is their ability to establish latent infection within the nervous system by colonizing peripheral sensory ganglia, which results in subsequent episodic outbreaks of infection triggered by precipitating events. Despite the latent nature of both herpes simplex virus type 1 (HSV-1) and varicella-zoster virus (VZV) within these sensory ganglia, simultaneous outbreaks of these viruses are uncommon. This is generally attributed to the differing reactivation features of these 2 viruses. Four cases of concurrent HSV-1 and VZV infection are described in the literature. We report concurrent infection of HSV-1 and VZV within the same V2 dermatome in an immunocompetent patient.
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5/26. Oesophagobronchial fistula caused by varicella zoster virus in a patient with AIDS: a unique case.

    Human herpesvirus oesophagitis in human immunodeficiency virus positive patients is caused by cytomegalovirus and herpes simplex virus; no cases of oesophagitis and oesophagobrochial fistula as a result of varicella zoster virus (VZV) have been reported to date. This report describes the case of a patient with a 2-3 mm deep oesophageal ulcer whose viral culture was positive for VZV. The patient was treated with acyclovir with resolution of the symptomatology. After the end of the induction treatment, because of the onset of fever and fits of coughing during eating, the patient underwent oesophagography, which showed an ulcer with an oesophagobronchial fistula in the middle and lower third of the oesophagus. This case report stresses the role of VZV infection as a possible cause of oesophagobronchial fistula, a rare but benign condition in patients with AIDS.
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6/26. granuloma annulare in a site of healed herpes zoster: Wolf's isotopic response.

    A case of granuloma annulare that developed in a site of healed herpes zoster is reported. polymerase chain reaction failed to detect VZV dna in a biopsy specimen. The occurrence of different types of cutaneous reactions in a body area previously affected by herpes virus infection is known as Wolf's isotopic response. Pathogenesis may be due to a local neuroimmune dysregulation set off by herpesvirus-induced lesions of dermal sensory nerve fibres.
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7/26. vidarabine therapy for severe herpesvirus infections. An unusual syndrome of chronic varicella and transient immunologic deficiency.

    Six patients with severe herpesvirus infections were successfully treated with vidarabine. One patient had a previously undescribed syndrome of chronic cutaneous varicella infection of eight months' duration, associated with transient but complete duppression of lymphocyte response to conconavalin A. Other diagnoses were severe varicella pneumonia, progressive cytomegalovirus pneumonia associated with acute lymphocytic leukemia, herpes simplex encephalitis, severe zoster associated with stage IV lymphoma, and disseminated herpes simplex in a patient receiving high doses of steroids. All patients showed cessation of new lesions or abrupt clinical improvement between days 2 and 4 after initiation of therapy, and all were cured of their clinical infection. Dramatic improvement in all of our patients and the minimal toxicity observed make vidarabine suitable for use in severe herpesvirus infections.
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8/26. Disseminated ecthymatous herpes varicella-zoster virus infection in patients with acquired immunodeficiency syndrome.

    Herpesvirus infections are among the most common and debilitating opportunistic infections in patients with acquired immunodeficiency syndrome (AIDS), and they may have atypical clinical features. We describe the cases of three patients with AIDS in whom atypical persistent ulcerative skin lesions developed as a result of varicella-zoster virus infection. Two patients had disseminated infection without a vesicular stage; one patient had underlying asteatotic eczema. All responded well to acyclovir. One patient was treated with azidothymidine, and typical dermatomal herpes zoster subsequently developed. The profound loss of helper T cell function in AIDS may lead to multiple abnormalities in local immune response to cutaneous herpesvirus infections and may be responsible for the atypical morphology and a prolonged course.
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9/26. Chronic progressive varicella-zoster virus encephalitis in an AIDS patient.

    A patient with AIDS developed chronic, progressive encephalitis. Pathologic changes indicated that the encephalitis was produced primarily by a human herpesvirus. Hybridization of radiolabeled rna probes transcribed from cloned dna fragments of varicella-zoster virus (VZV), herpes simplex virus, cytomegalovirus, and the human immunodeficiency virus to dna extracted from the patient's brain identified VZV as the causative agent. The results suggest that VZV should be considered in the differential diagnosis of chronic encephalitis of unknown etiology, particularly in immunosuppressed patients.
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10/26. Reactivation of herpesvirus in neurosurgical patients.

    The authors are presenting seven patients who had operations between July 1984 and July 1985 and who developed herpes infections postoperatively. Four of the patients developed their infections in a dermatomal distribution that correlated with the nerve roots manipulated at operation. A spectrum of localized herpes reactivation is demonstrated in this series. The use of corticosteroids and other associated variables are discussed. Like reactivation of herpes simplex after trigeminal nerve operation, we believe reactivation of herpes simplex and herpes zoster can occur in operation of the cervical, thoracic, or lumbosacral spine.
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