Cases reported "Herpes Simplex"

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1/11. Multiple herpetic whitlow lesions in a patient with chronic lymphocytic leukemia.

    Herpetic whitlow, a herpes simplex virus infection involving the digits, most commonly presents as a vesicular eruption involving a single digit. diagnosis of herpetic whitlow can usually be made with the history of exposure, the characteristic vesicular eruption, and a positive Tzank smear and/or viral culture. We describe a case of herpetic whitlow in a patient finishing 6 cycles of chemotherapy for refractory chronic lymphocytic leukemia that presented with a bilateral, multi-digit, crusted eruption of the hands. This is an illustrative case of an immunocompromised host status altering appearance and course of cutaneous disease such that the history and physical exam alone may not help in diagnosing atypical presentations of herpetic infections. This case underscores the necessity for clinico-histopathologic correlation.
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2/11. Case study: inoculation herpes barbae.

    A 21-year-old white man in otherwise excellent general health was referred for a painful, progressive, facial eruption with associated fever, malaise, and cervicofacial lymphadenopathy. The patient reported that a vesicular eruption progressed from the left side of his face to also involve the right side of his face over the 48 hours preceding his clinic visit. He also reported some lesions in his throat and the back of his mouth causing pain and difficulty swallowing. Four to 7 days before presentation to us, the patient noted exposure to his girlfriend's cold sore. Additionally, he complained of a personal history of cold sores, but had no recent outbreaks. physical examination revealed a somewhat ill man with numerous vesicles and donut-shaped, 2-4 mm, crusted erosions predominantly on the left side of the bearded facial skin. There were fewer, but similar-appearing lesions, on the right-bearded skin. The lesions appeared folliculocentric (Figure). Cervical and submandibular lymphadenopathy was present. Oral exam showed shallow erosions on the tonsillar pillars and soft palate. Genital examination was normal. The remainder of the physical exam was unremarkable. A Tzanck smear of vesicular lesions was positive for balloon cells and many multinucleated giant cells with nuclear molding. A viral culture was performed which, in several days, came back positive for herpes simplex virus. The complete blood cell count documented a white blood cell count of 8000/mm3 with 82.6% neutrophils and 9.0% lymphocytes. Based on the clinical presentation and the positive Tzanck smear, the patient was diagnosed with herpes simplex barbae, most likely spread by shaving. The patient was started on acyclovir 200 mg p.o. five times daily for 10 days. oxycodone 5 mg in addition to acetaminophen 325 mg (Percocet; Endo Pharmaceuticals, Chadds Ford, PA) was prescribed for pain relief. A 1:1:1 suspension of viscous lidocaine (Xylocaine; AstraZeneca Pharmaceuticals LP, Wilmington, DE), diphenhydramine (Benadryl; Pfizer Inc., New York, NY), and attapulgite (Kaopectate; Pfizer Inc., new york, NY) was given as a swish and spit to relieve the oral discomfort. Good hygiene, no skin-to-skin contact with others, and no further shaving to prevent autoinoculation were stressed. He was advised to discard his old razor.
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3/11. A case study of the cognitive and behavioral deficits of temporal lobe damage in herpes simplex encephalitis.

    herpes simplex viral encephalitis is a fairly common nonepidemic encephalitis which produces severe neurological sequelae in survivors. Most viral infections of the central nervous system produce diffuse damage, but the herpes simplex virus demonstrates a predilection for localization in the temporal and orbitofrontal regions of the brain. This case study illustrates the highly significant language difficulties, marked memory deficits, and propensity for physical aggression following temporal lobe damage brought about by herpes encephalitis, and presents the usefulness of a new diagnostic measure in delineating such a variable cognitive pattern.
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4/11. Sudden death in a neonate as a result of herpes simplex infection.

    This paper describes a case of a neonate with disseminated herpes simplex born to a 14-year-old asymptomatic mother. The infant's physical examination was normal at birth, and subsequent abnormalities were so subtle that infection was not recognized during life. Postmortem cultures of liver and spleen grew herpes simplex virus, and immunofluorescent direct antibody typing revealed Type 2. A cervical culture of the mother obtained after the infant's death was negative.
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5/11. Exposure to chemicals, physical agents, and biologic agents in mycosis fungoides and the sezary syndrome.

    The history of occupational, environmental, and/or iatrogenic exposure to potential carcinogenic agents was obtained at the time of onset of skin disease in 43 of 44 patients with cutaneous T-cell lymphoma (mycosis fungoides and the sezary syndrome) entering a National Cancer Institute therapeutic trial. A history of multiple exposures to these agents was common, the two most frequent being chemicals (91% of patients) and drugs (86%). Mean duration of expsosure was 13 years for chemicals and 18 years for drugs. The most common chemicals were air pollutants (39%), pesticides (36%), solvents and vapors (30%), and detergents and disinfectants (14%). Increased severity of disease was seen with increaed duration of chemical exposure in stage V cutaneous T-cell lymphomas only. The most frequent drugs besides tobacco (86%) were analgesics (20%), tranquilizers (18%), and thiazides (14%). Second cancers occurred in four patients, including two renal cell carcinomas, and a family history of cancer was present in 11. Fourteen of 22 patients questioned had recurrent herpes simplex. patients with chronic skin disease who have long-term exposure to combinations of chemicals, physical agents, and biologic agents, are heavy smokers, or have recurrent herpes simplex appear to be prime candidates for developing mycosis fungoides or the sezary syndrome.
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6/11. Trial with human leucocyte interferon and vidarabine in herpes simplex virus encephalitis: diagnostic and therapeutic problems.

    A combination therapy of human interferon, vidarabine, and dexamethasone was administered to six patients with proven (patients I-III) or presumed (patients IV-VI) herpes simplex virus encephalitis (HSVE). Interferon combined with dexamethasone was given to one patient with presumed HSVE (Patient VII). Leucopenia and elevated serum transaminase levels appeared in all patients and a diffuse bleeding in one of them. patients II, III and IV died, 26, 43, and 209 days after the onset of encephalitis, respectively. patients I, V, VI, and VII were left with moderate brain damage although their physical condition was good. HSV encephalitis presents diagnostic difficulties, complementary diagnostic methods are needed, and current therapeutic trials must be considered as preliminary.
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7/11. herpes simplex viral pneumonitis in childhood.

    We report two cases of herpes simplex pneumonia in children. One patient had down syndrome, and the other was immunosuppressed by cancer therapy. Both had interstitial pneumonitis with nonspecific physical, radiographic, and laboratory findings, and both died. The diagnosis of herpes simplex pneumonia was made by isolation of herpes simplex virus from autopsy lung cultures as well as by demonstration of antigen in the tissue with an immunoperoxidase procedure. Inasmuch as herpes simplex pneumonia is a potentially treatable infection, early virologic studies are recommended in immunocompromised children with progressive pneumonitis of undetermined cause.
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8/11. Congenital absence of scalp skin and herpes simplex virus. A case report.

    A male infant, born at 40 weeks' gestation of a 27-year-old mother, presented at delivery with three scalp lesions, 2 to 4 cm in diam, covered with necrotic tissue and devoid of hair. The infant was born by natural vertex delivery within 2 hours of membrane rupture; birth weight was 3,300 g and apgar score 10. There were no other skin lesions, and physical and neurological examinations were normal. herpes simplex virus Type 2 was isolated from the lesions and the mother's cervix. High titers of IgG and IgM antibodies in the serum of mother and infant indicated an intrauterine infection. The skin ulcers healed within 1 month, with gradual epithelization and formation of a hairless atrophic scar.
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9/11. Neonatal herpes simplex virus infection introduced by fetal-monitor scalp electrodes.

    An infant was severely infected with herpes simplex virus as a result of fetal monitoring with scalp electrodes on the buttocks. The first vesicles appeared at the site where the electrodes had been placed and, by day 9 after birth, additional lesions covered the entire perineum and lower extremities. The child developed acute meningoencephalitis and pneumatosis intestinalis. herpes simplex virus was isolated from cultures of skin vesicle fluid, cornea, saliva, blood, and spinal fluid. The infection resolved after treatment with adenosine arabinoside, administered intravenously for 11 days and applied topically for another 15 days. A follow-up examination when the child was 2 years old disclosed no physical or neurologic abnormalities. This case illustrates the risk of introducing herpes simplex infection by internal fetal monitoring.
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10/11. Waldenstrom's macroglobulinemia and neuropathy. Deposition of M-component on myelin sheaths.

    Chronic idiopathic polyneuropathy of a primary demyelinating type developed in a man who had had recurrent herpes simplex 2 for 10 years. A serum IgM kappa M-component was demonstrated on the myelin of individual sural nerve fibers by direct immunofluorescence microscopy. Marrow lymphocytosis and serum M-component increased with time. Attempts to confirm antibody activity of the M-component were negative. The evidence suggests that the attachment of M-component to nerve is a physical-chemical one. Interaction of M-component and nerve appears to have led to the neuropathy as an early manifestation of Waldenstrom's macroglobulinemia.
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