1/7. Fetal varicella syndrome: disruption of neural development and persistent inflammation of non-neural tissues.Primary varicella zoster virus (VZV) infection during pregnancy is rare. If it occurs between the 8th and 20th week of gestation, fetal varicella syndrome results in 1-2% of the fetuses. We report about a varicella infection that affected a pregnant mother in the 12th week of gestation. At 33 weeks, a premature girl was born with destruction of neurons in spinal cord, spinal ganglia and plexus myentericus, and secondary developmental disturbance including mummification of one arm and segmental intestinal atresia. The brain did not show any abnormalities. However, VZV dna could be detected by PCR in tissues from the brain and spinal ganglia. Chronic necrotizing inflammation was found in the placenta, fetal membranes, and one ovary. These locations showed nuclear inclusions which by in-situ-hybridization were proven to be VZV derived. This case demonstrates that in the fetal age, 'neurotropism' of VZV signifies severe destruction but not necessarily persistent inflammation of neural tissue. However, due to the inefficient fetal immune system, inflammation can go on for weeks, preferentially in non-neural tissues.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
2/7. Atypical recurrent varicella in 4 patients with hemopathies.Relapsing varicella may occur in children with hiv infection and more rarely in younger adults. Our aim was to report unusual clinical, histologic, and virologic aspects of 4 elderly patients with malignant hemopathies who had an unusual form of recurrent varicella develop. Conventional microscopy, immunohistochemistry, and in situ hybridization were applied to smears and skin biopsy specimens. The patients presented a few dozen, scattered, large, papulovesicular lesions with central crusting. No zoster-associated pain or dermatomal distribution of the lesions was noted. Conventional microscopy revealed vascular changes and epidermal alterations typical for alpha-herpes virus infection. The varicella zoster virus major viral envelope glycoproteins gE and gB, and the immediate-early varicella zoster virus IE63 protein and the corresponding genome sequence for gE were detected on Tzanck smears; they were localized in endothelial cells and keratinocytes on skin biopsy specimens. The varicella zoster virus infection in endothelial cells, the vascular involvement, and the widespread distribution of the lesions suggest that the reported eruptions are vascular rather than neural in origin. These findings invalidate the diagnosis of herpes zoster but strongly support the diagnosis of recurrent varicella in an indolent and yet unreported presentation. Furthermore, these eruptions differ from relapsing varicella in children and young adults by the age of the patients, the paucity of clinical lesions, the larger diameter of the lesions and their peculiar clinical aspect, the significantly longer time interval between primary varicella and the recurrence, the prolonged healing time of the lesions, their mild disease course, and the fact that all the lesions are in the same stage of development.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
3/7. Distribution of varicella-zoster virus dna and gene products in tissues of a first-trimester varicella-infected fetus.Precise information about varicella-zoster virus (VZV) infection in first-trimester fetuses remains sketchy. After varicella infection was diagnosed in a woman, her 12-week-old fetus was aborted and was investigated, by histological examination, virus culturing, polymerase chain reaction, in situ hybridization (ISH), and immunohistochemistry (IHC), for the presence of VZV infection. Only the results of the histological examination suggested the presence of alpha -herpesvirus infection, in the gastrointestinal tract and liver; results of ISH were positive for VZV, and results of IHC staining were positive for intermediate early protein 63 (IE63) but negative for glycoprotein E (gE), in the dorsal root ganglia (DRG), meninges, gastrointestinal tract, pancreas, smooth muscle, liver, and placental trophoblast, indicating the presence of a nonproductive, latency-like VZV infection. Only the gastrointestinal tract and liver exhibited simultaneous staining for IE63 and gE, a result suggesting that active replication of VZV was present. In conclusion, widespread nonproductive VZV infection in the absence of histological clues is an early event in VZV infection in fetuses. The observed gene-expression pattern in most tissues resembles that of latent VZV infection in DRG. Latency-like infection in nonneural cell types may potentially reactivate, leading to multifocal necrosis, fibrosis, and dystrophic calcifications, as observed in advanced congenital varicella syndrome.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
4/7. Virus detection in the fetal tissue of a premature delivery with a congenital varicella syndrome. A case report.Cases of congenital varicella syndrome have been published, to date, a single case reports. Isolation attempts of Varicella-Zoster virus from fetal tissues have, thus far, been unsuccessful. This is a first report of detection of Varicella-Zoster virus in fetal tissue by means of dna hybridization technique in a typical case of congenital varicella syndrome in a premature delivery of the 27th gestational week. The case is documented anamnestically, sonographically, pathologically and virologically. In women with primary varicella infection during pregnancy good sonographical controls are recommended. In cases with sonographically characteristical signs prenatal diagnosis with puncture of the umbilical vein cord and placentocentesis may be considered. The varicella dna detection should be supplemented, however, by the polymerase chain reaction.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
5/7. Varicella infection complicated with meningitis after immunization.A healthy 45 month old boy who had received varicella vaccine 21 months previously developed aseptic meningitis along with an episode of varicella. The presence of viral dna in cerebrospinal fluid (CSF) detected by polymerase chain reaction (PCR) with Southern blot hybridization confirmed the relationship between the symptoms and the CSF pleocytosis. This is the first reported case of this complication of varicella meningitis occurring in a child with documented immunization and seroconversion.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
6/7. Detection of varicella-zoster virus in congenital varicella syndrome: a case report.BACKGROUND: We studied the possibility of detecting varicella-zoster virus in formalin-fixed tissue samples from a still-born infant with congenital anomalies in order to verify the relationship with maternal varicella. CASE: A girl with hypoplasia of extremities, skin lesions, and microphthalmos was stillborn at 34 weeks' gestation. Her mother had had chickenpox between the 13th and 15th gestational weeks. Varicella-zoster virus dna could be detected in formalin-fixed tissue samples of lungs, spleen, adrenal glands, bulbus oculi, and placenta by polymerase chain reaction (PCR). The method, with the use of primers from gene 29 encoding the major dna-binding protein, proved to be highly sensitive. In addition, varicella-zoster virus dna/antigens were localized in some organs by in situ hybridization/monoclonal antibodies. CONCLUSION: The PCR method should be included in the diagnosis of congenital varicella syndrome. The varicella-zoster virus can be detected in formalin-fixed tissue samples using this technique.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |
7/7. Varicella-zoster virus infection associated with acute liver failure.Although acute liver failure due to the varicella-zoster virus is rare, it is frequently fatal. Immunologic impairment is a significant predisposing factor. Classic symptoms at presentation are rash, abdominal pain, and fever. After some days patients go on to develop full-blown liver failure. The diagnosis can be confirmed by histological examination and electron microscopy with fluorescent staining, immunohistochemistry, and in situ hybridization of the liver. In cases of high suspicion, acyclovir therapy should not be delayed.- - - - - - - - - - ranking = 1keywords = hybridization (Clic here for more details about this article) |