[On the clinical aspects of concomitant course of adenovirus and enterovirus infection].
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Adenoviridae↗
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Results for “ENTEROVIRUS INFECTIONS”
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ENTEROVIRUS INFECTIONS: ETIOLOGIC, EPIDEMIOLOGIC AND CLINICAL ASPECTS.
The term enteroviruses was introduced in 1957 to bring together in one large family the polioviruses, Coxsackie A and B and echoviruses, all agents for which the human alimentary tract is the natural habitat. At present more than 60 distinct members are recognized: three polioviruses, 24 Coxsackie A, six Coxsackie B and 30 echoviruses. The list of new members, particularly in the echo-group, grows regularly. The viruses are frequently widely disseminated in the summer and fall of the year, circulating chiefly among young children, causing both apparent and inapparent infection. The enteroviruses are responsible for a wide spectrum of clinical manifestations, including non-specific febrile illness, sometimes with rash, aseptic meningitis, paralytic disease, respiratory infections, pericarditis and myocarditis. There is considerable overlap in biologic behavior, and the same syndrome can be induced by many different agents. In a few instances the clinical pattern is distinct enough to suggest the group of agents involved. Thus, herpangina is associated with the Coxsackie A viruses and epidemic myalgia (devil's grip) with the Coxsackie B group. Paralytic disease is caused primarily by the polioviruses, but recently it has been found that other members, particularly the Coxsackie B viruses and Coxsackie A7 can also cause "paralytic poliomyelitis."The ultimate potential of enteroviruses in terms of central nervous system disease and other manifestations is unpredictable. Great variety in terms of clinical and epidemiologic behavior of known and "new" viruses has been the pattern in the past, and is likely to continue.
Central Nervous System Diseases↗
Detection of enterovirus RNA in clinical samples by nested polymerase chain reaction for rapid diagnosis of enterovirus infection.
Employing a nested polymerase chain reaction with primers from the 5' non-translated region of the enterovirus genome, we detected enteroviral RNA from patients with a variety of enterovirus-associated clinical syndromes. This technique was found to be sensitive (detecting enteroviral RNA extracted from 0.1 50% tissue culture infectious dose) and specific; no specific PCR product was detected from RNA extracts of a variety of non-enterovirus isolates. Although the technique is of comparable sensitivity to single round polymerase chain reaction followed by Southern blot hybridization, it was more rapid, since it enabled a diagnosis to be made within 1 day. Thus, using nested polymerase chain reaction we were able to detect enteroviral RNA in 31 of 46 clinical specimens from 17 of 23 patients with suspected enterovirus infections. The samples included cerebrospinal fluid, throat swabs, stool, vesicle fluid, peripheral blood lymphocytes, whole blood and pericardial effusion. In contrast virus was isolated in only 17 of 42 clinical specimens from 12 of 22 these patients. In preliminary studies, restriction endonuclease analysis of polymerase chain reaction products enabled us to distinguish between non-polio enteroviruses and poliovirus types 1, 2, and 3. This additional technique may be useful in distinguishing between such infections in polio-endemic countries where rapid public health measures may be required.
Adult↗
[Specific clinical, epidemiological patterns and laboratory diagnostics of enterovirus infection in the Republic of Belarus].
The clinical and epidemiological patterns as well as the results of the laboratory verification of the outbreak of enterovirus infection (EVI) in Minsk during the period of summer-autumn, 2000, are presented. During this outbreak a variety of clinical forms were observed, the serous meningitis being prevalent (57.5%). Practically simultaneous occurrence of infection on the territory of all administrative districts of the city, the predominant involvement of children aged up to 14 years into the outbreak, a high proportion of simultaneous casualities in the multiple foci. A number of circulating enteroviruses (EV)--ECHO 30, ECHO 6 of three serotypes and Coxsackie B5--were simultaneously isolated from clinical material. EV of the same serotypes were isolated from tap drinking water, and neutralizing antibodies to these serotypes were often detected in the patients blood sera. Infectious EV were also present in samples of bottled water and in water reservoirs used for bathing. The routes of EV transmission and the improvement of EVI control are discussed.
Adolescent↗
The inactivation of enterovirus infectivity by the sulfhydryl reagent p-chloromercuribenzoate.
The infectivity of several enteroviruses was inactivated by the sulfhydryl reagent p-chloromercuribenzoate (PCMB). The rate of inactivation was dependent on the ionic environment in which the reaction was carried out. Inactivation of infectivity was reversed by the thiol compound, reduced glutathione. Under certain conditions, PCMB prevented the adsorption of some enteroviruses to monolayer cultures of monkey kidney cells. The results suggest that enterovirus sulfhydryl groups are involved in the establishment of infection, and that they play a role in the adsorption of virus to host cells.
Benzoates↗
Adverse effects of maternal enterovirus infection on the fetus and placenta.
Gestational outcome in a murine model of congenital enterovirus infection was evaluated. Pregnant mice were inoculated intravenously with Theiler's murine encephalomyelitis virus (TMEV), a murine enterovirus, or with BHK 21 cell lysate (control) at 6-7 days of gestation (early) and sacrificed 6 or 12 days later, and their placentas and fetuses were studied. High rates of gross and histologic abnormalities (50%-87%) were seen in placentas and fetuses from dams infected with TMEV and sacrificed 6 days later. TMEV-infected dams sacrificed 12 days after inoculation had lower rates of placental-fetal abnormalities (25%-57%) but an additional 42% rate of complete pregnancy loss. Pregnancy loss (9%) and placental-fetal abnormalities (4%-7%) were uncommon in control animals. Rates of fetal abnormalities and placental infection in infected dams exceeded fetal viral infection, suggesting that TMEV infection adversely affects pregnancy either directly by fetal damage or indirectly by placental compromise.
Abortion, Spontaneous↗
Intrauterine fetal demise associated with enterovirus infection.
We have presented a case of fetal intrauterine enterovirus (coxsackievirus A) infection at 36 weeks' gestation. Viral infection should be suspected when there is a history compatible with viral illness in the mother during pregnancy. Although an increased level of IgM antibodies in cord blood suggests a previous intrauterine infection, the diagnosis of fetal or neonatal viral infection ultimately depends upon the isolation of the viral agent.
Adult↗
Enterovirus infections of the central nervous system.
The genus Enterovirus is a large group of viruses belonging to the family Picornaviridae. They have a worldwide distribution, cause a wide spectrum of disease, and are a common cause of central nervous system disease. Included among the sixty-six enterovirus serotypes known to infect humans are the three poliovirus (PV) serotypes, the cause of paralytic poliomyelitis (PPM). PPM has been controlled in many parts of the world by vaccination. Molecular and functional comparison of PV vaccine strain and wild neurovirulent PV strains has provided an insight into mechanisms of neurovirulence. Enteroviruses are also the most commonly implicated viral agents of aseptic meningitis. Less commonly they cause a more serious encephalitis. Specific antiviral treatment for enterovirus infections is not currently available. Virological diagnosis is nonetheless important to distinguish between enterovirus-induced meningitis or encephalitis and other treatable causes of disease with a similar clinical picture.
Animals↗
Diagnosis of horizontal enterovirus infections in neonates by nested PCR and direct sequence analysis.
A hospital-acquired outbreak with febrile illness and/or rash occurred in our neonatal special care nursery (SCN) from September 1995 to September 1996. A total of 23 infants developed symptoms. We could not detect the etiological agents by routine virus isolation. In a retrospective study, however, enterovirus RNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) from four out of six cerebrospinal fluid (CSF) samples and from two of 12 sera. Thus six out of 16 patients from whom samples were obtained were diagnosed retrospectively as having enterovirus infection. Furthermore, we detected the enterovirus genome from four of 20 serum samples obtained from patients who had other clinical symptoms, and from infants hospitalized without noticeable clinical illness during the same periods. This outbreak was caused by two different enteroviruses, which we assumed were echovirus type 7 (Echo 7) and coxsackievirus B3 (Cox B3), because of the sequence results. We demonstrated the clinical advantage of the analysis of nucleotide sequencing as supportive evidence of transmission.
Base Sequence↗
[An experience in applying Watson's theory in caring for an enterovirus-infected child and his primary caregiver].
Enterovirus is commonly seen in children. Its morbidity and mortality rate is about 18% (Department of Health, the Executive Yuan, 2003). This paper documents the use of Watson's theory in the care of a child aged two years and seven months and his primary caregiver. During the nursing process, the application of care and concern for the child and primary caregiver provided confidence, comfort, and relief of fear and anxiety caused by hospitalization, enabling the patient, during his time in hospital, to make physical and psychological progress. The caregiver was also able to gain an understanding of how to care for a child with enterovirus, which diminished some of the pressure caused by his admission to hospital and placed him and his family at the center of the nursing care.
Caregivers↗
Enterovirus infections in children.
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Child↗
The effect of immunosuppression with cyclophosphamide on an experimental porcine enterovirus infection in piglets.
Eleven specific pathogen-free, five week old piglets were infected orally with the T80 strain of porcine enterovirus type 2. Three days after infection, five of the piglets were treated with cyclophosphamide, together with two of four uninfected control piglets. The treated, infected piglets developed severe diarrhea, and one showed signs of encephalomyelitis. These piglets showed no virological evidence of recovery from the infection, since the virus persisted throughout the intestinal tract, and they failed to mount a serological response. It was concluded that immunosuppression with cyclophosphamide impaired the normal recovery mechanisms in this infection, providing further evidence that the humoral immune response is an important defence mechanism against porcine enterovirus infection in piglets.
Animals↗
[Limiting surface-active substances and enterovirus infection].
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Detergents↗
Characterization of the placental barrier to murine enterovirus infection.
We performed studies to characterize the mechanisms responsible for development during gestation of a placental barrier to Theiler's murine encephalomyelitis virus (TMEV) in a murine model of gestational enterovirus infection. Electron microscopy of placentae infected in early gestation revealed TMEV-induced changes in the decidua, giant cell, spongiotrophoblast, and labyrinth layers; in contrast, placentae infected in middle and late pregnancy demonstrated degenerative changes in the decidua, giant cell, and spongiotrophoblast layers but not in the labyrinth. Immunohistochemistry and in situ hybridization of placentae infected in early or late gestation demonstrated accumulation of monocytes/macrophages in infected, histologically damaged labyrinths, but no infiltration of immune cells into infected but histologically normal placental regions. Silver staining of placentae from dams inoculated in late gestation with inert gold beads the size of TMEV virions revealed beads within the decidua, giant cell, and spongiotrophoblast layers, but restriction of beads from labyrinths, similar to the usual distribution of TMEV in placentae infected in late pregnancy. These experiments suggest that anatomical relationships, and not systemic immune response, appear to be a major contributor to the murine placental barrier to TMEV.
Animals↗
Enterovirus infection--a possible trigger for Graves' disease?
Viruses are potential environmental factors in autoimmune disease. Some evidence suggests a relationship between enteroviral infection (especially Coxsackie B virus) and autoimmunity. We investigated 21 individuals with recent onset of Graves' hyperthyroidism in regard of (subclinical) enterovirus infection. Thyrotoxic symptoms had started about two months before blood sample collection. The patients were from Upper Austria and mainly female (17/21). Their mean free thyroxin levels in blood were twice the maximum normal value and the majority achieved a euthyroid state 1 1/2 years later, after antithyroid medication. We employed a nested PCR reaction with primers of the enterovirus genome on blood samples. All were negative for RNA of the enterovirus group. Coxsackie and related viruses were not identified as a trigger factor in autoimmune thyrotoxic disease.
Adult↗
Rapid differentiation of rocky mountain spotted fever from chickenpox, measles, and enterovirus infections and bacterial meningitis by frequency-pulsed electron capture gas-liquid chromatographic analysis of sera.
Normal sera and sera from patients with Rocky Mountain spotted fever, chickenpox, enterovirus infections, measles, and Neisseria meningitidis infections were extracted with organic solvents under acidic and basic conditions and then derivatized with trichloroethanol or heptafluorobutyric anhydride-ethanol to form electron-capturing derivatives of organic acids, alcohols, and amines. The derivatives were analyzed by frequency-pulsed electron capture gas-liquid chromatography (FPEC-GLC). There were unique differences in the FPEC-GLC profiles of sera obtained from patients with these respective diseases. With Rocky Mountain spotted fever patients, typical profiles were detected as early as 1 day after onset of disease and before antibody could be detected in the serum. Rapid diagnosis of Rocky Mountain spotted fever by FPEC-GLC could permit early and effective therapy, thus preventing many deaths from this disease.
Adolescent↗
Enterovirus infection in human pancreatic islet cells, islet tropism in vivo and receptor involvement in cultured islet beta cells.
AIMS/HYPOTHESIS: It is thought that enterovirus infections cause beta-cell damage and contribute to the development of Type 1 diabetes by replicating in the pancreatic islets. We sought evidence for this through autopsy studies and by investigating known enterovirus receptors in cultured human islets. METHODS: Autopsy pancreases from 12 newborn infants who died of fulminant coxsackievirus infections and from 65 Type 1 diabetic patients were studied for presence of enteroviral ribonucleic acid by in situ hybridisation. Forty non-diabetic control pancreases were included in the study. The expression and role of receptor candidates in cultured human islets were investigated with receptor-specific antibodies using immunocytochemistry and functional assays. RESULTS: Enterovirus-positive islet cells were found in some of both autopsy specimen collections, but not in control pancreases. No infected cells were seen in exocrine tissue. The cell surface molecules, poliovirus receptor and integrin alphavbeta3, which act as enterovirus receptors in established cell lines, were expressed in beta cells. Antibodies to poliovirus receptor, human coxsackievirus and adenovirus receptor and integrin alphavbeta3 protected islets and beta cells from adverse effects of poliovirus, coxsackie B viruses, and several of the arginine-glycine-aspartic acid motifs containing enteroviruses and human parechovirus 1 respectively. No evidence was found for expression of the decay-accelerating factor which acts as a receptor for several islet-cell-replicating echoviruses in established cell lines. CONCLUSIONS/INTERPRETATION: The results show a definite islet-cell tropism of enteroviruses in the human pancreas. Some enteroviruses seem to use previously identified cell surface molecules as receptors in beta cells, whereas the identity of receptors used by other enteroviruses remains unknown.
Adolescent↗