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Biomedical subjects

G Beards

Publications and source records attributed to G Beards.

7 recordsLinked to original sources

Management of hospital outbreaks of gastro-enteritis due to small roundstructured viruses.

Small round structured viruses (SRSVs, Norwalk-like viruses, NLVs) are the most common cause of outbreaks of gastro-enteritis in hospitals and also cause outbreaks in other settings such as schools, hotels, nursing homes and cruise ships. Hospital outbreaks often lead to ward closure and major disruption in hospital activity. Outbreaks usually affect both patients and staff, sometimes with attack rates in excess of 50%. For this reason, staff shortages can be severe, particularly if several wards are involved at the same time. SRSVs may be spread by several routes: faecal-oral; vomiting/aerosols; food and water. Viruses may be introduced into the ward environment by any of these routes and then propagated by person-to-person spread. In an outbreak setting, the diagnosis can usually be made rapidly and confidently on clinical and epidemiological grounds, particularly if vomiting is a prominent symptom. By the time an SRSV outbreak has been recognized at ward level, most susceptible individuals will have been exposed to the virus and infection control efforts must prioritize the prevention of spread of infection to other clinical areas bycontainment of infected/exposed individuals (especially the prevention of patient and staff movements to other areas), hand-hygiene and effective environmental decontamination. This report of the Public Health Laboratory Service Viral Gastro-enteritis Working Group reviews the epidemiology of outbreaks of infection due to SRSVs and makes recommendations for their management in the hospital setting. The basic principles which underpin these recommendations will also be applicable to the management of some community-based institutional outbreaks.

Caliciviridae Infections↗

Analysis of hepatitis B virus quasispecies changes during emergence and reversion of lamivudine resistance in liver transplantation.

This report describes nucleotide sequence analysis of part of the polymerase gene of hepatitis B virus (HBV) during the development of lamivudine-resistant HBV in five patients who received lamivudine treatment in conjunction with liver transplantation. Samples from patients were analysed before, during and after drug treatment in conjunction with serum HBV quantification by PCR. Lamivudine resistance was found to be associated with L526M and M550V changes in two patients and M550I change in three patients. Other changes associated with lamivudine resistance in some patients were V509I, A546V, S565A and A568T. The effects on HBV surface antigen are also described. Some patients were subsequently treated with famciclovir and/or ganciclovir with variable outcomes. In two out of three patients who stopped lamivudine treatment, reversion (partial or complete) to wild-type virus was observed after about 5 months. In contrast, a complex mixture of mutant viruses emerged in a third patient who stopped lamivudine treatment.

Antiviral Agents↗

Investigation of vesicular rashes for HSV and VZV by PCR.

Vesicular fluid from rashes of 132 patients was tested by a multiplex PCR shown to be specific for herpes simplex virus (HSV) type 1 and 2, and varicella zoster virus (VZV) genomic DNA. The results were compared with those obtained by examination by electron microscopy and virus isolation by cell culture. The PCR did not differentiate between HSV 1 and 2. By PCR, 64 HSV infections and 53 VZV infections were identified, with presumed 100% sensitivity and specificity. Fifteen specimens tested negative by PCR, electron microscopy, and virus isolation for herpes viruses. The sensitivities of virus isolation and electron microscopy for detection of herpes simplex virus were 56% and 80%. For varicella zoster virus, the sensitivities of virus isolation and electron microscopy were 47% and 60%. These data illustrate the advantage of rapid PCR diagnosis of herpes simplex virus and varicella zoster virus in vesicle fluids.

Adolescent↗

Temporal distribution of rotavirus G-serotypes in the West Midlands region of the United Kingdom, 1983-1994.

Samples of rotavirus from cases of acute gastroenteritis, occurring in the West Midlands region of the United Kingdom during the winter months of 1983 to 1994, were tested by enzyme-immunoassay for G-serotype (VP7). Statistically significant changes in the relative prevalence of serotypes occurred each year (p-values in chi-square tests were: p < 0.05 or p < 0.01). No consistent pattern was associated with these changes. G1, G2, G3, and G4 were the most common serotypes detected throughout the study period, accounting for 93.2%. Serotypes G5, G8, and G10 were detected in 0.4% samples, and serotypes other than G1 to G4 were detected in 6.8% samples. Thus, the rotavirus serotypes are less diverse here compared to other locations. These data are important for the development of an appropriate rotavirus vaccine.

Chi-Square Distribution↗

A serotype 10 human rotavirus.

Rotaviruses with genome rearrangements isolated from a chronically infected immunodeficient child (F. Hundley, M. McIntyre, B. Clark, G. Beards, D. Wood, I. Chrystie, and U. Desselberger, J. Virol 61:3365-3372, 1987) are the first recognized human isolates of serotype 10. This was shown by both a direct enzyme-linked immunosorbent assay and virus neutralization assays using serotype specific monoclonal antibodies. The serotype was confirmed by sequence analysis of the gene encoding VP7, which revealed a 96% amino acid homology to the bovine serotype 10 isolate B223.

Amino Acid Sequence↗

Heterogeneity of genome rearrangements in rotaviruses isolated from a chronically infected immunodeficient child.

Rotaviruses with genome rearrangements, isolated from a chronically infected immunodeficient child, were adapted to growth in BSC-1 cells. Preparations of viral RNA from fecal extracts showed a mixed atypical rotavirus RNA profile, which was due to the presence of at least 12 subpopulations of viruses grossly differing in genotype. Besides various forms of genome rearrangements involving segment 8-, 10-, and 11-specific sequences, reassortment in vivo was likely to have occurred during the emergence of these viruses. The protein products of viral genomes with various forms of segmental rearrangements seemed to be largely unaltered. Genome rearrangement is proposed to be a third mechanism directing the evolution of rotaviruses.

Animals↗