Biomedical subjects
A M Field
Publications and source records attributed to A M Field.
Use of a molecular probe for detecting JCV DNA directly in human brain material.
A hybridot assay using a radiolabelled JC virus probe has been used to detect the presence of JCV DNA in brain biopsy and postmortem brain samples from patients with neurological disease and possible progressive multifocal leucoencephalopathy. Sixty-nine brain samples from 45 patients were examined. Eleven samples from eight patients had detectable JCV DNA sequences. In seven of the eight patients this result was confirmed by electron microscopy and/or virus isolation or immunofluorescence.
The possession of three novel coli surface antigens by enterotoxigenic Escherichia coli strains positive for the putative colonization factor PCF8775.
A possible colonization factor, E8775, has previously been described for enterotoxigenic Escherichia coli strains of serogroups O25, O115 and O167. Re-examination of these strains by immunodiffusion has revealed that the antigenic nature of this factor, renamed putative colonization factor (PCF) 8775, is more complex than was first thought. All the strains of serogroup O25 tested possessed two antigenic components, termed CS4 and CS6, and gave mannose-resistant haemagglutination (MRHA) of human and bovine erythrocytes. Spontaneous variants possessing CS6 only did not give MRHA. Strains of serogroups O115 and O167 had the antigenic components CS5 and CS6, and gave MRHA of human, bovine and guinea-pig erythrocytes. Using immune electron microscopy, the components CS4 and CS5 were identified as fimbriae. No fimbriae were associated with CS6.
Properties of wild-type strains of enterotoxigenic Escherichia coli which produce colonization factor antigen II, and belong to serogroups other than O6.
Enterotoxigenic strains of Escherichia coli, which belonged to serogroups other than O6 and produced colonization factor antigen II, usually produced only coli surface antigen 3 (CS3) and gave weak mannose-resistant haemagglutination of bovine erythrocytes. A non-autotransferring plasmid, NTP165, from a strain of E. coli O168. H16 coded for heat-stable enterotoxin, heat-labile enterotoxin and CS antigens. The CS antigens expressed after acquisition of plasmid NTP165 depended on the recipient strain: a biotype A strain of serotype O6. H16 expressed CS1 and CS3; a biotype C strain of serotype O6. H16 expressed CS2 and CS3; strain K12 and strain E19446 of serotype O139. H28 expressed only CS3. An exceptional wild-type strain, E24377, of serotype O139. H28 produced CS1 and CS3 when isolated; a variant of E24377 which had lost the plasmid coding for CS antigens produced both CS1 and CS3 after the introduction of NTP165.
BK virus specific IgM responses in cord sera, young children and healthy adults detected by RIA.
An IgM capture solid-phase radioimmunoassay (MACRIA) for BK virus (BKV) specific IgM is described. This test was found to be more sensitive in detecting BKV specific IgM than both haemagglutination inhibition and immune electron microscopy with serum fractions from sucrose density gradients. The use of this specific assay allowed large numbers of sera to be examined with ease so that the distribution of BKV specific IgM in different populations could be studied more fully. BKV specific IgM was detected in 11/300 sera from London blood donors, in 24/114 sera from children aged between 2 and 11 years admitted to a paediatric unit and 14/79 sera taken from children aged between 2 and 5 years for the investigation of anti-streptolysin 0 titres. BKV specific IgM was not detected in 404 cord sera examined to investigate the transplacental transmission of BK virus.
Expression of plasmids coding for colonization factor antigen II (CFA/II) and enterotoxin production in Escherichia coli.
Two plasmids transferred from enterotoxigenic Escherichia coli (ETEC) of serotype O6. H16 and biotypes A and C coded for mannose-resistant haemagglutination (MRHA) and production of heat-stable enterotoxin (ST) and heat-labile enterotoxin (LT). Both plasmids were nonautotransferring being mobilized most efficiently by the R plasmid R100-1. They were similar in their genetic properties being incompatible with each other and plasmids of the Inc group FI. The wild-type strains produced the colonization factor antigen II (CFA/II) which was made up of different coli surface antigens (CS). The biotype A strains produced CS1 and CS3 while the biotype C strains produced CS2 and CS3. These three antigens have the ability to cause MRHA. When plasmids coding for MRHA were transferred to K12 strains, the degree of haemagglutination was markedly reduced and only CS3 was produced. When both plasmids were transferred back into biotype A strains, good MRHA was restored and the strains produced CS1 and CS3. In a biotype C strain CS2 and CS3 were formed. The production of the antigens was compared by enzyme-linked immunosorbent assay (ELISA). The strains were also examined by electron microscopy where it was found that CS1 and CS2 were fimbrial antigens while CS3 was not.
Diagnostic virology using electron microscopic techniques.
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Plasmids coding for colonization factor antigen I and heat-stable enterotoxin production isolated from enterotoxigenic Escherichia coli: comparison of their properties.
We examined seven enterotoxigenic Escherichia coli strains which produced colonization factor antigen I (CFA/I). Four of these strains were from South Africa (three serotype O78:H12 and one serotype O63:H-), one was from Ethiopia (O78:H12), and two were from Bangladesh (O78:H11 and O78:H12). Plasmids coding for CFA/I were mobilized from six of these strains by using resistance or enterotoxin factors. No plasmid was mobilized from the serotype O78:H12 Bangladesh strain. The transconjugants obtained from crosses with the O78 strains also produced heat-stable enterotoxin (ST), and additional investigations showed that CFA/I and ST were coded for by a single non-autotransferring plasmid. These plasmids were fertility inhibition negative, did not restrict any of the coliphages with which they were tested, and were incompatible with each other. Four had molecular weights of approximately 60 X 10(6), and one had a molecular weight of 52 X 10(6). Like the other CFA/I plasmids, the CFA/I plasmid transferred from the O63:H- strain coded for ST, but this plasmid also coded for heat-labile enterotoxin. In most other respects the properties of this plasmid were similar to those of the CFA/I-ST plasmids previously described. The molecular weight of this plasmid was 65 X 10(6). The IncT R-factor Rtsl was marked with a transposon for tetracycline resistance and then transferred into the two Bangladesh wild-type strains. Plasmids which coded for tetracycline resistance, CFA/I, and ST were transferred from these strains. These plasmids were incompatible with Rtsl and with the CFA/I-ST plasmids described above and were recombinants between Rtsl and a CFA/I-ST plasmid. Their properties are also described.
Occurrence of IgM antibodies against BK and JC polyomaviruses during pregnancy.
In a serological survey of 430 pregnant women 45 had high or rising titres of BK-virus haemagglutination-inhibiting antibodies. The presence of BK-virus-specific IgM was confirmed in 10 of these women. No BK-virus-specific IgM was detected in the samples of cord blood from the babies born to these women. The sera from 40 women known to be excreting inclusion-bearing cells during pregnancy were tested for the presence of BK-virus and JC-virus-specific IgM and IgG. The presence of BK-virus-specific IgM was confirmed in three cases and JC-virus-specific IgM in seven cases. Specific IgM persisted for several months in some pregnant women. No Bk-virus-specific IgM was detected in any of the samples of cord blood from the babies born to these women with evidence of polyomavirus infection. No JC-virus-specific IgM was detected in 36 out of 37 of the cord bloods; however, in one it is possible that minute amounts of JC-virus-specific IgM were present.
A prospective study of human polyomavirus infection in pregnancy.
Urine samples from 1,235 pregnant women were examined by light microscopy for cytologic evidence of virus infection. Smears of urine sediment from 40 women (3.2%) were observed to contain inclusion-bearing cells; polyomavirus infection was confirmed by virologic methods in 24 (60%). A polyomavirus was isolated from 12 women. Five isolates were identified as JC virus and one as BK virus. Another isolate designated AS virus appeared to be unique. Serologic studies on the 40 women were consistent with a high frequency of reactivation of JC virus, and virus excretion was related to gestation. The evidence suggests that selective excretion of JC virus may occur in pregnancy. Among 390 pregnant women without inclusion-bearing cells in their urine, 78 (20%) had a high or rising titer of serum antibody to JC or BK virus or both, a result suggesting virus reactivation, but virus excretion was not detected. In contrast to other reports, no evidence was found for transmission of BK virus to the fetus.
Polyoma virus in urine during pregnancy.
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Parvovirus-like particles in human sera.
A parvovirus-like antigen has been found in sera of nine healthy blood-donors and two patients. Its pathogenicity is unknown, but 30% of adults possess specific antibody. The new agent can be confused with hepatitis-B antigen both morphologically and serologically.
Identity of a newly isolated human polyomavirus from a patient with progressive multifocal leucoencephalopathy.
Isolation of a strain of polyomavirus, designated COL, from the brain of a patient with progressive multifocal leucoencephalopathy is described. The COL strain is antigenically similar to JC polyomavirus, previously isolated from a brain affected by progressive multifocal leucoencephalopathy and is unrelated to BK, another human polyomavirus isolated from urine. Immunological cross testing of viruses in the Polyomavirus genus shows that there are at least six antigenic types in this group.
Human polyomavirus infection in renal allograft recipients.
Cytological and virological studies on 74 patients with functioning renal allografts were undertaken to detect polyomavirus infection of the renal tract. Ten patients (13.5%) were excreting polyomavirus. Virus particles were seen in the electron microscope in urine samples from eight patients. B.K. polyomavirus was isolated from four patients. Infection with a different polyomavirus was probable in one patient. Virus isolation was most readily achieved when large numbers of intact virus particles were seen in the urine. Patients who were excreting large amounts of polyomavirus shed numerous inclusion-bearing cells which could be detected by cytology. A serological study showed that the prevalence of B.K. antibody was similar to that found in the general population and 38% of this series of transplant patients had evidence of active infection with B.K. virus.
Virus-induced obstruction of the ureteric and cystic duct in allograft recipients.
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Latex test for AU antigen.
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Evidence for oral excretion of E.B. virus in infectious mononucleosis.
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Specificity of Au antibodies.
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