A panel of eight murine monoclonal antibodies (Mabs) was raised against the surface antigens of Aeromonas sobria isolated from a patient with diarrhoea. Antibodies to the LPS core and O‐antigen and to protein antigens were generated. Three Mabs of the IgM isotype against either protein or LPS agglutinated 34/75 Aeromonas isolates from clinical and environmental sources. Similar numbers of A. hydrophila, A. sobria and A. caviae isolates were agglutinated. The Mabs were screened for their ability to inhibit A. sobria adhesion to HEp‐2 cells, and haemagglutination (HA). Two Mabs directed against conformationally dependent epitopes on a 43‐kDa protein blocked both functions. Of the anti‐LPS Mabs one blocked adhesion only, and another blocked HA but not adhesion. Immunoprecipitation studies suggested that LPS‐protein complexes may be involved in these potential virulence functions of A. sobria.
We have recorded the systemic and mammary/mucosal immune responses of women following natural infection with RS virus during the second and third trimesters of pregnancy. Anti-RS virus IgG antibody levels in the sera of women collected in the first trimester of pregnancy showed a bimodal distribution with high and low antibody groups. Antibody levels increased after exposure to the winter RS virus epidemic in the second trimester of pregnancy, probably as a result of infection but only for women in the low antibody group. Despite the increases, antibody levels for these women remained well below those of the high antibody group. There was no rise in mean antibody levels after exposure in the third trimester, even among women with low antibody, suggesting a degree of immunosuppression in late pregnancy. There was no evidence that infection during pregnancy was associated with adverse consequences for the infant. Exposure to RS virus in the first two trimesters, but not the third, was associated with high colostral IgA antibody levels that were maintained in the milk throughout the first 7 weeks of lactation. There was a significant correlation between colostral and maternal nasal IgA antibody levels at delivery. Levels of blood or colostral lymphocyte transformation responses at delivery were unaffected by exposure to RS virus in pregnancy. These observations upon natural infection suggest that vaccination during pregnancy is likely to achieve only marginal effects upon serum antibody levels but boost maternal mammary/mucosal immunity.
Seven of 230 breast fed infants followed prospectively from birth through their first winter contracted RS virus infections. The colostral from five of the mothers of these infants contained antiviral IgA antibodies. In each case antibody levels were above the mean for a group of 36 mothers whose infants were age matched to infected infants but for whom there was no evidence of RS virus infection in their first winter. Four colostral samples from mothers of infected infants also contained antiviral IgG antibody. Colostral lymphocyte reactivity to RS virus antigen was tested in three mothers of infected infants and two showed significant proliferation. There was, therefore, no evidence that mothers of infected infants lacked mammary immunity to the virus. Maternal mammary IgA and IgG responses following diagnosis of RS virus infection in the infant were followed for the seven cases identified prospectively and for a further 23 infants admitted to hospital with RS virus infections of varying severity. There was no evidence that the mothers of more severely affected infants were deficient in IgA or IgG milk antibody.
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