Cellular and humoral immune response to group B streptococci

Klesius, Phillip H.; Zimmerman, Robert A.; Mathews, James H.; Krushak, Donald H.

doi:10.1016/s0022-3476(73)80525-6

Cited by 54 publications

(28 citation statements)

References 6 publications

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“…Deficiency of Glm(l) is known not to influence the IgG l level and thus could not explain the low IgG 1 levels found. The IgG subclass deficiencies fit well with earlier known deficiency o f type-specific antibodies to GBS in m others o f infants with severe GBS infections [13]. The m others are frequently colonized with GBS in the urogenital tract over years without producing IgG an tibodies [4], Previous results have shown that the an tibody response after vaccination with carbohydrate antigen [26] as well as after clinical infections with bacteria carrying carbohydrate antigen [20] might be restricted to IgG2.…”

Section: Discussionsupporting

confidence: 83%

Deficiency of IgG Subclasses in Mothers of Infants with Group B Streptococcal Septicemia

Oxelius¹,

Lindén²,

Christensen³

et al. 1983

Int Arch Allergy Immunol

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Serum IgG subclasses were studied in 19 mothers of infants with serious infections caused by group B streptococci (GBS) and compared with a control group of 20 mothers of healthy infants. 13 of 19 mothers showed decreased subclass levels: 10 of 19 low IgG2, 9 of 19 low IgG1 and 4 of 19 low IgG3. The levels of IgG1, IgG2 and IgG3 were significantly lower among mothers of GBS-infected infants than among the controls. Thus, there is indirect evidence that the infants were immunodeficient at birth.

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Section: Discussionsupporting

confidence: 83%

Deficiency of IgG Subclasses in Mothers of Infants with Group B Streptococcal Septicemia

Oxelius¹,

Lindén²,

Christensen³

et al. 1983

Int Arch Allergy Immunol

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“…Dossett et al detected opsonins to group B streptococci in whole blood and serum in 1969 (20). Subsequently Klesius et al (21) and Mathews et al (22) reported that serum from humans and experimentally infected baboons contained opsonins directed against types Ta, Tb, Ic, II, and III organisms. Their studies, which were carried out by visually determining phagocytic uptake and the percentage of PMNs ingesting microorganisms, suggested that types Tb, Ic, II, and III streptococci were naturally and nonspecifically opsonized by 95% of human and baboon sera.…”

Section: Discussionmentioning

confidence: 99%

Assessment of group B streptococcal opsonins in human and rabbit serum by neutrophil chemiluminescence.

Hemming¹,

Hall²,

Rhodes³

et al. 1976

J. Clin. Invest.

215

102

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A B S T R A C T The factors important in host defense against group B streptococci are not well understood. The role ofantibody and complement in the prevention of serious infection by these organisms is not known because, to date, a reliable measure of functional opsonic activity has not been developed. Recently, it has been shown that neutrophils produce a chemiluminescence after ingestion of particulate matter, and that this event can be detected and quantitated in a liquid scintillation system. We have adapted the chemiluminescence procedure to examine rabbit hyperimmune and human serum for the presence of group B streptococcal opsonins. Group B streptococci of types Ia, II, and III that were opsonized in homologous but not heterologous type serum produced a peak in chemiluminescence when added to normal human neutrophils. Such activity was correlated, in each instance, with ingestion of bacteria by neutrophils and deposition of immunoglobulin and C3 on the bacterial surface as detected by indirect immunofluorescence.With this assay, we have examined sera from colonized and diseased patients for the presence of opsonins to types Ia, II, and III group B streptococci. Maternal sera often contained type-specific opsonins which resided in the IgG fraction and which crossed the placenta to appear in paired cord specimens. 63% of patients colonized with group B streptococci had serum opsonins to their colonizing type of organism. In contrast, none of the 15 patients with sepsis or meningitis had opsonins directed against their infecting strain.

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“…Antibody against type-specific polysaccharide, and against the protein antigen Ic, protects mice (Lancefield et al, 1975) against lethal infection. In vitro studies of the blood of parturient women reveal several factors that might be concerned in defence against the organism (Klesius et al, 1973;Mathews, Klesius and Zimmerman, 1974). According to Baker and Kasper (1976), the sera of women whose infants suffered from invasive type-III infection were devoid of antibody against this type but it was present in the sera of vaginal carriers of type-III organisms.…”

Section: Susceptibility To Infectionmentioning

confidence: 99%

Neonatal streptococcal infections

Parker

1977

Postgraduate Medical Journal

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Summary Most serious neonatal streptococcal infections are caused by group-B streptococci. The pattern of serious group-B neonatal disease in Britain resembles that described in other countries; both "early-onset" and "late-onset" forms are seen, but reliable incidence rates have not yet been determined. Serological-type III strains predominate in neonatal meningitis in Britain, but not so markedly as in some parts of the U.S.A. A deficiency of group-II strains in meningitis is, however, apparent in both countries. Present information about the carriage of group-B streptococci suggests that antibiotic prophylaxis administered to mothers or infants is unlikely to reduce greatly the frequency of "early-onset" disease. The continuous presence of a suitable chemical disinfectant in the vagina during labour might be more effective. Insufficient is known about the epidemiology of "late-onset" neonatal disease for rational preventive measures to be designed. More information is required about the postnatal acquisition of group-B streptococci by neonates and its sources, and about passive transfer of type-specific antibody from the mother to her child.

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Cellular and humoral immune response to group B streptococci

Cited by 54 publications

References 6 publications

Deficiency of IgG Subclasses in Mothers of Infants with Group B Streptococcal Septicemia

Deficiency of IgG Subclasses in Mothers of Infants with Group B Streptococcal Septicemia

Assessment of group B streptococcal opsonins in human and rabbit serum by neutrophil chemiluminescence.

Neonatal streptococcal infections

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