Plaque-forming cells in mice after experimental infection with Brucella abortus. (49/11816)

Cells producing antibody to brucella lipopolysaccharide were detected in spleens of mice infected with Brucella abortus 19 by a hemolytic plaque assay. The appearance of immunoglobulin M-producing cells preceded humoral antibodies. The primary plaques were observed 5 days after inoculation, and they were still present by day 70.  (+info)

Role of antibody and complement in opsonization of group B streptococci. (50/11816)

A requirement for the classic complement pathway in opsonization of group B streptococci was observed by using both a chemiluminescence and a radiolabeled bacterial uptake technique. The classic pathway increased levels of opsonization for types Ia and II stock and wild strains and for some type III wild strains. In contrast, other type III wild strains and the type III stock strain had accelerated kinetics of uptake in the presence of an intact classic pathway, but the level of opsonization was unchanged from that with antibody alone. We could not demonstrate a significant role for the alternative pathway in opsonizing stock or wild strains of group B streptococci. Futhermore, electrophoretic and complement consumption analysis by hemolytic titration failed to reveal alternative pathway activation by the majority of strains of this group. Therapy aimed at supplying opsonins for these organisms will require the presence of type-specific antibody.  (+info)

Role of nonagglutinating antibody in the protracted immunity of vaccinated mice to Pseudomonas aeruginosa infection. (51/11816)

Effective immunization against infection with Pseudomonas aeruginosa is difficult to evaluate because agglutinin levels decline rapidly. Because fractionation of hyperimmune sera often yields more specific antibody than can be accounted for by direct agglutination tests, an immunoglobulin-specific assay based on antiglobulin augmentation was used to characterize antibody responses of C3H/HeJ mice vaccinated with P. aeruginosa type 2 lipopolysaccharide. Nonagglutinating antibodies, initially detected at 2 weeks post-primary vaccination, were predominantly immunoglobulin G after 5 weeks, and they remained elevated at levels usually 32-fold higher than the direct titer throughout the 4-month study period. The sequential production of immunoglobulin M, then immunoglobulin G, followed that found in orthodox immunological responses. Sera that contained nonagglutinating antibodies but not direct agglutinins (14 to 16 weeks) enhanced phagocytosis of P. aeruginosa type 2 by macrophages from unimmunized mice and passively immunized mice against lethal challenge doses; bactericidal activity of these sera was not demonstrated in the presence or absence of complement. When challenged with 1, 10, and 100 50% lethal doses at 16 weeks, survival rates of actively immunized mice were significantly higher than those of unvaccinated mice (P < 0.001). Thus, at a time when no direct agglutinins were detectable, the augmented system detected nonagglutinating antibodies that could confer protracted resistance in vaccinated mice to pseudomonas infection.  (+info)

Pneumococcal conjugate vaccine primes for polysaccharide-inducible IgG2 antibody response in children with recurrent otitis media acuta. (52/11816)

Children with frequent recurrent episodes of otitis media may have a deficient IgG2 antibody response to polysaccharide antigens. Five otitis-prone children were vaccinated with heptavalent pneumococcal conjugate vaccine. While all had an IgG1 antibody response to all pneumococcal serotypes included in the conjugate vaccine, the IgG2 response, especially to serotypes 6B, 9V, 19F, and 23F, was poor. However, vaccination with a 23-valent polysaccharide vaccine 6 months after conjugate vaccination induced an 11.5- to 163-fold increase in IgG2 anti-polysaccharide antibody titers. Thus, an IgG2 polysaccharide antibody deficiency can be overcome by priming with a pneumococcal conjugate vaccine followed by a booster with a polyvalent polysaccharide vaccine.  (+info)

Vertical transmission of Treponema pallidum to various litters and generations of guinea pigs. (53/11816)

The transmission of congenital syphilis was studied in a 4-generation guinea pig family with 10 litters and 38 offspring. By use of one or all of the following tests (ELISA-IgM, polymerase chain reaction, and rabbit infectivity), transplacental infection was demonstrated through 5 litters and up to 4 generations. Twenty-eight (93%) of 30 animals were positive by >/=1 test, and 2 (7%) were negative by 1 or 3 tests. While transmission of the pathogen appeared to be unaffected by the maternal acquisition of immunity, signs of smoldering infection in the young was suggested by the decline in humoral responses in successive progeny and by unusual rabbit infectivity test results. With each pregnancy there was a remarkable booster in the maternal humoral response, which dropped significantly prior to term. These findings shed new light on the understanding and interpretation of serologic testing during pregnancy and the perinatal period.  (+info)

Experimental infection of human volunteers with Haemophilus ducreyi does not confer protection against subsequent challenge. (54/11816)

Two groups of human volunteers were inoculated with 2 doses of live Haemophilus ducreyi 35000HP. The reinfection group consisted of 7 subjects who previously had participated in experimental infection with 35000HP to the pustular stage of disease. The control group consisted of 7 naive subjects. Papules developed at 92.8% (95% confidence interval [CI], 66.1%-99.8%) of sites inoculated with live bacteria, in the reinfection group, and at 85.7% (95% CI, 57.2%-98. 2%) of sites in the control group. Sixty-nine percent (95% CI, 36. 8%-90.9%) of papules evolved into pustules in the reinfection group, compared with 41% (95% CI, 15.2%-72.3%) in the control group. The recovery rates of H. ducreyi from surface cultures and the histopathology of biopsies obtained from both groups were similar. Thus, experimental infection to the pustular stage of disease does not provide protective immunity against subsequent challenge.  (+info)

Production of antibodies to staphylococcal superantigens in atopic dermatitis. (55/11816)

Staphylococcal superantigens (SAG) are implicated in the inflammation of atopic dermatitis. As SAG mediated diseases may be modified by specific antibodies, the antibody response to SAG in atopic dermatitis was investigated. Immunoglobulin (Ig) G to staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB), and toxic shock syndrome toxin 1 (TSST-1) were measured by sandwich enzyme linked immunosorbent assay (ELISA) in 74 children with atopic dermatitis and 111 controls. Controls had detectable IgG to SEA, SEB, and TSST-1, which increased with age. Atopic dermatitis subjects had an increased response to SEB at 6 months to 2 years (76% v 42%) and 2 to 7 years (79% v 57%), and equivalent responses to SEA and TSST-1, compared to controls. It is suggested that increased responses to SEB relate to increased colonisation and hence exposure to superantigen producing staphylococcus in atopic dermatitis, and that inflammation of atopic dermatitis is not caused by an inability to make antibody to SAG.  (+info)

An immunoblotting procedure comprising O = 9,12 and H = d antigens as an alternative to the Widal agglutination assay. (56/11816)

AIMS: To compare the established Widal agglutination assay with an immunoblotting procedure. METHODS: 110 sera were used to compare the established Widal agglutination assay with an immunoblotting procedure incorporating lipopolysaccharide (LPS) (O = 9,12) and flagellar (H = d) antigens. RESULTS: Antibodies to the LPS antigens were detected in 18 sera by the Widal assay and in 37 by immunoblotting. Antibodies to the flagellar antigens were detected in 27 sera by Widal assay and in 25 by immunoblotting. CONCLUSIONS: An immunoblotting procedure incorporating O = 9,12 LPS and H = d flagellar antigens was rapid and more sensitive than the established Widal agglutination assay for providing evidence of infection with S typhi.  (+info)