T-cell deprived mice heavily infected with Schistosoma mansoni suffer from severe microvesicular damage to hepatocytes within seven weeks of infection. The damage can be prevented by administration of serum (CIS) obtained from mice chronically infected with S. mansoni or from mice immunized with intact or homogenized S. mansoni eggs. Reaction of serum samples from individual chronically infected mice in immunoelectrophoresis with S. mansoni egg homogenate has enabled the identification of at least 12 distinct immuno precipitation reactions. Precipitating antibody against one S. mansoni egg antigen, omega 1, has been detected in all mice with patent chronic infections, and anti-omega 1 antibody is the most concentrated of the precipitating anti-egg antibody species in pooled CIS. Pooled serum obtained from infected intact mice reacting predominantly against omega 1 was found partially to prevent the hepatotoxicity reaction on transfer to infected deprived mice. Serum samples from mice injected with egg homogenate fractionated either by preparative electrophoresis or by cation exchange chromatography, and containing antibodies reactive with antigen omega 1 in immunoprecipitation, were fully protective against liver cell damage induced by S. mansoni in deprived mice. Sera from mice immunized with other S. mansoni egg fractions, and which did not contain antibodies reactive with omega 1, were not hepatoprotective. Antigen omega 1 is compared and contrasted with other S. mansoni egg antigens that have been described.
The penetration of three antibiotics, penicillin, chloramphenicol and erythromycin into bovine neutrophils, either alone or containing previously ingested Staphylococcus aureus, was determined, and their intracellular activity against these bacteria was measured. Uptake of radiolabelled antibiotics was assessed by rapidly separating neutrophils from extracellular antibiotic by centrifugation through silicone oil. Intracellular activity was estimated by comparing the numbers of bacteria surviving intracellularly in neutrophils exposed to antibiotic for 3 h at ten times the MBC, with those surviving intracellularly in untreated neutrophils. Penicillin was slightly concentrated within the neutrophils, reaching a maximum intracellular concentration 1.75 times that of the extracellular concentration; this is the C/E ratio. Chloramphenicol entered to a greater extent with a maximum C/E ratio of 7.08. Erythromycin became highly concentrated within the neutrophils with a C/E ratio of 11.46 after 90 min incubation. The presence of ingested staphylococci significantly reduced the uptake of chloramphenicol, but had no significant effect on the penetration of the other antibiotics. Intracellular activity studies indicated that, at ten times MBC, only penicillin had any significant activity against intracellular staphylococci, reducing survival by 28%. This work demonstrates that penetration of certain antibiotics can be altered by the presence of ingested staphylococci and that high intracellular levels of antibiotics do not necessarily ensure good intracellular activity against pathogenic micro-organisms.
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