The inhibitory and bactericidal activity of N-formimidoyl-thienamycin in vitro against 131 clinical isolates selected for their gentamicin resistance was compared with that of cefotaxime and moxalactam. All strains were inhibited by N-formimidoyl-thienamycin concentrations within a range of 0.12-4 mg/l. N-formimidoyl-thienamycin was less active than cefotaxime and moxalactam against Escherichia coli and Klebsiella spp., and more active than all other antibiotics tested against Serratia spp., Enterobacter cloacae, Pseudomonas aeruginosa and Acinetobacter spp. In contrast to the other antibiotics N-formimidoyl-thienamycin showed a narrow margin of difference between minimal inhibitory and minimal bactericidal concentrations. N-formimidoyl-thienamycin is a promising antibiotic for the treatment of hospital infections with multi-resistant organisms.
In 20 patients suffering for several years from serious chronic relapsing Crohn's disease the following immunological tests were carried out: (1) in-vitro stimulation of blood lymphocytes by PHA-P, (2) identification of T and B cells by formation of spontaneous rosettes and complement receptor rosettes, (3) effect of Crohn's serum on mixed lymphocyte reaction (MLR) of normal allogeneic lymphocytes, (4) in-vitro phagocytosis and intracellular killing of E. coli by polymorphonuclear granulocytes. The results indicate an immune defect of lymphocyte function and the effect of humoral factor(s) on T cell mediated immune reactions: (1) Lymphocyte stimulation by PHA-P was reduced significantly in Crohn's disease. In PHA-P dose response, maximal stimulation has shown a decrease and a shift to higher doses. (2) An increase in the absolute number of B cells caused a decrease in the mean percentage of T cells. The absolute number of T cells did not differ significantly from those of the controls. (3) Crohn's serum has shown an inhibitory effect in MLR of normal lymphocytes. (4) No impairment of phagocytosis or intracellular killing by polymorphonuclear granulocytes has been observed. The results suggest a symptomatic immune defect syndrome in a wasting disease. There is no evidence of a primary immune defect in Crohn's disease.
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