Abstract
Summary and Conclusions
(1) In experimental spirochetal infections BAL reverses the therapeutic activity of penicillin, bacitracin, Chloromycetin, oxophenarsine and gold compounds (Myochrysin), while it has no influence on streptomycin, terramycin and aureomycin. (In most cases subtilin has not been affected, occasionally it has been potentiated by BAL and by cysteine). (2) Monothiols (cysteine and glutathione) do not induce the reversal obtained with BAL. (3) In trypanosomal infection BAL reverses the therapeutic activity of arsenicals and Fuadin, while it has no influence on Naphuride, Stil-bamidine and Aeriflavine. The toxicity of Fuadin for the host(24) is noticeably increased by BAL treatment. (4) In experimental streptococcal infection none of these antibiotics has been influenced by BAL (or monothiols), except Myochrysin, which has been inhibited by BAL. (5) In the E. coli infection only penicillin was influenced by BAL: its activity was increased. This apparent potentiation was found to be due to a blood level increase determined by BAL with higher penicillin doses. (6) It is concluded that a number of chemically different therapeutic agents (penicillin, bacitracin, Chloromycetin, Au, Sb, As compounds) act by a similar mechanism involving the dithiol function in the protozoan infection, while their activity is of a different nature in bacterial infections (probably with the exception of the gold compound). It is considered that BAL inhibition of the drug does not take place with an identical mechanism for the host and the parasite. The specific BAL reversal in the spirochetal infection (and not in others) proves that this is due to a biological effect and not to a chemical inactivation of the drug.
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