To demonstrate that an enhancement phenomenon might be involved during the development of bacterial infections, one has to establish that specific humoral antibodies protect, in some way, microorganisms against the defence reations of the host. This report presents the evidence that specific antibodies could be evolved in assuming a certain survival of bacterial cells in host's tissue. (1) Homologues antistaphylococcal sera passively potentiated the development of experimental staphylococcal synovitis infection of chickens. The enhancement activity of the antisera was associated with a relatively high level of immune adherence antibodies and seemed not be correlated with their agglutinin titers. (2) The passive transfer of chicken anti-Brucella immune globulins promote the survival of B. abortus in the spleen of chickens infected with these bacteria. This enhancing effect was reduced significantly when the immune globulins were absorbed with heat-killed Brucella cells to remove all the anti-Brucella agglutinins and immune adherence antibodies. (3) The passive transfer of rabbit antimycobacterial immunoglobulins directed against either living or soluble extracts of Mycobacterium tuberculosis strain H37Rv, promotes the multiplication of the BCG stain of M. tuberculosis in the spleen of mice infected with low doses of this latter strain. This enhancing effect was reduced significantly when antisera were absorbed with living BCG. Morever, such treatment led to the removal of all haemagglutinating antibodies when antisera were tested aganist either BCG or H37Rv soluble extracts.

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Enhancing effect of passive immunization with mycobacterial antibodies on humoral and cellular immunity in BCG-infected mice.

The present paper is an attempt to get insight about the mechanisms involved in the enhancing phenomenon that occurs in bacterial infections. Mice infected with small doses of the BCG strain of M. bovis and treated with a M. tuberculosis H37Rv antiserum investigated at various intervals for their capacity to synthesize haemagglutinating antimyco-bacterial antibodies and to develop delayed hypersensitivity to PPD. As controls, BCG-infected mice were treated with the antiserum freed from its mycobacterial antibodies. It was found that the passive immunization of BCG-infected mice promotes the growth of bacilli in their spleen and induces a late formation of antimycobacterial antibodies which do not seem to be related to the development of delayed hypersensitivity.

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