Gonococci in pus appear in in which they are surrounded by organelles and granules derived from the host cells in which they multiplied. These clusters have been named because (1) the cocci multiply within them, (2) the whole complex makes contact with epithelial cells, (3) the cocci in the units are not recognised by polymorphs as long as the coating of granules is dense enough, and (4) the cocci are probably protected against humoral defence mechanisms. During multiplication of bacteria in infectious units, soluble antigenic material is probably produced. No morphological evidence of multiplication of gonococci outside infectious units was observed in pus from patients with gonorrhoea. Attempts to reproduce typical infectious units in animal models have so far failed.

The identity of the surrounding granular coating was established morphologically and with appropriate sera labelled with I and horseradish peroxidase. It is proposed that the mechanism of gonococcal pathogenicity is primarily based on the internal disorganisation of the regulatory mechanism of human macrophages. A sequence of events in the infection is discussed.

The anatomical changes observed in subcutaneously implanted plastic chambers in guinea-pigs infected with gonococci may be attributable to partial interference with the internal regulation of phagocytes. The effect of drugs on bacterial counts in the chamber cavity was studied. Under the influence of colchicine the number of colony-forming units increased 100 times within 8 h; vinblastine was without effect. Neither of these drugs had any effect on the growth of gonococci In studies by immune electron microscopy with sera from patients with gonococcal septicaemia, IgG was shown to react strongly with the gonococcal surface, free endotoxin, ring structures (pits) liberated from the lipopolysaccharide backbone and with unspecified soluble antigenic material. The detection of pilar antibodies in these sera was rare.


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