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The characteristics of Gram-negative organisms and some of the underlying reasons for their adjuvant action with diphtheria toxoid are described.The adjuvant effect was shown by an earlier production of antitoxin, with a maintained differential advantage over controls, but with the usual decline in titre with passage of time. The adjuvant effect only occurred with a primary stimulus. There was no adsorption between toxoid and vaccine and mixture of the two was not necessary, but the vaccine had to be given simultaneously with or within 24 hr. following injection of the toxoid. There was evidence for believing that these adjuvants decreased the minimal stimulating dose of antigen and caused hyperplasia of antibody-producing cells. No direct link could be found between the characteristic stress symptoms caused by lipopolysaccharides and their ability to enhance antibody formation.

SUMMARYFifteen strains of Haemophilus injuenxae were found to require for growth, in addition to coenzyme 1 (diphosphopyridine nucleotide ; DPN) and haematin, the following substances : pantothenic acid, thiamine, uracil. Some of the strains also required a purine, accepting xanthine, hypoxanthine or guanine, but not adenine. Cysteine (or glutathione) was also needed for luxuriant growth. A medium is described which yields crops of about 1010 organisms/ml. after incubation for 18 hr. at 34". Sheep red cells, but not horse red cells, contain a DPN-ase, located in the stroma, which rapidly destroys any DPN added to them and also destroys the contained DPN when the cells are lysed.

The survival rate of mice actively or passively immunized against intracerebral challenge with Bordetella pertussis, was independent of the size of challenge dose within the range of 20–2000 LD.This unexpected result appears to be due to the anatomical peculiarities of the infected organ, in which circulating antibody does not pass the normal blood-brain barrier easily. The pertussis infection does not cause sufficient inflammation to induce a pathological increase in the permeability of the barrier until the number of living microbes in the brain reaches 10 to 10. Since this stage in the brain consistently occurs after 4–5 days, independently of the size of the inoculum within the range 20–2000 LD, the outcome of infection in the immunized animal depends solely on the degree of specific immunity.In the non-immune mouse, the increase in permeability of the barrier persists until death. In the immunized mouse, the elimination of the infection leads to a restoration of the normal barrier at about the 6th day.

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