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Pseudomembranous colitis: Presence of clostridial toxin.

A toxin was found in the faeces of nine out of nine patients with pseudomembranous colitis and two out of two with antibiotic-associated non-specific colitis. The toxin was neutralised by Clostridium sordellii antitoxin but not by a commercial mixture of C. welchii, oedematiens, and septicum antitoxins. The in-vitro and in-vivo properties of pseudomembranous-colitis toxin closely resemble those of the toxin of C. sordellii.

Adolescent↗

Determination of diphtheria toxin neutralizing antibody titers with a cell protein synthesis inhibition assay.

A method which allows an accurate determination of very low titers of antibodies able to neutralize diphtheria toxin has been developed. The assay is based on the incubation of a reference amount of diphtheria toxin with different dilution of the serum and the evaluation of the residual toxicity of diphtheria toxin on Vero cells. The cells are seeded in 96-well plastic plates with the toxin-serum mixtures and the residual toxin activity is measured as the block of cell protein synthesis after incubation with [14C]leucine. Antitoxin titers as low as 0.002 IU can be reproducibly and accurately measured and the method gives a linear response in the range 0.002 to 8.0 IU/ml.

Animals↗

Pathogenesis of experimental shock. II. Absence of endotoxic activity in blood of rabbits subjected to graded hemorrhage.

A series of biological test reactions was used in order to establish the presence of bacterial endotoxins in the blood of rabbits during the progression of hemorrhagic shock. 1. When the shocked animal was used as the test object, it was not possible to induce either the generalized Shwartzman reaction or the dermal Shwartzman phenomenon with exogenous endotoxin (S. enteritidis or E. coli) as one of the two provocative factors. 2. Epinephrine instilled into the skin of rabbits either before, during, or after an episode of hemorrhagic shock did not result in the hemorrhagic skin reaction which occurs in the presence of as little as 1 microg of endotoxin intravenously. 3. Passive transfer from a donor in the irreversible phase of shock of 20 to 25 ml of blood into a primed recipient (B.P. at 40 mm Hg for 1 hour) was uniformly lethal. 4. Similar amounts of blood from such shocked donor failed upon intravenous injection to elicit a protective hemorrhagic reaction in skin sites which were infiltrated with 100 microg of epinephrine. In the same animals 1 microg of endotoxin added to the blood samples caused a positive dermal response. 5. Blood was taken from rabbits which had been pretreated with S. enteritidis endotoxin and then subjected to hemorrhagic shock (35 mm Hg for 2 hours). Such samples upon passive transfer produced positive skin reactions in epinephrine sites but were not lethal to the primed test recipient used in these studies. It is concluded that the contribution of bacterial endotoxemia to the genesis of hemorrhagic shock remains to be determined.

Animals↗

AFLATOXIN B2: CHEMICAL IDENTITY AND BIOLOGICAL ACTIVITY.

Aflatoxin B(2), a blue-fluorescent metabolite of Aspergillus flavus, was isolated from cultures grown on crushed wheat. Chemical structure of the compound was elucidated as dihydroaflatoxin B(1). Biological activity was determined in day-old male white Pekin ducklings. The criteria of activity were reduction in growth and liver size and the extent of bile-duct hyperplasia.

Aflatoxins↗