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Biomedical subjects

G Sakaguchi

Publications and source records attributed to G Sakaguchi.

At least 109 records · Page 6Linked to original sources
PubMed1979

Fluid accumulation in mouse ligated intestine inoculated with Clostridium perfringens enterotoxin.

Clostridium perfringens enterotoxin, when inoculated into the ligated intestinal loop of mice, caused marked distension due to fluid accumulation. The increase in weight of the intestinal loop was proportional to the log dose of enterotoxin within a range from 1 to 16 micrograms. The fluid accumulation was arrested by washing the loop with saline or by injection of the specific anti-enterotoxin serum into the loop 5 or even 30 min after inoculation of the enterotoxin. A significant increase in weight of the loop was found as early as 10 min after inoculation of the toxin. These results may suggest that entergotoxin is neither bound firmly to the mucosal membrane nor permeates into the cells of the intestinal wall. The mouse intestinal loop test is economical, simple to perform, and applicable for quantitative determination of the enteropathogenic activity of C. perfringens enterotoxin.

Animals↗
PubMed1979

Antibodies to Clostridium botulinum toxins in free-living birds and mammals.

Naturally-occuring antibodies against Clostridium botulinum toxins were found in Cathartes aura (turkey vultures), Canis latrans (coyotes) and Corvus brachyrhynchos (crows) by the passive hemagglutination (PHA) test and verified by the serum neutralization (SN) test. The prevalence of IHA antibodies was 18 of 20 vultures (90%), 5 of 12 crows (42%) and 25 to 110 coyotes (23%). Vultures and coyotes were seropositive by the PHA test against A, B, C, D, and F toxins. The highest antibody titer 1:8192 was in vulture serum against type C. In descending order, the highest antibody levels were against type C, D, F, E, A and B toxins.

Animal Population Groups↗
PubMed1978

Sporulation and C2 toxin production by Clostridium botulinum type C strains producing no C1 toxin.

All of the 8 strains that were previously assumed to be nontoxigenic Clostridium botulinum type C were re-examined for their toxigenicity and were demonstrated by trypsinization of the culture filtrates to produce C2 toxin under improved cultural conditions. One per cent glucose added to trypticase peptone medium enhanced C2 toxin production. The larger the spore population, the higher the C2 toxicity and when spore population was smaller than a level of 10(4)/ml, no C2 toxicity was demonstrated. The C2 toxin was produced only during sporulation and not during vegetative growth.

Clostridium botulinum↗
PubMed1978

Experimental botulism in chickens: the cecum as the site of production and absorption of botulinum toxin.

Highly purified preparations of Clostridium botulinum toxins were administered to chickens by various routes. Chickens were highly susceptible to type A toxin, but relatively resistant to toxins of other types. Type C toxin (12S) at a dose of 1 X 10(7) mouse ip LD50 failed to kill the chicken by the oral route. Oral administration of 10 or more of type A, C, or D spores killed normal chickens, whereas cecoligated chickens were insusceptible to oral administration of 10(6) spores. These results show that the site of production and absorption of botulinum toxin in chickens is the cecum. Peroral administration of spores of a type C strain cured of its prophages and producing the C2 factor only also killed normal chickens. Chickens appeared to the more susceptible to the C2 factor than to the C1 toxin. The C2 factor, therefore, may play more important role in chicken deaths from toxico-infection with type C organisms. The optimum temperature for growth of C. botulinum types C and D was found to be 40-42 C. Type C and D toxins were significantly more stable than type A toxin in the cecum contents with pH above 7. These characteristics and the high density of distribution of type C spores in the environment may explain prevailing cases of type C botulism among broiler chickens.

Animals↗
PubMed1977

Oral toxicities of Clostridium botulinum toxins in response to molecular size.

Clostridium botulinum type A, B, and F toxins of different molecular sizes were fed to mice to compare the oral toxicities. The progenitor toxin, a complex of a toxic and nontoxic component, of any type was higher in oral toxicity to mice than the dissociated toxic component or the derivative toxin. The former may no doubt play a more important role in the pathogenesis of food-borne botulism. The higher oral toxicity possessed by the progenitor toxin, including the exceptionally high one found with type B-L toxin, can be explained solely by the protection afforded by the nontoxic component attached to the toxic component. The possibility of the highest oral toxicity of type B-L toxin to humans is discussed.

Administration, Oral↗
PubMed1977

Correlation between oral toxicity and in vitro stability of Clostridium botulinum type A and B toxins of different molecular sizes.

The in vitro sensitivity to acid and pepsin differed markedly among Clostridium botulinum type A and B toxins of different molecular sizes. The larger the molecular size of the toxin, the higher the resistance to these agents. Tye B derivative toxin was rapidly inactivated, but the progenitor toxins resisted in vitro exposure to rat intestinal juice. The molecular dissociation of the progenitor toxins did not occur in rat intestinal juice of pH 7.0, but did occur in a buffer solution of the same pH. The oral toxicity may depend mostly on the stability of toxin molecules in the stomach and, to a less extent, in the intestine. The present results seem to justify the conclusion that C. botulinum type A and B progenitor toxins with molecular sizes larger than 16S are more potent oral toxins than 12S progenitor toxins.

Administration, Oral↗
PubMed1977

Clostridium botulinum type D toxin: purification, molecular structure, and some immunological properties.

Clostridium botulinum type D progenitor toxin was purified. The addition of ribonucleic acid to the whole culture helped initial acid precipitation of the toxin. As with type B, both L (16S) and M toxins (12S) obtained from a hemagglutinin-positive strain, whereas M toxin only was produced by a hemagglutinin-negative strain. M toxin (molecular weight, 300,000) consisted of one molecule each of a toxic (molecular weight, 170,000) and a nontoxic component (molecular weight, 130,000); L toxin consisted of both components plus hemagglutinin. The specific toxicity of M toxin was 5 X 10(8) mean lethal doses per mg of N; that of L toxin was 2.4 X 10(8) mean lethal doses per mg of N. These toxins were fully or nearly fully active, but in un-nicked form. Trypsinization caused nicking in the toxic component, forming a molecule made up of two peptide chains with molecular weights of 110,000 and 60,000; there was little or no increase in toxicity. The toxic component of type D was not antigenically related to that of type C, whereas the nontoxic component was antigenically indistinguishable from that of type C. The toxicities of both L nad M toxins of the hemagglutinin-positive strain were increased twofold by trypsinization. Neither toxin contained the C2 toxic factor elaborated by C and D strain.

Bacterial Proteins↗
PubMed1977

Activation of botulinum toxins in the absence of nicking.

The derivative toxins purified from cultures of proteolytic strains of Clostridium botulinum types A and F were found to have been only partially nicked but were fully activated. Trypsinization of C. botulinum type B derivative toxin at pH 6.0 resulted in simultaneous activation and nicking, whereas at pH 4.5, activation preceded nicking. The toxin was split by trypsin at pH 6.0 into two fragments with molecular weights of 112, ooo and 57,000. The toxin contained at least three trypsin-sensitive peptide bonds, one of which was more sensitive than the others at pH 6.0. These results indicate that activation of botulinum toxins by trypsin or endogenous protease (s) is not a direct result of nicking.

Botulinum Toxins↗
PubMed1977

Intestinal absorption of botulinum toxins of different molecular sizes in rats.

During a period of 10 to 12 h after injection of type B 16S (L) toxin into the ligated duodenum of rats, 0.01 to 0.1% of the total toxicity administered was found in the lymph drawn by cannulation of the thoracic duct. The recovery was 50 to 100 times higher than that of the rat given type B 12S (M) or 7S (S) toxin. During the same period, 0.6 to 1.5% of the specific antigens were recovered, regardless of the molecular size of the toxin that had been administered. In lymph of the B-L or B-M toxin recipient, the toxic and nontoxic components were detected in comparable quantities, indicating that the undissociated progenitor toxin molecule is absorbed through the intestinal wall. Although the toxic component had lost its toxic activity, the two components of B-M toxin appearing in lymph reassembled to reconstruct the 12S molecule, whereas those of B-L toxin did not, although the toxic component was still active. Type B-L, B-M, and B-S toxins showed similar stabilities to in vitro exposure to rat lymph (pH 8.2), but B-L toxin showed a considerably higher stability to intestinal juice (pH 7.0) than did B-M toxin. Thus, the toxicity of lymph of rats administered botulinum toxin intraduodenally depends not upon the rate of absorption, but largely upon the stability in the intestine.

Animals↗