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W Stenzel

Publications and source records attributed to W Stenzel.

At least 37 records · Page 2Linked to original sources
PubMed1978

[The influence of non-metabolizable alpha- and beta-glycosides on the regulation of sorbose fermentation of salmonellae (author's transl)].

Fermentation of sorbose by late positive Salmonella wildtype cultures and by mutant strains splitting this sugar promptly is restrained by the beta-glucoside salicine and likewise by 1-o-methyl-alpha-D-glucopyranoside (MGP), but is not influenced by lactose or sucrose. In growing cultures salicine works more powerful on sorbose utilization than MGP while in dense suspensions of non-multiplying bacteria the relations are reversed. Among the majority of wildtype strains this suppressive effect is diminished or abolished by dimethylsulfoxide (DMSO), but there are strains in which the glucoside effect is enhanced by DMSO. The sorbose fermentation lag in the presence of salicine or MGP is detectable, too, in dense suspensions of promptly splitting Salmonella mutant strains in media poorly supplied with nitrogen and must therefore be attributed to a non-mutative event. From prior work (Stenzel, 1977c) we got some evidence that this event might depend on an inhibition of enzyme induction. Targets and mode of action of the alpha- and beta-glucoside largely seem to be identical, though possibly there might exist minor differences.

Benzyl Alcohols↗
PubMed1977

[Suppression of sorbose fermentation of Salmonellae by salicine (author's transl)].

Fermentation of sorbose by Salmonellae splitting this sugar with delay is restrained to a varying degree in presence of salicine, depending on the concentration of this glycoside. There is no support that salicine might become metabolized in this process. A similar salicine effect on the delayed fermentation of dulcitol has not been seen.

Fermentation↗
PubMed1977

[On the genetics of the delayed attack of substrates by strains of the Salmonella group (author's transl)].

The delayed attack of sugar alcohols by Salmonellae essentially goes back on a mutative event but doesnot represent a phenotypical or genotypical uniform phenomenon. The - frequently occuring - regularly split of sugars is caused by a simple looking fixed rate mutative event, and is characterized by an only moderate variation of the latent period preceding acid formation. In contrast, irregularly delayed splitting strains attack the substrate varying and, when occasion arises, with an extremely uncertain latency. Fermentation capacity of some strains attacking dulcitol irregularly can be induced by irradiation with ultraviolet light, and can be reduced to a certain degree by treatment with acridine orange, but cannot be transferred to other strains by conjugation. We presume that at least the uv inducible type of irregularly delayed splitting is governed by an episomal genetical element which is active only in the autonomous state but is repressed when being integrated within the chromosome.

Culture Media↗
PubMed1977

[Effects of dimethylsulfoxide and salicine on the delayed adaption on sorbose and dulcitol of Salmonellae (author's transl)].

Among the majority of Salmonella strains splitting sorbose or dulcitol with delay dimethylsulfoxide shortens the latent period preceding acid formation and abolishes the deceleration of sorbose adaption caused by salicine. In other strains, especially S. paratyphi B cultures, DMSO doesn't touch sorbose adaption directly but amplifies the restraing effect of salicine. From the whole of our findings it can be concluded that in the first group of strains sorbose adaption starts with segregation of adaptive sorbose permease positive mutants, followed by the - salicin-sensitive - induction of this permease, the appearance of mutants aditionally metabolizing sorbose constitutively, and, finally, the substrate-promoted particular growth of adapted cells. The latter category of strains, however, apparently possesses a wild type (constitutive or adaptive?) sorbose permease but splits off mutants with adaptive metabolizing enzymes the induction of which is salicine-sensitive. The amplification of the salicine effect by DMSO found in these strains might be refered to an enhancement of salicine uptake caused by DMSO.

Adaptation, Physiological↗
PubMed1976

[Sorbose in Salmonella diagnosis (author's transl)].

From 1525 Salmonella strains checked for fermentation of sorbose the majority failed to attack this sugar or split it with distinct delay. None of these cultures showed production of acid from sorbose prior to the third day of incubation. In contrast, sorbose was attacked within 24 hours by 74 out of 100 Ballerup-Bethesda strains. As an easy and reliable basis test combination for performing a minimal biochemical Salmonella diagnosis a series consisting of Kligler's medium and media containing urea, lysine, lactose, sucrose, sorbose, and salicin is suggested.

Salmonella↗
PubMed1975

[Serotype 185 and E. coli O115 - two distinct bioseropathotypes (author's transl)].

E. coli O115 strain 27w and TRABULSI's serotype 185 have been subjected by us to comparing examinations of the serological behaviour of their cell wall and their protoplasmatic antigens, of their biochemical and cultural behaviour and their pathogenicity for the mucous membranes of guinea-pigs. As a result of this inquiry it was found, that E. coli O115 27w and the dysentery-provoking serotype 185 are biological distinct bacteria which only share a minor cross relationship of their O-antigens, and which should not be classified together.

Animals↗
PubMed1975

[Occurrence of the cathode-bound group antigen of the dysentery bacilli in Escherichieae types of intermediate character (author's transl)].

Protoplasmatic antigens of 28 strains of 27 Escherichieae types not accepted as Shigellae have been examined for the occurrence of a cathode-bound group antigen (KGA). From the tested cultures of non-dysentery-provoking types E. coli O28 E1073(z) TAYLOR, E. coli O32, E. coli O115 (27w), Alkalescens-Dispar O1, A.-D. O1 var. Koji, A.-D. O2, A.-D. O3, A.-D. O4, A.-D. O5, A.-D. O6, A.-D. O7, and the intermediate serotypes H62 and 6275-52 no one possessed KGA, and likewise one of the two examined E. coli O136 cultures proved to be KGA-negative. In contrast, KGA was found in the dysentery types 147, 792, 185, Sh. guanabara, E. coli O124, E. coli O136 (one strain), E. coli O143, E. coli O144, and E. coli O152, in the Shigella-like serotypes 2044-54 and 1831, in the E. coli serotypes O112a,b:K68 and RUCHMAN, which have been suspected to provoke dysentery but are showing the biochemical behavior of typical E. coli, finally in Alkalescens-Dispar O8, which is known to be apathogenic for mucous membranes. After, all, KGA seems to be a constituent of all dysentery bacilli, but might be absent in individual cultures. On the other hand, KGA exceptionally seems to be found also in Escherichieae types not enteropathogenic for men.

Antigens, Bacterial↗
PubMed1975

[Pathogenicity factors of gramnegative enteropathogenic bacteria and pathogenesis of intestinal diseases (author's transl)].

Enterotoxins as produced by the majority of enteropathogenic bacteria play a central role in the pathogenesis of cholera and E. coli enteritis but are obviously of little significance as to the development of Salmonella enteritis and dysentery. Pathology of Salmonella enteritis and dysentery results from multiplication of bacteria within the bowel wall and from the damage of tissue caused thereby. The lipopolysaccharides (endotoxins) of invasive enteropathogenic bacteria do not possess the character of a primary pathogenicity factor but operate as a protective agent versus bactericidal mechanisms of the macroorganism and probably also as an agent toxic for the tissue.

Animals↗
PubMed1975

[The cathode bound group antigen of dysentery-provoking escherichieae (author's transl)].

Antigens from disrupted cells of dysentery-provoking and of non-enteropathogenic Escherichieae were submitted to immunoelectrophoresis on cellulose acetate stripes at pH 8.0. Among 6 immune sera produced for this purpose by immunizing rabbits against desintegrated dysentery bacteria, only one contained a precipitine reacting with an antigen similar to the "generic antigen" of BELAYA. This - at pH 8.0 - cathode-bound group antigen (KGA) could not only be found in virulent but also in 5 attenuated cultures and in 5 from 6 avirulent strains of several dysentery types. Only the - apathogenic - type culture 1111/55 of dysentery-provoking E. coli O 136 showed no KGA-reaction. Some sources of methodical errors responsible for false outcomes of immunopherogrammes have been discussed.

Antigens, Bacterial↗