Examination of the L Forms of Group a Streptococci for the Group-Specific Polysaccharide and M Protein

Sharp, John T.; Hijmans, W.; Dienes, L.

doi:10.1084/jem.105.2.153

Cited by 54 publications

(26 citation statements)

References 15 publications

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“…Group A streptococcus L forms do not possess the group specific polysaccharide (8); they are capable of producing the M protein, but the M protein is not fixed in the cell but diffuses into the medium (8). The works of Cram ford (1) and Lynn and Muellenhery (6) suggest that group A streptococcus L forms contain an extra antigenic component not shared by the parent bacterial strain.…”

mentioning

confidence: 99%

Antigenic Structure of <i>Streptococcus pyogenes L </i>Forms

Havlíček¹,

Havlíčková²

1967

Pathobiology

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mentioning

confidence: 99%

Antigenic Structure of <i>Streptococcus pyogenes L </i>Forms

Havlíček¹,

Havlíčková²

1967

Pathobiology

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“…Further evidence for a deficiency in cell-wall components from L-forms has been provided by serological techniques; for example, the L-forms of group A streptococci were found to lack group-specific polysaccharide (Sharp, Hijmans & Dienes, 1957). Similar results had earlier been obtained in the cases of L-forms of Streptobacillus moniliformis (Klieneberger, 1942) and Proteus (Dienes, Weinberger & Madoff, 1950), although these studies antedated much important work on cell-wall structures.…”

Section: Introductionmentioning

confidence: 53%

“…Since the precise structural relationship between the cell-wall teichoic acid and the muramic-acid-containing mucopeptide is unknown, it is impossible to judge whether the non-production of ribitol teichoic acid might be caused by the absence of rigid mucopeptide or is a more direct consequence of antibiotic action. In L-forms of group A streptococci, the M protein, which is normally found in the cell wall, is still produced but is liberated into the culture medium (Sharp, Hijmans & Dienes, 1957). The possibility was considered that the teichoic acid of the staphylococci might behave in the same way but no evidence for this was found.…”

Section: Discussionmentioning

confidence: 99%

Cell-Wall Deficiencies in L-forms of Staphylococcus aureus

Pratt¹

1966

Journal of General Microbiology

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SUMMARYThree strains of penicillin-induced and one strain of D-cycloserineinduced L-forms of Staphylococcus aureus were investigated for components of the normal bacterial cell wall. None of the 4 strains was found to contain more than 0.008 yo of its dry weight as muramic acid, indicating the lack of mucopeptide. These forms also lacked the cell-wall ribitol teichoic acid as shown by the failure to yield any material containing ribitol. Neither muramic acid nor ribitol was detected as acid-soluble nucleotides in the L-forms, and teichoic acid was not released into the supernatant medium. Serological evidence for polysaccharide A was not found, but there was serological identity between extracts of membranes obtained from staphylococci and extracts of membranes isolated from the L-forms.

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“…This view has received confirmation by chemical and serological studies of group A /&haemolytic streptococci (Sharp, Hijmans & Dienes, 1957) and other species as reviewed by Roberts, McQuillen & Roberts (1959). The accumulation of a N-acetylamino sugar precursor of cell walls of Staphylococcus uureus incubated with penicillin was reported by Park & Strominger (1957), and explained as a consequence of deficient cell-wall formation following the action of the antibiotic.…”

Section: Discussionmentioning

confidence: 87%

The Additive Effect of Glycine and other Amino Acids on the Induction of the L-Phase of Group A -Haemolytic Streptococci by Penicillin and D-Cycloserine

Michel

Hijmans

1960

Journal of General Microbiology

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SUMMARYThe ability of glycine to induce L-phase of bacteria did not apply to group A 8-haemolytic streptococci. In the presence of penicillin, glycine in a bacterial inhibitory concentration had a notably additive L-phase inducing property for streptococci. Reasons are given to support the view that this activity o€ glycine is limited to the induction of L-phase growth. A sharp increase in the yield of L-phase colonies was also observed when serine, threonine, methionine or alanine were tested under similar conditions. When the effectiveness of the racemate and both the isomers of these amino acids was compared, the D-isomer was the active substance in most cases. In one strain, the L-inducing and bacterial inhibitory action of the racemate and both isomers of methionine was tested simultaneously. The yield of L-phase colonies was found to be inversely proportional to the effect of the different stereoisomers on bacterial growth.D-Cycloserine had a weak L-inducing effect on group A streptococci, but the combined action of D-cycloserine and glycine or DL-serine was equal to that obtained with penicillin and the same amino acids. Propagation of these L-phase organisms was possible in the presence of 1 yo (w/v) glycine and within a narrow range of concentrations of D-cycloserine. The additive effect of the amino acids cited towards penicillin and D-cycloserine for the induction of L-phase structures can be explained by the antibiotic property of high concentrations of glycine and some of the D-amino acids.

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Examination of the L Forms of Group a Streptococci for the Group-Specific Polysaccharide and M Protein

Cited by 54 publications

References 15 publications

Antigenic Structure of <i>Streptococcus pyogenes L </i>Forms

Antigenic Structure of <i>Streptococcus pyogenes L </i>Forms

Cell-Wall Deficiencies in L-forms of Staphylococcus aureus

The Additive Effect of Glycine and other Amino Acids on the Induction of the L-Phase of Group A -Haemolytic Streptococci by Penicillin and D-Cycloserine

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