scholarly journals THE EFFECT OF A POLYSACCHARIDE-SPLITTING ENZYME ON STREPTOCOCCAL INFECTION

1941 ◽  
Vol 73 (4) ◽  
pp. 493-506 ◽  
Author(s):  
George K. Hirst
Keyword(s):  
Molecular Weight ◽  
Streptococcal Infection ◽  
Protective Action ◽  
Intraperitoneal Administration ◽  
Group A Streptococci ◽  
Group A ◽  
Intraperitoneal Infection ◽  
Virulent Group

1. Confirming the observations of other experimenters, it has been found that group A hemolytic streptococci produce a capsule containing a polysaccharide which is similar to, if not identical with, certain high molecular weight sugars found in the mammalian body. 2. Leech extract possesses a powerful enzyme capable of splitting one of the linkages in this polysaccharide and of decapsulating group A and group C hemolytic streptococci in vitro and in vivo. 3. Mice and guinea pigs can be protected from intraperitoneal infection with a virulent group C streptococcus by the intraperitoneal administration of leech extract. In contrast there is little protective action of leech extract in mice infected with group A hemolytic streptococci. 4. The protective effect of leech extract against streptococcal group C infection is probably due to the removal of the capsule in vivo. 5. The capsule of mouse virulent group C streptococci plays a major rôle in the virulence of that microorganism, while the capsule of certain mouse virulent group A streptococci plays little, if any, rôle in virulence, at least when the infection is intraperitoneal in the mouse.

scholarly journals CROSS-REACTIONS AMONG GROUP A STREPTOCOCCI

1968 ◽  
Vol 128 (5) ◽  
pp. 959-968 ◽  
Author(s):  
Grove G. Wiley ◽  
Pauline N. Bruno
Keyword(s):  
Streptococcal Infection ◽  
Cross Protection ◽  
The Other ◽  
Group A Streptococci ◽  
Agar Gel ◽  
Cross Reactions ◽  
Group A ◽  
Spur Formation ◽  
Homologous Reaction

Strains of four streptococcal types, 33, 41, 43, 52, and a nontypable strain, Ross, cross-reacted in precipitin and bactericidal tests. The homologous reactions, which determined the type, afforded the major protection and developed promptly and regularly in the serum of rabbits during immunization. The associated cross-reactions, on the other hand, appeared in the serum of certain rabbits only, were often not as strong as the associated homologous reactions, and required for their presence a longer period of immunization than the homologous reactions. Agar gel analysis of the homologous precipitin reactions revealed, as would be expected, reactions of serological identity, while those cross-reactions which were strong enough to test in this way formed bands of precipitate which joined with spur formation on the side of the homologous reaction. These experiments and others referred to in the text suggest that cross-protection, as demonstrated in bactericidal tests, is sufficiently widespread to be a factor in streptococcal immunity, if a corresponding protection occurs in vivo. Thus, streptococcal infection with one of the cross-reacting strains might confer, in addition to strong homologous protection, a certain amount of cross-protection.

scholarly journals FATE OF NON-VIRULENT GROUP A STREPTOCOCCI PHAGOCYTIZED BY HUMAN AND MOUSE NEUTROPHILS

1957 ◽  
Vol 106 (6) ◽  
pp. 777-786 ◽  
Author(s):  
Armine T. Wilson ◽  
Grove G. Wiley ◽  
Pauline Bruno
Keyword(s):  
Electric Current ◽  
Peripheral Blood ◽  
Group A Streptococci ◽  
Blood Neutrophils ◽  
Group A ◽  
Time Required ◽  
Human And Mouse ◽  
Virulent Group

The fate of non-virulent group A streptococci phagocytized in vitro has been investigated by destroying the phagocyte with electric current and observing whether the liberated cocci multiply. Human and mouse peripheral blood neutrophils quickly injure ingested cocci, the time required to produce 50 per cent non-survival of chains being 8 and 6¾ minutes, respectively.

scholarly journals ENHANCED RESISTANCE TO STREPTOCOCCAL INFECTION INDUCED IN MICE BY CELL WALL MUCOPEPTIDE

1965 ◽  
Vol 122 (5) ◽  
pp. 877-890 ◽  
Author(s):  
Jiri Rotta ◽  
Thomas J. Prendergast ◽  
Walter W. Karakawa ◽  
Charles K. Harmon ◽  
Richard M. Krause
Keyword(s):  
Cell Wall ◽  
Cell Walls ◽  
Streptococcal Infection ◽  
Group A Streptococci ◽  
Streptococcal Cell Wall ◽  
Enhanced Resistance ◽  
Group A ◽  
Late Recovery ◽  
Fever Response ◽  
Virulent Group

The streptococcal cell wall mucopeptide when injected into mice either intraperitoneally or intravenously enhances the resitance to subsequent challenge with virulent Group A streptococci. Rabbits which are injected intravenously with solubilized mucopeptide develop a fever response which has a resemblance to that achieved with endotoxin. Mice which survive 6 to 7 weeks after challenge with virulent Group A streptococci yield at autopsy search Group A streptococci serologically identical to the challenge organisms. A preparative dose of cell walls injected into mice prior to challenge diminished this late recovery of streptococci. Group A-variant streptococci were recovered from mice which survived challenge and carried the organisms for several weeks. Filterable bacterial forms, which grew on L form media, were recovered from infected mice. The serologic type of the L forms was identical to that of the challenge organisms.

scholarly journals THE RÔLE OF THE MUCOID POLYSACCHARIDE (HYALURONIC ACID) IN THE VIRULENCE OF GROUP A HEMOLYTIC STREPTOCOCCI

1944 ◽  
Vol 79 (3) ◽  
pp. 319-330 ◽  
Author(s):  
E. H. Kass ◽  
C. V. Seastone
Keyword(s):  
Hyaluronic Acid ◽  
Human Blood ◽  
Bactericidal Activity ◽  
Streptococcal Infection ◽  
Protective Action ◽  
Type I ◽  
Group A Streptococci ◽  
Hyaluronidase Activity ◽  
Turbidimetric Method ◽  
Group A

1. A quantitative turbidimetric method for the estimation of hyaluronidase activity, based on the ability of the enzyme to decrease the capacity of the polysaccharide to precipitate acidified protein has been developed. Two units of hyaluronidase, by this method, are equivalent to one viscosity-reducing unit. 2. Hyaluronidase added to a phagocytic system containing defibrinated human blood, immune or non-immune, greatly increases the rate of phagocytosis of group A streptococci. Phagocytosis of Type I pneumococci is not affected by hyaluronidase under the same conditions. 3. The bactericidal activity of non-immune blood against group A streptococci is increased by hyaluronidase; the activity of immune blood is, however, somewhat inhibited by the enzyme. Killing of pneumococci is not affected by the presence of the enzyme. 4. Mice can be protected against group A streptococcal infection by frequent treatment with 200 turbidity-reducing units of hyaluronidase; the protective action of the enzyme is removed by heating at 60°C. for 1 hour. Mice infected with Type I pneumococcus and treated with hyaluronidase die somewhat sooner than the untreated controls.

scholarly journals Influences of Linezolid, Penicillin, and Clindamycin, Alone and in Combination, on Streptococcal Pyrogenic Exotoxin A Release

2003 ◽  
Vol 47 (5) ◽  
pp. 1752-1755 ◽  
Author(s):  
Elizabeth A. Coyle ◽  
Raymond Cha ◽  
Michael J. Rybak
Keyword(s):  
In Vitro Model ◽  
Group A Streptococci ◽  
Bacterial Burden ◽  
Exotoxin A ◽  
Group A ◽  
Vitro Model ◽  
Virulent Group

ABSTRACT An in vitro model was used to compare the effects of linezolid, clindamycin, and penicillin, alone and in combination, on streptococcal pyrogenic exotoxin A (SPE A) release against virulent group A streptococci (GAS). All regimens exhibited lower (P < 0.05) SPE A release at 1 h than those with penicillin alone. Linezolid and clindamycin, alone or in combination with penicillin, may optimize the treatment of GAS infections by reducing bacterial burden and exotoxin release.

Anti-invasive activity of bovine lactoferrin towards group A streptococci

2002 ◽  
Vol 80 (1) ◽  
pp. 119-124 ◽  
Author(s):  
Maria Ajello ◽  
Rita Greco ◽  
Francesco Giansanti ◽  
Maria Teresa Massucci ◽  
Giovanni Antonini ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Host Cells ◽  
Bovine Lactoferrin ◽  
Group A Streptococci ◽  
Intracellular Replication ◽  
In Vitro Invasion ◽  
Cultured Epithelial Cells ◽  
Group A

Group A streptococci (GAS) are able to invade cultured epithelial and endothelial cells without evidence of intracellular replication. GAS, like other facultative intracellular bacterial pathogens, evolved such ability to enter and to survive within host cells avoiding the host defences, and bacterial intracellular survival could explain the recurrence of infections. We report here that 1 mg bovine lactoferrin (bLf)/mL significantly hindered the in vitro invasion of cultured epithelial cells by GAS isolated from patients suffering from pharyngitis and completely inhibited the invasiveness of GAS pretreated with subinhibiting concentrations of erythromycin or ampicillin. One milligram of bLf per millilitre was also able to increase the number of epithelial cells undergoing apoptosis following GAS invasion, although the number of intracellular GAS in the presence of bLf decreased by about 10-fold. The ability of bLf to decrease GAS invasion was confirmed by an in vivo trial carried out on 12 children suffering from pharyngitis and already scheduled for tonsillectomy. In tonsil specimens from children treated for 15 days before tonsillectomy with both oral erythromycin (500 mg t.i.d. (three times daily)) and bLf gargles (100 mg t.i.d.), a lower number of intracellular GAS was found in comparison with that retrieved in tonsil specimens from children treated with erythromycin alone (500 mg t.i.d.).Key words: lactoferrin, group A streptococci, invasiveness, anti-invasive activity, apoptosis.

Effects of Unfractionated and Low Molecular Weight Heparins on Platelet Thromboxane Biosynthesis “In Vivo”

1994 ◽  
Vol 72 (06) ◽  
pp. 942-946 ◽  
Author(s):  
Raffaele Landolfi ◽  
Erica De Candia ◽  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Armando Antinori ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Unfractionated Heparin ◽  
Low Molecular Weight Heparin ◽  
Primary Source ◽  
In Vivo Studies ◽  
Low Molecular Weight ◽  
Heparin Administration ◽  
To Receive

SummarySeveral “in vitro” and “in vivo” studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis “in vivo”, as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionaed heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 ± 1388 vs 2092 ±777, p <0.05; 2,3-dinor-TxB2: 2737 ± 808 vs 1535 ± 771 pg/mg creatinine, p <0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation “in vivo” and suggest that the use of low molecular weight heparin may avoid this complication.

Action of Lysolecithin on Blood Platelets

1963 ◽  
Vol 09 (03) ◽  
pp. 512-524 ◽  
Author(s):  
Chava Kirschmann ◽  
Sara Aloof ◽  
Andre de Vries
Keyword(s):  
Blood Platelets ◽  
Protective Action ◽  
Platelet Surface ◽  
Washed Platelet ◽  
Sufficient Concentration ◽  
Saline Medium

SummaryLysolecithin is adsorbed to washed blood platelets and, at sufficient concentration, lyses them, inhibits their clot-retracting activity and promotes their thromboplastin-generating activity. Lysolecithin adsorption to the platelet was studied by using P32-labelled lysolecithin obtained from the liver of rats injected with labelled orthophosphate. The amount of lysolecithin adsorbed to the surface of the washed platelet in saline medium is dependent on the concentration of lysolecithin in solution and reaches saturation — 5 × 10-8 jig per platelet — at a concentration of 9—10 µg per ml. Platelet lysis in saline medium begins at a lysolecithin concentration higher than 18 jig per ml. Plasma and albumin prevent adsorption of lysolecithin to the platelet and protect the platelet from damage by lysolecithin. Albumin is able to remove previously adsorbed lysolecithin from the platelet surface. The protective action of plasma explains the lack of platelet damage in blood, the plasma lecithin of which has been converted to lysolecithin by the action of Vipera palestinae venom phosphatidase, in vitro and in vivo.

Toxicity of Heparinoids, with Special Reference to the Precipitation of Fibrinogen

1964 ◽  
Vol 12 (01) ◽  
pp. 232-261 ◽  
Author(s):  
S Sasaki ◽  
T Takemoto ◽  
S Oka
Keyword(s):  
Molecular Weight ◽  
Dextran Sulfate ◽  
Anticoagulant Activity ◽  
Molecular Structures ◽  
Severe Reaction ◽  
Clinical Use ◽  
Molecular Weights ◽  
Close Relationship

SummaryTo demonstrate whether the intravascular precipitation of fibrinogen is responsible for the toxicity of heparinoid, the relation between the toxicity of heparinoid in vivo and the precipitation of fibrinogen in vitro was investigated, using dextran sulfate of various molecular weights and various heparinoids.1. There are close relationships between the molecular weight of dextran sulfate, its toxicity, and the quantity of fibrinogen precipitated.2. The close relationship between the toxicity and the precipitation of fibrinogen found for dextran sulfate holds good for other heparinoids regardless of their molecular structures.3. Histological findings suggest strongly that the pathological changes produced with dextran sulfate are caused primarily by the intravascular precipitates with occlusion of the capillaries.From these facts, it is concluded that the precipitates of fibrinogen with heparinoid may be the cause or at least the major cause of the toxicity of heparinoid.4. The most suitable molecular weight of dextran sulfate for clinical use was found to be 5,300 ~ 6,700, from the maximum value of the product (LD50 · Anticoagulant activity). This product (LD50 · Anticoagulant activity) can be employed generally to assess the comparative merits of various heparinoids.5. Clinical use of the dextran sulfate prepared on this basis gave satisfactory results. No severe reaction was observed. However, two delayed reactions, alopecia and thrombocytopenia, were observed. These two reactions seem to come from the cause other than intravascular precipitation.

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