fibrin and Streptococcal-Infections

Group A streptococci (GAS) express soluble and surface-bound virulence factors. Secreted streptokinase (SK) allelic variants exhibit varying abilities to activate host plasminogen (Pg), and GAS pathogenicity is associated with Pg activation and localization of the resulting plasmin (Pm) on the bacterial surface to promote dissemination. The various mechanisms by which GAS usurp the host proteolytic system are discussed, including the molecular sexuality mechanism of conformational activation of the Pg zymogen (Pg*) and subsequent proteolytic activation of substrate Pg by the S•KPg* and SK•Pm catalytic complexes. Substantial progress has been made to delineate both processes in a unified mechanism. Pm coats the bacteria by direct and indirect binding pathways involving plasminogen-binding group A streptococcal M-like (PAM) protein and host fibrin(ogen). Transgenic mouse models using human Pg are being optimized to mimic infections by SK variants in humans and to define in vivo combined mechanisms of these variants and PAM.

Topics: Animals; Bacterial Proteins; Carrier Proteins; Fibrin; Fibrinolysin; Fibrinolysis; Host-Pathogen Interactions; Humans; Models, Molecular; Plasminogen; Protein Binding; Streptococcal Infections; Streptococcus pyogenes; Streptokinase; Virulence; Virulence Factors

Infective endocarditis is characterized by the formation of septic masses of platelets on the surfaces of heart valves and is most commonly caused by viridans streptococci. Streptococcal virulence in endocarditis involves factors that promote infectivity and pathogenicity. Adhesins and exopolysaccharide (glycocalyx) contribute to infectivity. Although many factors may contribute to pathogenicity, the platelet aggregation-associated protein (PAAP) of Streptococcus sanguis contributes directly to the development of experimental endocarditis. PAAP is synthesized as a rhamnose-rich glycoprotein of 115 kDa and contains a collagen-like platelet-interactive domain, pro-gly-glu-gln-gly-pro-lys. Expressed on the cell wall of platelet aggregation-inducing strains (Agg+) of S. sanguis, PAAP apparently interacts with a signal-transducing receptor complex on platelets, which includes a novel 175-kDa alpha 2-integrin-associated protein and a 65-kDa collagen-binding component. From available data, the role of PAAP in the pathogenesis of experimental endocarditis may be explained by a proposed mechanistic model. On injured heart valves, PAAP first enhances platelet accumulation into a fibrin-enmeshed thrombus (vegetation), within which S. sanguis colonizes. Colonizing bacteria must resist platelet microbicidal protein (PMPR). The aggregation of platelets on the heart valve may be potentiated by an ectoATPase expressed on the surface of the S. sanguis and platelet alpha-adrenoreceptors that respond to endogenous catecholamines. The expression of PAAP may be modified during infection. Collagen is exposed on damaged heart valves; fever (heat shock) occurs during endocarditis. In response to heat shock or collagen in vitro, PAAP expression is altered. After colonization, streptococcal exotoxin(s) may cause fever. Proteases and other enzymes from streptococci and host sources may directly destroy the heart valves. When PAAP is unexpressed or neutralized with specific antibodies, experimental endocarditis runs a milder course and vegetations are smaller. The data suggest strongly, therefore, that the role of PAAP may overlap the colonization function of putative adhesins such as FimA or SsaB. Finally, PAAP also contributes to the development of the characteristic septic mural thrombus (vegetation) of infective endocarditis and the signs of valvular pathology.

Topics: Adenosine Triphosphatases; Adhesins, Bacterial; Bacterial Proteins; Bacterial Toxins; beta-Thromboglobulin; Blood Platelets; Blood Proteins; Chemokines; Collagen; Endocarditis, Bacterial; Fibrin; Gene Expression Regulation; Glycoproteins; Heart Valves; Humans; Integrins; Platelet Aggregation; Polysaccharides, Bacterial; Receptors, Adrenergic, alpha; Rhamnose; Signal Transduction; Streptococcal Infections; Streptococcus; Streptococcus sanguis; Virulence

Topics: Acute Disease; Adolescent; Adult; Child; Child, Preschool; Chronic Disease; Female; Fibrin; Fibrinogen; Glomerulonephritis; Hemolytic-Uremic Syndrome; Humans; Immune Complex Diseases; Immunoglobulin A; Immunoglobulin G; Kidney Diseases; Lupus Erythematosus, Systemic; Male; Middle Aged; Nephritis; Nephrosis; Nephrotic Syndrome; Purpura; Streptococcal Infections

Invasive bacterial infections remain a major cause of human morbidity. Group B streptococcus (GBS) are Gram-positive bacteria that cause invasive infections in humans. Here, we show that factor XIIIA-deficient (FXIIIA-deficient) female mice exhibited significantly increased susceptibility to GBS infections. Additionally, female WT mice had increased levels of FXIIIA and were more resistant to GBS infection compared with isogenic male mice. We observed that administration of exogenous FXIIIA to male mice increased host resistance to GBS infection. Conversely, administration of a FXIIIA transglutaminase inhibitor to female mice decreased host resistance to GBS infection. Interestingly, male gonadectomized mice exhibited decreased sensitivity to GBS infection, suggesting a role for gonadal androgens in host susceptibility. FXIIIA promoted GBS entrapment within fibrin clots by crosslinking fibronectin with ScpB, a fibronectin-binding GBS surface protein. Thus, ScpB-deficient GBS exhibited decreased entrapment within fibrin clots in vitro and increased dissemination during systemic infections. Finally, using mice in which FXIIIA expression was depleted in mast cells, we observed that mast cell-derived FXIIIA contributes to host defense against GBS infection. Our studies provide insights into the effects of sexual dimorphism and mast cells on FXIIIA expression and its interactions with GBS adhesins that mediate bacterial dissemination and pathogenesis.

Topics: Androgens; Animals; Factor XIIIa; Female; Fibrin; Fibronectins; Humans; Male; Mast Cells; Mice; Streptococcal Infections; Streptococcus agalactiae; Transglutaminases

Platelets and coagulation are involved in bacterial colonisation of the host. Streptocococcus pneumoniae (pneumococcus) are important etiologic agents of respiratory tract infections in humans. The formation of pneumococci-platelet associations may facilitate haematogenous dissemination of pneumococci by providing an adhesive surface on damaged endothelium. However, the formation of platelet-pneumococci associations and the factors involved in this process have not been described so far. The formation of platelet-pneumococci associates was analysed and quantified using flow cytometry. Binding of pneumococci to platelets was significantly increased after activation of platelets with thrombin, while platelet activation by ADP or collagen did not promote formation of platelet-pneumococci associates. In addition to be a platelet agonist, thrombin cleaves fibrinogen, which results in the generation of fibrin. The simultaneous formation of fibrin and activation of platelets was shown to be a prerequisite for a high number of platelet-pneumococci associates. Moreover, exogenously added human thrombospondin-1 (TSP-1) significantly enhanced the association of pneumococci with activated platelets. Soluble fibrin and TSP-1 are key co-factors of platelet-pneumococci-association. Similar results were recently demonstrated for S. aureus-platelet adhesion. Consequently, we hypothesise that the described mechanism of platelet-bacteria-association might represent a general and important strategy of Gram-positive bacteria during development of invasive diseases.

Topics: Adenosine Diphosphate; Blood Platelets; Cell Adhesion; Cells, Cultured; Fibrin; Fibrinogen; Host-Pathogen Interactions; Humans; Platelet Activation; Respiratory Tract Infections; Streptococcal Infections; Streptococcus pneumoniae; Thrombin; Thrombospondin 1

Group A streptococci, a common human pathogen, secrete streptokinase, which activates the host's blood clot-dissolving protein, plasminogen. Streptokinase is highly specific for human plasminogen, exhibiting little or no activity against other mammalian species, including mouse. Here, a transgene expressing human plasminogen markedly increased mortality in mice infected with streptococci, and this susceptibility was dependent on bacterial streptokinase expression. Thus, streptokinase is a key pathogenicity factor and the primary determinant of host species specificity for group A streptococcal infection. In addition, local fibrin clot formation may be implicated in host defense against microbial pathogens.

Topics: Ancrod; Animals; Anticoagulants; Bacterial Proteins; Carrier Proteins; Colony Count, Microbial; Disease Susceptibility; Fibrin; Fibrinolysin; Fibrinolysis; Gene Deletion; Humans; Immunity, Innate; Mice; Mice, Inbred C57BL; Plasminogen; Skin; Species Specificity; Spleen; Streptococcal Infections; Streptococcus pyogenes; Streptokinase; Transgenes; Virulence

Invasive and toxic infections caused by Streptococcus pyogenes are connected with high morbidity and mortality. Typical symptoms of these infections are hypotension, edema formation, tissue necrosis, and bleeding disorders. Here we report that components of the coagulation system including fibrinogen, factors V, XI, and XII, and H-kininogen, are assembled at the surface of S. pyogenes through specific interactions with bacterial surface proteins. In plasma environment, absorption of fibrinogen by S. pyogenes causes a hypocoagulatory state resulting in prolonged clotting times and impaired fibrin network formation. Moreover, the binding of coagulation factors and the subsequent activation of the coagulation system at the bacterial surface lead to the formation of a fibrin network covering S. pyogenes bacteria adhering to epithelial cells. The results suggest that interactions between S. pyogenes and components of the coagulation system contribute to some of the symptoms seen in severe infections caused by this important human pathogen.

Topics: Antigens, Bacterial; Bacterial Adhesion; Bacterial Outer Membrane Proteins; Bacterial Proteins; Blood Coagulation; Blood Coagulation Factors; Carrier Proteins; Cell Line; Epithelial Cells; Fibrin; Fibrinolysis; Humans; In Vitro Techniques; Membrane Proteins; Microscopy, Electron; Microscopy, Electron, Scanning; Streptococcal Infections; Streptococcus pyogenes

In Streptococcus sanguinis (sanguis) induced experimental endocarditis, we sought evidence that the development of aortic valvular vegetation depends on the availability of fibrin. Endocarditis was induced in New Zealand white rabbits by catheter placement into the left ventricle and inoculation of the bacteria. Fibrin was localized in the developing vegetation with 99mTechnetium (Tc)-labeled anti-fibrin antibody one or three days later. When rabbit anti-fibrin antibody was given intravenously on day 1, the mass of aortic valvular vegetation was significantly reduced at day 3; infusion of non-specific rabbit IgG showed no effect. The 99mTc-labeled anti-fibrin antibody also labeled kidneys that showed macroscopic subcapsular hemorrhage. To learn if the deposition of fibrin in the kidneys was a consequence of endocarditis required a comparison of farm-bred and specific pathogen-free rabbits before and after the induction of endocarditis. Before induction, the kidneys of farm-bred rabbits were labeled, but specific pathogen-free rabbits were free of labeling and signs of macroscopic hemorrhage. After 3 days of endocarditis, kidneys of 10 of 14 specific pathogen-free rabbits labeled with 99mTc-labeled anti-fibrin antibody and showed hemorrhage. Kidney lesions were suggested to be a frequent sequellae of S. sanguinis infective endocarditis. For the first time, fibrin was shown to be required for the continued development of aortic valvular vegetations.

Topics: Animals; Antibodies; Aortic Valve; Disease Models, Animal; Endocarditis, Bacterial; Fibrin; Kidney; Rabbits; Streptococcal Infections; Streptococcus sanguis; Technetium

The model of experimental endocarditis can be used for the investigation of the different steps in the physiopathologic process leading to the formation of the infected cardiac vegetation. It has also greatly contributed to the knowledge of the characteristics of the infected vegetation. These data allow a better understanding of the therapeutic consequences (both preventive and curative) of the physiopathologic process.

Topics: Animals; Antibiotic Prophylaxis; Bacterial Adhesion; Disease Models, Animal; Endocarditis, Bacterial; Endothelium; Fibrin; Heart Valves; Humans; Rabbits; Streptococcal Infections; Streptococcus; Thrombosis

The "Streptococcus milleri" (SMG) group have been shown to possess factors in vitro that may be involved in pathogenesis. All SMG strains are able to bind fibronectin via a cell-surface protein; the binding ranged from 12 to 198 mol/cell. Strains also bound to platelet-fibrin or fibrin clots and fibrinogen, giving maximum adhesion values of 16.5%, 21.8% and 151 mol/cell respectively. Members of the species S. constellatus produced thrombin-like activity. Lancefield group C SMG aggregated rat platelets, a bacterial cell-surface protein acting as mediator in the reaction. Most of the in-vitro factors did not correlate with each other, an indication that SMG strains possess a wide variety of pathogenic properties that may be involved in the production of abscesses or endocarditis. However, there was a correlation between the binding of large amounts of fibrinogen ( > 100 mol/cell) and the ability to aggregate platelets. This suggests that fibrinogen binding may aid in platelet aggregation.

Topics: Abscess; Animals; Bacterial Adhesion; Blood Platelets; Endocarditis, Bacterial; Fibrin; Fibrinogen; Fibronectins; Platelet Aggregation; Rats; Serotyping; Streptococcal Infections; Streptococcus; Surface Properties

Adherence of group A, B, and C streptococci to fibrin thrombi was studied by using a novel fluorochrome microassay carried out in microdilution plates in which fibrin thrombi had been prepared by clotting citrated human, cattle, or horse plasma. Substantial adherence was observed with various strains of group A and C streptococci, whereas little was observed with group B streptococci. Adherence of all group A and C streptococcal strains decreased by up to 40% when fibronectin was depleted from the plasmas used for preparing fibrin thrombi, and fibronectin repletion increased adherence of streptococci in a dose-dependent manner. Addition of the 210-kilodalton C-terminal fragment of fibronectin to fibronectin-depleted plasma restored the adherence of group C but not group A streptococci, whereas addition of the 29-kilodalton N-terminal fragment was without any effect for all tested streptococcal strains. Prior incubation of group A and C streptococcal strains with fibronectin markedly increased their adherence, but treatment with proteases abolished their ability to adhere to fibrin thrombi. Adherence of group B streptococci was not affected by either fibronectin depletion or proteolytic digestion. These results indicate that both fibronectin incorporated into the fibrin matrix of thrombi and soluble fibronectin can mediate adherence of group A and C streptococci to fibrin thrombi and that binding sites for fibronectin located on the bacterial surface mediate this adherence.

Topics: Animals; Bacterial Adhesion; Cattle; Fibrin; Fibronectins; Horses; Humans; Hydrolysis; Streptococcal Infections; Streptococcus pyogenes; Trypsin; Wound Infection

In-vivo diffusion of labelled spiramycin into fibrin was investigated in a rabbit model of left sided subacute endocarditis caused by a nutritionally variant streptococcus that produces large fibrin vegetations. Animals received one 30 min infusion of different doses of 3H spiramycin alone (73.4 +/- 3.5 microCi and 846 microCi) or 57.5 +/- 3.5 microCi in combination with 50 mg/kg 'cold' spiramycin. Thirty minutes after the end of infusion (T30) these vegetation/blood and vegetation/muscle ratios were between 1 and 2 and the vegetation/plasma ratio was between 2 and 4 for the three doses tested. Autoradiography showed that 3H spiramycin was homogeneously distributed throughout the vegetation in comparison with some other drugs. On the other hand, there were considerable differences in antibiotic concentration among different vegetations in a single animal.

Topics: Animals; Autoradiography; Endocarditis, Subacute Bacterial; Female; Fibrin; Leucomycins; Rabbits; Streptococcal Infections

The adhesion to fibrin-platelet clots in vitro of 21 strains of streptococci isolated from the blood of patients with sub-acute bacterial endocarditis (SABE) was measured. The species, in order of greatest adhesion, were Streptococcus faecalis, Streptococcus mutans, Streptococcus milleri, Streptococcus sanguis, dextran-positive Streptococcus mitior, dextran-negative Streptococcus mitior and Streptococcus salivarius. Individual strains within species, however, cannot be assumed to be representative of their species and may exhibit unusually high or low adhesion. Adhesion depended upon both bacterial concentration and period of contact. There was no simple relationship between ability to adhere and liability to cause endocarditis. Formation of dextran did not increase adhesion. The streptococci were more adhesive than strains of Escherichia coli and Neisseria sicca and less adhesive than strains of Staphylococcus aureus and Streptococcus pyogenes.

Topics: Adhesiveness; Blood Coagulation; Blood Platelets; Dextrans; Endocarditis, Subacute Bacterial; Enterococcus faecalis; Escherichia coli; Fibrin; Humans; Neisseria; Sepsis; Staphylococcus aureus; Streptococcal Infections; Streptococcus; Streptococcus mutans; Streptococcus pyogenes; Streptococcus sanguis

Infectious endocarditis (IE) develops following bacteremic episodes during which bacteria may attach to sterile thrombotic vegetations. Such thrombotic vegetations result from the deposition of platelets and fibrin on lesioned endothelium. These sterile vegetations are the most susceptible to infection in the left side of the heart, since this localization is found in as much as 80% of the patients with IE. Any circulating bacterial or mycotic organism may induce endocarditis, but streptococci are most often responsible, possibly because of their high capacity to adhere to thrombotic vegetations. The host cell defenses apparently cannot penetrate the dense network of platelet and fibrin in the vegetation, and humoral immunity (antibodies and complement) are of no help against gram-positive cocci. Thus, the infected vegetation has been compared to a localized agranulocytic focus, permitting the survival of infection and allowing bacteria to be released freely and continuously into the circulation (hence the constant bacteremia, a hallmark of IE). In the subacute and chronic evolution of IE, the clinical findings are mainly due to immunization of the host against the infecting microbe, resulting in antigen-antibody-complex-mediated vasculitis, and in nonspecific symptoms. Only positive blood cultures at this stage will confirm the clinical suspicion of endocarditis. Embolism may occur in any organ and falsify the diagnosis because of focal signs. Local complications of IE are the major cause of mortality in this disease, and are due to valve perforation, paravalvular abscesses, cardiac metastatic abscesses etc. If these complications occur early in the course of IE, the course may be acute.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Agranulocytosis; Endocarditis, Bacterial; Endocarditis, Subacute Bacterial; Fibrin; Humans; Platelet Aggregation; Sepsis; Streptococcal Infections; Streptococcus

Immunofluorescence was performed on lung tissue obtained at necropsy from 18 newborn infants, including five with group B streptococcal (GBS) sepsis, seven with idiopathic respiratory distress syndrome (IRDS), and six control infants who died from other causes. Deposits of C3, IgG, and fibrin were found within hyaline membranes of infants who died with GBS sepsis or IRDS within 48 hours after birth. In some cases C4, factor B, and IgM were also observed. In five infants with IRDS who died more than five days after birth, immunofluorescent lung findings were less common and less intense. Hyaline membranes, attributed to mechanical ventilators and oxygen therapy in two infants who did not have GBS infection or IRDS, were negative for complement and immunoglobulins although fibrin was detected in one specimen. These data suggest that immunologic processes may contribute to the pathogenesis of certain types of acute lung injury, particularly in infants who die from GBS infection or IRDS during the early neonatal period.

Topics: Antigen-Antibody Complex; Complement C3; Fibrin; Fluorescent Antibody Technique; Humans; Immunoglobulin G; Infant, Newborn; Infant, Newborn, Diseases; Lung; Lung Diseases; Respiratory Distress Syndrome, Newborn; Streptococcal Infections; Streptococcus agalactiae

A new procedure, plasma fibrinogen chromatography, has been utilized, together with other blood coagulation assays, to quantify fibrin formation in 43 children with acute poststreptococcal glomerulonephritis (AGN) from the time of hospitalization until recovery. During the prediuretic phase of AGN, significant evidence for substantial increase in fibrin formation (intravascular coagulation) included gross increase in plasma high molecular weight fibrinogen complexes (HMWFC), the development of either hypo- or hyperfibrinogenemia and gross depression of coagulation factor XIII concentration and of alpha2-macroglobulin concentration. During the diuretic phase of the disease, these abnormalities regressed and evidence of enhanced plasma fibrinolytic activity, documented by an increase in fibrinogen first derivative, was detected. Concomitantly, urinary excretion of fibrin(ogen) degradation products (FDP) underwent substantial increase. With disease recovery, which occurred in all children, urinary FDP excretion ceased and all coagulation findings normalized.

Topics: Acute Disease; Adolescent; Blood Coagulation Factors; Blood Coagulation Tests; Child; Child, Preschool; Chromatography, Gel; Disseminated Intravascular Coagulation; Diuresis; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Fibrinolysis; Glomerulonephritis; Humans; Kidney Function Tests; Molecular Weight; Prognosis; Streptococcal Infections

Compared with streptokinase, thrombolytic treatment with urokinase has the advantages of being better tolerated and of practically unlimited applicability. Its disadvantage is the high cost. A good lytic action can be obtained with a dosage of 150,000 Ploug Units/12 hours for a duration of lysis of 8-14 days combined with heparin, the therapy being monitored by determination of the products of fibrinolysis. This dosage is not possible if the time factor plays a decisive role in the success of the treatment, e.g. in myocardial infarction. Urokinase is indicated when streptokinase cannot be used, or if continuation of the streptokinase therapy is necessary because of extensive thromboses.

Topics: Adult; Costs and Cost Analysis; Drug Therapy, Combination; Endopeptidases; Female; Femoral Vein; Fibrin; Fibrinolysin; Heparin; Humans; Male; Middle Aged; Myocardial Infarction; Pelvis; Streptococcal Infections; Streptokinase; Thrombosis; Time Factors; Urokinase-Type Plasminogen Activator; Venae Cavae

Topics: Arteritis; Biopsy; Child; Complement System Proteins; Diagnosis, Differential; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immunoglobulin G; Kidney; Kidney Glomerulus; Male; Microscopy, Electron; Streptococcal Infections

Topics: Acute Kidney Injury; Biopsy; Cell Migration Inhibition; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Immune Complex Diseases; Male; Necrosis; Peritoneal Dialysis; Proteinuria; Remission, Spontaneous; Streptococcal Infections

Topics: Blood Coagulation Tests; Blood Sedimentation; Cold Temperature; Fibrin; Fibrinogen; Fibrinolysis; Humans; Methods; Microchemistry; Plasminogen; Streptococcal Infections; Streptokinase

Topics: Animals; Basement Membrane; Cattle; Cell Membrane; Cell Nucleus; Collagen; Connective Tissue; Cytoplasm; Cytoplasmic Granules; Endoplasmic Reticulum; Epithelium; Extracellular Space; Female; Fibrin; Glycogen; Inflammation; Leukocytes; Lipids; Mammary Glands, Animal; Mastitis, Bovine; Microscopy, Electron; Milk Proteins; Organoids; Staphylococcal Infections; Streptococcal Infections

Topics: Adolescent; Child; Child, Preschool; Complement System Proteins; Female; Fibrin; Fluorescent Antibody Technique; Glomerulonephritis; Humans; Male; Streptococcal Infections

Topics: Adult; Age Factors; Antibodies; Antigen-Antibody Reactions; Autopsy; Basement Membrane; Biopsy; Complement System Proteins; Female; Fibrin; Glomerular Filtration Rate; Glomerulonephritis; Humans; Immunoelectrophoresis; Immunoglobulin G; Kidney Failure, Chronic; Kidney Glomerulus; Kidney Transplantation; Male; Middle Aged; Neutrophils; Streptococcal Infections; Transplantation, Homologous

Topics: Acute Disease; Blood Coagulation Factors; Blood Urea Nitrogen; Child; Creatinine; Female; Fibrin; Fibrinolysis; Glomerulonephritis; Heparin; Humans; Penicillin V; Prednisolone; Streptococcal Infections; Uremia

Topics: Deoxyribonucleases; Enzymes; Fibrin; Humans; Streptococcal Infections; Streptococcus

A method for the measurement of fibrinolysin production by beta hemolytic streptococci is described. The test was shown to be highly accurate in that repeated determinations showed only small variations. A study of 766 strains of beta hemolytic streptococci isolated from normal soldiers and patients with respiratory disease showed that fibrinolysin was produced by Lancefield groups A, C, and G, and, in addition, by a few strains of groups B and F. Group A streptococci produced more fibrinolysin on the average than the other groups. The median titers were 117 for group A, 61 for group C, and 20 for group G streptococci. In a study of 388 typed group A streptococci from different subjects the fibrinolytic capacity of an organism was shown to be related to the serological type. The importance of this observation in relation to the role of streptococcal fibrinolysis in infections is discussed. Finally, it was demonstrated that strains of streptococci which produced large amounts of fibrinolysin were capable of stimulating antifibrinolysin formation in patients whereas strains that produced small amounts only occasionally caused antibody formation.

Topics: Antifibrinolytic Agents; Blood; Fibrin; Fibrinolysin; Fibrinolysis; Humans; In Vitro Techniques; Streptococcal Infections; Streptococcus; Streptococcus pyogenes

Topics: Antifibrinolytic Agents; Blood; Fibrin; Humans; Immunity; Streptococcal Infections; Streptococcus

Topics: Blood; Fibrin; Fibrinolysin; Humans; Streptococcal Infections; Streptococcus

Topics: Blood; Endopeptidases; Enteropeptidase; Fibrin; Fibrinolysin; Fibrinolysis; Humans; Hydrolases; Peptide Hydrolases; Streptococcal Infections; Streptococcus; Trypsin

Topics: Antifibrinolytic Agents; Blood; Fibrin; Fibrinolysis; Humans; Streptococcal Infections; Streptococcus

Topics: Antifibrinolytic Agents; Blood; Fibrin; Fibrinolysis; Humans; Streptococcal Infections; Streptococcus