streptococci Flashcards
gram stain and catalase status/ oxidase status of streptococci
gram positive cocci in chains or pairs, catalase negative, oxidase negative, aerotolerant bacteria that ferment carbs to produce lactic acid
list the members of the streptococci family
Streptococcus pyogenes (group A), S. agalactiae (group B), S. equinus (Group D), viridians streptococci, and S. pneumoniae (pneumococcus)
Describe the classification system of streptococci based on visible hemolysis on sheep blood agar.
Some strains of streptococci can hemolyze red blood cells.
alpha hemolysis and strep groups
Incomplete destruction of erythrocytes, resulting in a green coloration of the medium surrounding the colonies. The green pigment is due to biliverdin and other heme compounds. Many of the oral streptococci and S. pneumoniae are alpha hemolytic.
beta hemolysis and strep groups
Complete lysis of RBCs results in a distinct clear zone around the colonies. Beta hemolysis usually is visualized better under reduced oxygen tension (i.e., by stabbing the organisms into the agar) because of the oxygen lability of the hemolysin. Lancefield groups A, B and C streptococci usually are beta-hemolytic.
gamma hemolysis
conventional designation for strains which produce no hemolysis effect on sheep blood agar. The term “nonhemolytic streptococci” is more precise
Describe Lancefield classification of streptococci and the antigens involved in classification
Beta hemolytic strep can be classified into 21 serological groups (A-U) based on antigen differences in cell wall carbohydrates. Certain alpha and nonhemolytic groups can also be classified this way. Group A strep antigen is the M protein of the cell wall. For S. pneumoniae it is the capsular polysaccharide
Assign the common streptococci species to the correct Lancefield groups.
A (bacitracin sensitive): S. pyogenes (beta hemolytic). B (Camp test positive): S. agalactiae (beta hemolytic or none). D (Bile-Esculin hydrolysis positive and 6.5% NaCl tolerance): Enterococcus faecalis, Non-typable: S. Salivarius, S. sanguis
Describe the structure of streptococci
Contains outer capsule > cell wall (M, T, R antigens) > carbohydrates > peptidoglycan > cytoplasmic membrane. And teichoic acids (lipotechoic acids associated with M protein). M proteins project from the cell surface
hyaluronic acid capsule
surrounds Group A strep- anti phagocytic.
M protein
The major virulence determinant of S. pyogenes. Prevents interaction of bacteria with complement. Phagocytes kill strains without M-protein.
Antibody against M-protein allows killing to occur.
80 different M-protein serotypes- vary at the N terminalThe major virulence determinant of S. pyogenes. Prevents interaction of bacteria with complement. Phagocytes kill strains without M-protein.
Antibody against M-protein allows killing to occur.
80 different M-protein serotypes- vary at the N terminalThe major virulence determinant of S. pyogenes. Prevents interaction of bacteria with complement. Phagocytes kill strains without M-protein.
Antibody against M-protein allows killing to occur.
80 different M-protein serotypes- vary at the N terminal
lipoteichoic acid
Virulence factor for group A strep which mediates initial adherence of the streptococci to mucosal cells. M protein aids by binding to LTA in correct orientation
T and R antigens
Cell wall proteins on Group A strep- not virulence factors
List extracellular products produced by S. Pyogenes
Streptolysin O, Streptolysin S, pyrogenic exotoxins A, B and C, Spreading factors (streptokinase, hyaluronidase, DNAse and proteinase)
Streptolysin O functions
hemolysin- binds cholesterol in RBCs and Causes hemolysis by inserting as a pore. Does not lyse neutrophils. Cardiotoxic. Inhibited by oxygen and inactivated by cholesterol. Anti-streptolysin O antibody increases after infection
Streptolysin S functions
hemolytic and cytotoxic
Pyrogenic exotoxins functions
pyrogenic, immunosuppressive, enhance host susceptibility to endotoxin shock. Rash (scarlet fever)
streptokinase functions
Activates human plasminogen which cleaves fibrin and fibrinogen. Facilitates spread.
Hyaluronidase functions
Breaks down CT and allows spread
DNAses functions
digests DNA, especially in pus.
Suppurative Group A strep infections
Pus forming- pharyngitis, pneumonia, osteomyelitis, cellulitis (bacteria gain access to subcutaneous tissues and spread rapidly), impetigo (superficial skin infection from break in skin), scarlet fever (fever, red rash, strawberry tongue, pyrogenic exotoxins)
List non suppurative Group A strep complications
Acute rheumatic fever and post-streptococcal glomerulonephritis
Acute rheumatic fever onset, mechanisms
3-6 weeks after S. pyogenes infection (pharyngitis). Inflammation of heart valve, skin, joints and CNS plus fever. Damage to heart valves may occur. Most likely model is autoimmune disease. Prevention possible by therapy of acute infection.
Post-streptococcal glomerulonephritis onset, mechanism
Inflammation of glomerulus 2-4 weeks after strep pyogenes infection of skin or throat. May cause acute renal failure. Most likely model is immune complex disease. Immune complexes get trapped in glomerular basement membrane resulting in complement deposition and neutrophil recruitment/ damage to kidney. Prevention most likely not possible with therapy of acute infection
