STREPTOCOCCUS PYOGENES (GROUP A): Gram (+) Cocci in pairs or chains of 4 to 8.
STREPTOCOCCI
GRAM (+) COCCI, LACTOSE (+)
STREPTOCOCCUS PYOGENES (GROUP A): Gram (+) Cocci in pairs or chains of 4 to 8.
Epidemiology / At Risk: Spread by aerosolized droplets
Manifestations:
SUPPURATIVE:
Pharyngitis: 5-15 yrs old.
Scarlet Fever: Pronounced oropharyngeal infection and rash.
Strawberry tongue, with desquamation ------> raspberry tongue.
Desquamation of outer skin layer on trunk.
Caused by the virulence factor, Erythrogenic Toxin.
Toxic-Shock Like Syndrome: Similar to Staph, it occurs as a result of Superantigen Erythrogenic Toxin A (SEA).
Pyoderma:
IMPETIGO: Cutaneous lesions in kids, usually on face. Very similar to the Staph bullous lesions, except that these are vesicular lesions because these are actually full of bugs.
ERYSIPELAS: Cutaneous lesions in adults. Painful. Again contains organisms.
Pneumonia:
Bacteremia: Can lead to arthritis, osteomyelitis, endocarditis, meningitis.
NON-SUPPURATIVE: Sequelae
Rheumatic Fever: 2-3 weeks after soar throat, low-grade fever and polyarthritis.
Heart Murmur found, due to inflammatory process in heart.
Theories to cause:
Antibody to MAP protein cross-reacting with heart muscle.
Small Strep protein may bind to cardiac muscle.
Strep actually infect the heart valve, exposing our own antigens which are not normally exposed.
Acute Glomerulonephritis: Can follow skin or throat infections.
Associated with T-Antigen. Presence of DNAse Type B antigen is diagnostic.
Renal shutdown, oliguria, and hypertension.
Thought to be immune-complex disease.
Processing:
Specimen:
Stain: Cannot do smear on throat culture -- normal flora (such as Strep Pneumoniae) would interfere.
Culture:
Large zones of beta-Hemolysis seen on blood agar plate.
Appearance of colonies goes from mucoid ------> smooth ------> rough.
MUCOID: Producing a capsule.
SMOOTH: Hyaluronidase attacks the bacteria's own capsules.
ROUGH: In chronic patient, lots of protein being made.
Todd-Hewitt Broth: Done when few organisms were recovered.
Strep: Granular precipitates on sides and bottom of tube.
Staph: Diffuse turbidity.
Identification:
BACITRACIN: Group-A Strep = SENSITIVE. Group-B Strep is resistant.
OFFICE TEST, SWAB: Agglutination antibody to Group-A antigen. Positive test is diagnostic. Negative test -- get culture.
Swab is put in nitrous acid to extract the Group-A antigen.
CATALASE (-): Compare to Staph.
ANTIBODY to STREP-O (ASO) TEST: Streptolysin-O is immunogenic and is found in Strep A, C, and G. Presence of ASO antibodies indicates that we have Strep A, C, or G, but does not indicate which one.
Test: RBC's. If antibody is present, then the cells are not hemolytic, and the RBC's will settle at the bottom in the center of the colony, giving it the appearance of a button.
Virulence:
Cell-Associated:
Cell-Wall Carbohydrate: Not an effective human antigen
Peptidoglycan: Induces inflammation
Lipotechoic Acid: Adheres to buccal mucosa, allowing colonization. Adhesin.
M-Protein: Fibers extending from surface.
Antigenically diverse (85 types) and immunogenic, to which we make protective antibodies.
This means we could get 85 strep-throats in our lifetime.
Antiphagocytic:
Clumps PMN's and white cells.
Interferes with alternate complement by binding Factor H
Interferes with classical complement by inhibiting C3B deposition onto cells.
M-Associated Protein (MAP): Antigenic, can cause cross-reaction with myocardial sarcolemma.
T-Antigen: Associated with Glomerulonephritis.
G-Protein: Binds Fc portion of IgG.
Streptococcal Chemotactic Factor: Inactivates C5a. Shuts down inflammatory response in host.
Capsule: During early inflammation, it is made antiphagocytic due to hyaluronidase. We can't develop antibody to the bugs until the capsule is lost.
Capsule accounts for the smooth texture in colony.
Extracellular: Release right outside of cellular environment.
DNAase: Four Types
Type B: Is antigenic and is diagnostic for glomerulonephritis. Most prevalent in skin infections.
Streptokinase: Works with TPA to digest clots. Can be immunogenic. Repeated therapies with streptokinase as a blood-thinner can result in hypersensitivity.
Hyaluronidase: Degrades its own capsule, plus host connective tissue.
Proteinase: Used to digest its own M-Protein.
Exotoxins
Streptolysin O: Oxygen labile and not expressed in vitro. It is hemolytic in vivo.
It lyses RBC's and WBC's under reduced oxygen tension. Damages platelets.
Antigenic: Basis for the ASO test.
Streptolysin S: Oxygen-stable. Hemolytic, but there is no lysis in vivo. Very small and not antigenic.
Erythrogenic Toxin: Three types. Causes the rash seen in Scarlet Fever.
Type-A also known as Superantigen Erythrogenic Toxin A (SEA), and causes Toxic-Shock Like Syndrome in the elderly.
Host Immune Response:
Antibody to M-Protein is protective.
Antibody to Streptolysin O (ASO) is diagnostic for suppurative infection to Strep A, C, or G.
Antibody to DNAse B is diagnostic for non-suppurative sequelae.
Vaccine / Prevention:
Treatment: Penicillin-G will work. Strep to date is not resistant.
STREPTOCOCCUS AGALACTIAE (GROUP -B): Gram (+) Diplococci
Name-Derivation: Agalactiae = associated with milk.
Epidemiology / At Risk:
Manifestations:
Neonatal Meningitis and Sepsis. Can be infected during birth by asymptomatic (normal flora) vaginal colonies.
Processing:
Specimen: CSF or blood.
Stain:
Culture:
Small zones of beta-Hemolysis. Larger beta-Hemolytic zones would be Group A Strep.
Identification:
BACITRACIN: Group-B Strep = RESISTANT. Group-A Strep - Sensitive.
CAMP TEST: Mix normally non-hemolytic Staph Aureus with specimen, and hemolytic zone is augmented. Staph Aureus is normally only hemolytic at 4C.
SEROTYPES: 5 serotypes
Group III is predominant one in meningitis. IgG vaccine for the mother is being worked on.
Virulence:
Capsular Antigens: Type III is associated with neonatal meningitis.
Can withstand bile in GI tract.
Vaccine / Prevention: Under development for mother.
STREPTOCOCCUS EQUI (GROUP C):
Name-Derivation: Equi = horse
Epidemiology / At Risk: Major pathogen of horses, or person-to-person.
Manifestations:
Skin suppuration: Cellulitis from skin breaks.
Identification:
Agglutination with Group-C antiserum.
Virulence:
Streptolysin O: Oxygen labile hemolysin, ASO (+).
Streptokinase: Antigenically distinct from Strep Group A.
This one is used as a blood thinner. It is immunogenic and hypersensitivity can develop.
STREPTOCOCCUS BOVIS (GROUP D): Very similar to E. Faecalis
Name-Derivation: Bovis = from cattle.
Epidemiology / At Risk: Opportunistic
Manifestations:
Respiratory, peritoneal infections.
Processing:
Culture: alpha-Hemolysis (partial hemolysis) = green clearing close to the colonies. Source of color unknown.
Identification: Compared to Enterococcus Faecalis
Penicillin sensitive.:
Treatment:
Sensitive to penicillin.
ENTEROCOCCUS FAECALIS (GROUP D): Very similar to Strep Bovis
Name-Derivation: feces.
Epidemiology / At Risk: Normal GI flora.
Manifestations: Multiple infections. Often a complication of cholecystitis.
GI obstruction may lead to bacteremia and endocarditis, due to bacterial resistances.
Processing:
Stain:
GRAM-VARIABLE -- both Gram (+) and Gram (-) found, alive.
Culture: Use blood agar with 40% bile and 6.5% NaCl. All three types of hemolysis found in culture.
Identification: Compared to Strep Bovis (Group D)
Grows in the presence of bile.
Penicillin resistant.
Virulence:
LIPOTECHOIC acid, very lipid rich, leads to gram-variable appearance.
Treatment: Penicillin resistant, strongly, due to altered Penicillin-binding proteins.
Also have acquired vancomycin and gentamycin resistance.
GROUP G STREPTOCOCCI:
Epidemiology / At Risk: Major animal pathogen, minor cause of human infections.
Manifestations:
Cellulitis.
Synovium.
Bacteremia, endocarditis.
Processing:
Specimen:
Stain:
Culture:
Identification: ASO (+)
Virulence:
Streptolysin O: Oxygen labile hemolysin.
DNAse: Invasive.
Streptokinase: Antigenically unique.
STREPTOCOCCUS PNEUMONIAE (PNEUMOCOCCUS, DIPLOCOCCUS):
Epidemiology / At Risk: #1 cause of community-acquired pneumonia.
Normal flora of oropharynx.
Viral flu, smoking, alcohol, old age, CHF predispose to infection.
Manifestations:
Pneumonia:
Lobar pneumonia with diffuse widespread consolidation.
Sudden onset of symptoms.
Productive cough, with mucopurulent rusty sputum.
Pericarditis and Pleurisy: Continuous spread from lungs can cause empyema and invasion of pericardium.
Bacteremia: 15-25% of cases.
Otitis Media: Infants.
Processing:
Specimen: Sputum sample is very fragile.
Stain: Gram (+) lancet-shaped Diplococci.
Culture: Very large capsule gives a halo appearance to the colonies. Smooth colonies.
Smooth colonies; alpha-hemolysis.
Autolysis occurs after continued incubation -- center of colony becomes sunken inward.
Identification:
Counter-Immune Electrophoresis (CIE): Can be done to look for capsular antigens. The capsule is not degraded and shows up in blood, urine, and sometimes CSF.
OPTOCHIN SENSITIVE: Compare to Strep Viridans.
Quellung Reaction: Would show positive Quellung with specific antisera against the sputum sample. Test not done anymore, 85 different serotypes are too many.
SEROTYPES: 85 serotypes; They are immunogenic, and antibodies are protective.
Virulence:
Polysaccharide Capsule: #1 virulence factor. 85 different types.
Type 3 can stick around post-infection and cause damage in lungs via antigen-antibody reactions. It is the most virulent and makes tons of capsule.
Extracellular Enzymes:
Amidase: Causes autolysis, which releases Pneumo lysin-O.
Neuraminidase: Helps to penetrate mucin and thus colonize the nasopharynx.
Protease: Digest antibodies.
PNEUMO LYSIN-O: Factor released upon autolysis. Oxygen-labile hemolysin.
Inhibits respiratory burst when inside PMN's.
Cytotoxic for epithelial cells.
Cell-Associated:
Forssman (F) Antigen: Inhibits amidase, therefore inhibits autolysis in vivo.
M-Protein: Antigenic, but not protective.
C-Polysaccharide: In cell wall. In acute infection, it induces inflammation. Promotes release of host C-Reactive Protein, which then acts with IgG to induce complement.
Peptidoglycan Fragments: Induce inflammation and chronic necrosis.
Host Immune Response:
Vaccine / Prevention: PNEUMO-VAC VACCINE. It only includes the most virulent 25 or so serotypes -- those that cause bacteremia.
Given to at-risk folks: Splenectomy, old, HIV, diabetes, COPD, CVD. Latest recommendation says every 6 years. Flu shot is also recommended for prevention.
Kids under 2 can't get the pure vaccine (preventative for otitis media) -- must be conjugated to protein. Kid's vaccine is under development.
Treatment: Penicillin is effective. Little resistance developed yet, but it is due to PBP's when present.
VIRIDANS STREPTOCOCCUS:
Name-Derivation: Viridans = green, as it appears in culture.
Manifestations: Important opportunistic organism in periodontal disease.
Bacteremia will lead to endocarditis, especially if heart valves were already damaged.
Processing:
Culture: alpha-Hemolysis, appearing green.
Identification:
OPTOCHIN-RESISTANT: Compare to Strep. Pneumoniae.
Treatment: Penicillin-resistant. Combination therapy (aminoglycoside) required.
GRAM (+) COCCI, LACTOSE (+)
STREPTOCOCCUS PYOGENES (GROUP A): Gram (+) Cocci in pairs or chains of 4 to 8.
Epidemiology / At Risk: Spread by aerosolized droplets
Manifestations:
SUPPURATIVE:
Pharyngitis: 5-15 yrs old.
Scarlet Fever: Pronounced oropharyngeal infection and rash.
Strawberry tongue, with desquamation ------> raspberry tongue.
Desquamation of outer skin layer on trunk.
Caused by the virulence factor, Erythrogenic Toxin.
Toxic-Shock Like Syndrome: Similar to Staph, it occurs as a result of Superantigen Erythrogenic Toxin A (SEA).
Pyoderma:
IMPETIGO: Cutaneous lesions in kids, usually on face. Very similar to the Staph bullous lesions, except that these are vesicular lesions because these are actually full of bugs.
ERYSIPELAS: Cutaneous lesions in adults. Painful. Again contains organisms.
Pneumonia:
Bacteremia: Can lead to arthritis, osteomyelitis, endocarditis, meningitis.
NON-SUPPURATIVE: Sequelae
Rheumatic Fever: 2-3 weeks after soar throat, low-grade fever and polyarthritis.
Heart Murmur found, due to inflammatory process in heart.
Theories to cause:
Antibody to MAP protein cross-reacting with heart muscle.
Small Strep protein may bind to cardiac muscle.
Strep actually infect the heart valve, exposing our own antigens which are not normally exposed.
Acute Glomerulonephritis: Can follow skin or throat infections.
Associated with T-Antigen. Presence of DNAse Type B antigen is diagnostic.
Renal shutdown, oliguria, and hypertension.
Thought to be immune-complex disease.
Processing:
Specimen:
Stain: Cannot do smear on throat culture -- normal flora (such as Strep Pneumoniae) would interfere.
Culture:
Large zones of beta-Hemolysis seen on blood agar plate.
Appearance of colonies goes from mucoid ------> smooth ------> rough.
MUCOID: Producing a capsule.
SMOOTH: Hyaluronidase attacks the bacteria's own capsules.
ROUGH: In chronic patient, lots of protein being made.
Todd-Hewitt Broth: Done when few organisms were recovered.
Strep: Granular precipitates on sides and bottom of tube.
Staph: Diffuse turbidity.
Identification:
BACITRACIN: Group-A Strep = SENSITIVE. Group-B Strep is resistant.
OFFICE TEST, SWAB: Agglutination antibody to Group-A antigen. Positive test is diagnostic. Negative test -- get culture.
Swab is put in nitrous acid to extract the Group-A antigen.
CATALASE (-): Compare to Staph.
ANTIBODY to STREP-O (ASO) TEST: Streptolysin-O is immunogenic and is found in Strep A, C, and G. Presence of ASO antibodies indicates that we have Strep A, C, or G, but does not indicate which one.
Test: RBC's. If antibody is present, then the cells are not hemolytic, and the RBC's will settle at the bottom in the center of the colony, giving it the appearance of a button.
Virulence:
Cell-Associated:
Cell-Wall Carbohydrate: Not an effective human antigen
Peptidoglycan: Induces inflammation
Lipotechoic Acid: Adheres to buccal mucosa, allowing colonization. Adhesin.
M-Protein: Fibers extending from surface.
Antigenically diverse (85 types) and immunogenic, to which we make protective antibodies.
This means we could get 85 strep-throats in our lifetime.
Antiphagocytic:
Clumps PMN's and white cells.
Interferes with alternate complement by binding Factor H
Interferes with classical complement by inhibiting C3B deposition onto cells.
M-Associated Protein (MAP): Antigenic, can cause cross-reaction with myocardial sarcolemma.
T-Antigen: Associated with Glomerulonephritis.
G-Protein: Binds Fc portion of IgG.
Streptococcal Chemotactic Factor: Inactivates C5a. Shuts down inflammatory response in host.
Capsule: During early inflammation, it is made antiphagocytic due to hyaluronidase. We can't develop antibody to the bugs until the capsule is lost.
Capsule accounts for the smooth texture in colony.
Extracellular: Release right outside of cellular environment.
DNAase: Four Types
Type B: Is antigenic and is diagnostic for glomerulonephritis. Most prevalent in skin infections.
Streptokinase: Works with TPA to digest clots. Can be immunogenic. Repeated therapies with streptokinase as a blood-thinner can result in hypersensitivity.
Hyaluronidase: Degrades its own capsule, plus host connective tissue.
Proteinase: Used to digest its own M-Protein.
Exotoxins
Streptolysin O: Oxygen labile and not expressed in vitro. It is hemolytic in vivo.
It lyses RBC's and WBC's under reduced oxygen tension. Damages platelets.
Antigenic: Basis for the ASO test.
Streptolysin S: Oxygen-stable. Hemolytic, but there is no lysis in vivo. Very small and not antigenic.
Erythrogenic Toxin: Three types. Causes the rash seen in Scarlet Fever.
Type-A also known as Superantigen Erythrogenic Toxin A (SEA), and causes Toxic-Shock Like Syndrome in the elderly.
Host Immune Response:
Antibody to M-Protein is protective.
Antibody to Streptolysin O (ASO) is diagnostic for suppurative infection to Strep A, C, or G.
Antibody to DNAse B is diagnostic for non-suppurative sequelae.
Vaccine / Prevention:
Treatment: Penicillin-G will work. Strep to date is not resistant.
STREPTOCOCCUS AGALACTIAE (GROUP -B): Gram (+) Diplococci
Name-Derivation: Agalactiae = associated with milk.
Epidemiology / At Risk:
Manifestations:
Neonatal Meningitis and Sepsis. Can be infected during birth by asymptomatic (normal flora) vaginal colonies.
Processing:
Specimen: CSF or blood.
Stain:
Culture:
Small zones of beta-Hemolysis. Larger beta-Hemolytic zones would be Group A Strep.
Identification:
BACITRACIN: Group-B Strep = RESISTANT. Group-A Strep - Sensitive.
CAMP TEST: Mix normally non-hemolytic Staph Aureus with specimen, and hemolytic zone is augmented. Staph Aureus is normally only hemolytic at 4C.
SEROTYPES: 5 serotypes
Group III is predominant one in meningitis. IgG vaccine for the mother is being worked on.
Virulence:
Capsular Antigens: Type III is associated with neonatal meningitis.
Can withstand bile in GI tract.
Vaccine / Prevention: Under development for mother.
STREPTOCOCCUS EQUI (GROUP C):
Name-Derivation: Equi = horse
Epidemiology / At Risk: Major pathogen of horses, or person-to-person.
Manifestations:
Skin suppuration: Cellulitis from skin breaks.
Identification:
Agglutination with Group-C antiserum.
Virulence:
Streptolysin O: Oxygen labile hemolysin, ASO (+).
Streptokinase: Antigenically distinct from Strep Group A.
This one is used as a blood thinner. It is immunogenic and hypersensitivity can develop.
STREPTOCOCCUS BOVIS (GROUP D): Very similar to E. Faecalis
Name-Derivation: Bovis = from cattle.
Epidemiology / At Risk: Opportunistic
Manifestations:
Respiratory, peritoneal infections.
Processing:
Culture: alpha-Hemolysis (partial hemolysis) = green clearing close to the colonies. Source of color unknown.
Identification: Compared to Enterococcus Faecalis
Penicillin sensitive.:
Treatment:
Sensitive to penicillin.
ENTEROCOCCUS FAECALIS (GROUP D): Very similar to Strep Bovis
Name-Derivation: feces.
Epidemiology / At Risk: Normal GI flora.
Manifestations: Multiple infections. Often a complication of cholecystitis.
GI obstruction may lead to bacteremia and endocarditis, due to bacterial resistances.
Processing:
Stain:
GRAM-VARIABLE -- both Gram (+) and Gram (-) found, alive.
Culture: Use blood agar with 40% bile and 6.5% NaCl. All three types of hemolysis found in culture.
Identification: Compared to Strep Bovis (Group D)
Grows in the presence of bile.
Penicillin resistant.
Virulence:
LIPOTECHOIC acid, very lipid rich, leads to gram-variable appearance.
Treatment: Penicillin resistant, strongly, due to altered Penicillin-binding proteins.
Also have acquired vancomycin and gentamycin resistance.
GROUP G STREPTOCOCCI:
Epidemiology / At Risk: Major animal pathogen, minor cause of human infections.
Manifestations:
Cellulitis.
Synovium.
Bacteremia, endocarditis.
Processing:
Specimen:
Stain:
Culture:
Identification: ASO (+)
Virulence:
Streptolysin O: Oxygen labile hemolysin.
DNAse: Invasive.
Streptokinase: Antigenically unique.
STREPTOCOCCUS PNEUMONIAE (PNEUMOCOCCUS, DIPLOCOCCUS):
Epidemiology / At Risk: #1 cause of community-acquired pneumonia.
Normal flora of oropharynx.
Viral flu, smoking, alcohol, old age, CHF predispose to infection.
Manifestations:
Pneumonia:
Lobar pneumonia with diffuse widespread consolidation.
Sudden onset of symptoms.
Productive cough, with mucopurulent rusty sputum.
Pericarditis and Pleurisy: Continuous spread from lungs can cause empyema and invasion of pericardium.
Bacteremia: 15-25% of cases.
Otitis Media: Infants.
Processing:
Specimen: Sputum sample is very fragile.
Stain: Gram (+) lancet-shaped Diplococci.
Culture: Very large capsule gives a halo appearance to the colonies. Smooth colonies.
Smooth colonies; alpha-hemolysis.
Autolysis occurs after continued incubation -- center of colony becomes sunken inward.
Identification:
Counter-Immune Electrophoresis (CIE): Can be done to look for capsular antigens. The capsule is not degraded and shows up in blood, urine, and sometimes CSF.
OPTOCHIN SENSITIVE: Compare to Strep Viridans.
Quellung Reaction: Would show positive Quellung with specific antisera against the sputum sample. Test not done anymore, 85 different serotypes are too many.
SEROTYPES: 85 serotypes; They are immunogenic, and antibodies are protective.
Virulence:
Polysaccharide Capsule: #1 virulence factor. 85 different types.
Type 3 can stick around post-infection and cause damage in lungs via antigen-antibody reactions. It is the most virulent and makes tons of capsule.
Extracellular Enzymes:
Amidase: Causes autolysis, which releases Pneumo lysin-O.
Neuraminidase: Helps to penetrate mucin and thus colonize the nasopharynx.
Protease: Digest antibodies.
PNEUMO LYSIN-O: Factor released upon autolysis. Oxygen-labile hemolysin.
Inhibits respiratory burst when inside PMN's.
Cytotoxic for epithelial cells.
Cell-Associated:
Forssman (F) Antigen: Inhibits amidase, therefore inhibits autolysis in vivo.
M-Protein: Antigenic, but not protective.
C-Polysaccharide: In cell wall. In acute infection, it induces inflammation. Promotes release of host C-Reactive Protein, which then acts with IgG to induce complement.
Peptidoglycan Fragments: Induce inflammation and chronic necrosis.
Host Immune Response:
Vaccine / Prevention: PNEUMO-VAC VACCINE. It only includes the most virulent 25 or so serotypes -- those that cause bacteremia.
Given to at-risk folks: Splenectomy, old, HIV, diabetes, COPD, CVD. Latest recommendation says every 6 years. Flu shot is also recommended for prevention.
Kids under 2 can't get the pure vaccine (preventative for otitis media) -- must be conjugated to protein. Kid's vaccine is under development.
Treatment: Penicillin is effective. Little resistance developed yet, but it is due to PBP's when present.
VIRIDANS STREPTOCOCCUS:
Name-Derivation: Viridans = green, as it appears in culture.
Manifestations: Important opportunistic organism in periodontal disease.
Bacteremia will lead to endocarditis, especially if heart valves were already damaged.
Processing:
Culture: alpha-Hemolysis, appearing green.
Identification:
OPTOCHIN-RESISTANT: Compare to Strep. Pneumoniae.
Treatment: Penicillin-resistant. Combination therapy (aminoglycoside) required.
