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STREPTOCOCCUS
DR. EBUNIKHE I. KADU
INTORDUCTION
Domain: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaeceae
Genus: Streptococcus.
• Gram +ve, Spherical
• Most catalase -ve, Oxidase –ve
• Most facultative anaerobes
• Small pin pointed white gray, chains or
pairs
• Capsulated, Non spore forming, Non
motile
• Hemolytic BA.
CLASSIFICATION
1. HEMOLYTIC REACTION.
A. Alpha hemolysis.
• Partial green discoloration non groupable
• Eg S. Pneumoniae and S. Viridans
B. Beta hemolysis
• Complete hemolysis, clear zone, groupable
• Eg S. Pyogenes and S. Agalactiae
C. Gamma hemolysis
• non hemolytic
2. LANCEFIELD/ SEROTYPING.
• Beta hemolytic further classification, based on surface carbohydrates.
• 21 serotypes, Group A-W (excluding I and J)
• Eg S. Pyogenes, E. Faecalis, S. Agalactiae
3. OXYGEN NEEDS.
• Anaerobes
• Facultative
S. VIRIDANS.
INTRODUCTION.
• Gram +ve, Alpha hemolytic
• No lancefield hence low pathogenicity
• Oral cavity flora, nasopharynx, genital and skin
• Groups include: S. Anginosus, S. Mitis, S. Sanguinis, S. Salivarus, S. Mutans, S.
Milleri
• Entrance via dental and surgical instruments.
CLINICAL MANIFESTATIONS.
• Dental caries, gingivitis, oral infections others
• Subacute endocarditis
• Brain and abdominal abscess
• Neonatal infections.
LABORATORY DIAGNOSIS.
• Specimen collections from pus, blood, swabs
• Gram stain, +ve
• Blood agar, alpha hemolytic in aerobic condotions, beta in anaerobic (37
celcius, 18-24 hrs)
• Biochemical tests: Catalase –ve, Oxidase –ve, Optochin resistant, Bile
insoluble
• PCR
TREATMENT
• Prophylaxis
• Penicillin and other Beta lactams
• Ampicillin and gentamicin
• Vancomycin for penicillin allergic
S. PNEUMONIAE
INTRODUCTION
• Gram +ve, facultative, diplococci
• Alpha hemolytic, non spore, non motile
• Colonizes respiratory tract, sinuses and nasal cavity.
• Direct spread via respiratory droplets, neonatal infections
• Most cause of community acquired pneumoniae and meningitis in
children and elderly, sepsis in immunocompromised.
• Invasive pneumococcal diseases include: Bronchitis, Rhinitis, Acute
sinusitis, Septic arthritis, Brain abscess, Otitis media,
Conjuctivitis, Meningitis and Pericarditis
VIRULENCE FACTORS.
• Capsule, polysaccharide and antiphagocytic.
• IgA protease
• Pneumolysins- slows ciliary beating by respiratory tract, toxic to pulmomary
endothelial, spread to blood.
• Autolysins- breaks peptide crosslinking of cell wall
LABORATORY DIAGNOSIS
• Gram +ve
• Catalase –ve
• Optochin sensitive
• Inulin ferment +ve
• Bile solubility +ve
• Blood agar alpha hemolytic
• Quelling reaction +ve
TREATMENT
• Penicillin
• Ceftriaxone, Cefotaxime,
• Carbapenems
• Fluoroquinolones
• Erythromycin, Chloramphenicol, Vancomycin
• Prevention via conjugated vaccines.
INTERACTION WITH HAEMOPHILIS INFLUENZA
H. Influenza and S. Pneumoniae can both be found in human respiratory
system but Influenza when dead and expresses in neutrophils is more
aggressive in attacking Pneumoniae.
S. VIRIDANS S. PNEUMONIAE
Lysed in bile Insoluble Soluble
Inulin fermentation -ve +ve
Optochin sensitivity -ve +ve
Pathogenicity in mice -ve +ve
Quelling test -ve +ve
GROUP A STREPTOCOCCUS- GAS ( S.
PYOGENES)
INTRODUCTION
• Gram +ve, beta hemolytic (GABHS)
• Non motile, non spore, round
• Microbiota, infrequent pathogenic
• S. Pyogenes often called GAS
• Other GAS include: S. Anginosus, S. Dysgalactiae.
• Pyogenes means pus forming
• Can be cultured in fresh blood 1-3days
• Catalase –ve, facultative
• Lysogeny- meaning can carry more than one phages
• Transmission mainly by droplets.
CLINICAL MANIFESTATIONS.
• Superficial: Pharyngitis, Skin lesions, Vaginitis, Post partum infections.
• Deep: Bacteremia, Sepsis, Cellutitis, Flesh eating bacteria, Myositis,
Pericarditis, Meningitis, Pneumonia, Septic arthristis
• Immunologically mediated: Rheumatic fever, Reactive arthrisits,
Scarlet fever
• Toxix mediated: Scarletina, Toxic shock syndrome
VIRULENCE FACTORS.
• Bacterial capsule, antiphagocytic.
• Exotoxins: Streptolysin O, Streptolysin S poison against neutrophils,
Exotoxin A(SpeA) superantigen, SpeC degrades cytokines and ECM
• Enzymes: Streptokinase digest fibrin, Hyaluronidase spreads bacteria,
Streptodornase is a DNases, C5a peptidase against compliment system,
Streptococcal chemokine protease inhibits neutrophil migration.
COMPLICATIONS OF STREP THROAT.
• Acute rheumatic fever
• Acute poststreptococcal glomerulonephritis
LABORATORY DIAGNOSIS
• Gram +ve
• BA beta hemolytic
• Catalase –ve
• Bacitracin sensitive
TREATMENT AND PREVENTION
• Cephalosporins
• Tetracyclines
• Erythromycin
• Chloramphenicol
• No vaccines
• Treat pharyngitis early
GROUP B STREPTOCOCCUS (GBS)- S.
AGALACTIAE
 INTRODUCTION
• Gram +ve, round, form chains
• Beta hemolytica, catalase –ve, facultative
• Capsulated with exopolysaccharide
• Microbiota colonizing gastrointenstinal and genitourinary tracts
• 30% infections are asymptomatics
• Non motile, non spore
 LABORATORY DIAGNOSIS.
• Blood agar, beta hemolytic
• Gram stain, +ve
• Latex agglutination
• CAMP test, +ve
• Penicillin sensitive, catalase –ve
• Bacitracin resistance.
GBS INFECTIONS IN NEWBORNS
• Leading cause of neonatal infections
• Chorioamnionitis, postpartum infections and fetal deaths
• Neonatal sepsis, Meningitis, Pneumoniae or long term sequele
• Prevention of neonatal infections is by: Intrapartum antibiotics
prophylaxis, IV penicillin/ampicillin atleast 4hrs before delivery.
• In penicillin allergic mothers, cefazolin, clindamycin, vancomycin.
TREATMENT.
• Penicillin is drug of choice and can be combined with gentamicin
GROUP D STREPTOCOCCUS (GDS)/
ENTEROCOCCUS
INTRODUCTION.
• Have been reclassified to enterococcus
• They include: E. Faecalis, E. Faecium, E. Durans, E. Avium
• Non enerococcal group D include: S. Bovis, S. Equinis, S. Gallolyticus, S. Infantarius
E. FAECALIS
 Introduction.
• Gram +ve, GIT, catalase -ve
• High antibiotic resistance (together with E. Faecium
• More common in reinfected root canal
• Non motile, non spore, facultative
• Can grow in high temperutures 60 degrees and high alkaline pH 9.6
• Can resist bile salts, detergents, heavy metals, dessication etc
• Can cause endocardidtis, sepsis, UTI, Meningitis.
Virulence factors.
• Binds to dentine
• Suppresses lymphocytes
• Lytic enzymes- cytolysins
• pH homeostasis
• Biofilm
• Protease plasminogen
Multi drug resistance
• Aminoglycosides, Aztreonam, Cephalosporins, Vancomycin, Clindamycin,
Semisynthetic penicillins, Trimethoprim-sulfamethoxazole
Treatment.
• Nitrofurantoin, Linezolid, Daptomycin, NaOCl and Chlorhexidine, Ampicillin
E. FAECIUM
• Gram +ve, alpha hemolytic
• Vancomycin and multi drug resistant like Faecalis
• Tolerance to alcohol based solutions
• Treatment- Linezolid, Daptomycin, Sultamicillin, Tigecycline,
Streptogramins.
S. BOVIS
• Gram +ve, Esculin +ve, Sorbitol –ve, produce acetoin, Catalase –ve,
Oxidase –ve
• Non motile, Non spore, Gamma hemolytic
• Associated with UTI, endocarditis, Sepsis and colorectal cancer
• Can cause neonatal sepsis and meningitis

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Streptococcus

  • 2. INTORDUCTION Domain: Bacteria Phylum: Firmicutes Class: Bacilli Order: Lactobacillales Family: Streptococcaeceae Genus: Streptococcus. • Gram +ve, Spherical • Most catalase -ve, Oxidase –ve • Most facultative anaerobes • Small pin pointed white gray, chains or pairs • Capsulated, Non spore forming, Non motile • Hemolytic BA.
  • 3. CLASSIFICATION 1. HEMOLYTIC REACTION. A. Alpha hemolysis. • Partial green discoloration non groupable • Eg S. Pneumoniae and S. Viridans B. Beta hemolysis • Complete hemolysis, clear zone, groupable • Eg S. Pyogenes and S. Agalactiae C. Gamma hemolysis • non hemolytic
  • 4. 2. LANCEFIELD/ SEROTYPING. • Beta hemolytic further classification, based on surface carbohydrates. • 21 serotypes, Group A-W (excluding I and J) • Eg S. Pyogenes, E. Faecalis, S. Agalactiae 3. OXYGEN NEEDS. • Anaerobes • Facultative
  • 5. S. VIRIDANS. INTRODUCTION. • Gram +ve, Alpha hemolytic • No lancefield hence low pathogenicity • Oral cavity flora, nasopharynx, genital and skin • Groups include: S. Anginosus, S. Mitis, S. Sanguinis, S. Salivarus, S. Mutans, S. Milleri • Entrance via dental and surgical instruments. CLINICAL MANIFESTATIONS. • Dental caries, gingivitis, oral infections others • Subacute endocarditis • Brain and abdominal abscess • Neonatal infections.
  • 6. LABORATORY DIAGNOSIS. • Specimen collections from pus, blood, swabs • Gram stain, +ve • Blood agar, alpha hemolytic in aerobic condotions, beta in anaerobic (37 celcius, 18-24 hrs) • Biochemical tests: Catalase –ve, Oxidase –ve, Optochin resistant, Bile insoluble • PCR TREATMENT • Prophylaxis • Penicillin and other Beta lactams • Ampicillin and gentamicin • Vancomycin for penicillin allergic
  • 7. S. PNEUMONIAE INTRODUCTION • Gram +ve, facultative, diplococci • Alpha hemolytic, non spore, non motile • Colonizes respiratory tract, sinuses and nasal cavity. • Direct spread via respiratory droplets, neonatal infections • Most cause of community acquired pneumoniae and meningitis in children and elderly, sepsis in immunocompromised. • Invasive pneumococcal diseases include: Bronchitis, Rhinitis, Acute sinusitis, Septic arthritis, Brain abscess, Otitis media, Conjuctivitis, Meningitis and Pericarditis
  • 8. VIRULENCE FACTORS. • Capsule, polysaccharide and antiphagocytic. • IgA protease • Pneumolysins- slows ciliary beating by respiratory tract, toxic to pulmomary endothelial, spread to blood. • Autolysins- breaks peptide crosslinking of cell wall LABORATORY DIAGNOSIS • Gram +ve • Catalase –ve • Optochin sensitive • Inulin ferment +ve • Bile solubility +ve • Blood agar alpha hemolytic • Quelling reaction +ve
  • 9. TREATMENT • Penicillin • Ceftriaxone, Cefotaxime, • Carbapenems • Fluoroquinolones • Erythromycin, Chloramphenicol, Vancomycin • Prevention via conjugated vaccines. INTERACTION WITH HAEMOPHILIS INFLUENZA H. Influenza and S. Pneumoniae can both be found in human respiratory system but Influenza when dead and expresses in neutrophils is more aggressive in attacking Pneumoniae.
  • 10. S. VIRIDANS S. PNEUMONIAE Lysed in bile Insoluble Soluble Inulin fermentation -ve +ve Optochin sensitivity -ve +ve Pathogenicity in mice -ve +ve Quelling test -ve +ve
  • 11. GROUP A STREPTOCOCCUS- GAS ( S. PYOGENES) INTRODUCTION • Gram +ve, beta hemolytic (GABHS) • Non motile, non spore, round • Microbiota, infrequent pathogenic • S. Pyogenes often called GAS • Other GAS include: S. Anginosus, S. Dysgalactiae. • Pyogenes means pus forming • Can be cultured in fresh blood 1-3days • Catalase –ve, facultative • Lysogeny- meaning can carry more than one phages • Transmission mainly by droplets.
  • 12. CLINICAL MANIFESTATIONS. • Superficial: Pharyngitis, Skin lesions, Vaginitis, Post partum infections. • Deep: Bacteremia, Sepsis, Cellutitis, Flesh eating bacteria, Myositis, Pericarditis, Meningitis, Pneumonia, Septic arthristis • Immunologically mediated: Rheumatic fever, Reactive arthrisits, Scarlet fever • Toxix mediated: Scarletina, Toxic shock syndrome VIRULENCE FACTORS. • Bacterial capsule, antiphagocytic. • Exotoxins: Streptolysin O, Streptolysin S poison against neutrophils, Exotoxin A(SpeA) superantigen, SpeC degrades cytokines and ECM • Enzymes: Streptokinase digest fibrin, Hyaluronidase spreads bacteria, Streptodornase is a DNases, C5a peptidase against compliment system, Streptococcal chemokine protease inhibits neutrophil migration.
  • 13. COMPLICATIONS OF STREP THROAT. • Acute rheumatic fever • Acute poststreptococcal glomerulonephritis LABORATORY DIAGNOSIS • Gram +ve • BA beta hemolytic • Catalase –ve • Bacitracin sensitive TREATMENT AND PREVENTION • Cephalosporins • Tetracyclines • Erythromycin • Chloramphenicol • No vaccines • Treat pharyngitis early
  • 14. GROUP B STREPTOCOCCUS (GBS)- S. AGALACTIAE  INTRODUCTION • Gram +ve, round, form chains • Beta hemolytica, catalase –ve, facultative • Capsulated with exopolysaccharide • Microbiota colonizing gastrointenstinal and genitourinary tracts • 30% infections are asymptomatics • Non motile, non spore  LABORATORY DIAGNOSIS. • Blood agar, beta hemolytic • Gram stain, +ve • Latex agglutination • CAMP test, +ve • Penicillin sensitive, catalase –ve • Bacitracin resistance.
  • 15. GBS INFECTIONS IN NEWBORNS • Leading cause of neonatal infections • Chorioamnionitis, postpartum infections and fetal deaths • Neonatal sepsis, Meningitis, Pneumoniae or long term sequele • Prevention of neonatal infections is by: Intrapartum antibiotics prophylaxis, IV penicillin/ampicillin atleast 4hrs before delivery. • In penicillin allergic mothers, cefazolin, clindamycin, vancomycin. TREATMENT. • Penicillin is drug of choice and can be combined with gentamicin
  • 16. GROUP D STREPTOCOCCUS (GDS)/ ENTEROCOCCUS INTRODUCTION. • Have been reclassified to enterococcus • They include: E. Faecalis, E. Faecium, E. Durans, E. Avium • Non enerococcal group D include: S. Bovis, S. Equinis, S. Gallolyticus, S. Infantarius E. FAECALIS  Introduction. • Gram +ve, GIT, catalase -ve • High antibiotic resistance (together with E. Faecium • More common in reinfected root canal • Non motile, non spore, facultative • Can grow in high temperutures 60 degrees and high alkaline pH 9.6 • Can resist bile salts, detergents, heavy metals, dessication etc • Can cause endocardidtis, sepsis, UTI, Meningitis.
  • 17. Virulence factors. • Binds to dentine • Suppresses lymphocytes • Lytic enzymes- cytolysins • pH homeostasis • Biofilm • Protease plasminogen Multi drug resistance • Aminoglycosides, Aztreonam, Cephalosporins, Vancomycin, Clindamycin, Semisynthetic penicillins, Trimethoprim-sulfamethoxazole Treatment. • Nitrofurantoin, Linezolid, Daptomycin, NaOCl and Chlorhexidine, Ampicillin
  • 18. E. FAECIUM • Gram +ve, alpha hemolytic • Vancomycin and multi drug resistant like Faecalis • Tolerance to alcohol based solutions • Treatment- Linezolid, Daptomycin, Sultamicillin, Tigecycline, Streptogramins. S. BOVIS • Gram +ve, Esculin +ve, Sorbitol –ve, produce acetoin, Catalase –ve, Oxidase –ve • Non motile, Non spore, Gamma hemolytic • Associated with UTI, endocarditis, Sepsis and colorectal cancer • Can cause neonatal sepsis and meningitis