STREP Flashcards
(30 cards)
What are the General Features of Streptococci (with “why”)
- Gram-positive, catalase-negative cocci
➡️ Lacks catalase enzyme, unlike staphylococci; helps differentiate them in the lab.
- Oval or coccoid cells (\~2 µm), arranged in pairs or chains
➡️ “Strepto-” means twisted chain; typical microscopic appearance.
- Facultative anaerobes or capnophilic
➡️ Can grow with or without oxygen; some prefer CO₂-rich environments, helping survival in various host tissues.
- Homofermentative metabolism (produces lactic acid without gas)
➡️ End-product of glucose metabolism is lactic acid, which can contribute to local tissue damage or acidification.
What’s the Taxonomy of streptococcus?
- Kingdom: Eubacteria
- Phylum: Firmicutes
- Class: Bacilli
- Order: Lactobacillales
- Family: Streptococcaceae
- Genus: Streptococcus
Classify streptococcus bacteria with examples of each
Classification Methods (with “why”)
- Hemolytic Reaction on Blood Agar
➡️ Shows how the bacteria interact with red blood cells:
- Beta-hemolysis: Complete lysis ⏩clear zone (e.g., S. pyogenes)
- Alpha-hemolysis: Partial lysis ⏩ greenish zone (e.g., S. pneumoniae)
- Gamma-hemolysis: No lysis (e.g., some enterococci)
Why it matters: Hemolysis helps quickly narrow down species groups.
- Lancefield Grouping (A–H, K–U)
➡️ Based on specific carbohydrate antigens in the cell wall.
- Group A: S. pyogenes
- Group B: S. agalactiae
Why it matters: Helps identify pathogens responsible for different infections.
- Capsular Polysaccharide Typing
➡️ Used especially for S. pneumoniae (over 90 serotypes) and Group B strep.
Why: Capsule determines virulence and immunity; typing aids in vaccine development.
- Biochemical Reactions
➡️ Needed when antigen-based grouping fails.
- Used for identifying viridans group streptococci and others that don’t fit Lancefield types.
Why: Viridans strep lack Lancefield antigens but cause diseases like endocarditis; require alternative ID methods.
List examples of medically relevant streptococcus
- Streptococcus pyogenes (Group A β-haemolytic streptococcus)
What are the core characteristics of Streptococcus pyogenes (Group A β-haemolytic streptococcus)
- Gram-positive cocci, 0.6–1.0 µm, arranged in chains.
- Beta-haemolytic on blood agar → complete RBC lysis.
- Group A (Lancefield antigen).
- Natural reservoir: Humans.
- Transmission: Person-to-person via respiratory droplets.
- Peak age: 5–15 years (pharyngitis most common).
Molecular Typing
- >150 strains identified based on M-protein types.
Carriage Rates
- Pharyngeal carriage in children: 15–20% (varies by season/location).
- Lower in adults → natural immunity or reduced exposure .
What are the Virulence Factors S. Pyognes(with clinical “why”)
1. Surface Structures
- Hyaluronic acid capsule
⏩ Mimics host tissues, inhibits phagocytosis.
- Lipoteichoic acid
⏩ Promotes initial adherence to pharyngeal cells.
- M-protein (major virulence factor)
- Inhibits complement activation (antiphagocytic).
- Facilitates adherence to mucosa.
⏩ Correlates with invasiveness and immune evasion.
- Adhesins (Fibronectin-binding proteins)
⏩ Promote tight attachment to epithelial surfaces.
- Opacity factor
⏩ M-protein–linked, binds fibronectin; contributes to invasion and immune modulation.
2. Toxins
- Streptolysin O (SLO)
- Oxygen-labile, antigenic, best detected anaerobically.
- Pore-forming; lyses RBCs, WBCs.
- Streptolysin S (SLS)
- Oxygen-stable, non-antigenic, causes beta-hemolysis on agar.
- Damages host cell membranes.
- Streptococcal pyrogenic exotoxins (SpeA, B, C…)
- Superantigens ➡️ massive cytokine release.
- Cause:
- Toxic shock syndrome
- Necrotizing fasciitis
- Scarlet fever rash
3. Enzymes
- DNases (A–D) ➡️ liquefy pus (reduce viscosity of neutrophil DNA).
- Streptokinase ➡️ activates plasminogen ➡️ dissolves fibrin clots.
- Hyaluronidase ➡️ degrades connective tissue; promotes spread.
- C5a peptidase ➡️ cleaves C5a, inhibits PMN recruitment.
Clinical Takeaway
- S. pyogenes uses a multi-pronged attack:
- Evades immunity (capsule, M-protein).
- Adheres and invades (adhesins, enzymes).
- Destroys tissues and immune cells (toxins, haemolysins).
- Spreads rapidly (streptokinase, hyaluronidase, DNases).
What are the clinical significance of Streptococcus pyogenes
1. Streptococcal Pharyngitis
- Onset: Abrupt; 2–4 days post-exposure.
- Features: Fever, headache, sore throat, malaise, gray-white tonsillar exudate.
- Why: Local infection of pharyngeal mucosa; inflammation + toxin-mediated symptoms.
2. Scarlet Fever
- Cause: Spe exotoxins (superantigens).
- Rash: Diffuse, red, starts upper chest ➡️ spreads to trunk/extremities.
- Why: Immune response to circulating exotoxins.
3. Toxic Shock–Like Syndrome (STSS)
- Features: Bacteremia + necrotizing fasciitis, shock, multiorgan failure.
- Cause: Superantigen (SpeA).
- Why: Cytokine storm due to non-specific T-cell activation.
4. Puerperal Sepsis
- Postpartum: Endometritis, sepsis, necrotizing fasciitis, TSS.
- Neonates: Stillbirth, neonatal sepsis, cellulitis.
- Complications: Pelvic cellulitis, peritonitis, abscess.
- Why: Invasion of genital tract mucosa during delivery.
5. Impetigo
- Features: Vesicles ➡️ pustules ➡️ crusted lesions.
- Common in: Children.
- Why: Superficial skin infection from minor trauma or insect bites.
6. Cellulitis
- Features: Red, warm, swollen spreading skin infection.
- Why: Infection of dermis/subcutis; often follows skin injury.
7. Erysipelas
- Distinct feature: Sharply demarcated skin swelling + fever.
- Why: Lymphatic spread of infection; involves superficial dermis and lymphatics.
8. Non-Suppurative Sequelae
Acute Rheumatic Fever (ARF)
- Triggered by: Pharyngitis (M1, 3, 5, 6, 14, 18, 19).
- Why: Molecular mimicry ➡️ autoimmune attack on heart, joints, CNS.
Acute Glomerulonephritis (AGN)
- Triggered by: Skin (M2, 9, 55, 57, etc.) or pharyngeal infection (M1, 4, 12…).
- Why: Immune complex deposition in glomeruli ➡️ inflammation.
What are the Basic Characteristics of Streptococcus pneumoniae (Pneumococcus)
- Gram-positive, alpha-hemolytic, lancet-shaped diplococcus.
- Capsulated: >92 serotypes; capsule is the major virulence factor.
- Reservoir: Human nasopharynx.
- Transmission: Respiratory droplets.
Carriage & Risk Factors of Pneumococcus
- High carriage: 70–100% in infants; decreases with age (\~10% in adults).
- Invasive risk: <2yrs, >65yrs, immunocompromised, chronic diseases.
What are the Virulence Factors & Function of pneumococcus
| Capsular polysaccharide ➡️ Inhibits phagocytosis; key for invasion
Cell wall polysaccharide ➡️Triggers inflammation via cytokine and complement activation |
Pneumolysin ➡️ Cytotoxic; damages cilia, activates complement
PspA & PspC ➡️Inhibit complement binding and phagocytosis
PsaA ➡️Promotes adhesion to mucosal cells
Autolysin ➡️Lyses bacteria to release inflammatory components
Neuraminidases (NanA, NanB) ➡️Aid adherence, especially in respiratory tract
Factor | Function
Clinical significance of S. Pneumonia
1. Community-Acquired Pneumonia (CAP)
- Most common cause.
- Presentation: Sudden fever, productive cough, pleuritic chest pain, consolidation.
- Why: Inhaled or aspirated into alveoli ➡️ inflammation, consolidation.
2. Bacterial Meningitis
- Leading cause in adults and children <5yrs.
- Why: Nasopharyngeal colonization ➡️ bloodstream ➡️ meningeal invasion.
3. Otitis Media, Sinusitis, Mastoiditis
- Accounts for \~40–50% of acute otitis media in children.
- Why: Eustachian tube dysfunction allows migration from nasopharynx.
4. Bacteremia/Sepsis
- Often follows pneumonia or otitis media in high-risk groups.
5. Less Common Infections
- Endocarditis, pericarditis, arthritis, osteomyelitis, neonatal sepsis, skin/soft tissue infections.
What are the Age-Related Serotype Patterns of S. Pneumonia?
- Children: 6, 14, 18, 19, 23.
- Adults: 1, 3, 4, 7, 8, 12.
What are the key characteristics of III. Streptococcus agalactiae (GBS)
- Gram-positive, beta-hemolytic, Group B Streptococcus.
- Colonizes vagina, rectum, and GI tract.
- Higher colonization in Black women, DM, immunosuppressed.
- Transmission: Maternal ➡️ neonatal (in utero or during delivery).
- Group B antigen: Acid-stable rhamnose-glucosamine polymer.
- Capsular serotypes: Ia, Ib, II–VIII.
Whatre the Virulence Factors of Streptococcus agalactiae (GBS)
Capsule ➡️ Inhibits phagocytosis and complement activation
| Sialic acid ➡️Blocks alternate complement pathway
| Beta-hemolysin/cytolysin ➡️Damages lung/endothelial cells; aids CNS invasion
| Lipoteichoic acid ➡️Promotes epithelial adherence
| C5a peptidase ➡️Disrupts neutrophil recruitment
| c-antigen proteins ➡️Promote invasion of cervical cells, protect intracellularly
| Others ➡️➡️Hyaluronidase, CAMP factor, proteases, nucleases
Factor | Function
What are the Clinical Significance GBS
Neonatal Disease
- Early-onset (<7 days): Sepsis, pneumonia, meningitis.
- Late-onset (7–89 days): Sepsis, meningitis, focal infections (e.g., bone, joints).
Adults
- Risk factors: Immunosuppression, comorbidities.
- Diseases: Pneumonia, septic arthritis, osteomyelitis, endocarditis, meningitis, soft tissue infections.
Women
- UTI, postpartum endometritis, post-Caesarean bacteraemia.
What are the key features of Viridans Streptococci
Key Features
- Alpha or non-hemolytic, gram-positive cocci.
- Normal flora: Mouth, respiratory, urogenital tracts.
- its of Low virulence, but opportunistic.
What are the conditions Viridian can cause and it’s mechanism
| Dental caries (S. mutans) ⏩Glucosyltransferases ➡️ which hydrolyse dietary sucrose, form insoluble glucans that adhere to teeth ➡️dental plaque
| Infective endocarditis ⏩Especially in damaged valves (e.g., rheumatic heart disease) |
| Bacteraemia ⏩In neutropenic patients |
| Meningitis ⏩ In congenital craniofacial abnormalities or head trauma
Condition | Mechanism
What are the Classification Groups of S. Viridian?
Classification Groups
Group Species
Mitis ➡️ S. mitis, S. oralis, S. infantis, etc.
Mutans ➡️ S. mutans, S. sobrinus, etc.
Salivarius ➡️ S. salivarius, S. thermophilus, etc.
Sanguinis ➡️ S. sanguinis, S. gordonii, etc.
Anginosus ➡️ S. anginosus, S. intermedius, etc.
Bovis ➡️ S. gallolyticus, S. pasteurianus, etc.
Based on the different infection type how are samples collected in STREP?
| Pharyngitis ➡️Depress tongue, swab posterior pharynx and tonsils. Avoid tongue/uvula contact.
| GBS screening ➡️Vaginal + rectal swab at 35–37 weeks gestation. Cervical swabs not useful.
| Meningitis ➡️Lumbar puncture using aseptic technique.
| Bacteraemia/sepsis ➡️Blood cultures. Multiple sets improve yield.
| Lung infections ➡️Collect good-quality sputum (low epithelial cells, high neutrophils).
| Wound infections ➡️Priority: Tissue biopsy > Aspirate > Swab. Use aseptic technique.
Infection Type | Sample & Notes
How do you culture STREP?
Media ⏩ Sheep Blood Agar (SBA) or Chocolate Agar for fastidious growth.
Incubation ⏩ 24–48 hours at 35–37°C, CO₂-enriched environment.
Haemolysis ⏩ Observe under anaerobic conditions: beta (clear), alpha (green), gamma (none), or alpha-prime.
Microscopy (Direct Gram Stain)
Appearance: Gram-positive cocci in pairs and chains.
Seen in specimens that later yield Streptococci on culture.
What are the Presumptive Identification Methods for GAS
1. Group A Streptococcus (GAS – S. pyogenes)
- Bacitracin Susceptibility
- Positive test = any zone of inhibition on blood agar.
- GAS is bacitracin-sensitive (used for presumptive ID).
- SXT Susceptibility
- GAS is SXT-resistant.
- Helps exclude other beta-hemolytic groups (C, F, G are SXT-sensitive).
- PYR Test
- GAS is PYR-positive (red color after hydrolysis).
- Highly sensitive and specific.
What are the Presumptive Identification Methods for GBS
2. Group B Streptococcus (GBS – S. agalactiae)
- CAMP Test
- GBS produces arrowhead hemolysis when streaked near beta-hemolysin-producing S. aureus.
- Highly sensitive for GBS.
- Pigment Production
- GBS may produce orange/red pigment (less commonly used diagnostically).
- SXT Resistance
- GBS is SXT-resistant, like GAS.
