Streptococci Flashcards
Characteristics of Streptococci?
What is unique about them?
How are they classified?
- Gram positive, coccus shaped, grows in chains
- Grow in chains because they divide in a plane, unlike staph for example
- “Streptos” genus = bent/twisted in greek
- Non-motile, non-endospore forming (despite being positive)
- Classified by pattern of hemolysis on blood agar (make toxins that destroy RBCs)
Classification types?
- α-hemolytic - partial hemolysis (oxidation of hemoglobin)
- β-hemolytic - total lysis
- γ-hemolytic - no hemolysis
List the α-hemolytic species
Describe the function of each bacteria in the virdians group
- S. pneumoniae (pneumococcus) (no. 4 killer)
- Viridans group:
- S. viridans - gets into blood, pre-existing damaged heart tissue = endocarditis
- S. mutans - Kit Kat is fermented by this (on your teeth) = tooth decay
- S. thermophilus - used industrially to make dairy products; non-pathogenic
List the β-hemolytic species (group A-C) and describe their function
- S. pyogenes (Group A strep) - strep throat (no. 5 killer)
- S. agalactiae (Group B strep) - can cause meningitis (neonatal)
- S. equi (Group C strep) - horse pathogen
List the γ-hemolytic species (group D, N)
What is unique about this group?
- Enterococcus species (Group D strep) - drug resistant pathogen
- Lactococcus lactis (Group N strep) - food grade organism
Not considered streps - too genetically distinct
How are strep groups (ex., strep A) decided?
Rebecca Lancefield: classified groups using surface carbohydrate antigens which successfuly distinguishes strains
Describe the pathogen S. pyogenes
- A common human specific pathogen w/ human reservoir
- Extracellular; inflammation, neutrophil recruitment, abscesses
- Pyo = pus
- 5-15% asymptomatic carriage in school age kids
- Can carry for >2 years without infection; thus great colonizer
- Master at hiding from immune system using virulence factors (inhibit innate)
What is the main virulence factor for S. pyogenes? What does it do?
Describe the main serotypes
- M. protein
- Anti-phagocytic cell surface protein
- Binds to C4 binding protein (complement proteins) which protects own cells from complement system
- Strep takes it = protection from complement
- Antibodies can target M. protein
- Workaround = strep makes >100 M protein serotypes (1 antibody targets only 1 serotypes)
- M1, M3 = pharyngitis, invasive disease
- M18 = rheumatic fever -
- Unsure why the associations exist
- Workaround = strep makes >100 M protein serotypes (1 antibody targets only 1 serotypes)
What are the other 3 virulence factors?
- Hyaluronic acid capsule
- Polysaccharide on surface
- Protects strep from complement (blocks receptor binding to C3b) -
- Major component of our OWN tissue as well, thus, cannot make vaccine against capsule
- Hemolysins
- Makes O and S streptolysins
- Made by all group A strains - important
- S: produces β-hemolysins
- O: oxygen turns it off
- Superantigens
- Secreted exotoxins (Spe’s)
- Function as potent activators of T cells –> cytokine storm –> TSS
- Not emetic (vomit-inducing) like staph enterotoxins (SE’s) in Staph Food Poisoning
Characteristic of pharyngitis a.k.a. strep throat?
How is it treated?
- Common in school age children, teenagers
- Severe sore throat; no cough
- Swollen lymph nodes, pus (tonsillar exudate)
- Skin rash
- Treatment:
- β-lactams (no documented resistance until recently…)
- Erythromycin (resistant strain exists); used in case of penicillin allergy
Characteristics of impetigo?
- Also caused by S. aureus (staph)
- Superficial skin infection; red sores
- Highly contagious
- Topical ABx
Characteristics of scarlet fever?
- Rash develops during strep throat
- Strawberry tongue, fever
-
Caused by “scarlet fever toxins”; Streptococcal pyogenic exotoxins (SpeA, SpeC)
- Thus this rash is NOT a sign of bacteremia
What is Rheumatic Fever? What does it cause?
- Occurs 2-3 weeks after infection (of strep throat or scarlet fever)
- Autoimmunity caused by antibody cross-reactivity with M protein (strep –> response to M –> attack host tissue when no strep left)
- Acute rheumatic fever = initial, acute, painful swollen joints
- Rheumatic heart disease = damaged heart valves (chronic)
- Congestive heart failure = increase risk of infective endocarditis by other pathogens
Rare in developed because strep is treated quickly
What causes Invasive Streptococcal disease?
- Bacteremia: blood isolation
- Soft tissue: necrotizing fasciitis
- Muscle: necrotizing myositis
- TSS
- Combine 2-4 to get flesh eating disease; as dangerous as bubonic plague
Describe the risk factors and treatment for invasive strep
Risk factor
- Tissue injury
- Use of nonsteroidal anti-inflammatory agents
- Chicken pox (60 fold increase) as the lesions from pox = portal of entry
- Postpartum
- Lack of immunity to superantigens and M protein
- MHC class 2 halotypes; by chance, may bind the superantigens really well = more likely to develop invasive disease
Treatment
- ABx
- Amputation, debridement
- IVIG (intravenous immunoglobulin)
- To neutralise superantigen activity, opsonize S. pyogenes
What is genetic variability in S. pyogenes caused by?
Genetic variability in strep is due to mobile elements that have inserted around the chromosome
Describe the findings of the mouse model
- Deletion of SpeA decreases virulence significantly, same with deleting all superantigens
- Therefore injecting SpeA antibodies = decrease infection in mice (superantigens = potential future vaccine)
- Deletion of T cells = inhibition of infection!
- Making mice immunodeficient = infection goes away
- Therefore, functional T cells are required for nasopharyngeal infection (unique to S. pyogenes)
What is important about the MHC class 2 during a strep infection?
Strep is a human-specific pathogen and so is only adapted to the MHC class 2; mouse model with mouse MHC class 2 = minimal colonisation
- Therefore, MHC class II is an important contributor to host-specific tropism by S. pyogenes
