Streptococci Flashcards
(48 cards)
What happens in alpha hemolysis?
erythocytes NOT destroyed; greenish discoloration
What happens in beta hemolysis?
erythrocytes ARE destroyed; clearing underneath growth
What happens in gamma hemolysis?
non-hemolytic; anything that’s not alpha or beta
What’s the basis of lancefield classification?
C-carbohydrates and glycerol teichoic acid
What are the classifcations of Strep?
Group A = S. pyogenes
Group B = S. agalactiae
Group D = E. faecalis
*strep pneumoniae and viridans= NONE
What hemoylitic pattern is seen in Strep Pneuomoniae and Strep Viridans?
Pneumoniae = alpha/beta/none
Viridans=alpha
What are some characteristics of Strep Pyogenes?
- transient flora
- not always symptomatic
- not common to culture
What is the mode of transmission for Strep Pyogenes?
- from asymptomatic carriers via respiratory droplets and skin-to-skin
- via fomites and insect vectors
- for soft tissue infections, breakage in skin
What are GAS virulence factors?
- fibronectin binding proteins
- M protein: binds fibronectin and fibrinogen -> antiphagocytic
- toxins: Streptococcal Shock Syndrome
- capsule: antiphagocytic and anti-Ig
- DNAases: pus that’s less viscous than Staph Aureus
What’s the difference between the pus of Staph Aureus vs Strep Pyogenes?
GAS has a more liquefying pus
When do we do a rapid strep test?
need 2, 3, or 4 criteria of: tonsilar exudates, tender cervical adenopathy, absence of cough, fever
if positive: treat with antibiotics
if negative: back to square one
When do we not do rapid strep test?
patients with history of RF, vascular heart disease, immunosuppression, recurrent/chronic pharyngitis
Define cellulitis.
diffuse inflammation of CT that spread along the fascial planes
often occuring where skin has previously broken
What layers do erysipelas infect?
superficial infections of dermis and upper subcutaneous layer (have well defined edge)
How do we treat the skin infections related to Strep Pyogenes? (impetigo, cellulitis, erysipelas)
antibiotics!
What are the streptococcal pyrogenic exotoxins?
superantigens (cytokine storm)= interacting with macrophages & helper T cells to release IL-1, IL-2, IL-6, TNF-alpha, TNK-beta, and gamma-IFN
SpeA and SpeC = encoded by lysogenic phages
SpeB = located in bacterial chromosome (found in all GAS)
What’s the treatment for necrotizing fascititis?
surgical removal of all the affected areas + empiric antibiotics like vancomycin
What is special about the M protein?
shares same epitopes as heart muscles (molecular mimcry) -> so when make Abs to M protein, may make Abs to heart muscles too
What are the theories for post-streptococcal glomerulonephritis?
- IgG-streptococcal antigen complexes depositing on glomerular tissue
- cross-reactivity between unidentified streptococcal Ags and glomerular membrane components
- deposition of nephrostreptokinase-plasmin complexes on glomerular basement membrane and subsequent damage by host plasmin
What should be done to prevent spread from S. Agalactiae positive mother to neonate?
prophylactic antibiotics for positive MOM to decrease colony size and reduce risk of transmisson
What is virulence factor for S. Agalactiae that’s important for preventing phagocytosis?
capsule
Type II: adult disease
Type III: infant disease
What’s the clinical presentations for early onset GBS?
symptoms within day 0-1
respiratory distress, apnea, sepsis (bacteremia is most common form), pneumonia, meningitis
What treatment can be utilized for the severe cases of early onset GBS?
extracorporeal membrane oxygenation (ECMO): temporizing, supportive treatment to effectively bypass severely diseased lungs while they’re given time to heal from infection
What group have a higher proportion of maternal colonization?
African Americans and nonsmokers
