Cocci Flashcards
Virulence factors of Group A streptococci
Structural: Pili; M protein (infect surfaces because of pili)
Toxins: Streptokinase (breaks blood clots, spread b/c break down blood clots); Streptodornase; Hyaluronidase; Pyrogenic toxin (cause fever); Erythrogenic toxin (red skin rash, scarlet fever)
What is the spread of streptococci from a sore throat?
Oropharynx -> tonsils; floor of mouth; middle ear; mastoids; meninges
What are the reservoirs and transmission of Group A streptococci?
From Carriers + infected patients in direct contact with a susceptible person, dogs might be carriers/reservoirs
What are some post-streptococcal conditions (2 weeks, lesions are sterile)?
- Skin infections -> recovery -> pain, blood and protein in urine = post streptococcal nephritis, autoimmune nephritis, no bacteria in kidney
- Sore throat -> recovery -> fever, arthritis, endocarditis = rheumatic fever
- Syndenham’s chorea - neurological symptoms (OCD?)
Two ways to diagnose Group A streptococcal infection
- Swab - culture - Gram stain - bacitracin sensitivity (accurate but slow)
- Rapid office tests with antibody assays (quick but less sensitive)
What are the virulence factors for Group B strep? What is the reservoir and transmission?
Structural : capsule; resistant to phagocytosis
R - genital tract of 25% of women, T - neonatal (fatal meningitis)
How do you prevent neonatal Group B strep infection? (4)
Penicillin prophylaxis if vaginal/rectal swab shows Group B, previous baby with Group B, fever or membranes ruptured for > 18 hrs
What are the virulence factors of pneumococci?
Structural: capsule - anti-phagocytic; polysaccharide antigen; stimulates opsonizing antibody; 80 types; basis of typing sera (can type which pneumonia is going around) and vaccines(no vaccines against other cocci); basis of ‘quellung’ rxn (polyvalent antibody, swelling rxn on agar plate)
Pathogenesis of bacterial pneumonia
Natural resistance to lung infections via mechanical clearance by mucus/cilia - this brings up the pneumococci and then you digest them with stomach acid, inhibition of natural resistance to lung infection (mechanical obstruction disease) smoking; virus; allergy (too much fluid being produced, can’t sweep it away); immobility; mechanical obstruction (tumors and foreign bodies); depressed cough reflex; HF
pneumococci are not very virulent, but these things cause it
How do you manage bacterial pneumonia?
Offer vaccine to susceptible groups; identify and treat the underlying cause; antibiotic sensitivity tests and offer antibiotics - now they are resistant to penicillin
Reservoir and virulence factors of viridans streptococci
Reservoir: Mouth (100% of people)
Virulence factors: Sugar-metabolizing enzymes
Pathogenesis of dental caries and endocarditis
Low MW sugars -> V. streptococci EITHER acids-> decalcification OR High MW sugars -> dental plaque -> bacteremia (biofilm, causes gum disease) -> endocarditis
Following dental surgery, can get into blood and stickiness allows them to clot the heart
What are some other ways of classifying S. aureus?
Coagulase test (clotting) -> positive OR DNAse pos., salt resistant, beta hemolytic
What are the virulence factors of S. aureus?
Structural: Protein A, Capsule, Coagulase (causes clotting, localized tissue death, stops antibiotics from geting in THEREFORE need to drain the abcess)
Toxins: DNase, enterotoxin, exfoliatin, leukocidin, TSS toxin
What is problematic with Staphlococci?
they have accumulated mutations leading to multi-drug resistance - at least 6 resistance genes, 8 strains in existence now
