4 pyogenic cocci Flashcards
pyogenic
pus forming
pyogenic cocci
streptococcus + staphylococcus
what is pus made of
dead neutrophils, bacteria, inflammatory exudate, and tissue debris
why is pus formed
battle between neutrophils + bacteria
how is pus formed
- bacterial substances recruit neutrophils
- bacteria resist pahgocytosis
- bacteria are NOT killed by neutrophils
- bacteria instead kill neutrophils, which die and release lysosomal enzymes
- enzymes damage surrounding tissues
streptococcus mechanism for avoiding phagocytosis
- M protein is the most important factor
2. Hyaluronic acid capsule
how does strep avoid phagocytosis
interferes with opsonization due to complement deposition by causing bacteria to be coated with fibrinogen + fibrin
staphylococcus mechanism for avoiding phagocytosis
- protein A
- cell wall components
- leukocidin
how does protein A allow staph to avoid neutrophils
protein A binds antibodies using their constant regions
-antibodies are backwards so they don’t bind Fc receptors on phagocytes
streptococcus
gram positive coccus
gram positive
purple
hemolysis diseases of group A streptococci (aka strep pyogenes)
beta hemolytic strep throat + rheumatic fever
hemolysis diseases of viridans streptococci (group like strep mutans, organisms that cause caries)
alpha hemolytic caries + endocarditis
hemolysis diseases of streptococcus pneumoniae (pneumococcus)
alpha hemolytic pneumonia + meningitis+ otitis
which two look similar (group A streptocci, viridans streptococci, streptococcus pneumoniae)?
viridans strep + strep pneumoniae look similar because they are both alpha hemolytic
which bacteria have alpha hemolytic colonies
strep viridans + strep pneumoniae
alpha hemolysis on blood agar
when bacteria surrounds it like a ring or halo
beta hemolytic agar plate
area around colony is completely cleared - strep pyogenes
group A streptococci
classified into “lancefield groups” based on carbohydrate antigens called Ccarbohydrate beta hemolytic
encounter
group A streptococci colonize the skin + mucous membranes
-are sperad by infected droplets from person to person, often asymptomatically
entry
the bacteria adhere to epithelial surfaces, e.g. in the thoat; lipoteichoic acid, a constituent of the Gram positive cell surface, is an ADHESIN which makes the organism sticky
spread
spreading depends on how the infection was acquired
- skin + mucous membrane infections usually localized
e. g. in the throat, infection usually remains localized
wound infections in deeper tissue (e.g. surgical wounds, battle wounds) spread
rapidly
streptococci secrete a number of digestive enzymes including proteases, hyaluronidase, and DNAase. during its spread. Describe the pus
thin and runny
multiplication
M protein + hyaluronic acid capsule help streptococci resist phagocytosis
how do M proteins interfere with multiplication
bind host molecules that prevent complement deposition on the bacterial surface. interferes with opsonization
how does hyaluronic acid capsule interfere with multiplication
interferes with attachment of phagocytes
Damage
damage may be caused by intense inflammatory response
streptococci damage
produce many toxins such as streptococcal pyrogenic exotoxins (Associated with scarlet fever and shock inducing infections)
how do streptococcoal pyrogenic exotoxins SPEs act by?
influencing host reponses
diseases
strep throat, tonisllitis, scarlet fever, pyoderma
invasive diseases
cellulitis, necrotizing fasciiitis
what is flesh eating bacteira
necrotizing fasciitis
nonsuppurative sequelae
rheumatic fever + glomerulonephritis
scarlet fever
strawberry tongue, strep throat with a rash, lasts a couple of weeks, after rash resolves..skin desquamates
pyoderma
skin infectio nlike a mosquito bite