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Flashcards in 4 pyogenic cocci Deck (90):
1

pyogenic

pus forming

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pyogenic cocci

streptococcus + staphylococcus

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what is pus made of

dead neutrophils, bacteria, inflammatory exudate, and tissue debris

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why is pus formed

battle between neutrophils + bacteria

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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

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streptococcus mechanism for avoiding phagocytosis

1. M protein is the most important factor
2. Hyaluronic acid capsule

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how does strep avoid phagocytosis

interferes with opsonization due to complement deposition by causing bacteria to be coated with fibrinogen + fibrin

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staphylococcus mechanism for avoiding phagocytosis

1. protein A
2. cell wall components
3. leukocidin

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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

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streptococcus

gram positive coccus

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gram positive

purple

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hemolysis diseases of group A streptococci (aka strep pyogenes)

beta hemolytic strep throat + rheumatic fever

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hemolysis diseases of viridans streptococci (group like strep mutans, organisms that cause caries)

alpha hemolytic caries + endocarditis

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hemolysis diseases of streptococcus pneumoniae (pneumococcus)

alpha hemolytic pneumonia + meningitis+ otitis

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which two look similar (group A streptocci, viridans streptococci, streptococcus pneumoniae)?

viridans strep + strep pneumoniae look similar because they are both alpha hemolytic

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which bacteria have alpha hemolytic colonies

strep viridans + strep pneumoniae

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alpha hemolysis on blood agar

when bacteria surrounds it like a ring or halo

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beta hemolytic agar plate

area around colony is completely cleared - strep pyogenes

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group A streptococci

classified into "lancefield groups" based on carbohydrate antigens called Ccarbohydrate beta hemolytic

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encounter

group A streptococci colonize the skin + mucous membranes
-are sperad by infected droplets from person to person, often asymptomatically

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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

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spread

spreading depends on how the infection was acquired
-skin + mucous membrane infections usually localized
e.g. in the throat, infection usually remains localized

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wound infections in deeper tissue (e.g. surgical wounds, battle wounds) spread

rapidly

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streptococci secrete a number of digestive enzymes including proteases, hyaluronidase, and DNAase. during its spread. Describe the pus

thin and runny

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multiplication

M protein + hyaluronic acid capsule help streptococci resist phagocytosis

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how do M proteins interfere with multiplication

bind host molecules that prevent complement deposition on the bacterial surface. interferes with opsonization

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how does hyaluronic acid capsule interfere with multiplication

interferes with attachment of phagocytes

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Damage

damage may be caused by intense inflammatory response

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streptococci damage

produce many toxins such as streptococcal pyrogenic exotoxins (Associated with scarlet fever and shock inducing infections)

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how do streptococcoal pyrogenic exotoxins SPEs act by?

influencing host reponses

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diseases

strep throat, tonisllitis, scarlet fever, pyoderma

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invasive diseases

cellulitis, necrotizing fasciiitis

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what is flesh eating bacteira

necrotizing fasciitis

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nonsuppurative sequelae

rheumatic fever + glomerulonephritis

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scarlet fever

strawberry tongue, strep throat with a rash, lasts a couple of weeks, after rash resolves..skin desquamates

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pyoderma

skin infectio nlike a mosquito bite

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suppurative diseases

strep throat, tonsillitis, scarlet fever, pyoderma??

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cellulitis

infection of subcutaneous tissue + skin

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necrotizin fascitis

affects deeper in the subcutaneous tissues and fascia

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what is a nonsuppurative sequelae of strep

rheumatic fever

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acute rheumatic fever

only follows strep throat caused by group A streptococci

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what characterizes acute rheumatic fever

carditis, polyarthritis, neurological disorder, rash

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st. vitus dance

neurological disorder during acute rheumatic fever

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what may be fatal or cause severe damage to the heart valves

acute rheumatic fever

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how can we prevent acute rheumatic fever

treat strep throat with penicillin

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once you have progressed to rheumatic fever after strep

you cannot treat it with penicillin anymore
-does not respond to penicillin treatment

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rheumatic fever is thought to be an autoimmune disease, somehow evoked by infection by

group A strep

48

viridans streptococci

-alpha hemolytic
-not sensitive to P disk
-30-60% of the normal oral flora

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examples of viridans streptococci

streptococcus mutans invovled in caries and plaque
-most common cause of subacute bacterial endocarditis
-causes severe sepsis in immunocompromised patients

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P disk

distinguishes between viridans + strep pneumonia, which are both hemolytic

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what is sensitive to the P disk

strep pneumonia

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infective endocarditis

-infection of the inner surfaces of the heart and valves

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subacute endocarditis patients

mild fever
anorexia
weakness
weigh loss for several weeks durations

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60% of infections of infective endocarditis are caused by

viridans streptococci

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predisposing factors of infective endocarditis

-usually affects heart valves whose surfaces have already been damaged
- rheumatic fever
-congenital heart defects
-degenerative disease
-mitral valve prolapse
-prosthetic heart valves

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emia

presence of something in blood

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bacteremia

presence of bacteria in blood

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sepsis or septicemia

growth of bacteria in blood

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endocarditis + dentistry

bloody dental procedures are associated with transient bacteremia which can lead to endocarditis

60

if a cause of endocarditis is determined, 67% of cases it is a

dental procedure

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prophylactic actibiotics are recommended for

at risk patients with endocarditis

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bacteria related to bacterial endocarditis

viridans streptococci

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how do we treat bacterial endocarditis

iv penicillin + gentamicin

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staphylococci stain

purple

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coagulase

enzyme that clots plasma

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staphylococcus aureus

pathogenic

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staphylococcus epidermidis

nonpathogenic

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staphylococcus aureus

colonization common, coagulase positive, bronze colony, positive mannitol

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staphylococcus epidermidis

colonization common, coagulase negative, white colony, negative mannitol

70

encounter of staph

s. epidermidis commonly colonizes humans
s. aureus colonizes about 20-30% of people

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staph colonizes

skin, nose, + mucous membranes

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staph tolerates

high salt and can grow in salt concentrations that inhibit growth of other bacteria

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what can bread down fatty acids found on skin

staphyloccoci

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what can be spread from person to person by HAND contact

staphyloccocci

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staphylococci ENTRY, SPREAD, MULTIPLICATION, DAMAGE

-enters deep tissues via a wound
-highly vascularized organs, bones, lungs, kidneys are sites of abscesses in hematogenous spread
-area of inflammation usually remains localized

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localized diseases caused by staphylococci

abscesses (boils)
wound infections
osteomyelitis

77

generalized diseases caused by staphylococci

bacteremia with metastatic abscesses + endocarditis

78

toxins that caused staphylococci

scalded skin syndrome (exfoliatin)
toxic shock syndrome
gastroenteritis

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one of the major causes of bacterial infections in the oral cavity

staphylococci

80

infected root canals, osteomyelitis of the jaws, facial cellulitis, dentoalveolar abscesses

staphylococci

81

virulence factors of staphylococci

1. capsule, cell wall components
2 protein A
3 leukocidin
4 catalase
5 coagulase
6 toxins

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protein A as a virulence factor

resists phagocytosis

83

leukocidin as a virulence factor

resist phagocytosis

84

catalase as a virulence factor

reduces killing by neutrophils

85

coagulase as a virulence factor

causes plasma to clot

86

toxins as virulence factors

scalded skin syndrome- exfoliatin
-toxic shock syndrome
-food poisoning enterotoxins

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two types of organisms

streptococci + staphylococci

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strep + staph

colonize people, spread from person to person, produce pyogenic infections bc they have mech that allow them to resist phagocytosis

89

staph

localized infections - boils

90

strep

spreading infections- cellulitis + necrotizing cellulitis