4/18 Gram Positive Bacteria

Front 1

list three gram positive cocci bacteria classes?

Back 1

staphylococcus, streptococcus, and enterococcus

Front 2

sources of staph aureus

Back 2

gram positive clusters found on people's skin, 50-80% healthcare workers, spread by hand contact

Front 3

suppurative skin infections assoc with staph aureus

Back 3

suppurative infections (skin) assoc – impetigo, folliculitis, furuncles, boils, carbuncles (numerous boils fused tog), cellulitis (infection of deeper layers of skin)

Front 4

systemic infections assoc with staph aureus

Back 4

- systemic infections - bacteremia, endocarditis (rt side of heart in intravenous drug users, 50% mortality), pneuomonia (aspiration of oral secretions, or following hematogenous dissemination), osteomyelitis (secondary to trauma. Or hematogenous dissemination to bone), septic arthritis (most common cause)

Front 5

enterotoxin mediated disease assoc with staph aureus

Back 5

enterotoxin mediated dx – food poisoning, toxic shock syndrome (TSST-1 super antigen or enterotoxins), scalded skin syndrome (mediated by exfoliative toxins, with intense inflammation and desquamation), bullous impetigo

Front 6

virulence factors assoc with staph aureus

Back 6

 capsule – inhibits phagocytosis; facilitate adherence
 peptidoglycan – endotoxin-like activity, attracts leukocytes
 teichoic acid – polymer of ribitol and glycerophosphates, involved in complement activation, facilitates adherence
 protein A – binds to Fc region of IgG, reduces binding of phagocytes via FcR, inhibits complement activation; protective factor
 catalase – converts hydrogen peroxide from neutropohils to water, counteracts neutrophil ability to kill bacteria via production of oxygen free radicals
 coagulase – converts fibrinogen to fibrin, clots plasma; bacteria can hide within the clot; white cells, Ab, and even antibiotics do not penetrate clots well
 enzymes promote bacterial spread in tissue – fibrinolysin, hyaluronidase, lipase, nucleases
 cytotoxins – membrane damaging toxins that lyse eukaryotic cells
• enterotoxins (diarrhea and vomiting)
• toxic shock syndrome toxin – cause of toxic shock syndrome
• exfoliative toxin – causes scalded skin syndrome in neonates
 some strains break down B-lactam because in antibiotic wall

Front 7

how can you be exposed to staph saphyophyticus

Back 7

inadequately cooked food. inhabits the GI tract.

Front 8

what is the 2nd most common cause of UTI in sexually active women?

Back 8

S. saphrophyticus. young women are more susceptible.

Front 9

clinical manifestations of staph epidermitis

Back 9

endocarditis, infections of prosthetic joints and shunts/catheters

Front 10

virulence factors of staph epidermitis

Back 10

oability to bind to foreign materials
obiofilm production

Front 11

what are 3 methods used to differentiate streptococci?

Back 11

1. hemolysis (beta clear (pyogenes, agalactiae), alpha incomplete green)
2. serologic activity (Lancefield Groups based on antigenic differences in carbohydrates on cell wall – mainly in b-hemolytic strains) – pyogenes A, agalactiae B, pneumoniae – not grouped
3. biochemical reactions

Front 12

diseases assoc with S. pyogens

Back 12

pharyngitis, skin and soft tissue infections (impetigo, cellulitis (involves deeper layers of skin), erysipeias (involves upper layers of skin), scarlet fever, necrotizing fascilitis), bacteremia, sepsis, toxic shock syndrome (M protein bind fibrinogen and to adhesion molec – release of heparin binding protein from neutrophil. Endothelium gate control for inflammation), strep throat, scarlet fever

Front 13

sequellae assoc with S. pyogens

Back 13

- sequellae – rheumatic fever (after ONLY throat infections - less than 1% cross reaction btw M protein and heart tissue – permanent damage to heart valves), acute glomerulonephritis (sequellae of throat OR skin infections that is immune mediated)

Front 14

virulence factors assoc with S. pyogens

Back 14

Capsule – antiphagocytic, adhesive
M protein – mediates internalization by host cells, degrades C3b,
Pyrogenic exotoxins – A (most imp), B, C; temperate phage assoc with STSS and scarlet fever
Streptolysin O – lyses cells
Streptokinase – lyses blood clots – facilitates spread

Front 15

give hemolysis and group category for S. pyogenes and S. agalactiae

Back 15

S.pyogens - B hemolysis; Group A (GAS)
S.agalactiae - B hemolysis; Group B (GBS)

Front 16

what bacteria is the leading cause of infectious death in newborns?

Back 16

S. agalactiae

Front 17

what is the most common cause of community acquired bacterial pneumonia?

Back 17

S. pneumoniae

Front 18

what is the most common cause of bacterial endocarditis in the US?

Back 18

viridans group streptococci.

Front 19

what is the source of S. agalactiae?

Back 19

source – colonizes GI and genitourinary tracts; transmitted neonates in utero or birthing

Front 20

what are the diseases assoc with S. pneumoniae

Back 20

pneumonia, otitis media in children, sinusitis, meningitis

Front 21

list two commensal organisms found in GIT within the Enterococcus sp.

Back 21

E. faecium, E. faecalis

Front 22

what are three main groups of aerobic gram positive rods that we studied

Back 22

bacillus, corynebacterium, listeria

Front 23

what are unique char of bacillus

Back 23

spore forming, large boxy rods; ubiquitous, found in soil

Front 24

what are clinical manifestations of bacillus anthracis

Back 24

a. dx primarily in herbivores. Clinical manifestations – cutaneous black eschar, inhalation – lungs, cough, chest pain, fever. GI: NV, enlarged mediastinal lymph nodes

Front 25

bacillus cereus is associated with two types of food poisoning different the causes and effects of the two?

Back 25

spores live in food after heating
1. diarrheal form, 6-15hrs after ingestion, rarely vomiting - heat labile toxin (caused diarrhea by inc cAMP levels in gut)
2. emetic form - 30min-6hrs; nausea and vomiting, no diarrhea, associated with heat stable toxin.

Front 26

besides food poisoning, what other effect can bacillus cereus have on the body?

Back 26

eye infections (follows eye trauma) – rapid blindness

Front 27

what are the symptoms and clinical manifestations of corynebacterium diphtheriae?

Back 27

a. symptoms toxin pseudomembrane on tonsils, edema formation, bullneck appearance – B binds to cell; A inactivates elongation factor-2; leading cause of death – cardiomyopathy
b. clinical manifestations – cutaneous (skin from microabrasions)

Front 28

what are the clinical manifestations and transmission methods of listeria monocytogenes?

Back 28

a. clinical manifestations – neonatal dx – congenital – stillbirth, systemic infection, septicemia, meningitis, encephalitis. Immunocompromised – fever, nausea, diarrhea.
b. neonatal sepsis, meningitis
c. transmission – feces, food-borne infection, person to person – congenital and during labor and delivery

Front 29

what are three main groups of aerobic gram positive rods that we studied

Back 29

bacillus, corynebacterium, listeria

Front 30

what are unique char of bacillus

Back 30

spore forming, large boxy rods; ubiquitous, found in soil

Front 31

what are clinical manifestations of bacillus anthracis

Back 31

a. dx primarily in herbivores. Clinical manifestations – cutaneous black eschar, inhalation – lungs, cough, chest pain, fever. GI: NV, enlarged mediastinal lymph nodes

Front 32

bacillus cereus is associated with two types of food poisoning different the causes and effects of the two?

Back 32

spores live in food after heating
1. diarrheal form, 6-15hrs after ingestion, rarely vomiting - heat labile toxin (caused diarrhea by inc cAMP levels in gut)
2. emetic form - 30min-6hrs; nausea and vomiting, no diarrhea, associated with heat stable toxin.

Front 33

besides food poisoning, what other effect can bacillus cereus have on the body?

Back 33

eye infections (follows eye trauma) – rapid blindness

Front 34

what are the symptoms and clinical manifestations of corynebacterium diphtheriae?

Back 34

a. symptoms toxin pseudomembrane on tonsils, edema formation, bullneck appearance – B binds to cell; A inactivates elongation factor-2; leading cause of death – cardiomyopathy
b. clinical manifestations – cutaneous (skin from microabrasions)

Front 35

what are the clinical manifestations and transmission methods of listeria monocytogenes?

Back 35

a. clinical manifestations – neonatal dx – congenital – stillbirth, systemic infection, septicemia, meningitis, encephalitis. Immunocompromised – fever, nausea, diarrhea.
b. neonatal sepsis, meningitis
c. transmission – feces, food-borne infection, person to person – congenital and during labor and delivery

Front 36

what bacteria is the leading cause of infectious death in newborns?

Back 36

S. agalactiae

Front 37

what is the most common cause of community acquired bacterial pneumonia?

Back 37

S. pneumoniae

Front 38

what is the most common cause of bacterial endocarditis in the US?

Back 38

viridans group streptococci.

Front 39

what is the source of S. agalactiae?

Back 39

source – colonizes GI and genitourinary tracts; transmitted neonates in utero or birthing

Front 40

what are the diseases assoc with S. pneumoniae

Back 40

pneumonia, otitis media in children, sinusitis, meningitis

Front 41

list two commensal organisms found in GIT within the Enterococcus sp.

Back 41

E. faecium, E. faecalis