Gram Positive Cocci

Front 1

T/F: all of these pathogens cannot colonize asymptomatically.

Back 1

F

Front 2

are these pathogens primarily intra or extracellular?

Back 2

extracellular

Front 3

why is handwashing very important with S. aureus?

Back 3

bc it can survive for a long time on dry surfaces (it exists virtually everywhere)

Front 4

T/F: S. aureus can grow in high salt concentrations.

Back 4

T. Salting foods will not prevent food poisoning from S. aureus

Front 5

metabolically, how do you distinguish staph from strep?

Back 5

staph is catalase positive

Front 6

biochemically how do you differentiate between A. aureus and S. epidermis?

Back 6

S. aureus is coagulase positive

Front 7

most asymptomatic S. aureus colonizations are found where in the body?

Back 7

in the nares, more likely if a health care worker

Front 8

describe the two basic lesions caused by S. aureus.

Back 8

an abscess is walled off bacs by fibrin (the bacs can break through via staphylokinase and cause bacteremia thus it is important to drain the absesses) or pyogenic exudate (pus)

Front 9

define bacteremia.

Back 9

presence of bacs in blood

Front 10

define systemic inflammatory response syndrome (SIRS)

Back 10

response of the body to systemic release of inflammatory mediators and must include at least two of the following: fever or hypothermia, tachypenia, leukocytosis or leukopenia

Front 11

define sepsis, severe sepsis, and septic shock.

Back 11

SIRS that is caused by a microbial etiology. sepsis with one or more signs of organ dysfunction. sepsis with hypotension.

Front 12

describe multiorgan dysfunction syndrome.

Back 12

SIRS with persistant hypotension leading to clotting, renal, hepatic, cardiac, or cognitive failure and acculmulation of products of metabolism that cannot be cleared

Front 13

describe impetigo

Back 13

pyogenic S. aureus infection superficial infection of the skin, primarily hits face and limbs, culture it bc Strep pyogenes can also cause it, and treat with antibiotics.

Front 14

differentiate between foliculitis, furuncles, and carbuncles.

Back 14

all from S. aureue and are pyogenic skin infections. Foliculitis is infection of hair folicle with a small pus pocket. furuncle are more severe extension of folliculitis and are large, painful with an underlying collection of dead/necrotic tissue. Carbuncles are furuncles that coalesce and extend into deeper tissue causing bacteremia and systemic symptoms

Front 15

describe cellulitis.

Back 15

nasty skin infection that can be due to staph aureus causing fever, severe pain, sometimes bacterema as the org penetrates

Front 16

staph aureus wound infections usually occur when what?

Back 16

after surgery, in immunocompromised, on foreign objects like dirt or suture in wound

Front 17

differentiate between the types of pneumonia caused by staph aureus. What is the treatment for these diseases?

Back 17

aspiration pneumonia develops after aspiration of oral sectretion, usually in young or CF, flu, or COPD pts, and has abscesses in the lung. Hematogenous pneumonia is common for pts with bacteremia. Necrotizing pneumonia is the most dangerous, is community aquired, can lead to septic shock, and has a high mortality rate. usually oxacillin or lactamase resistant antibiotic unless it is MRSA

Front 18

in terms of staphyloccocal osteomyelitis, where does it normally effect adults and what are the treatment outcomes?

Back 18

usually vertebral. with antibiotics and surgery it has good treatment outcomes

Front 19

bacteremia of staph can lead to what mortal illness and what is the visible sign of this disease?

Back 19

endocarditis seen with septic emboli which are occlusions of capillaries with micro colonies of staph aureus

Front 20

septic arthritis usually occurs in tose who...

Back 20

receive intrarticular injections

Front 21

describe staphylococccal scladed skin syndrome AKA Ritter's disease.

Back 21

caused by staph toxin, usually in neonates, redness and inflammation of mouth, blisters without orgs in the fluid, and finally desquamation of the epithelium. Rarely fatal

Front 22

describe bullous impetigo.

Back 22

a form of staphylococcal scalded skin syndrome that is localized and produced from toxins of S. aureus infected with a phage, but these blisters will have orgs in it unlike other forms of SSSS.

Front 23

give facts about toxic shock syndrome.

Back 23

Caused by TSST1 of staph aureus. causes fever, hypotension, and diffuse rash. complete desquaitization usually occurs. 90% of ppl have antibodies against TSST. 3-7% of menstruating women have vag staph. High risk of recurrence. ~50% of pts with TSS fail to develop antibody to TSST1 after

Front 24

what causes staphylococcal food poisonoing? what are some characteristics of it?

Back 24

the enterotoxins from staph, not the orgs themselves, thus you do not need infection, just the toxin. cannot reheat food bc the toxxin is very heat reresistant. Symptoms occur about 4 hours after ingestion, can only treat the symptoms

Front 25

MRSA isolates can be categorized how?

Back 25

heterogenous is a small fraction of the population while homogeneous is the entire pop is resistant

Front 26

what are the treatments for MRSA?

Back 26

vancomycin, is staph is just MSSA (sensitive) can use oxacillin. topical mupirocin can be used to decolonize nasal carriers. Also note that VRE has transferred its vanc resistance to some MRSA strains

Front 27

T/F: a lot of staph and strep toxins are superantigens.

Back 27

T

Front 28

describe the virulence factors of staph aureus.

Back 28

capsular polysaccharide inhibits neutrophil phag and chemotaxis. protein A binds the Fc portion of some IgG's thus neutralizing the ability of phagocytic cells to recognize it, but immuntiy to the bug can still develop. cytotxins a,b,d,g can kill various euk cells. panton valentine leukocidin lyses neutrophils and is responsible for necrotizing pneumonia. exofoliative toxins A and B are responsible for scalded skin syndrome. enterotoxins are responsible for food poisoning and are superantigens. TSST1 for toxic shock syndrome - massive cytokine release and thus shock and death, they are superantigens. peptidoglycan - like an endotoxin, stimulates pyrogens, activates complement, produces IL1, aggregates neutrophils (part of abscess formation. MSCRAMMs/adhesins which bind to the ECM and host cells

Front 29

T/F staph epidermidis is normal flora?

Back 29

T

Front 30

what diseases does staph epidermidis cause?

Back 30

infected catheters, or skin wounds it is almoust exclusively nocosomial

Front 31

describe the bacteremia and sepsis caused by staph epidermidis

Back 31

bacteremia can lead to seeding of damaged heart valves and subsequent endocarditis while sepsis can occur via the host's response to infection

Front 32

describe the virulence factors of staph epidermidis.

Back 32

capsular polysaccharides: slime that protects bacterium from antibiotics and immune cells and a glue (biofilm)

Front 33

what special circumstances exist when culturing S. epidermidis

Back 33

need multiple blood cultures in order not to contaminate with normal S. epi flora

Front 34

treatment of S. epi?

Back 34

vanc

Front 35

what is the morphology of strep pneumoniae

Back 35

diplococci

Front 36

What are the alpha hemolytic strep? what does they look like on agar and what causes this effect?

Back 36

S. pneumoniae and "viridans" strep. This is not actual RBC lysis, but is a greening of the agar due to H2O2 that is released from the bacs

Front 37

what are the beta hemolytic strep species? what causes this?

Back 37

S. pyogens and S. agalactiae. Exotoxins cause this via GAS in pyogenes and GBS in agalactiae

Front 38

what surface antigens are associated with what strep species?

Back 38

A is for pyogenes, B is for agalactiae and D is for enterococci. pneumniae is ungroupable

Front 39

what is the key way to diagnose strep species?

Back 39

by physiological means

Front 40

what mode of respiration does S. pyogenes utilize?

Back 40

facultative respiration

Front 41

which protein is used for serotyping S. pyrogens and what can this protein do to evade the immune system?

Back 41

M protein and it can undergo phase variation

Front 42

what defense mechanism does S.pyogenes utilize to evade phagocytosis?

Back 42

it is usually encapsulated

Front 43

is S. pyogenes usually found intra or extracellularly?

Back 43

extra

Front 44

are strep orgs catalse + or -?

Back 44

negative

Front 45

where is S. pyogenes found in nature?

Back 45

asymptomatically colonizes upper respiratory tract and skin of those with wounds or disease as well as those with poor hygeine

Front 46

how is S. pyogenes spread?

Back 46

it can survive on dry surfaces for a long period of time, can be spread through droplets, food, and water. It can also be spread via breaks in the skin after direct contact with the infected/colonized person, fomite, or arthropod vector

Front 47

what strep species can cause disease in an otherwise healthy person?

Back 47

S. pyogenes

Front 48

what are the difficulties in diagnosing strep throat?

Back 48

most pharyngitis cases are due to a virus and some ppl have an asymptomatic colonization of strep pyogenes. Thus lab tests show strep but the culprit is a virus this leading to the misuse of antibiotics

Front 49

strep throat symptoms include what

Back 49

sore throat, fever, malaise, headache

Front 50

what types of complications may arise from untreated strep throat?

Back 50

non suppurative and suppurative (pus producing). suppurative complications include otitis media, peritonsillar cellulitis, mastoiditis, peritonsillar or retropharyngeal abscesses. Non suppurative include acute rheumatic fever which involves inflammatory changes in heart, joints, blood vessels, and SQ tissues (includes carditis, polyarthritis, and chorea).

Front 51

describe scarlet fever.

Back 51

complication of S. pyogens infection of throat or skin. Strain of pyogenes is infected by bacteriophage which elaborate the exotoxins causing rash, high fever, strawberry tongue, eventual desquamation of the skin.

Front 52

describe acute glomerulonephritis.

Back 52

nonsupporative complication following pharyngitis or polyderma infection of S pyogenes. causes acute inflammation of renal glomeruli with edema, hypertension, hematuria, and proteinuria. mechanism of disease is unknown and can lead to loss of renal function in some adults whereas most younger patients recover with no problem

Front 53

describe impetigo pyroderma.

Back 53

very difficult to distinguish between streo and staph infection. Colonization occurs first and then infection at sight where skin integrity is compromised. red papules first and eventually to postules. spreads from original infection sight and is most common in young children; associated with poor hygeine and moist climate

Front 54

describe erysipelas. cellultits.

Back 54

local pain, inmflammation, fever, chills lymph node enlargement from S. pyogenes. cellulitis is another skin infection of pyogenes as well as staph aureus that occurs when the skin is compromised

Front 55

what is the fatal progression of strep disease (pyogenes)

Back 55

flu like symptoms, pneumonia, bacteremia, then fatal toxic shock. Note this pneumonia is different than S. pneumoniae in that it is more rapidly progressive

Front 56

describe the process of streptococcal toxic shock syndrome.

Back 56

GAS penetrates a skin lesion or introduced during surgery or due to pneumonia and dissemination into the blood stream. associated with strains that cause skin disease not pharyngitis. GAS multiply at site of infection and produce toxins (dif here bw staph and strep is strep has much more bacs at sight of infection). systemic symptoms then occur, the patient becomes bacteremic and many develop necrotizing fasciitis, hypotension, and impaired clotting

Front 57

what are some differences between staph and strep toxic shock syndrome?

Back 57

rash and desquamation are uncommon in strep. bacteremia is frequent in strep. mortality is much higher in strep

Front 58

if a patient presents with infected skin lesion, SEVERE pain, and fever then think...

Back 58

toxic shock syndrome

Front 59

how do you treat strep toxic shock.

Back 59

not penicillin bc the bacs are in stationary phase. use clindamycin and penicillin, may need surgical exploration and debridement of infected tissue if necrotizing fasciitis. IV fluids maybe needed

Front 60

how does complement effect strep?

Back 60

it cannot lyse it bc of thick peptidoglycan, but it can opsonize it (C3b) since it is extracellular

Front 61

GAS means what?

Back 61

group A strep toxin (S. pyogenes)

Front 62

what are the major virulence factors of GAS M protein?

Back 62

antiphagocytic against neutrophils, binds fibrinogen, sequesters C4b binding protein which decreases C3b deposition. sequesters Factor H which also decreases C3b deposition

Front 63

what are S. pyogenes virulence factors?

Back 63

capsule of hyaluronic acid (makes host think it is endogenous) that makes em antiphagocytic. DNAse which digests DNA in pus to allow the org to move around. Streptolysin S and O: lyses leukocytes, platelets, and erythrocytes. C5a peptidase: degrades complement component C5a thus impairing neutrophil chemotaxis. Superantigens that promote excesive T cells, cytokines and thus shock. Lipoteichoic acid acts synergistically with superantigen to promote shock

Front 64

what kind of colony formation do hyperencapsulated strains of S. pyogenes have?

Back 64

mucoid

Front 65

what age group does strep pneumoniae usually effect?

Back 65

very young, elderly or somehow immunocompromised

Front 66

what are the key properties of S. pneumoniae?

Back 66

gram pos diplococcus, facultative anaerobe, aerotolerant, virulent strains are encapsulated with dif polysaccharides than S. pyogenes. usually soluble in bile

Front 67

can ppl have an asymptomatic colony of S pneumoniae?

Back 67

yes about 1/3 of ppl have an asymptomatic colonization at some point in their lives, but it usually only effects those that are immunocompromised with an antecedent resp infection

Front 68

what are the symptoms of pneumonia from S. pneumoniae?

Back 68

shaking chills, productive cough, blood in sputum, chest pain, can become cyanotic due to damaged ciliated cells and lack of oxygen

Front 69

what other diseases of S. pneumoniae are usually preceded by viral infection oof the upper resp tract?

Back 69

otitis media and sinusitis

Front 70

what are ways that S. pneumoniae can reach the CNS o cause meningitis?

Back 70

bacteremia from pneumonia, infection of ear or sinus, trauma that causes communication bw subarachnoid space and nasopharynx

Front 71

what are the symptoms of meningitis caused by S. pneumoniae?

Back 71

fever, irritability, drowsiness, neck stiffness, seizure, coma... can lead to blindness, hearing loss, learning disabilities, paralysis, and death

Front 72

what can cause S.pneumoniae to become bacteremic and what can this cause?

Back 72

1/4 of pneumonia patients will become bacteremic, and 80%+ of meningitis patients will also. It usually does not occur in sinusitis/otitis media. it can result in endocarditis

Front 73

what is the most useful tool against the S. pneumoniae capsule and how does the org fight back?

Back 73

antibodies against the capsule, but the org can change the composition and antigenicity of the capsule

Front 74

what org contains pneumolysin and what does it do?

Back 74

S. pneumoniae and it is toxic for many cell types, activates complement, and suppresses oxidative bursts of phagoytes.

Front 75

what bac uses teichoic acid and peptidoglycan fragments to activate complement and thus cause more damage to the infected tissues?

Back 75

S. pneumoniae

Front 76

what is the major contributor to damage of the host tissue in S. pneumoniae infections?

Back 76

the host immune response that is illicited by the bug

Front 77

what makes S. pneumoniae able to aquire drug resistance as well as new capsular polypeptide antigens?

Back 77

it is naturally transformable

Front 78

what are the treatment options for S. pneumoniae?

Back 78

penicillin, but many strains are resistant now. Can use vanc. vaccine against the capsule is available but it is not very effective

Front 79

how is S. pneumoniae spread?

Back 79

by intensive close contact

Front 80

what strep species is group B strep?

Back 80

Strep agalactiae

Front 81

describe the key properties of GBS.

Back 81

gram pos, chain cocci, commensal as well as pathogenic, extracellular with a capsule that has different polysaccharides and is more effective than S. pneumoniae, usually infects elderly and immunocompromised

Front 82

what is the resevoir for GBS?

Back 82

normal member of GI flora as well as 10 to 30% of healthy vaginas

Front 83

describe the early onset disease of GBS.

Back 83

severly immunocompromised newborn (usually premie) gets it from asymptomatic mother. leads to sepsis and meningitis. all encapsulated serotypes can cause this

Front 84

describe the late onset disease of GBS.

Back 84

occurs after 7th day of childbirth. bacteremia, meningitis, bone/joint involvement, usually term baby with no risk factors, serotype III predominates. NOT PNEUMONIA, lung is npot sight of initial infection

Front 85

what are the symptoms of early onset GBS disease?

Back 85

lethargy, poor feeding, jaundice, hypotension... if meningitis, 1/2 have seizures, 5-10% mortality, as well as 25-50% chance of permanent neurologic sequelae from meningitis

Front 86

how does a pre term baby aquire GBS?

Back 86

mother has it in vagina, it then penetrates placental membranes, child aspirates large amounts of infected amniotic fluid, hits the lungs and causes pneumonia, then invades the pulmonary epithelial and endothelial cells to the blood stream and thus sepsis.

Front 87

what are the risk factors used to determine if a baby is susceptable to GBS?

Back 87

high inoculum of bacs, virulent strain, chorioamnionitis, gestation < 37 wks, ROM> 18 hours, lack of anti capsule antibodies from mom

Front 88

what adults are susceptable to GBS infection?

Back 88

pregnant - cesarean related wound infection. Immunocompromised or those with an underlying medical condition

Front 89

what diseases can GBS cause in adults?

Back 89

septic arthritis, meningitis, endocarditis, skin and soft tissue infection

Front 90

how can an infant become infected with late onset GBS?

Back 90

from mom or from another exogenous source

Front 91

what is the mortality rate for adult GBS?

Back 91

21-34%

Front 92

what diseases can GBS cause in adults?

Back 92

bacteremia is most common and if it does not kill you, it will reoccur usually. pneumonia, endocarditis, meningitis, arthritis and osteomyelitis, skin and soft tissue infections

Front 93

what are the main virulence factors of GBS?

Back 93

the capsule which inhibits phagocytosis and is antigenically variable bc of a terminal sialic acid, hemolysin which is toxic for many cell types, C5a peptidase

Front 94

how is GBS controlled/treated?

Back 94

pregnant women are tested 2 wks before birth and are given penicillin if needed.

Front 95

what are the indications for intrapartum antibiotic prophylaxis for gbs?

Back 95

previous infant with GBS, GBS bacteremia during pregnancy, positive GBS screenig culture, delivery at <37 wks, membrane rupture over 18 hrs, intrapartum temp > 100.4. NOTE this will only reduce early onset disease not late onset

Front 96

how is GBS spread between asymptomatic carriers?

Back 96

sexual contact (though it is not considered an STD), fecal oral route, some ppl have it asymptomatically in their throat

Front 97

what antibiotics and vaccines are used for GBS?

Back 97

penicillin or ampicillin, some resistance has been reported. for big time infections do ampicilin and aminoglycoside, vanc in pts allergic to penicillin. new vaccines being developed against the capsule and the surface proteins

Front 98

what are key characteristics and properties of the enterococci?

Back 98

gram pos coccus, in pairs or short chains, hardy on dry surfaces, microscopically indistinguishable from S. pneumoniae, facultative, often resistant to antibiotics (VRE), not as virulent as strep or staff, but can transfer resistance to other species! normal resident of healthy human colon as well as hands of health care workers

Front 99

what can cause enteroccoci to become cause disease?

Back 99

usually an opportunist, it becomes dangerous with prolonged hospitilization with long periods of antibiotic treatment, thus everything else is killed but it. It is 1st in causes of nosocomial bacteremia

Front 100

describe the diseases caused by enterococci.

Back 100

bacteremia can hit through urinary tract, pelvic sepsis, or wounds; it is usually transient but death rate is high bc pts usually have some other problem. Endocarditis usually in pt with underlying heart valve issue. UTI is most common in faecalis and usually associated with catheter that is contaminated. wound infection/pelvic infection/ intraab infection all usually found with other bacs, some can be septic.

Front 101

how is enterococci spread?

Back 101

thinking is now get an expgenous infection not endogenous normal flora. may be from hospital care workers

Front 102

what are the control protocols of VRE?

Back 102

isolate patient, all persons entering or leaving the room should wear gloves/gown, non critical items should remain in room, wash hands with antibac agent after contact, keep infected patient isolated until 3 stool cultures are negative

Front 103

what are the antibiotics for enterococci?

Back 103

1st try is aminoglycosides plus cell wall active antibiotic. If VRE do linezolid or quinupristin/Dalfopristen