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Microbiology > Gram positives lec 7 > Flashcards

Gram positives lec 7 Flashcards

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Biology 101 flashcards
1
Q

How does staph aureus cause infections and intoxication?

A

Due to bacteria and due to toxins secreted by the bacteria. It can also be carried on the skin as part of the normal flora.

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2
Q

What is a carrier

A

asymptomatic carriage on skin or mucous membranes of anterior nares.

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3
Q

Intoxication

A

when toxin is ingested, food poisoning, contaminated food sources, gastroenteritis.

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4
Q

toxins produced during infection:

A

toxic shock syndrome, scalded skin syndrome

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5
Q

Infection at localized surface-

A

furuncles, carbuncles, impetigo, stye

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6
Q

infection at deep

A

osteomyelitis, arthritis

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7
Q

systemic infection

A

pneumonia, endocarditis, UTI, enterocolitis, septicemia

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8
Q

What are common surface lesions?

A

impetigo, furuncle (boil) hair follicle, stye, carbuncles

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9
Q

What do Staph aureus lesions often produce?

A

Large amounts of pus

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10
Q

What binds the bacteria during surface infections?

A

fibronectin binding proteins. Coagulase causes fibrin to clot walling off the bacteria, and protein A binds the Fc portion of IgG helping to protect the bacteria from immune response.

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11
Q

How does S aureus spread?

A

Spread is accompanied by the production of a number of toxins.

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12
Q

fibronectin

A

binding proteins, adherence to fibronectin

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13
Q

protein A

A

binds Fc portion of IgG protects cell from phagocytosis

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14
Q

coagulase

A

induces fibrin clotting on the bacteria protecting the cell from phagocytosis

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15
Q

What aids is dissolution and spreading that leads to infections?

A

hylauronidase, fibrinolysin

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16
Q

fibrinolysin

A

lysis the fibrin

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17
Q

hylauronidase

A

promotes spread through CT

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18
Q

hemolysins

A

toxins for nutrient scavenging.

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19
Q

deep lesions

A

cellulitis, osteomyelitis, arthritis

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20
Q

other infections

A

pneumonia, endocarditis , bacteremia

21
Q

What are Tsst 1 and SEs

A

super antigens! they bind to the outside of the Vbeta chain of the TCR and crosslink it to MHC class II. All T cells with V beta chain will be activated. *activation does not require antigen. Activation causes CYTOKINE STORM and causes toxic shock

22
Q

what is toxic shock

A

similar to endotoxic shock except it is mediated by an exotoxin rather than lps

23
Q

What is toxic shock syndrome

A

caused by TSST and SEs. hallmarks are fever, malaise, rash, lethal hypotension, multi-organ changes. Can be a local cause, originally associated with high absorbancy tampons.

24
Q

staphylococcal scalded skin sydrome

A

in children and neonates, follows URT, inner ear infection, blisters develop on 90% of body surface, skin sheds, associated with prod of exfoliative toxin(causitive agent)

25
Q

How can s aureus be carried?

A

asymptomatically on the skin and nares of mucus membranes. persistent carriers = ALWAYS CARRY S aureus.

26
Q

How do carriers spread S aureus?

A

direct contact, fomites, contamination of food. Carriers can also infect themselves.

27
Q

Intoxication by food poisoning:

A

if food is at warm temp, bacteria grow and produce Staph exotoxin (SE) which are HEAT STABLE. Once formed, temp makes no difference. SE acts as a superantigen at GI lining leading to diah and vomit. Cooking kills the bacteria and disease is transient and self- limiting.

28
Q

MRSA methicillin res. staph aureus highlights

A

contains mec A gene which encodes an alt penicillin binding pro. PBP , is resistant to ALL beta lactam antibiotics

29
Q

HA- MRSA

A

hospital associated, often resistant to other antibiotics too

30
Q

CA MRSA

A

community associated- found in community and is associated with death of healthy individuals. can grow better in host in communities. virulence factors allow growth on skin ( can survive on surfaces)

31
Q

S Aureus can be resistant to :

A

penicillin- changes in PBP mec A gene, beta lactamases , chloramphenicol- efflux pumps, prod of acetylases, erythromycin - changes in ribosome proteins, sulfonamides- alt pteridine synthetase

32
Q

Staph Aureus characteristics

A

gram + cocci in grape like clusters, catalase positive, coagulase positive, Beta hemolytic usually slightly yellowish/gold colonies

33
Q

what distinguishes Staph aureus from streptococci?

A

catalase postive trait

34
Q

What is Staph epidermidis

A

part normal flora, forms biofilms on indwelling devices

35
Q

Why do recurrent bouts of septicemia occur?

A

septicemia is due to planktonic free living bacteria that can be killed by antibiotics. The Killing is not as effective in the biofilm, so the biofilm survives and can cause another bout of septicemia. THE only way to clear infection is to remove the indwelling device.

36
Q

what can S epidermidis form biofilms on ?

A

prosthetic valves, contact lenses, intravasc catheters, endo trach tubes, joint rep, voice prosthesis

37
Q

S epidermis characteristics

A

gram postive cocci in grape like clusters , gamma hemolytic, catalase positive, coagulase negative

38
Q

S saprophyticus

A

gram + cocci in clusters GI tract normal flora, causes UTI, most likely wont be on exam

39
Q

How are streptocci classified?

A

Lancefield serotyping against surface structures. Cell wall specific polysac LTA components. S pyogenes serotyped based on M protein serotypes. S agalctiae and S pneumoniae based on caps polysac antigenicity

40
Q

Group A include:

A

Streptococcus pyogenes

41
Q

Group B :

A

streptococcus agalactiae

42
Q

Group D:

A

enterococcus faecalis and faecium

43
Q

Group H:

A

streptococcus sanguis

44
Q

Streptococcus pyogenes group A disease:

A

infection localized: tonsilitis, impetigo, erysipelas, deep- necrotizing fascitis Tss, immune response: rheumatic fever, rheum heart disease, glumeruloneph

45
Q

non invasive diseases:

A

pharyngitis , impetigo( superinfected with S aureus), cellulitis( can occur with S pyogenes- chicken pox)

46
Q

ARF post streptococcal sequelae

A

antibodies react with heart sarcolemma following throat infection, m protein induction of cross reactive antibodies, RHDisease results

47
Q

glomerulonephritis

A

deposition of immune complexes in the kidney leading to inflammation

48
Q

What protein is an important virulence factor for S. pyogenes

A

M protein ( strains are grouped by M-types) Differences include SNPs, high variance between strains

49
Q

Streptococcus pyogenes Group A strep

A

gram positive in cocci in chains, beta helolytic on blood agar, catalase negative (dist from staph) bacitracin sensitive, PYR positive

Microbiology (7 decks)

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