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micro/id > staphylococci > Flashcards

staphylococci Flashcards

1
Q

pyogenic

A

pus-forming

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2
Q

staphylococci are able to survive in ____ environments

A

salty

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3
Q

Mannitol Salt Agar (MSA)

S. aureus ferments the mannitol, releasing acid byproduct, causing phenol red pH indicator in agar to change to ______

A

yellow.

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4
Q

Responsible for a broad spectrum of clinical syndromes

A

Staphylococcus aureus

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5
Q

Medical device-related infections

A

Staphylococcus epidermidis

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6
Q

Urinary tract infections

A

Staphylococcus saprophyticus

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7
Q

Hospital Acquired S. aureus are mostly drug resistant (e.g. Methicillin Resistant S. aureus [MRSA], Vancomycin Resistant S. aureus [VRSA]).

A

yep

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8
Q

Community Acquired S. aureus infections (CA-SA) generally have more treatment options, but

A

drug resistance is emerging

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9
Q

The reservoir for S. aureus in adults is the human axillae (armpits), nares, and external genitalia. In neonates, S. aureus is found in the umbilical stump, perineum, skin and gastrointestinal tract.

The carriage rate is approximately 30% in the general population. Health care workers as well as diabetics, intravenous drug users and patients on hemodialysis have higher carriage rates.

A

yep

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10
Q

main rout of entry for S.aureus

A

S. aureus gains entry to deeper tissues after trauma, surgery or instrumentation breach integrity of the skin or mucous membranes.

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11
Q

S. aureus is specialized for survival in the host as an

A

extracellular pathogen

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12
Q

S. aureus has Many Potent Virulence Factors (4)

A
  1. Inhibitors of phagocytosis
  2. Cell-associated adhesins for tissue colonization (many bind extracellular matrix proteins)
  3. Secreted proteins for the creation of a hospitable extracellular milieu
  4. Secreted toxins for nutrient acquisition and immune escape
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13
Q

inhibitors of phagocytosis that S. aureus has (3)

A
  1. Protein A.
  2. polysaccharide capsule
  3. coagulase
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14
Q

Release nutrients from host
tissue aiding growth, and also
also allow for dissemination of
bacteria (3)

A
  1. proteases
  2. lipases
  3. DNases
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15
Q

numerous exotoxins exist like membrane-damaging toxins and superantigens

A

yep

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16
Q

superatnigens

A

activates t-cells (high 20%) with a high cytokine release by bridging TCR and MHC II

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17
Q

superantigen toxin-related disease

A
  1. toxic shock syndrome
  2. menstrual
  3. non-menstrual
  4. food poisoning
  5. S. scalded skin syndrome
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18
Q

resistant to many beta-lactams due to acquisition of mecA gene encoding alt. peptidoglycan synthesis protein

A

MRSA- methicillin-resistant

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19
Q

Is the result of a thickened peptidoglycan layer.

Vancomycin is less able to penetrate.

A

VISA-Vancomycin-intermediate

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20
Q

Acquisition of the vanA gene, originally from vancomycin-resistant
Enterococcus. (VanA makes D-alanine-D-lactate peptide cross-bridge
precursors in cell wall instead of the usual D-alanine-D-alanine.)

A

VRSA- Vancomycin-resistant

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21
Q

S. epidermidis is a normal inhabitant of human skin.

A

yep

In the normal host, S. epidemidis cannot cause
infection in the absence of a foreign body,
even if the skin has been compromised.
Exceptions are neonates, IV drug users.

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22
Q

S.epidermis adhesins (3) to biomaterials

A
  1. fimbriae- surface structures
  2. AtlE
  3. capsular polysaccharide
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23
Q

threapy for device related S. epidermidis

A

removal of the foreign body and then treat vancomycin

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24
Q

therapy to S. saprophyticus

A

no different than other UTI pthogens

25
Q

golden, Beta-hemolytic colonies, can ferment mannitol.

26
Q

white, non-hemolytic, cannot

ferment mannitol.

A

S. epidermidis

27
Q

Gram-positive cocci, chains or diplococci,

catalase-negative

A

streptococci

28
Q

Group A Strep (GAS)

A

S. pyogenes –

29
Q

Group B Strep (GBS)

A

S. agalactiae –

30
Q

Group D Strep (GDS)

A

S. bovis –

31
Q

serotyping scheme based on cell wall carbohydrate antigens

A

Lancefield groups—

32
Q

type of hemolysis green/brown zone

around colonies

A

Alpha-hemolysis

***Alpha is due to breakdown of hemoglobin and other molecules in RBSs, not really lysis of RBCs.

33
Q

type of hemolysis:
complete lysis,
and clearing

A

Beta-hemolysis

34
Q

type of hemolysis:

non-hemolytic

A

gamma-hemolysis

35
Q

S. pyogenes is found

A

on skin and mucosal surfaces of humans

36
Q

Skin and mucous membrane infections
Strep throat
-Colder weather; spread mainly by aerosol
Impetigo
-Warmer weather; contact transmission
Erysipelas
-Infection of the upper levels of dermis
Deep tissue and blood infection
Cellulitis
Necrotizing fasciitis, myositis
Pneumonia, puerperal fever (infection of placenta)
Toxigenic manifestations
Scarlet Fever (erythrogenic toxin [a superantigen])
Streptococcal toxic shock syndrome (strep TSS) due
to superantigen expression

A

suppurative GAS disesase

37
Q

cellulitis

A

deeper infection of skin and can rapidly spread

tx. with oral antibiotics

38
Q

strawberyy tongue associated with

A

Scarlet fever - GAS toxigenic manifestations

39
Q

A. Glomerulonephritis

  • Follows pharyngitis or impetigo, 10-15% attack rate
  • Antigen-antibody-complement complex deposited in kidney
  • Edema, smoky or rust colored urine, hypertension

B. Acute rheumatic fever
Valvular Heart Disease
Follows untreated pharyngitis and/or scarlet fever, not impetigo
Presents 1-5 weeks post-pharyngitis
Fever, rash, arthritis, carditis, movement disorder (chorea)
Caused by specific subset of GAS strains
Proposed pathogenesis: autoimmunity
Generation of cross-reactive antibodies recognizing heart
Prevention: Rx pharyngitis with 10 d of antibiotics
Now rare in US, but in developing countries a major cause of heart disease

A

non-suppurative complications of GAS infection

40
Q

major GAS virulence factor

A

surface localized “M protein”

41
Q

roles of M protein (3)

A
  1. attachment
  2. resistance of phagocytosis
  3. resistance to complement
42
Q

M protein importance in immunity

A

Anti-M protein IgG is protective

43
Q

pore forming toxins in GAS exotoxins which important for necrotizing fascitis cause what type of hemolysis

44
Q

Therapy for GAS

A
  1. penicillin-sensitive
45
Q

S. agalactiae normally found in

A

lower GI tract which can colonize female genital tract leading to infection during birth

46
Q

S. bovis a GDS species is common in

A

bowel flora however when found in bloodstream it correlates with colon cancer and it is a significant cause of endocarditis

47
Q

enterococci normally inhabit the

48
Q

enterococci can cause _____ and it is resistant to _____ and it is inhibited but not killed by _____

A

enterococci can cause endocarditis and it is resistant to cephalosporins and it is inhibited but not killed by penicillin

49
Q

Group of a-hemolytic , and some g-hemolytic (non-hemolytic) streptococcal species, that are commensals, and are of low virulence.
Most are oral commensal bacteria isolated from dental plaque
Cause of subacute endocarditis

A

viridans streptococci

50
Q

alpha–hemolytic (green/brown zone), not in a Lancefield group
Mucosal pathogen, typically extracellular
Asymptomatic nasopharynx carriage rate of ~15-25%
Common cause of otitis media and community-acquired pneumonia
Less frequently causes bacteremia and bacterial meningitis
Estimated 1.6M annual deaths worldwide
Capsular polysaccharide-based vaccines are protective but don’t cover most serogroups

A

s. pneumoniae- pneumococcus

51
Q

pneumoccocal lung infection causes

A

lobar pneumonia characterized by inflammatory exudate within the intra-alveolar space

** patchy bronchopneumonia can also occur

52
Q

severe complication of pneumococcal that causes the brain to be covered with inflammatory exudate (pus)

A

pneumococcal meningitis

53
Q

encounter of oneumococcus

A

aerosols, mucus exchange and formites

54
Q

host immunity that is protective of pneumococcus from inflammed lung to bloodstream (bacterimia”

A

anti-capsular antibody

55
Q

virulence factors of pneumococcus (4)

A
  1. surface and secreted IgA1 protease
  2. surface phosphoryl choline- resists antimicrobial peptides
  3. pneumolysin: pore forming toxin that impairs mucociliary clearance and kills neutrophils
  4. polysaccharide capsule- essential for colonization and virulence and protective of anticapsular ab
56
Q

capsular polysacchrides each conjugated to a protein to promote T-cell-dependent response

1999: (PCV7 [pneumococcal conjugate vaccine 7-valent ])
2010: 13-valent (PCV13 or Prevnar13)

A

Conjugative vaccine for children < 5 yo and elderly >64 yo for pneumococcal

57
Q

(PPSV23 [pneumococcal polysaccharide vaccine 23-valent])
People with splenectomy
Elderly—every 10 years or so (along with PCV13)
Pre-existing lung conditions

A

nonconjugated vaccine of 23 common capsular polysacchrides for pneumococcal

58
Q

therapy for pneumococcal infection

A
  1. penicillin-sensitive but some resistant so treat with ceftriaxoneand vancomycin
    * *** penicillin allergic pt. treat with fluroquinoline
59
Q

identification of pneumococcus:

  1. Gram stain:
  2. Culture on blood agar:
  3. Serotype determination by Quellung reaction
A
  1. Gram stain: Gram-positive diplococci
  2. Culture on blood agar:
    • a-hemolytic
    • Optochin-sensitive (disk diffusion test)
  3. Serotype determination by Quellung reaction - Serotype-specific antibody causes cross-linking of cells and apparent swelling

micro/id (41 decks)

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