Staphylococci Flashcards Preview

Rheum/Musculoskeletal/Derm Week 3 > Staphylococci > Flashcards

Flashcards in Staphylococci Deck (62):
1

T or F. All staph produce catalase

T. All can hydrolase H2O2 (not all have coagulase). Bacteria that make catalase can survive the killing effect of H2O2 within neutrophils.

 

2

What is this?

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Staph (Gram positive cocci in grapelike clusters)

3

Describe staph aureus

gram positive cocci that produces both coagulase and catalase, produces beta hemolysis on BAP, and is a member of normal flora

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4

What are the virulence determinants of Staph aureus?

-catalase and coagulase

-the vast majority produce beta-lactamase 

-some strains contain mecA genes which code for altered PBPs (these strains are known as MRSA)

-staphyloxanthin (carotenoid)

-Hemolysins (liberates iron)

-protein A

-teichoic acids

-polysaccharide capsule

-peptidoglycan 

-alpga toxin.hemolysin (membrane-damaging hemolyitc toxin)

-Panton Valentine (P-V) leukocidin

-•Gamma-toxin/leukotoxin (membrane-damaging hemolytic toxin)

5

What are some common sites of colonization of staph aureus?

nose (30% of people are colonized at any given time with chronic carriers being at icnreased risk of infection)

-skin

-vagina in 5% of women 

6

Staph aureus infections are common in what populations?

childcare centers, IVDUs, prisons, sports teams

7

What does staphyloxanthin do?

•causes golden color to colonies.

–Enhances pathogenicity by inactivating microbicidal effect of superoxides and other ROSs within neutrophils

8

What does coagulase do? What is its function in staph aureus?

–Causes plasma to clot by activating prothrombin to form thrombin which catalyzes activation of fibrinogen to form fibrin clot

       –Serves to wall off infected site, delaying migration of neutrophils to the site

9

What does protein A do?

Major protein in cell wall. Binds to Fc portion of IgG at complement binding site and prevents complement activation; no C3b produced so phagocytosis of organisms is greatly reduced

10

What do teichoic acids do?

–Mediate adherence of staph to mucosal cells 

–Lipoteichoic acid induces IL-1 and TNF from macrophages

11

Note on the polysacchardide capsule of staph aureus

 –11 serotypes; 5 and 8 most commonly cause infection 

–Capsule allows bacteria to attach to artificial materials and resist host cell phagocytosis

12

What does peptidoglycan do?

–Stimulates macrophages to produce cytokines, activates complement/coagulation cascades

endotoxin like properties.  Reason for septic shock but no endotoxin

13

What does alpha toxin do?

–Forms holes in host cells

–Causes necrosis of skin and hemolysis

14

What does Panton Valentine (P-V) leukocidin do?

(membrane-damaging hemolytic toxin)

This is a pore-forming cytotoxin that causes leukocyte destruction by damaging cell membranes and causes tissue necrosis. Cell contents then leak out of a pore which the toxin forms and can cause severe skin/soft tissue infections as well as severe necrotizing pneumonia

–Produced by MRSA strains, typically community-acquired

 

Model for emergence of PVL producing CA-MRSA: a methicillin-susceptible S. aureus (MSSA) strain is infected and lysogenized by a phage (phiSLT) that harbors the lukS-PV and lukF-PV genes (pvl) encoding the PVL. Subsequently, a methicillin resistance cassette (SCCmec IV, V or VT) carrying the mecA gene is horizontally transferred into the pvl-positive MSSA strain and integrates into the genome in a location that is distinct from that of the phiSLT integration site. 

 

15

What does Gamma-toxin/leukotoxin do?

(membrane-damaging hemolytic toxin)–Lyses phagocytes/RBCs

16

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17

What causes Staphylcoccal Scalded skin syndrome?

This is a toxin mediated complication of Staph aureus that is caused by exfoliative toxins A and B that act as proteases to cleave desmogleins in desmosomes, leading to seperation of the epidermis layer of the skin. 

18

How does SSSS present?

 

–Very common in newborns, typically 3-7 days of age

–Febrile, irritable, diffuse blanching erythema with blisters/bullae appearing 1-2 days later starts around the mouth.

–Serous fluid exudates, dehydration, electrolyte imbalance

–Flaky desquamation/sloughing occurs as lesions heal

–Mucous membranes are not involved–Recovery 10 days

 

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19

T or F. SSSS will not result in scarring

T.  Because the cleavage plane of the blisters is intraepidermal

20

How can S. aureus cause food poisoning?

This is a toxin mediated sequelae of Staph aureus caused by enterotoxin A which causes prominent vomiting and watery, non-bloody diarrhea. Enterotoxin A acts as a superantigen in the GI tract, and stimulates IL-1 and IL-2 from macrophages and helper T cells which causes vomiting via activation of the vomiting center in the brain. 

This toxin is heat resistant and not inactivated by brief cooking and is resistant to stomach acid/enzymes 

21

What is Bullous impetigo?

A sequelae of Stpah aureus caused by exfoliative toxins that presents as enlarged vesicles at localized to the site of infection filled with clear, yellow fluid which later becomes darker and more turbid. 

These vesicles are more common on the trunk and typicall leave a thin brown crust when ruptured

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22

What causes staph toxic shock syndrome?

This is another toxin mediated complication of Staph aureus in which toxin is produced locally in the vagina/nose/post-op wounds by S. aureus that enters the blood stream and stimulates release of large amounts of IL-1, IL-2, and TNF AND acts as a superantigen and binds to T-cell receptors, resulting in polyclonal T-cell activation. 

23

What are some common causes of TSST?

Leaving tampons in too long, nasal packing to stop bleeds, post-op infections, and other infections (sptic joints, etc.)

NOTE: 

The isolation of S. aureus is not required for the diagnosis of staphylococcal TSS. S. aureus is recovered from wound or mucosal sites in 80 to 90 percent of patients with TSS and recovered from blood cultures in approximately 5 percent of cases

24

How does Staph TSS present?

Almost all causes are in caucasions and it presents variably with symptoms including, fever, hypotension, N/V, sever myalgias, renal failure, and a diffuse macular erythroderma that desquamates 1-2 weeks after onset

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25

How do you treat MSSA?

Nafcillin/oxacillin

some cephalosporins (Cefazolin, ceftriaxone, cefepime, ceftaroline)

-vanco

-augmentin for mild cases

26

T or F. MSSA is resistant to PCN

T Most produce beta-lactamase

27

How is MRSA treated?

-vanco

-dapto, linezolid

-ceftaroline

-bactrim/clinda/doxycycline for mild infections 

28

How is VISA/VRSA treated?

Dapto, Linezolid, Ceftaroline 

29

What is the main resistance mechanism of MRSA?

•changes in PBP in cell membranes.  MecA genes on bacterial chromosome encode the altered PBPs.

30

What is the main resistance mechanism of VRSA?

•Genes encode enzymes that substitute D-lactate for D-alanine in the peptidoglycan.

31

What is the source of resistance in VISA?

synthesis of unusally thickened cell wall 

32

When testing a Gram-positive culture for sensitivity to clindamycin, it is common to perform a "D-Test" to determine if there is a macrolide-resistant subpopulation of bacteria present. This test is necessary because some bacteria express a phenotype known as MLSB, in which susceptibility tests will indicate the bacteria are susceptible to clindamycin, but in vitro the pathogen displays inducible resistance.

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33

How is TSS treated?

 

The treatment involves giving supportive fluids (10-20L/day) and vasopressors (dopamine, Nor) +

Surgical intervention AND

ABX

34

What ABX are recommended for TSS?

Vanc/Oxacillin (MRSA/MSSA) PLUS Clindamycin (to suppress protein synthesis and therefore toxin synthesis)

35

How can S. aureus infection be prevented before a surgery?

give peri-operative Cefazolin +/- Vanc depending on rate of MRSA in the area OR

intranasal mupirocin to reduce coloniztion, combined with Hibiclens (chlorhexidine gluconate) for bathing +/- ABX (doxy, bactrim) for about 1 week 

36

 

Describe S. epi

A gram + clustered cocci that is catalase positive but coag negative and DOES NOT ferment mannitol. 

Part of normal flora of skin, also mucous membranes and non-hemolytic (Novobiocin sensitive)

37

T or F. S. epi is urease positive

T. 

It is an enzyme that catalyzes the hydrolysis of urea into carbon dioxide and ammonia. The reaction occurs as follows:

(NH2)2CO + H2O → CO2 + 2NH3

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38

When do most S. epi infections occur?

•Most S. epi infections occur in setting of foreign devices

–Most likely prosthetic materials are inoculated with small numbers of staph at time of implant

•IV catheters, prosthetic heart valves, grafts, prosthetic joints

39

Pathogenesis of S. epi

•Bacterial adherence initial step

–Once introduced in body, foreign materials become coated with host proteins – fibrinogen, fibronectin, etc., which serve as potential receptors for various Staph surface proteins. 

–Strains of S. epi possess surface adhesins critical for interacting with host proteins and mediating more specific adherence

40

What happens after S. epi attaches?

•After attachment: Extracellular polysaccharide matrix or slime is produced which encases the bacteria.  Biofilm (below) functions as barrier to antibiotic penetration and may interfere with host defenses.

NOTE: S. aureus produces biofilm as well

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41

How is Staph epi treated?

The treatment involves removing the device if possible and ABX

Vanco (If MSSE, can use oxacillin/nafcillin)

and Rifampin and Gent should be added for prosthetic value endocarditis 

42

Describe staph saprophyticus 

Catalase positive, coagulase negative, non-hemolytic, urease positive, does not ferment mannitol, novobiocin resistant

43

What does S. sapro cause most often?

•2nd most common cause of community-acquired UTIs in women

•Most have had sex within the previous 24 hours.

44

Treatment of staph sapro UTI?

•Bactrim or Cipro

45

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E. 

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46

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B. 

47

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B. This is PVL (most likely comminuty aquired)

A= protein A

C= Teichoic Acid

D= Peptidoglycan

48

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E.

49

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B. This is SSSS

50

What is the only cephalosporin that covers MRSA?

Ceftaroline

51

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52

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B. 

53

Tx? Bug?

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C. This is staph epi (remember that staph epi wont cause you to get really ick but is commonly reisstant to a lot of drugs)

Tx: Vancomycin 

54

Note about using Rifampin as monotherapy for bacterial infection

Never do this, the bug will rapidly develop resistance. Only use as adjunct therapy such as in a prosthetic infection by staph epi

55

T or F. Cipro isnt really used for gram positives

T. Cipro cannot treat staph aureus or epi

56

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B. 

57

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C. This toxic shock syndrome (may have a tampon in)

58

What is the main difference between staph TSS and strep TSS?

Staph TSS will not present with any obvious signs of a source of infection (usually due to tampon use, nasal packing), while Strep TSS will usually present with an obvious cellulitis

59

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60

What is a common complication for staph TSS?

loss of limbs due to:

1) activation of DIC

2) massive vasopressor therpay can cause distal ischemia 

61

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A. To reduce organism density (might want to also give doxycycline or bactrim (you suspect this is MRSA))

62

What should be done?

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Repeat imaging, baseline labs, and get blood cultures