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Dermatological Block > Staph and Strep > Flashcards

Staph and Strep Flashcards

1
Q

Staphylococci general characteristics

A

nonmotile, do not produce spores, produce catalase (degrade hydrogen peroxide

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2
Q

Most common bacterial cause of conjunctivitis

A

Staph aureus

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3
Q

Staph aureus’ distinguishing lab features

A

Production of coagulase and sensitive to novobiocin

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4
Q

Common source of staph aureus infection in neonates

A

carriage by health care personnel

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5
Q

Carrier state

A

individual harbors potential pathogen and can spread it to others, though the carrier is either asymptomatic or has recovered from an infection by the organism already

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6
Q

Colonization

A

Acquisition of a new organism and it may cause infection or may be eliminated by host defenses

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7
Q

Colonization resistance

A

Nonpathogenic resistant bacteria occupy attachment sites on skin and mucosa, interfering with colonization by pathogenic bacteria

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8
Q

Primary site of colonization for staph epidermidis

A

Skin

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9
Q

Primary site of colonization for staph saprophyticus

A

Skin surrounding GU tract

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10
Q

Primary site of colonization for staph aureus

A

nose

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11
Q

Reason for yellow color of staph aureus on culture

A

Staphyloxanthin

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12
Q

Mechanism by which staph aureus causes necrotizing PNA

A

P-V Leukocidin: Pore-forming toxin kills cells, especially WBCs, by damaging cell membranes

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13
Q

Protein A

A

staph aureus virulence factor; binds to Fc portion of IgG at complement binding site and prevents complement activation; major component of cell wall; no C3b produced so phagocytosis of organisms is greatly reduced

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14
Q

Teichoic acid

A

staph aureus virulence factor; mediates adherence of staph to mucosal cells; induces release of cytokines (IL-1, TNF) from macrophages

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15
Q

Peptidoglycan

A

staph aureus virulence factor; endotoxin-like properties (can activate complement, coagulation cascade, stimulate macrophages to release cytokines); cause of septic shock

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16
Q

Staphyloxanthin

A

causes golden color to staph aureus colonies; virulence factor that enhances pathogenicity by inactivating microbicidal effect of superoxides and other ROS within neutrophils

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17
Q

Coagulase

A

staph aureus VF; causes plasma to clot by activating prothrombin to from thrombin which catalyzes activation of fibrinogen to form fibrin clot; serves to wall off infected site, delaying migration of neutrophils to the site.

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18
Q

Hemolysins

A

Staph aureus VF; hemolyze RBCs and use iron that is required for bacteria to grow; forms holes in host cells; causes necrosis of skin

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19
Q

Polysaccharide capsule

A

staph aureus VF; 11 serotypes with 5&8 most commonly causing infection; it allows bacteria to attach to artificial materials and resist host cell phagocytosis

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20
Q

Panton Valentine Leukocidin

A

Staph aureus VF; pore forming cytotoxin that causes leukocyte destruction by damaging cell membranes and causes tissue necrosis; cell content leak out of pore formed by the toxin causing severe skin/soft tissue infection and necrotizing pneumonia; produced by CA-MRSA

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21
Q

Gamma toxin/leukotoxin

A

staph aureus VF; lyses phagocytes/RBCs

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22
Q

Furuncle

A

boil; infection of hair follicle; purulent material extends through dermis into subcu tissue; abscess forms

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23
Q

Carbuncle

A

Coalescence of several inflamed follicles

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24
Q

Folliculitis

A

Superficial infection of hair follicles with purulent material in epidermis

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25
Q

Cellulitis

A

infection of soft tissue; involves deeper dermis and subcu fat

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26
Q
A

Furuncle

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27
Q
A

Carbuncle

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28
Q
A

Paronychia

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29
Q
A

Folliculitis

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30
Q
A

Cellulitis

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31
Q
A

Hordoleum

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32
Q
A

Blepharitis

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33
Q
A

Conjunctivitis

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34
Q

Pyogenic infection

A

Endocarditis, septic arthritis, osteomyelitis, postsurgical wound infections, pneumonia which can lead to empyema/abscess, sepsis, mastitis, abscessess (local and from blood stream)

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35
Q

MRSA population group

A

Childcare centers, IV drug users, wrestling teams, prisons

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36
Q

Cause of scarlet fever

A

Exofoliatin/Exfoliative toxins A and B; toxin acts as a protease that cleaves desmoglein in desmosomes

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37
Q

Clinical presentation of scalded skin sydrome

A

newborns (3-7days), febrile, irritable, diffuse blanching erythema with blisters 1-2 days later in flexural areas, buttocks, hands; serous fluid exudates, dehydration, electrolyte imbalance; mucous membranes are not involved and there is no scarring; lasts 10 days

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38
Q
A

Scalded skin syndrome

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39
Q

Enterotoxin

A

Toxin in staph aureus that causes food poisoning; it causes prominent vomiting and watery, non-bloody diarrhea; acts as superantigen in GI tracts, stimulates IL-1 and IL-2 from macrophages and helper T cells (cytokines stimulate enteric nervous system to activate vomiting); heat/acid resistant toxin; 1-8 hour incubation period

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40
Q

Bullous impetigo cause

A

caused by exfoliative toxin; localized at site of infection

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41
Q

Clinical presentation of bullous impetigo

A

Young children; vesicles that have enlarged to form flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust; usually on the child’s trunk

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42
Q
A

Bullous impetigo

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43
Q

Causes of Staph toxic shock

A

Toxin mediated/superantigen from tampons, nasal packing to stop bleeds, post op infections

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44
Q

Staph aureus TSS pathogenesis

A

Toxic shock syndrome toxin enters blood stream and stimulates release of large amounts of IL-1, IL-2, and TNF; blood cultures will be negative becasue the syndrome is caused by the toxin not the bacteria

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45
Q

Clinical presentation of staph TSS

A

Fever, hypotension, dizziness/syncope, diffure macular erthroderma that desquamates in 1-2 weeks after onset, V/D, severe myalgias with CPK elevation, renal failure, transaminits or hyperbilirubinemia, thrombocytopenia, AMS

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46
Q

Treatment options for MRSA

A

Vancomycin, Ceftaroline, Linezolid, Daptomycin, Bactrim/Clinda(mild)

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47
Q

Treatment options for MSSA

A

produces beta lactamase so resistant to some beta lactams; use Nafcillin/oxacillin, Cefazolin, Ceftriaxone, Cefepime, Ceftaroline, Vancomycin, Augmentin (mild)

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48
Q

VISA/VRSA treatment options

A

Daptomycin, Linezolid, Ceftaroline

49
Q

MRSA resistance mechanism

A

changes in PBP in their cell membranes; MecA genes on the bacterial chromosome encode these altered PBPs

50
Q

Resistance mechanism of VRSA

A

genes encode enzymes that substitute D-lactate for D-alanine in the peptidoglycan cell wall

51
Q

Resistance mechanism of VISA

A

Due to the synthesis of an unusually thickened cell wall

52
Q

Supportive treatment for TSS

A

Extensive fluid suppression (10-20L/day) and vasopressors (dopamine and NE)

53
Q

Surgical treatment of TSS

A

remove causative agent; if patient is post-surgical, surgical wounds must be explored and debrided

54
Q

Antibiotics for TSS

A

Vanc/Oxacillin plus Clindamycin

55
Q

Why Clindamycin is used in treatment of TSS

A

Clinda suppresses protein synthesis and therefore toxin synthesis; other antibiotics may suppress toxin synthesis too, such as Linezolid

56
Q

Prevention of Staph Aureus

A

For surgery: peri-operative Cefazolin and Vanc if high rate within population

Intranasal mupirocin to reduce colonization with Hibiclens for bathing +/- milds ABX (Doxy, Bactrim)

57
Q

Staph aureus micro properties

A

Catalase positive, coagulase positive, beta hemolytic, ferments mannitol

58
Q

Micro properties of Staph epi

A

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

59
Q

Micro properties of Staph Saprophyticus

A

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

60
Q

How is coagulase test done

A

with rabbit plasma

61
Q

Most common setting of staph epi infections

A

usually in the context of a foreign device implant (heart valve, hip), due to organisms on implant

62
Q

Pathogenesis of staph epi

A

Bacterial adherence - adhesins interact with host proteins that cover the prosthetic such as fibringoen and fibronectin; after attachement extracellular polysaccharide matrix or slime is produced which encases the bacteria creating a biofilm

63
Q

Treatment options for Staph epi

A

Vancomycin, (Oxacillin/Nafcillin if MSSE), Rifampin or Gentamicin can be added especially for prosthetic valve endocarditis (high resistance to Gent limits use); remove the device

64
Q

Staph saprophyticus presentation

A

2nd most common CA-UTI in women; most have had sex within previous 2-4 hours

65
Q

Treatment of S. saprophyticus

A

Bactrim or Cipro

66
Q

General characteristics of streptococci

A

Spherical GPCs arranged in pairs or chains; catalase negative, distinguished from each other based on hemolysis

67
Q

How group A strep causes disease

A

Pyogenic inflammation, exotoxin production, immunologic

68
Q

Method of diagnosing strep throat (GAS phayngitis)

A

Rapid antigen test

69
Q

How rapid strep antigen test works

A

high specificity, low sensitivity; takes ~10 min; anitgens are extracted from throat swab and reacted with antibody bound to latex particles; agglutination of latex particles occurs if GAS is present. If high suspicion and negative rapid test, do throat culture

70
Q

What does alpha hemolysis look like

A

green zone around colonies as result of incomplete lysis of RBCs

71
Q

What does beta hemolysis look like

A

clear zone around colonies due to complete lysis of RBCs

72
Q

What does gamma hemolysis look like

A

No lysis of RBCs

73
Q

Streptolysin O

A

hemolysin; oxygen labile; causes beta-hemolysis only when colonies grow under surface of blood agar plate; this is what antibodies exist after infection

74
Q

Streptolysin S

A

hemolysin, oxygen stable; causes beta-hemolysis on surface of plate

75
Q

M Protein

A

antiphagocytic VF of GAS; protrudes from outer surface of cell and interferes with ingestion by phagocytes; 80 serotypes

76
Q

GAS Polysaccharide capsule

A

antiphagocytic VF; it is made of Hyaluronic acid which is a native compound to humans so no antigens are formed against it.

77
Q

Hyaluronidase

A

GAS VF; degrades hyaluronic acid (in subcu tissue); known as spreading factor - facilitates spread of GAS in cellulitis/other skin infections

78
Q

Streptokinase

A

GAS VF; activates plasminogen to from plasmin which dissocles fibrin in clots, thrombi, and emboli; role in GAS infections is unclear

79
Q

DNase (streptodornase)

A

GAS VF; degrades DNA in exudates/necrotic tissue; protect the bacteria from being trapped in neutrophil extracellular traps (NETs)

80
Q

C5a peptidase

A

GAS VF; cleaves C5a produced by the complement system; minimizes influx of neutrophils early in infection

81
Q

Streptococcal chemokine protease

A

GAS VF; prevents migration of neutrophils into site of infection by degrading chemokine IL-8 which would recruit neutrophils to site

82
Q

Potential complications of untreated GAS pharyngitis

A

otitis media, sinusitis, mastoiditis, meningitis, peritonsillar/retropharyngeal abscess, rheumatic fever

83
Q

GAS Treatment

A

Oral Penicillin V, Amoxicillin, or Cephalexin (twice daily for 10 days); if Pen allergy - Azithromycin (Zpack), Clarithromycin (2x10days), Clindamycin (3x10days)

84
Q

Skin/soft tissue infections GAS

A

Erysipelas (rash across cheeks and nasal bridege), Impetigo, Cellulitis

85
Q

Erythrogenic toxin

A

GAS toxin; responsible for rash of scarlet fever, acts as superantigen

86
Q

Pyrogenic exotoxin A

A

GAS toxin; causes most cases of TSS. Superantigen - causes release of large amounts of cytokines

87
Q

Exotoxin B

A

GAS toxin; protease that rapidly destroys tissue and is produced in large amounts by the “flesh eating” strains of GAS that cause necrotizing fasciitis

88
Q

Clinical scenario for GAS TSS

A

In setting of GAS infection (most common entry points are skin, vagina, pharynx) or at site of minor trauma who develop skin infections within 3days; diffuse erythema, fever, chills, myalgia, n/v/d, hypothermia, hypotension, AMS

89
Q

Complications of GAS TSS

A

DIC, AKI, ARDS, puerperal sepsis, endometritis

90
Q

Diagnosis of GAS TSS

A

isolation of GAS from normally sterile site (blood, CSF, tissue biopsy) and hypotension plus other organ involvement

91
Q

Treatment of GAS TSS

A

Penicillin plus Clindamycin

92
Q

Post strep glomerulnephritis

A

caused by nephritogenic strains of GAS, frequently after skin infections; Ag-ab complex form against GBM; present with HTN, facial edema, LE edema, dark urine; early treatment does not stop it and most cases resolve completely

93
Q

Acute rheumatic fever

A

2 weeks after GAS pharyngitis, caused by rheumatogenic strain; antibodies against GAS proteins cross-react with host antigens

94
Q

Diagnosis of Rheumatic fever

A

polyarthritis, carditis, nodules, erythema marginatum, syndenham chorea (neuro disorder consisting of abrupt involuntary movements); ASO titer

95
Q

Treatment of Rheumatic Fever

A

Full course of anitbiotics to eradicate any residual GAS; then prevent further infections with prophylaxis (penicillin IM monthly for many years)

96
Q

Peptostreptococcus

A

anaerobe, members of normal flora of gut, mouth, female genital trac; commonly found in mixed anaerobic infections

97
Q

Treatment of peptostreptococcus

A

Penicillin

98
Q

Group D Strep

A

Hydrolyze esculin in presence of bile (produce black pigment on bile-esculin agar); includes Enterococcus sp, and Strep Bovis

99
Q

Enterococcus faecalis/faecium

A

can grow in hypertonic saline or in bile; low virulence; VF include capsule and enzymes that injure host tissue; part of normal colonic flora; cause hospital acquired UTIs, bactermeia, and endocarditis

100
Q

Treatment of Enterococcus faecalis/faecium

A

combination antibiotic therapy required - PCN/Vanc depending on resistance and aminoglycoside

101
Q

VRE

A

Most likely enterococcus faecium; treat with Linezolid or Daptomycin

102
Q

Streptoccocus bovis

A

causes endocarditis in patients with colon cancer (very strong association); will not grow in hypertonic saline

103
Q

Treatment of strep bovis

A

PCN, Ceftriaxone, or Vancomycin

104
Q

Mechanism of resistance for VRE

A

genes encode enzymes that substitute D-lactate for D-alanine in peptidoglycan

105
Q

Streptococcus agalactiae micro

A

GBS; narrow zone of beta hemolysis; lack of hydrolysis of bile esculin agar; hydrolyzes hippurate; Bacitracin resistant (GAS is sensitive); CAMP Test - protein is produced that enhances sheep blood hemolysis in presence of Staph Aureus; organism induces inflammatory response; polysaccharide capsule is antiphagocytic

106
Q

Strep agalactiae clinical scenario

A

Colonizes genital tract of some women; infection acquired in utero or during passage through the vagina; RF - PROM in women colonized, babies born <37wks; children whose mothers lack anitbodies

107
Q

Complications of strep agalactiae

A

neonatal sepsis, meningitis, PNA

108
Q

Clinical setting of strep agalactiae in adults

A

important cause of invasive infections such as septic arthritis, cellulitis, osteomyelitis. Diabetes is main predisposing factor, and breast cancer

109
Q

GBS diagnosis

A

Gram stain/culture; rapid test available in vaginal/rectal samples, detects DNA

110
Q

Treatment of GBS

A

Penicillin/Ampicillin (Vanc if resistant0

111
Q

GBS Prevention

A

screen all pregnant women between 35-37 weeks; administer Pen G/Ampicillin IV at time of delivery if positive

112
Q

Most common cause of subacute bacterial endocarditis

A

Viridans group strep

113
Q

Veridans strep micro characteristics

A

alpha hemolytic, resistant to lysis by bile, optochin resistant

114
Q

Viridans group strep typical locations

A

part of normal flora of mouth and colon; enter blood stream after dental surgery or in patients with cavities/poor dentation

115
Q

Streptococcus mutans

A

Cause of dental caries; synthesizes polysaccharides in dental plaque

116
Q

Pathogenesis of viridans strep

A

no enzymes or exotoxins; can produce glycocalyx allowing for organism to attach to heart valve; can cause brain abscesses, endocarditis, and liver/abdominal abscesses

117
Q

Treatment of viridans strep

A

Penicillin or Ceftriaxone; for endocaridits with intermediate susceptibility to PCN, add Gentamicin

118
Q
A

Dermatological Block (6 decks)

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