Micro Winter 2 Bacteria

Front 1

Staph aureus description (ID features)

Back 1

Gram positive, catalase positive, B-hemolytic, MSA

Front 2

Staph aureus toxins

Back 2

Exfoliative, TSST-1

Front 3

Staph aureus virulence factors

Back 3

Coagulase - clots plasma
Hemolysins - lyse blood cells
Leukocidin - damages membranes
Hyaluronidase - spreading factor
Staphylokinase - dissolves fibrin clots

Front 4

Strep pyogenes description

Back 4

Gram positive cocci
Group A Beta hemolytic (GAS or GABHS)

Front 5

Strep pyogenes toxins

Back 5

Spe - scarlet fever rash

Front 6

Strep pyogenes virulence factors

Back 6

Dnase - reduce viscosity of lysed cells
Hyaluronidase
Streptokinase
M protein - inhibits phagocytosis, cross-reacts with host cells

Front 7

Acne vulgaris pathogenesis

Back 7

- Genetics
- Keratinocyte hyperproliferation due to androgen hormones
- Excess sebum production
- Propionibacterium acnes
- Inflammation due to release of fatty acids, hypersensitivity to bacteria

Front 8

Progression of acne

Back 8

0. Normal hair follicle
1. Closed comedo/white head
2. Open comedo/black head
3. Papule
4. Pustile

3&4 are inflammatory

Front 9

Retinoids

Back 9

- Comedolytic & anti-inflammatory
- Decreaes keratinocyte cohesiveness
- Topical - adapalene, tretinoin
- Systemic - isotretinoin (teratogen!)

Front 10

Antibiotics used in acne

Back 10

- Less resistance when combined with benzoyl peroxide
- Topical - erythromycin, clindamycin
- Systemic - tetracyclines

Front 11

Pseudomonas aeruginosa description

Back 11

Gram negative bacilli
Pyocin & pyoverdin
Ubiquitous, opportunistic

Front 12

Folliculitis caused by S. aureus

Back 12

Barber's itch, sty

Front 13

Folliculitis caused by Psuedomonas

Back 13

Hot tub folliculitis
Systemic component - fever, headache, sore throat, malaise, may be due to LPS

Front 14

Furuncle

Back 14

- Single opening, purulent material, pinpoint
- S. aureus
- Involves skin and subcutaneous tissues
- Neck, axilla, buttocks

Front 15

Carbuncle

Back 15

- Aggregate of furuncles
- Neck, back, thighs
- S. Aureus

Front 16

Treatment of furuncles and carbuncles

Back 16

- Warm compress
- Incision and drainage
- Antimicrobials
- Recurrent - mupriocin

Front 17

Pyoderma

Back 17

Spreading bacterial skin inflammation marked by pus-filled lesions, confined to epidermis and dermis

Front 18

Nonbullous impetigo

Back 18

- S. aureus or GAS
- Vesicles/pustules
- Spreads rapidly via autoinoculation
- Children <6
- Exposed areas - face, arms, legs

Front 19

Bullous impetigo

Back 19

- S. aureus - exfoliative toxin producing strains
- Thin white blisters (intraepidermal)
- Children <2
- Face and legs

Front 20

Ecthyma

Back 20

- GAS
- Ulcerative pyoderma
- Extends into dermis
- Green-yellow crust, raised with induration
- Untreated impetigo
- Lower extremities

Front 21

Ecthyma & impetigo treatment

Back 21

- Personal hygeine
- Debridement
- Mupirocin
- Systemic abx - cephalosporin, penicillin OR B-lactam/lactamase inhibitor

Front 22

Cellulitis

Back 22

Non-necrotizing inflammation of dermis and hypodermis
Heat, erythema, edema, tenderness
"orange peel"

Front 23

Most common cellulitis pathogens

Back 23

GAS (post-operative) and S. aureus (doesn't spread as fast)

Front 24

Acinetobacter baumannii

Back 24

Aerobic, gram-negative coccobacilli
Hospital-acquired cellulitis
Assoc. w/ invasive devices and trauma
Multi-drug resistant

Front 25

Pasteurella multocida

Back 25

Cellulitis assoc. w/cat & dog bites
Purulent drainage

Front 26

Cellulitis assoc. w/water

Back 26

Aeromonas hydrophilia, Legionella spp., Vibrio vulnificus

Front 27

Creptiant cellulitis

Back 27

Gas accumulation in tissue due to anaerobic metabolism
Clostridium spp, Bacteroides, Prevotella, Peptostreptococcus, Peptococcus

Front 28

Erysipelas

Back 28

- Pathogens - GAS and staph aureus (rare)
- Special form of cellulitis but with: prodrome, induration, sharp borders, lymphangitis, and desquamation

Front 29

Treatment of cellulitis, erysipelas and folliculitis

Back 29

Penicillins

Front 30

Type 1 necrotizing fasciitis definition/risk factors

Back 30

- Polymicrobic (4-6 organisms) - damage from synergistic activity of anaerobe and aerobe
- Trunk, abdomen, perineum
- Risk factors - trauma, surgery, diabetes

Front 31

Type 1 necrotizing fasciitis microbes

Back 31

Facultative anaerobes - S. aureus, E.coli, Psuedomonas, Strep milleri, GAS, vibrio vulnificus

Anaerobes - Bacterioides fragilis, clostridium, peptostreptococcus, prevotella

**Normal flora

Front 32

Type 2 necrotizing fasciitis definition/risk factors

Back 32

- Monomicrobic: GABHS M-proteins 1&3
- Can follow blunt trauma, bug bite, chicken pox, IVDA, surgery
- 50% cases occur with STSS
- Risk factors - often immunocompetent, or NO significant past medical history

Front 33

Necrotizing fasciitis clinical manifestations

Back 33

- Pain out of proportion, then cutaneous anesthesia
- Hard wood feel of tissue
- Erythema: red-purple-blue
- Systemic toxicity
- Detection of gas in soft tissue (type 1)
- Putrid odor with anaerobic pathogen

Front 34

Type 1&2 necrotizing fasciitis treatment

Back 34

Ampicillin, clindamycin or metronidazole

Front 35

MRSA treatment

Back 35

Vancomycin

Front 36

Necrotizing fasciitis complications

Back 36

- 70-80% mortality
- Bacteremia
- TSS
- DIC
- Endotoxin shock
- Cutaneous gangrene and myonecrosis

Front 37

Spontaneous gangrenous myositis microbe

Back 37

GAS

Front 38

Spontaneous gangrenous myositis clinical manifestations

Back 38

Similar to necrotizing fasciitis
Rapid development - systemic toxicity, STSS, contiguous muscles
NO gas formation

Front 39

Spontaneous gangrenous myositis epidemiology

Back 39

Entry though abrasions and blunt trauma
Male = female
All age groups of healthy patients
Risk factors - NSAIDs delay diagnosis, Vimentin upregulated in injured muscle

Front 40

Spontaneous gangrenous myositis diagnosis

Back 40

Surgery - histopathology
- Infiltration of granulocytes
- Gram positive streptococci

Front 41

Spontaneous gangrenous myositis treatment

Back 41

Agressive debridement, poss. amputation
Clindamycin

Front 42

Clostridial Gangrene microbes

Back 42

Perfringens or Septicum

Front 43

Clostridial gangrene pathogenesis

Back 43

- Direct innoculation of wound via trauma/surgery
- Hematogenous spread from GI tract
- Toxins - alpha, theta, kappa
- Clostridium has fast doubling rate
- H2 gas production
- Oxygen depletion
- Extremities and trunk

Front 44

Alpha toxin/phospholipase C

Back 44

- C. perfingens
- Lyses RBCs, monocytes, fibroblasts, platelets, leukocytes
- Negative inotropic effect
- Triggers histamine release, platelet aggregation, thrombus formation

Front 45

Theta toxin

Back 45

- Perfringolysin
- Causes direct vascular injury, cytolysis, hemolysis
- PMN destruction

Front 46

Kappa toxin

Back 46

Collagenase - facilitates rapid spread

Front 47

Clostridal gangrene diagnosis

Back 47

- "Sweet mousy smell" - C. perfringens
- Toxemia, tachycardia, fever, shock
- Gas pockets - not neccessarily due to clostridium
- Crepitation
- Gram-positive culture
- NO inflammatory cells

Front 48

Scalded skin syndrome pathogen

Back 48

Staph aureus

Front 49

Staphylococcal Scalded skin Syndrome toxins

Back 49

Epidermolytic toxins - both serine proteases, superantigens
ET-A (chromosome)
ET-B (plasmid)

Front 50

Epidermolytic toxin (ET-A, ET-B) action

Back 50

- Cleave desmoglein-1 - component of desmosomes that mediates keratinocyte adhesion
- Produce intraepidermal splitting of tissue & necrosis

Front 51

Staphylococcal Scalded skin Syndrome epidemiology

Back 51

- Rare
- Children <5yr esp. neonates (most common)
- Adults >65 (high mortality rate)
- Immunocompromised
- Renal failure

Front 52

Staphylococcal Scalded skin Syndrome disease progression

Back 52

- Site of infection - oral/nasal cavities, throat, umbillicus, conjuctiva
- Early stage - fever, irritability, faint blanching rash
- Acute stage - Large blisters form, hyperemic mucous membranes, Nikolsky's sign (epidermal separation with pressure), desaquamation, conjuctivitis
- Decline stage- heals without scaring, adults freq. have bacteremia/pneumonia

Front 53

Staphylococcal Scalded skin Syndrome diagnosis

Back 53

- Culture and biopsy
- Toxin ID by ELISA or latex agluttination

Front 54

Staphylococcal Scalded skin Syndrome treatment

Back 54

- Nafcillin or oxacillin
- Emollients, fluids

Front 55

Toxic shock syndrome organisms

Back 55

Staphylococcus (TSS) and Streptococcus (STSS)

Front 56

Why tampons cause TSS

Back 56

- Increase pO2 of vagina
- Supply surfactant
- Bind magnesium

Front 57

Sites of infection of TSS

Back 57

- Menstration assoc.
- Postpartum
- Surgical wounds
- Sinusitis, arthritis, etc.
- Children - cuts

Front 58

TSS toxins

Back 58

TSST-1 (most common)
SEB and SEA (staphylococcal enterotoxin)

Front 59

STSS toxins

Back 59

Streptococcal pyrogenic exotoxins:
SPEA (primary), SPEB, SPEC

Front 60

STSS & TSS epidemiology

Back 60

- Yound adults, esp. menstruating women

Front 61

TSS predispositions

Back 61

- Cellulitis
- Influenza
- Sinusitis
- Tracheitis
- IVDA
- HIV
- Post-operative infection
- Gynecological infection

Front 62

STSS predispositions

Back 62

- Same as type II necrotizing fasciitis (co-occurs in 50%)
- Streptococcal myositis

Front 63

TSS diagnosis

Back 63

1. Fever
2. Rash
3. Desquamation
4. Hypotension
5. Multisystem involvement (3) - vomitting, diarrhea, myalgia, mucous membrane hyperemia, renal/liver damage, thrombocytopenia, disorientation/confusion

* Negative serology for rocky mountain fever, leptospirosis, measles, negative CSF/blood cultures (blood may have S aureus)

Front 64

STSS diagnosis

Back 64

Same as TSS but only need 2 multisystem involvements, may have DIC, ARDS, soft-tissue necrosis
* Lab isolation of GAS

Front 65

TSS & STSS treatment

Back 65

- Oxygen, fluids, IVIG
- Clindamycin

Front 66

Anaerobic bacteria characteristics

Back 66

- Predominant part of normal flora
- Can tolerate 2-8 % oxygen
- Use fermentation or anaerobic metabolism
- No detoxifying enzymes - SOD, catalase, peroxidase
- Prefer acidic conditions and low oxygen tissue
- Putrid odor

Front 67

Usual source of anaerobic infection

Back 67

Endogenous - our own flora

Front 68

Anaerobic bacterium in this unit

Back 68

Peptostreptococcus (Gram +)

(Gram -)
Bacteroides
Prevotella
Porphyromonas
Fusobacterium

Front 69

Bacteroides fragilis characteristics

Back 69

- Bile-resistant
- Gram neg bacillus
- Encapsulated
- Non-fastidious
- LPS does not contain Lipid A
- Most common anaerobic pathogen

Front 70

Bacteroides fragilis virulence factors

Back 70

- Capsule - antiphagocytic, stimulates abscess formation, inhibits macrophage migration
- Fimbrae - adhesion
- B-lactamase
- SOD & catalase - EXCEPTION
- Succinic acid - inhibits neutrophils
- IgA protease
- Extracellular enzymes that promote abscess formation - collagenase, fibrinolysin, hyaluronidase, heparinase

Front 71

Bacteroides fragilis pathogenesis

Back 71

- Non invasive, endogenous infection
- Displaced by trauma, disease state
- Can cause localized abscess in colon, rupture and cause peritonitis, hematogenous spread to other organs

Front 72

Bacteroides fragilis clinical & treatment

Back 72

- Acute abdominal pain
- Drain abscess
- Debridement of necrotic tissue
- Metronidazole, clindamycin, or B-lactam w/B-lactam inhibitor

Front 73

Porphyromonas & prevotella characteristics

Back 73

- Gram negative, encapsulated
- LPS = strong exotoxin
- Normal oral flora, GI&GU

Front 74

Porphyromonas clincal manifestations

Back 74

- Gingival & tooth infections
- Isolated from other infections - axillary, perianal, etc.

Front 75

Prevotella clinical manifestations

Back 75

P. melaninogenica -URI
P. bivia & disiens - femal GU

Front 76

Fusobacterium characteristics

Back 76

- Gram neg
- Fusiform = cigar-shaped
- Normal flora of oral cavity
- Produces sulfur and methylmercaptan (halitosis)

Front 77

Fusobacterium clinical manifestations

Back 77

- Trenchmouth
- Noma - gangrenous infection of face
- Osteomyelitis (monomicrobic)

Front 78

Peptostreptococcus characteristics

Back 78

- Only gram pos. anaerobic pathogen
- Normal flora of mouth, GI, GU

Front 79

Peptostreptococcus clinical manifestations

Back 79

- Aspiration pneumonia
- Brain abscesses
- GI and wound infections

Front 80

Clues for diganosing anaerobic infections

Back 80

- Foul or sickly sweet smelling discharge
- Mucosal surface infection
- Gas production
- Severe necrosis
- Gram stain shows polymicrobic infection
- Many antibiotics ineffective

Front 81

What makes a person more susceptible to TSS?

Back 81

No antibodies to toxin, may be genetic

Front 82

What antibiotics are ineffective in anaerobic infections?

Back 82

Aminoglycosides
Sulfa drugs
Penicillin

Front 83

What antibiotics are effective in anaerobic infections?

Back 83

Clindamycin, metronidazole
Combination therapy is best

Front 84

B-lactams are used in

Back 84

Impetigo, fasciitis (all), SSSS

Front 85

Clindamycin is used in

Back 85

Fasciitis, myositis, TSS, STTS, anaerobic infections

Front 86

Infections caused by strep pyogenes

Back 86

Ecthyma
Cellulitis*
Erysipelas*
Type 1 necrotizing fasciitis
Spontaneous gangrenous myositis
STSS

Front 87

Infections caused by staph aureus

Back 87

Folliculitis
Furuncle/carbuncle
Impetigo*
Bullous impetigo
Type II NF*
Scalded skin syndrome (SSSS)
TSS

Front 88

NSAIDs should be avoided in

Back 88

Cellulitis, myositis