Bac of skin, soft tissue, bone, and joint Flashcards

1
Q

Risk organisms for Diabetes mellitus

A

Staph aureus

Group B strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk organisms for neutropenia

A

pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Risk organisms for IV drug abuse:

A

MRSA

pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Risk organisms for hottubs

A

pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Impetigo - organism, what/where is it,

A

-srep pyogenes > Staph aureus
-most superficial of bacterial skin infections
causes honey crusts, bullae (Blisters) and erosions –> Small vesicles lead to pustules which crust over (“honeycrusts”)
-AROUND MOUTH
-most frequent bacterial skin inf in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

most frequent bacterial skin inf in chldren?

A

impetigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bullous Impetigo - organism, what/where is it,

A
  • staph aureus
  • Blisters are initially filled with cloudy fluid and later rupture, resulting in erosions and crusting
  • blister fluid has s aureus in it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ecthyma - organism, what/where is it,

A
  • -srep pyogenes > Staph aureus
  • Ecthyma is a slightly deeper form of impetigo with resultant scarring and ulceration
  • Causes punched-out ulcerative lesions**
  • may result from neglected or inadequately treated impetigo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Furuncle/Boi - organism, what/where is it,

A
  • Staph aureus
  • Deep-seated infection (abscess) involving the entire hair follicle and adjacent subcutaneous tissue
  • Large, painful, raised nodules that have an underlying collection of dead and necrotic tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Carbuncle - organism, what/where is it,

A
  • S. aureus Lesions
  • Multiple furuncles/boils can coalesce and extend into deeper subcutaneous tissue
  • Defining feature is that patients present with chills and fevers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

defining feature of carbuncle?

A

CHILLS AND FEVERS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Folliculitis - organism, what/where is it

A
  • Infection of the hair follicle

- Multiple species of bacteria have been implicated, as well as fungal organisms. (pseudomonas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Erysipelas - organism, what/where is it

A
  • S. pyogenes
  • Acute infection of skin - superficial
  • Inflammation (warmth)
  • Lymph node enlargement
  • Chills, fevers
  • -Involved skin is distinct from uninvolved skin*
  • Usually preceded by respiratory or skin S. pyogenes infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cellulitis - organism, what/where is it

A
  • S. pyogenes > S. aureus ( also GAS, pasturella multicoida, vibrio vulnificus)
  • Involves skin and deeper subcutaneous tissue
  • Local inflammation and systemic symptoms (ex. fever)
  • -Involved versus uninvolved tissue is unclear*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Paronychia - organism, what/where is it

A
  • S. aureus > S. pyogenes
  • Localized, superficial infection or abscess of the nailfolds
  • Most common infection of the hand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute paronychia - presentation, organism

A
  • usually presents as an acutely painful abscess in the nailfold
  • most commonly caused by S. aureus, followed by streptococci and Pseudomonas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chronic paronychia - presentation, organism

A
  • defined as being present for longer than 6 weeks’ duration

- Often results from C. albicans infection. More difficult to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Necrotizing fasciitis - organism, what/where is it

A
  • S. pyogenes > C. perfringens, mixed anaerobes, S. aureus
  • Acute infection of subcutaneous tissue
  • Diffuse redness, due to deep tissue involvement
  • Destruction of muscle and fat
  • Cellulitis, followed by bullae (blister) and gangrene
  • Toxicity, multi organ failure, and death are the hallmarks of this disease; thus prompt medical intervention is necessary to save the patient
  • Antibiotics and surgical debridement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

3 common bacteria that cause SSTI?

A

Staph aureus
strep pyogenes
pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Staphylococci - organism details

A
  • Gram +, facultative anaerobe, form grape-like clusters
  • Catalase + (unlike Strep)= Breaks down H2O2 to H2O and O2
  • Non flagellate, non-motile, non-spore forming
  • Found in skin and mucus membranes of humans
21
Q

S. aureus - spread? and cause what?

A
  • person to person, direct contact or exposure to contaminated fomites
  • -Nasal shedding*
  • skin infections, sepsis, endocarditis, pneumonia, osteomyelitis, septic arthritis, purulent meningitis, food poisoning, toxic shock
22
Q

S aureus on plates color and hemolysis?

A
  • White or golden

- Beta hemo

23
Q

S. aureus virulence factors

A
  • Structural: Capsule, biofilm, peptidoglycan, teichoic acid, protein A
  • Toxins: Cytotoxins (alpha, beta, delta, gamma), exfoliative toxins, enterotoxins, toxic shock syndrome toxin
  • Enzymes: Extracellular hydrolases
24
Q

S. aureus - purpose of capsule?

A
  • structural virulence factor
  • anti-phagocytic
  • Slime layer/biofilm: facilitates adherence to foreign bodies (catheters, prosthetic valves and joints), anti-phagocytic
25
Q

S. aureus - purpose of Peptidoglycan

A

-structural virulence factor

endotoxin like activity

26
Q

S. aureus - purpose of teichoic acid

A
  • structural virulence factor

- adhesion

27
Q

S. aureus - purpose of protein A

A
  • structural virulence factor
  • inhibits antibody mediated clearance by binding to IgG Fc domain –> the antibody cant communicate with the ijmmune system without Fc region
28
Q

S. aureus - virulence factor - toxins:

A

-Cytotoxins: Alpha (pore forming toxin), beta, delta, gamma, P-V leukocidin; Toxic for many cells, including leukocytes, erythrocytes, fibroblasts, macrophages, and platelets (LEADS TO NECROSIS)
-Exfoliative toxins: Two forms: ETA and ETB
Serine proteases that split the intraepidermal junctions; Mediates Staphylococcal scalded skin syndrome (SSSS) (LEADS TO BLISTERS)
-Enterotoxins: Superantigens (enterotoxin A (most common), B, C, D); Associated with development of food poisoning (insensitive to heat and gastric enzymes)
-Toxic shock syndrome toxin-1: Superantigen associated with toxic shock syndrome

29
Q

S. aureus - virulence factor - enzymes

A
  • Coagulase: Converts fibrinogen to fibrin (may wall off and protect bacteria)
  • *-A variety of enzymes can hydrolyze host tissue to aid in spread of S. aureus throughout the body**
  • Hyaluronidase: Hydrolyzes hyaluronic acids in connective tissue, promoting the spread of staphylococci in tissue
  • Fibrinolysin: Dissolves fibrin clots
  • Lipases: Hydrolyzes lipids
  • Nucleases: Hydrolyzes DNA
30
Q

S. aureus TOXIN MEDIATED diseases

A

Scalded skin syndrome

31
Q

S. aureus SUPPURATIVE diseases

A
Osteomyelitis
Septic arthritis
Impetigo
Folliculitis
Furuncles or boils
Carbuncles
32
Q

Staphylococcal Scalded Skin Syndrome (SSSS) - affects who most often? what causes?

A
  • neonates (High recovery) and immunodef (highly lethal)
  • Exfoliative toxin (ETA or ETB) cause exfoliation of superficial layers of skin (no scarring) Serine proteases that split the intraepidermal junctions; Mediates Staphylococcal scalded skin syndrome (SSSS) (LEADS TO BLISTERS)
33
Q

Staphylococcal Scalded Skin Syndrome (SSSS) - two important diagnostic features?

A
  • non-cultureable from skin –> no staph in blisters but bc its toxin but staph is in the nose or pharynx or soemthing
  • no leukocytes
34
Q

S. aureus - SSSS - exfoliatiative toxins:

A
  • serine proteases that split desmoglein-1 (desmoglein 1 forms intercellular bridges in the stratum granulosum epidermis)
  • neutralizing antibodies develop to resolve the toxic proces!!!**
35
Q

SSSS - disease progression

A
  • three phases: initial (erythroderma), exfoliative, and desquamative (recovery).
  • initial: redness around nose or mouth
  • exfoliative stage begins on the second day of the illness. The erythematous skin wrinkles and peels off at sites of minor trauma or with minimal lateral pressure by the examiner’s fingertip, illustrating the presence of Nikolsky sign
  • NEXT: fluid-filled bullae –> rupture and result in scalded skin appearance
  • NEXT: skin desquamates, leaving normal skin in 7 to 10 days
36
Q

SSSS - disease management/treatment:

A
  • fluid resuscitation,
  • correction of electrolyte abnormalities,
  • identification and treatment of the source of the toxigenic Staphylococcus with oxacillin or vancomycin
37
Q

SSSS - diagnosis:

A
  • disease presentation

- biopsy = cleavge plane in the upper epidermis

38
Q

Staph aureus - food poisoning - most common foods? symptoms?

A
  • processed meats, custard filled pastries, potato salad, ice cream
  • abrupt onset, short lived (24 hrs)
39
Q

toxic shock syndrome - causative organism? symptoms?

A
  • staph aureus
  • pharyngitis, vaginitis, vomiting, watery diarrhea, febrile, hypotensive, diffuse erythematous rash over entire body
  • peeling of palms and soles by 14th day
40
Q

toxic shock syndrome - how disease occurs?

A

-staph aureus invades local site and produces TSST1 toxin which is absorbed into body

41
Q

Localized cutaneous pyogenic staphylococcal infections of staph aureus?

A

impetigo
folliculitis
furuncles or boils

42
Q

Treatment of cutaneous infections

A
  • staph usually cant infect immunocompetent indiv unless stitches, splinter…etc
  • wound needs to be opened and foreign matter needs to be removed
  • can use
43
Q

MRSA: Methicillin-resistant Staphylococcus aureus - how are they so resistant?

A
  • MecA gene acquired on a mobile genetic element (PRETTY MUCH: EASY TO SPREAD RESISTANCE) is a PBP: penicillin binding protein that binds methicillin and related penicillins and cephalosporins NAFICILLIN OR OXACILLIN)
  • Resistant to beta-lactams (usually by plasmid exchange) and other antibiotics
44
Q

MRSA: Methicillin-resistant Staphylococcus aureus - most common infections?

A

skin infections

45
Q

MRSA: Methicillin-resistant Staphylococcus aureus - treatment??

A

vancomycin

46
Q

s. aureus treatment?

A

-Superficial lesions resolve
-Extensive lesions require drainage plus antibiotics
-Penicillinase-resistant penicillin (methicillin, NAFCILLIN, OXACILLIN) +/- aminoglycoside MRSA –>is a problem here… resistant to all Beta-lactams
For MRSA or hypersensitivities… clindamycin, vancomycin, erythromycin

47
Q

Osteomyelitis - symptoms, and associated with what kind of infection? organism

A
  • bone pain, fever, swelling malaise (cant walk well or arm hurts without visible issue)
  • bacterial infections –>staph aureus
48
Q

Septic arthritis - primary organism? where affects?

A
  • painful erythematous joint
  • usually in large joints..shoulder, knee, hip, elbow
  • staph aureus common in chidren and adults receiving intraarticular injections of who have mechanically abnormal joints
  • Neisseria gonorrhoeae is the most common cause in sexually active persons