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micro 8 > Bac of Skin, soft tissue, bone, and joint 2 > Flashcards

Bac of Skin, soft tissue, bone, and joint 2 Flashcards

1
Q

Streptococcus - organism details:

A
  • Gram positive cocci typically arranged in chains or pairs
  • Aerobic and facultative anaerobic (i.e. can switch to anaerobic respiration)
  • Culture typically on blood agar to determine hemolysis
  • Catalase negative (unlike Staph.)
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2
Q

α-hemolysis:

A

yields a dark and greenish appearance due to chemical change in the hemoglobin in the red cells

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3
Q

β-hemolysis:

A

complete hemolysis of blood around and under colony

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4
Q

γ-hemolysis:

A

no color change or lysis

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5
Q

Lancefield antigens

A

Distinct carbohydrate structures derived from cell wall extracts used to define species of Strep (primarily β- hemolytic) into groups A through U

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6
Q

group A strep=

A

pyogenes

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7
Q

group B strep=

A

agalactiae

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8
Q

organism SENSITIVE to Bacitracin?

A

Strep pyogenes - Group A strep

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9
Q

transient colonization of Group A strep where?

A

URT and skin surface

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10
Q

Group A strep Virulence factor - capsule:

A

hyaluronic acid capsule is a poor immunogen and interferes with phagocytosis (looks like our own stuff)

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11
Q

Group A strep Virulence factor -Adhesins

A
  • Pili/fimbrae
  • LTA: involved in adhering to fibronectin on epithelial cell surface
  • Protein F and M protein are involved in invasion of epithelial cell
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12
Q

Group A strep Virulence factor - m-protein

A
  • myosin-like
  • Binds many host molecules to facilitate cell invasion (fibrinogen, Ig, factor H) –> Inhibits complement activation
  • variable N-terminus which defines the serotype
  • Associated with virulent strains/invasion of epithelium
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13
Q

Group A strep Virulence factor -Toxins

A
  • Streptolysin O and Streptolysin S == Pore forming toxins

- Strep Super Antigens (SAgs) - Increase proinflammatory cytokine production= pyogenic results

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14
Q

pyoderma (impetigo) distinguishing feature?

A

-often seen aroudn the mouth = honeycrusts

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15
Q

erysipelas - distinguishing feature?

A

-lesion is distinct from surroudning skin (USUALLY CAUSED BY STREP PYOGENES)

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16
Q

cellulitis (inflammation) - distinguishing feature?

A

-lesion IS NOT distinct from surrounding skin

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17
Q

most common superficial skin infection in children? organism?

A
  • Impetigo - vesicles turn into pustules into honeycrust appearance
  • usually Strep pyogenes
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18
Q

bullous impetigo is due to? how is this distinguished from other similar disease presentations from other organisms?

A
  • Staph aureus
  • distinguished from typical streptococcal infection by more extensive, bullous lesions that break down and leave thin paper-like crusts instead of the thick amber crusts of streptococcal impetigo (blisters = exfoliative toxin)
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19
Q

Necrotizing fasciitis - most common organism? key symptoms?

A
  • group A strep = pyogenes

- starts out as not painful and looks slightly red but pain and tenderness become severe!

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20
Q

pain and tenderness is usually not very severe in which condition? In which condition is pain and tenderness very severe?

A

NOT-cellulitis

YES-necrotizing fasciitis

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21
Q

Necrotizing fasciitis - treatment?

A
  • remove the dead tissue and then skin graft

- antibiotis to help - broad spectrum

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22
Q

Glomerulonephritis - causative organism where? how does it happen?

A
  • group A strep BOTH PHARYNGEAL AND CUTANEOUS –> the kidney issues start after the pharyngeal/cutaneous
  • type 3 hypersensitivity = immune complexes get stuck in kidney and that damaging stuff
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23
Q

Acute poststreptococcal glomerulonephritis (APSGN) - symptoms:

A
  • hematuria, edema, hypertension, ± oliguria
  • Reduced serum complement (CH50 and C3 –> get used up in the kidney issues)
  • No evidence of systemic disease
  • Recent streptococcal infection (serology or culture)
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24
Q

Streptococcal Toxic Shock Syndrome - caused by and some extra info she bolded…

A
  • pyrogenic exotoxins = SpeA and SpeC
  • most patients with streptococcal disease are bacteremic and many have necrotizing fasciitis.
  • Shock and organ failure (e.g., kidney, lungs, liver, heart)
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25
Q

Streptococcal Toxic Shock Syndrome - Diagnosis, treatment and prevention

A
  • Culture followed by Lancefield grouping…Bacitracin susceptibility predicts group A
  • Direct Ag detection from a swab available but may be inaccurate
  • PCR detection also possible
  • **Anti-Streptolysin O (pore forming toxin) antibodies in serum - ASO test- documents previous exposure
  • PENICILLIN
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26
Q

Pseudomonas aeruginosa - organism details., transmission

A
  • Gram (-), aerobic, motile rod
  • xidase+(distinguishes from Enterobacteriaceae)
  • non-fermenter
  • Hemolytic on blood agar
  • Produces water soluble pigments - pyocanin
  • Antibiotic resistance is common*
  • Minimalist: grows over a wide temperature range (4-42OC)and with minimal nutrition (ammonia and CO2)
  • Primarily a nosocomial infection with many reservoirs: Soil, vegetation, water; Food, cut flowers, sinks, toilets, floor mops, respiratory therapy and dialysis equipment, disinfectant solutions
  • Transmission is by contact, food and water
  • Primarily an opportunistic pathogen (Cystic fibrosis, immunocompromised)
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27
Q

Pseudomonas aeruginosa virulence factors

A
  • Mucoid polysaccharide capsule=alginate
  • Adhesins: Pili, flagella, LPS, alginate
  • Secreted toxins and enzymes:
  • Phospholipase C (hemolysin), collagenase, lipase, elastase, pyocyanin (proinflammatory), pyoverdin (siderophore)
  • Exotoxin A (ETA)–>IMPORTANT FOR SPREAD OF INFECTION: A/B toxin: ExoA inactivates EF-2 via ADP ribosylation (similar to DT)=Blocks protein synthesis
  • Type III secretion system secretes toxins Exoenzyme S and T into target eukaryotic cells leading to cell damage and spread of infection
  • Antibiotic resistance: Mutation of porin proteins
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28
Q

blue green pigment produced===

A

pseudomonas aeruginosa

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29
Q

Pseudomonas aeruginosa - skin and soft tissue infectinos seen in…

A
  • Burn wounds
  • Folliculitis
  • Osteochondritis (inflammation of bone and cartilage) of the foot –> After a penetrating injury (stepping on a nail)
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30
Q

Common cause of otitis externa ‘swimmers ear’

Common cause of eye inf with contaminated contact lens’?

A

pseudomonas aeruginosa

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31
Q

causes pneumonia in immnodeficient or cystic fibrosis patients?

A

pseudomonas aeruginosa –> OPPORTUNISTIC INFECTION

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32
Q

bacterimic/septicemic pseudomaons infection identified by what kind of skin lesion?

A

ecthyma gangrenosum - infection of blood vessels that results in characteristic necrotic lesions

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33
Q

septic patient with skin lesions - organism?

A

pseudomonas

34
Q

hottub and you get pt with little red dots over body areas? treatment?

A
  • Pseudomonas folliculitis

- usually resolves on own in 5 days

35
Q

“Green nails” - major cause, what condition sets up for green naisl? what is it?

A
  • p. aeruginosa
  • candidial paronychia sets up the moist environment needed
  • grows as a biofilm on ventral or dorsal surface
36
Q

chronic paronychia most often casued by?

A

candida

37
Q

Webspace Intertrigo - common cause, presentation, what sets up for this condion? common other issue associated with this?

A
  • Presents as macerated and eroded skin on interdigital toes
  • Pseudomonas is the most common cause.
  • Usually occurs in the setting of excessive moisture
  • usually associated with athletes foot stuff
38
Q

Treatments and prevetion for pseudomonas aeruginosa?

A

treat- lots of antibiotic resistance –> need to do susceptibility testing –> combination therapy (aminoglycosides and Beta lactams
prevent- maintain dry conditions, dont treat with unnecessarry antibiotics, prevent contamination of equipent

39
Q

strep toxic shock syndrome has

A

bacteremia in the blood and wound!

40
Q

staph toxic shock syndrome has

A

ONLY TSST1 - nothing in blood and wound

41
Q

C. perfringens (hemolysin) causes:

A

gangrene, diarrhea/colitis

42
Q

C. difficile causes (enterotoxins)

A

diarrhea/colitis

43
Q

Clostridium perfringens infection/growth is usually associated with …

A

production of hydrogen and carbon dioxide gas

44
Q

C. perfringens Toxins

A
  • 1)-α-toxin is the most important*
  • Produced by all five types (A-E)
  • Phospholipase that hydrolyzes lecithin and sphingomyelin disrupting cell membranes
  • Lyses erythrocytes, platelets, leukocytes and endothelial cells
  • -Mediates massive hemolysis and tissue destruction**
    2) Beta toxin - destroy mucosa
    3) enterotoxin -small intestine stuff
45
Q

Gas Gangrene - organism and most occurs due to?

A
  • C. perfringens Disease
  • traumatic wound and or surgical wounds (especially colon surgery bc its normal flora)
  • –> LOTS OF GAS PRODUCTION
46
Q

differentiate gas gangrene from other necrotizing conditions?

A

-gas gangrene has foul smelling discharge and reddish brown discoloration of the wound

47
Q

C. perfringens treatment/diagnosis

A
  • diag: recognize symptoms, Microscopic detection of gram-positive rods in clinical specimens without leukocytes is useful (BC it kills any cells coming in with alpha toxin)
  • treat: high dose penicillin and demore dead tissue
48
Q

C. tetani - organism details:

A
  • motile, spore forming, Gram (+) rod
  • Strict anaerobe, difficult to culture
  • large terminal spores =drumstick
49
Q

C. perfringens- organism details

A
  • Large Gram (+) rods, non-motile

- Spores are rarely observed

50
Q

C. tetani - disease progression-

A
  • small wound –> entry

- Small local infection provides a source for Tetanospasmin, which makes its way to CNS (retrograde axonal transport)

51
Q

Tetanospasmin**

A

C tetani toxin –> heat labile neurotoxin

  • Inactivates proteins that control release of inhibitory neurotransmitters (glycine and γ-aminobutyric acid) => unregulated excitation
  • Causes spastic paralysis
  • rapidly degraded in GI –> BOTULINUM TOXIN IS NOT!
52
Q

C. tetani - diagnsis/treatment/revention

A
  • immunizaiton w/ 10 yr booster

- metronidazole cleaning of wound and human tetanus immunoglobulin vaccine

53
Q

Mycobacterium - organism details;

A
  • Weakly Gram-positive, strongly acid-fast (BRIGHT PINK), aerobic rods
  • Lipid-rich cell wall
  • crazy cell wall = difficult to treat and long term
  • slow growing
54
Q

M. tuberculosis - organism details and infection issue

A
  • acid fast
  • Slow growing
  • Nonpigmented or light/tan colonies
  • Grow on Löwenstein-Jensen or Middlebrooks media
  • normally pulmonary infection and can disseminate in immuno def
55
Q

M tuberculosis infects what types of cells?

A

livesinside macrophages! –> immune system T-cells wall it off = granuloma

56
Q

M tuberculosis - Treatment and prevention

A

treatm: long term: isoniazid and rifampin, as well as ethambutol, pyrazinamide
prevention: vaccine - useful in children and not adults

57
Q

Mycobacterium leprae organsm and disease details:

A

-acid fast bacteria!
-Human and armadillo reservoir
-Targets macrophages and Schwann cells
-Slow disease process, follows a chronic course, leading to granuloma formation
No classic endo or exotoxins
-Cell Wall: Proinflammatory; phenolic glycolipid I (PGL-1) is a unique antigen
phenolase

58
Q

Mycobacterium leprae - transmission

A

nasal secretions

59
Q

Two distinct stages of leprosy disease

A

1) Tuberculoid=Paucibacillary (containing few bacilli)
2) Lepromatous=Hansen’s Disease
Multibacillary (containing many bacilli)
Chronic disease of the
Skin – dermal macrophages
Peripheral nerves – schwann cells

60
Q

leprosy - people with Tuberculoid (TH1) vs Lepromatous (TH2)

A

TH1 can mount imune response while TH2 cannot

61
Q

Tuberculoid vs Lepromatous

A
  • Lesions: FEW with tuberculoid — MANY with lepromatous (NODULE LIKE)
  • infectivity: low with tuber HIGH with lepro
  • Immune response: DTH reaction to lepromin with tuberculoid. NO reactivity to lepromin Th2) with lepromatous
  • tuber= few or no acid fast rods observed vs lepromatous with numerous acid fast rods in skin lesions
  • lepromatous = generate many antibodies but this doesnt help since intracellular/walled off
62
Q

Lepromin test

A

-intradermal injection with inactivated M. leprae. Differentiates tuberculoid leprosy, in which there is a positive delayed reaction (DTH) at the injection site, from lepromatous leprosy, in which there is no reaction despite the active infection.

63
Q

can you culture M leprae

A

NO

64
Q

M leprae - diagnosis / treatment

A
  • need biopsy, lepromin test
  • Tuberculoid: sulfones (dapsone) and rifampin for 6 months
  • Lepromatous: Dapsone, rifampin, +clofazimine for 12 months
65
Q

Nocardiosis vs Actinomycosis

A
  • Nocardia = Aerobic Gram positive rod, weak acid fast, branched filaments that resemble hyphae, aerial hyphae
  • Actinomia= NOT ACID FAST!
66
Q

weakly acid fast organism?

A

nocardia

67
Q

Mycetoma - what is it ? what casues it? where is it? where is the most common site of infection?

A
  • -Nocardia: Cutaneous infections
  • FOOT MOST COMMON!
  • More frequent in the tropics
  • Slowly progressive, painless
  • begins with minor injury
68
Q

Lymphocutaneous disease -

A
  • -Nocardia: Cutaneous infections
  • Primary infection or secondary spread to cutaneous site characterized by chronic granuloma formation and erythematous subcutaneous nodules, with eventual ulcer formation
69
Q

Cellulitis and subcutaneous abscesses

A

Granulomatous ulcer formation with surrounding erythema but minimal or no involvement of the draining lymph nodes

70
Q

Nocardia: Diagnosis and treatment

A
  • history of working outside!
  • weakly acid fast organism on biopsy
  • grows slow
  • Treat with TMP-SMX
71
Q

Actinomyces israellii - organism details

A
  • filamentous rods
  • looks like teeth/molars
  • normal flora
  • sulfur granules=yellow/orange colonies of organisms resembling grains of sand
72
Q

Actinomyces israellii - assocaited with…

A

DENTAL WORK

73
Q

sulfur granules seen with

A

Actinomyces israellii - seen around the mouth

74
Q

Diagnosis and treatment: Actinomycosis

A
  • culture, and biopsy
  • The lack of staining with modified acid-fast stain separates Actinomyces from Nocardia
  • Treatment: penicillin
75
Q

acne vulgaris-

A
  • Common disorder of the pilosebaceous unit

- Propionibacterium acnes

76
Q

Propionibacterium acnes- casues? organism details

A
  • acne
  • Small, anaerobic, Gram-positive rod
  • common flora
77
Q

Gingivitis is…

A

is the inflammation of the gingiva (gums) - *reversible

78
Q

Periodontitis (periodontal disease) is

A

a chronic inflammatory disease, which includes gingivitis along with loss of connective tissue and bone support for the teeth- irreversible

79
Q

Periodontal diseases are caused by

A

bacteria in dental plaque ( polymicrobial anaerobic infection)

80
Q

Dental caries - dominant organism?

A

==cavities!

Streptococcus mutans

micro 8 (6 decks)

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