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.)
2
Q
α-hemolysis:
A
yields a dark and greenish appearance due to chemical change in the hemoglobin in the red cells
3
Q
β-hemolysis:
A
complete hemolysis of blood around and under colony
4
Q
γ-hemolysis:
A
no color change or lysis
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
6
Q
group A strep=
A
pyogenes
7
Q
group B strep=
A
agalactiae
8
Q
organism SENSITIVE to Bacitracin?
A
Strep pyogenes - Group A strep
9
Q
transient colonization of Group A strep where?
A
URT and skin surface
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)
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
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
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
14
Q
pyoderma (impetigo) distinguishing feature?
A
-often seen aroudn the mouth = honeycrusts
15
Q
erysipelas - distinguishing feature?
A
-lesion is distinct from surroudning skin (USUALLY CAUSED BY STREP PYOGENES)
16
Q
cellulitis (inflammation) - distinguishing feature?
A
-lesion IS NOT distinct from surrounding skin
17
Q
most common superficial skin infection in children? organism?
A
- Impetigo - vesicles turn into pustules into honeycrust appearance
- usually Strep pyogenes
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)
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!
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
21
Q
Necrotizing fasciitis - treatment?
A
- remove the dead tissue and then skin graft
- antibiotis to help - broad spectrum
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
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)
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)
25
Streptococcal Toxic Shock Syndrome - Diagnosis, treatment and prevention
- 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
26
Pseudomonas aeruginosa - organism details., transmission
- 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)
27
Pseudomonas aeruginosa virulence factors
- 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
28
blue green pigment produced===
pseudomonas aeruginosa
29
Pseudomonas aeruginosa - skin and soft tissue infectinos seen in...
- Burn wounds
- Folliculitis
- Osteochondritis (inflammation of bone and cartilage) of the foot --> After a penetrating injury (stepping on a nail)
30
Common cause of otitis externa ‘swimmers ear’
| Common cause of eye inf with contaminated contact lens'?
pseudomonas aeruginosa
31
causes pneumonia in immnodeficient or cystic fibrosis patients?
pseudomonas aeruginosa --> OPPORTUNISTIC INFECTION
32
bacterimic/septicemic pseudomaons infection identified by what kind of skin lesion?
ecthyma gangrenosum - infection of blood vessels that results in characteristic necrotic lesions
33
septic patient with skin lesions - organism?
pseudomonas
34
hottub and you get pt with little red dots over body areas? treatment?
- Pseudomonas folliculitis
| - usually resolves on own in 5 days
35
“Green nails” - major cause, what condition sets up for green naisl? what is it?
- p. aeruginosa
- candidial paronychia sets up the moist environment needed
- grows as a biofilm on ventral or dorsal surface
36
chronic paronychia most often casued by?
candida
37
Webspace Intertrigo - common cause, presentation, what sets up for this condion? common other issue associated with this?
- 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
Treatments and prevetion for pseudomonas aeruginosa?
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
strep toxic shock syndrome has
bacteremia in the blood and wound!
40
staph toxic shock syndrome has
ONLY TSST1 - nothing in blood and wound
41
C. perfringens (hemolysin) causes:
gangrene, diarrhea/colitis
42
C. difficile causes (enterotoxins)
diarrhea/colitis
43
Clostridium perfringens infection/growth is usually associated with ...
production of hydrogen and carbon dioxide gas
44
C. perfringens Toxins
* ***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
Gas Gangrene - organism and most occurs due to?
- C. perfringens Disease
- traumatic wound and or surgical wounds (especially colon surgery bc its normal flora)
- --> LOTS OF GAS PRODUCTION
46
differentiate gas gangrene from other necrotizing conditions?
-gas gangrene has foul smelling discharge and reddish brown discoloration of the wound
47
C. perfringens treatment/diagnosis
- 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
C. tetani - organism details:
- motile, spore forming, Gram (+) rod
- Strict anaerobe, difficult to culture
- large terminal spores =drumstick
49
C. perfringens- organism details
- Large Gram (+) rods, non-motile
| - Spores are rarely observed
50
C. tetani - disease progression-
- small wound --> entry
| - Small local infection provides a source for Tetanospasmin, which makes its way to CNS (retrograde axonal transport)
51
Tetanospasmin****
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
C. tetani - diagnsis/treatment/revention
- immunizaiton w/ 10 yr booster
| - metronidazole cleaning of wound and human tetanus immunoglobulin vaccine
53
Mycobacterium - organism details;
- 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
M. tuberculosis - organism details and infection issue
- 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
M tuberculosis infects what types of cells?
livesinside macrophages! --> immune system T-cells wall it off = granuloma
56
M tuberculosis - Treatment and prevention
treatm: long term: isoniazid and rifampin, as well as ethambutol, pyrazinamide
prevention: vaccine - useful in children and not adults
57
Mycobacterium leprae organsm and disease details:
-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
Mycobacterium leprae - transmission
nasal secretions
59
Two distinct stages of leprosy disease
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
leprosy - people with Tuberculoid (TH1) vs Lepromatous (TH2)
TH1 can mount imune response while TH2 cannot
61
Tuberculoid vs Lepromatous
- 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
Lepromin test
-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
can you culture M leprae
NO
64
M leprae - diagnosis / treatment
- need biopsy, lepromin test
- Tuberculoid: sulfones (dapsone) and rifampin for 6 months
- Lepromatous: Dapsone, rifampin, +clofazimine for 12 months
65
Nocardiosis vs Actinomycosis
- Nocardia = Aerobic Gram positive rod, ***weak acid fast***, branched filaments that resemble hyphae, aerial hyphae
- Actinomia= NOT ACID FAST!
66
weakly acid fast organism?
nocardia
67
Mycetoma - what is it ? what casues it? where is it? *where is the most common site of infection?*
- -Nocardia: Cutaneous infections
- FOOT MOST COMMON!
- More frequent in the tropics
- Slowly progressive, painless
- begins with minor injury
68
Lymphocutaneous disease -
- -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
Cellulitis and subcutaneous abscesses
Granulomatous ulcer formation with surrounding erythema but minimal or no involvement of the draining lymph nodes
70
Nocardia: Diagnosis and treatment
- history of working outside!
- weakly acid fast organism on biopsy
- grows slow
- Treat with TMP-SMX
71
Actinomyces israellii - organism details
- filamentous rods
- looks like teeth/molars
- normal flora
- sulfur granules=yellow/orange colonies of organisms resembling grains of sand
72
Actinomyces israellii - assocaited with...
DENTAL WORK
73
sulfur granules seen with
Actinomyces israellii - seen around the mouth
74
Diagnosis and treatment: Actinomycosis
- culture, and biopsy
- The lack of staining with modified acid-fast stain separates Actinomyces from Nocardia
- Treatment: penicillin
75
acne vulgaris-
- Common disorder of the pilosebaceous unit
| - Propionibacterium acnes
76
Propionibacterium acnes- casues? organism details
- acne
- Small, anaerobic, Gram-positive rod
- common flora
77
Gingivitis is...
is the inflammation of the gingiva (gums) - ****reversible***
78
Periodontitis (periodontal disease) is
a chronic inflammatory disease, which includes gingivitis along with loss of connective tissue and bone support for the teeth- ***irreversible***
79
Periodontal diseases are caused by
bacteria in dental plaque ( polymicrobial anaerobic infection)
80
Dental caries - dominant organism?
==cavities!
| Streptococcus mutans
