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Micro last plus one anatomy 5 > Bacterial infection of the skin and soft tissue joints and bone II > Flashcards

Bacterial infection of the skin and soft tissue joints and bone II Flashcards

1
Q

streptococcus type

A

catalase neg, gram pos cocci in chains

aerobic and facultative anaerobe

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2
Q

how are streptococcus organisms distinguished

A 
hemolytic props (hemolytic props)
serologic (lancefield) groupings (antigens)
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3
Q

what are lancefield antigen groupings? most common?

A

-looks for presence of certain antigens to differentiate beta hemolytic strep
-group in groups a-u
-A and B are the most common
D commonly found in enterococcus

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4
Q

what group is s. pyogenes? and what does it cause?

A
  • A

- causes strep throat, skin and soft tissue infections, rheumatic fever and glomerulonephritis

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5
Q

what is s. pyogenes (group A) sensitive to whereas other beta hemolytic strep groups are not?

A

bacitracin

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6
Q

what does s. pyogenes have in its capsule

A

hyaluronic acid -found in the ecm of our tissues so it looks like self material and thus we do not recognize it as a foreign substance and we dont phagocytose it

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7
Q

what does s. pyogenes have that allow it to adhere to its host?

A
  • pili
  • lipoteichoic acid- adheres to fibronectin
  • protein F and M protein = invasion of the epithelial cell
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8
Q

M protein

A
  • adhesion protein in s. pyogenes and are associated with invasion of epithelium
  • has many varying N termini so they are categorized that way
  • antiphagocytic
    -inhibits complement
    = IMPORTANT ADHESIN
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9
Q

what are some toxins used by s. pyogenes?

A
  • streptolysin O and Streptolysin S

- PORE FORMING TOXINS (like alpha toxin in s. aureus)

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10
Q

what are some super antigens used in s. pyogenes?

A
  • Spe- streptococcal pyrogenic exotoxins speA-C
  • increase proinflammatory cytokine production causing strep toxic shock syndrome, scarlet fever and necrotizing fasciitis
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11
Q

what is C5a peptidase?

A

peptidase made my s. pyogenes that degrades chemotactic C5a
C5a is an important in bringing neutrophils to the site of infection so if the Spe blocks its activity , you get no neutrophils to fight it off

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12
Q

pathogenesis of s. pyogenes

A
  • s. pyogenes binds via M protein
  • releases streptolysin O that creates a hole in the epithelial cell allowing s. pyo to enter
  • more streptolysin O is made in the cell leading to cell death
  • M protein and capsid prevent phagocytosis
  • C5a peptidase also allows for stoppage of chemtaxis by C5a
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13
Q 
impetigo
caused by?
when?
what occurs?
what can it be confused with?
A
  • formation of bullous lesions on the face-mostly around the mouth that is mostly in neonates. -HONEYCOMB like
    caused by s. pyogenes and s. aureus
    -usually during the warmer months
    -confused with chicken pox or herpes
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14
Q

how is bullous impetigo distinguished between the two bacterias?

A

s. aureaus- causes more extensive, bullous lesions that break down and leave thin paper-like crusts instead of thick amber crusts like in s. pyogenes
*** AMBER = PYOGENES
MROE EXTENSIVE, PAPERLIKE AND BROKEN DOWN= AUREUS

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15
Q

how do you know a skin infection is erysipelas

A
  • distinct border between diseased and not
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16
Q

what’s necrotizing fasciitis and what is it also referred to as?
what mostly causes it?

A
  • it is a gangrene or flesh eating bacteria

- caused mostly by group A strep

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17
Q

what does necrotizing fasciitis usually present as?

A
  • PAIN AND TENDERNESS SEVERE*** (looks grey) BUT LOOKS LIKE MINIMAL ERYTHYMA ON OVERLYING SKIN
  • for milder causes at superficial levels, skin is more abnormal but the pain and tenderness is only mild or moderate
  • as disease progresses over hrs, the pain worsens and get a change in skin look to more dusky or mottled erythema and edema
18
Q

how do you distinguish necrotizing fasciitis from cellulitis?

A
  • necrotizing fasciitis is very painful and appears grey over time
19
Q

treatment of necrotizing fasciitis

A
  • dead tissue block circulation to the wound and can easily colonized by the bacteria so you MUST debride the wound and create a clean margin
  • do so via skin graft
  • USE ANTIBIOTICS-BROADSPECTRUM
20
Q

what symptoms are known to be associated with s. pyogenes as pharyngitis

A
  • yellow white exudate
  • but also get SCARLET FEVER as a complication- which is release of exotoxin SpeA being released systemically and causing red spots on chest- strawberry tongue

endocarditis- M protein thought to mimic heart antigen to cause endocarditis of valves- react with heart sarcolemma membrane and myosin and synovium- occurs usually 3 weeks post strep pyogenes A infects for pharyngitis
=REMEMBER BOTH ARE FROM PHARANGITIS INFECTION

21
Q

*what can s. pyogenes infection of the skin cause?

A

-glomerulonephritis
-it can also be caused by a pharyngitis infection
-

22
Q

pathogenesis of glomerulonephritis

A

-type 3 sensitivity-
M antigen/streptokinase mimics self-antigen in the kidney and causes antigen- antibody complex that activates complement to attack it and attack the kidney cells causing inflammation
- occurs 1-4 weeks post pharyngitis and 3-6 wks post cutaneous infection

23
Q

acute poststreptococcal glomerulonephritis symptoms?

A
  • hematuria, oliguria (protein in blood), htn, edema
  • recent strep infection- see in culture
  • reduced serum complement
24
Q

streptococcal toxic shock syndrome

A
  • wound that progresses to necrotizing fasciitis and then turns to shock and death
  • initially pain and nonspecific flu-like symptoms
  • exotoxins of SpeA and C
25
Q

what is one of the main differences that distinguishes strep infection with staph infection?

A

strepto patients are mostly bacteremic and may get necrotizing fasciitis

26
Q

when diagnosing your patient, what dinstinguishes group A s. pyogenes from the rest

A

bacitracin suseptibility

27
Q

what can you look for serologically, that would indicate recent exposure to s. pyo in a patient that’s maybe coming in with glomerulitis

A
  • presence of anti-antigen O antibodies in the blood
28
Q

how is the treatment for s. pyogenes different from that of s. aureus

A

s pyogenes is PCN

s. aureus is vanco or oxacillin due to their b-lactamases

29
Q 
what kind of bacteria is  pseudomonas aeruginosa?
stain
movement
oxidase
fermentation
blood agar
produces
grows where?
how transmitted
A
  • gram neg rod
  • aerobic
  • motile
  • oxidase pos
  • non-fermenter
  • blood agar-hemolytic
  • produces PYOCANIN
  • minimalist that grows in many conditions-temps ad nutrition
  • nosocomial infection- pt with antibiotics
  • transmission be contact or food/water
  • opportunistic pathogen
30
Q

what are some virulence factors of p. aeruginosa?

A
  • capsule
  • adhesins like pilli, flagella, LPS and alginate
  • secretes phospholipase C (hemolysin), pyocyanin (proinflammatory), pyoverdin (siderophore) collagenase, lipase
  • HAS EXOTOXIN A- AN AB TOXIN THAT HAS B BIND HOST CELL AND A INACTIVATES EF-2 VIA ADP RIBOSYLATION AND BLOCKS PROTEIN SYNTHESIS CAUSING CELL DEATH
  • has a type 3 secretion system- exoenzyme s and t into target cells leading to cell damage and spread
31
Q

where does the antibiotics resistance come from in p. aeruginosa

A
  • mutation of the porin proteins
32
Q

*pathogenesis of p. aeruginosa

A
  • p. aeruginosa binds the cell
  • releases exotoxin A (AB toxin) that binds and A enters cell to bind EF-2
    -blockage of ribosylation and DNA synth
    release of exotoxin via type 3 secretion system of exoenzymes s and t
    -cell destruction
33
Q

where do you mostly see p. aeruginosa infection

A
  • CF pt
  • immnocompromised pt
  • burn victims
  • swimmer’s ear (otitis externa)
  • infection via contaminated contact lens
  • hot tub folliculitis
  • osteochondritis- inflammation of the bone or cartilage after cut in shoe with moisture
34
Q

what is a possible outcome of p aeruginosa on patients who are neutropenic, DM or have extensive burns?

A
  • pt can become bacteremic and it can lead to infection of blood vessels resulting in necrotic lesions known as ecthyma gangrenosum
35
Q

what is typical to find on a burn patient with a p. aeruginosa infection

A

-greenish blue color due to pyocyanin right on the moist surface of the wound that can eventually become bacteremic

36
Q

ecthyma gangrenosum

A
  • caused by p. aeruginosa septicemia

- starts with erythromatous or pupuric macule and then quickly develops into a hemorrhagic bulla that ruptures

37
Q

pseudomonas folliculitis

A
  • red papules that can turn into pruritic erythramatous pustules
  • can get it via hottub
  • will resolve in 5 days
  • p. aeruginosa infection
38
Q

green nails

A
  • pseudomonas infection of the nails
  • grows biofim on ventral or dorsal surface of skin
  • must have a pre-existing condition (candida paronychia-from s aureus) sets up moist environment for propagation of p. aeruginosa
  • can tell its aeruginosa cuz its green
39
Q

webspace intertrigo

A

-infection of s. aeruginosa between toes due to excessive moisture for it to grow

40
Q

how do you treat and prevent s. aeruginosa infections

A
  • treat- antibiotic resistance so do susceptibility testing- combo therapy of B lactam + aminoglycosides are used
  • prevent- clean medical equipment, don’t use unnecessary antibiotics, maintain dry conditions

Micro last plus one anatomy 5 (8 decks)

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