Flashcards in Bacterial infection of the skin and soft tissue joints and bone II Deck (40):
catalase neg, gram pos cocci in chains
aerobic and facultative anaerobe
how are streptococcus organisms distinguished
hemolytic props (hemolytic props)
serologic (lancefield) groupings (antigens)
what are lancefield antigen groupings? most common?
-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
what group is s. pyogenes? and what does it cause?
-causes strep throat, skin and soft tissue infections, rheumatic fever and glomerulonephritis
what is s. pyogenes (group A) sensitive to whereas other beta hemolytic strep groups are not?
what does s. pyogenes have in its capsule
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
what does s. pyogenes have that allow it to adhere to its host?
- lipoteichoic acid- adheres to fibronectin
-protein F and M protein = invasion of the epithelial cell
- adhesion protein in s. pyogenes and are associated with invasion of epithelium
- has many varying N termini so they are categorized that way
= IMPORTANT ADHESIN
what are some toxins used by s. pyogenes?
- streptolysin O and Streptolysin S
- PORE FORMING TOXINS (like alpha toxin in s. aureus)
what are some super antigens used in s. pyogenes?
- Spe- streptococcal pyrogenic exotoxins speA-C
-increase proinflammatory cytokine production causing strep toxic shock syndrome, scarlet fever and necrotizing fasciitis
what is C5a peptidase?
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
pathogenesis of s. pyogenes
- 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
what can it be confused with?
- 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
how is bullous impetigo distinguished between the two bacterias?
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
how do you know a skin infection is erysipelas
- distinct border between diseased and not
what's necrotizing fasciitis and what is it also referred to as?
what mostly causes it?
- it is a gangrene or flesh eating bacteria
- caused mostly by group A strep
what does necrotizing fasciitis usually present as?
- 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
how do you distinguish necrotizing fasciitis from cellulitis?
- necrotizing fasciitis is very painful and appears grey over time
treatment of necrotizing fasciitis
- 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
what symptoms are known to be associated with s. pyogenes as pharyngitis
- 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
*what can s. pyogenes infection of the skin cause?
-it can also be caused by a pharyngitis infection
pathogenesis of glomerulonephritis
-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
acute poststreptococcal glomerulonephritis symptoms?
-hematuria, oliguria (protein in blood), htn, edema
-recent strep infection- see in culture
- reduced serum complement
streptococcal toxic shock syndrome
- 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
what is one of the main differences that distinguishes strep infection with staph infection?
strepto patients are mostly bacteremic and may get necrotizing fasciitis
when diagnosing your patient, what dinstinguishes group A s. pyogenes from the rest
what can you look for serologically, that would indicate recent exposure to s. pyo in a patient that's maybe coming in with glomerulitis
- presence of anti-antigen O antibodies in the blood
how is the treatment for s. pyogenes different from that of s. aureus
s pyogenes is PCN
s. aureus is vanco or oxacillin due to their b-lactamases
what kind of bacteria is pseudomonas aeruginosa?
- gram neg rod
-minimalist that grows in many conditions-temps ad nutrition
-nosocomial infection- pt with antibiotics
-transmission be contact or food/water
what are some virulence factors of p. aeruginosa?
-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
where does the antibiotics resistance come from in p. aeruginosa
- mutation of the porin proteins
*pathogenesis of p. aeruginosa
- 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
where do you mostly see p. aeruginosa infection
- CF pt
- 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
what is a possible outcome of p aeruginosa on patients who are neutropenic, DM or have extensive burns?
- pt can become bacteremic and it can lead to infection of blood vessels resulting in necrotic lesions known as ecthyma gangrenosum
what is typical to find on a burn patient with a p. aeruginosa infection
-greenish blue color due to pyocyanin right on the moist surface of the wound that can eventually become bacteremic
-caused by p. aeruginosa septicemia
-starts with erythromatous or pupuric macule and then quickly develops into a hemorrhagic bulla that ruptures
-red papules that can turn into pruritic erythramatous pustules
-can get it via hottub
- will resolve in 5 days
-p. aeruginosa infection
-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
-infection of s. aeruginosa between toes due to excessive moisture for it to grow