Micro: Greenberg Flashcards
What are the virulence factors of strep?
adherence: *M protein - bind to skin cells, capsule, ECM binding proteins
immune evasion: *hyaluronate capsule (anti-phagocytic), M protein anti-complement, Ig binding proteins, C5a peptidase
invasion and spread: DNAase B, SpeB, streptolysins
toxicity: superantigens, pyrogenic exotoxins (SpeA & C)
What is the microbiology of clostridium?
gram positive rods, form spores
most strict anaerobes, some microaerotolerant
habitat = soil, intestines of animals and humans (feces)
What are the toxin mediated syndromes of c. perfringens?
*alpha toxin is most important: phospholipase C cleaves phosphatidyl choline, hemolytic (RBCs, WBCs, platelets, endothelial cells)
What are the skin diseases caused by c. perfringens?
cellulitis
necrotizing faciitis
*suppurative myositis and myonecrosis
What is the gastroenteritis dz caused by c. perfringens?
mild self-limited diarrhea
from storing meats too long at too warm after cooking - gives spores that survived cooking time to germinate
What are key differences in uncomplicated vs. complicated skin infections?
*monomicrobial, gram + (strep, staph) vs. polymicrobial
superficial layers w no underlying medical illness vs. deeper soft tissue layers w immunocompromised or vascular insufficiency
antibiotics alone vs. antibiotics and possible surgery
erysipelas, impetigo, cellulitis vs. abscesses, ulcers, necrotizing faciitis
Which forms of pyoderma are usually caused by strep and which by staph?*
strep - impetigo (*honey colored crusts, no scar), ecthyma (inf penetrates through epidermis, may ulcerate and leave scar)
staph - folliculitis, furuncle, carbuncle
What are the basics of impetigo?
associated w poor hygiene
year round in tropical environments, summer peak in temperate climates
*caused by both strep and staph
M serotypes more common
transmission by direct contact, fomites, insects - *person-to-person spread is common
What is the clinical manifestation of impetigo?
incubation 10-14 days
papule –> vesicle –> pustule (breaks open in 4-6 days)
superficial localized lesions w surrounding erythema
*honey colored exudate and crust - contains bacteria
What is the treatment for impetigo?
often self limited, or can resolve w soap and water
topical treatments: mupirocin gets strep and staph, bacitracin against group A strep, retapamulin for strep and staph inc MRSA
penicillin for strep, broader for staph
good hygiene! = prevention
What is the clinical presentation of erysipelas and how is it generally treated?
acute inflammation of skin w lymphatic involvement
advancing red *well-demarcated margins
facial often associated w prior pharyngitis and resolves spontaneously
trunk often surgical wound inf - can be fatal
penicillin is effective
What is cellulitis?
inf of dermis and subcutaneous tissue
usually following trauma
painful, red, swollen, tender
bacteremia in some cases
What is the clinical presentation of cellulitis?
*different than erysipelas - margins unclear, lesions may not be raised
more common in leg than arm
predisposing factors - DM, drug use, bypass
*staph and strep most common
What is lymphangitis?
spread of inf up the lymphatics get red linear streak progresses to bacteremia in 24-48 hrs often lymphadenitis fatal if not treated
What skin inf associations are there for psuedomonas, vibrio vulnificus, and pasteurella multocida?
- ecthyma gangrenosum
- diabetics and cirrhotics particularly vulnerable
- dog or cat bites
Aeromonas hydrophila
fresh water habitat, fish pathogen
usually causes gastroenteritis, can cause cellulitis
3rd generation cephalosporins
vibrio vulnificus
curved GNR, estuary reservoir
usually immunocompromised - *liver dz common
rapidly progressive - symptoms w/i 18 hrs of exposure
high mortality
treat w tetracyclines, cephalosporins, fluoroquinolones
pasteurella multocida
natural inhabitant of many animals, GN coccobacillus
causes pneumonia in rabbits, lethal for lots of animals
rapidly progressive cellulitis after *cat > dog bite
treat w augmentin (covers anaerobes in bite too)
erysipelothrix rhusiopathiae
GPR, found in many animals and fish
occupational illness - fish handlers, slaughterhouse workers
chronic and indolent
What is necrotizing fasciitis?
gangrenous destruction of skin, fascia and sometimes muscle
usually at site of trauma - *but may be inapparent
bacterial toxins prominent virulence factors - cause tissue separation and cell death
vascular thrombosis leads to ischemia and infarction
What is synergistic necrotizing cellulitis?
gram negative enteric flora and anaerobes
proximity to GI and GU tract
*Fournier’s gangrene - scrotum and external genitalia
What are the subtypes of necrotizing fasciitis?
progressive bacterial synergistic gangrene - often post-op
synergistic necrotizing cellulitis
streptococcal gangrene = flesh-eating bacteria (group A)
clostridial myonecrosis (gas gangrene) - follows trauma, war injuries
What are the clinical manifestations of necrotizing fasciitis?
described as “woody”
tender, *pain out of proportion to findings
red then dusky then purple, skin may slough
bullae may form, serous fluid in fascia
few PMNs, many bacteria
What are the features distinguishing necrotizing fasciitis from cellulitis?
systemic toxicity
prostration
rapidly spreading lesions
bullae
