Micro - Skin, Blood, Muscle Flashcards
S. aureus Alpha-toxin
Cause mammalian cell membranes to leak through pores formed by toxin.
S. aureus exfoliatins
Split epidermis between the stratum spinosum and stratum granulosum by disruption of intercellular junctions -> scalded skin syndrome
Toxin is absorbed in blood stream, w/erythema and intraepidermal desquamation at remote sites -> no S. aureus can be isolated from desquamation sites
S. aureus - coagulase
Coagulase is not a toxin, but plays role in pathogenesis -> fibrin coat makes Staph resistant to phagocytosis. Fibrin deposition in area of staph infxn helps localize the lesion
TSST-1 sx’s
High fever, vomiting, diarrhea, sore throat, muscle pain. Shock w/in 48 hours. Renal and hepatic dmg. Skin rash (followed by desquamatio at deeper level than toxic shock syndrome) and strawberry tongue
Coagulase negative Staph
Normal commensals. Non-beta-hemolytic (lack major virulence factors of S. aureus).
S. lugdunensis - primary pathogen like S. aureus. Occasional very serious infxns. Abscess formation. Can cause prosthetic joint infxn. Emerging pathogen
Staph. epidermidis
EPS or biofilm -> adhesion to catheters, artificial heart valves, etc. Biofilm -> protected from phagocytosis and abx, yet still obtain nutrients
Grp A Strep pyogenes
Pyrogenic exotoxin (SPE) -> cytokine release ->
- Red rash on skin (scarlet fever) cheeks, temples, buccal mucosa, strawberry tongue, punctate hemorrhages on palate, sandpaper rash on trunk, arms legs
- Pharyngitis (spread by direct contact or aerosols)
Poststreptococcal sequelae
Acute rheumatic fever ->
- Inflammatory dz -> fever, carditis, subcutaneous nodules, migratory polyarthritis
- Heart valve dmg -> murmurs, cardiac enlargement, repeat infxns -> progressive dmg
- Acute glomerulonephritis (children) -> 10 days after infxn, occasional renal failure, type III hypersensitivity
- Impetigo - starts at insect bite or minor abrasion. Small vesicles w/erythema become pustular and later crusted. Ecthyma
- Erysipelas - skin and subcut tissues. Spreading area of erythema and edema, often on face -> pain, fever, lymphadenopathy
- Strep pyogenes cellulitis, necrotizing fasciitis, TS-like S
Grp B Strep (GBS) - Strep agalactiae
- Neonate can acquire GBS during passage through birth canal unless preventative measures are taken
- Neonatal dz - lethargy, fever, sepsis, meningitis, resp distress
- Older children and adults - puerperal fever at delivery, gyn surgery infxns, skin and soft tissue infxns
Beta strep, NOT grps A or B
Grps C and G can cause pharyngitis -> no post infxn sequelae. Skin and soft tissue infxns, infxns of wounds, occasional bacteremias. Same txt as for grps A and B
Viridans strep (all other alpha strep once Strep pneumoniae has been ruled out)
Alpha hemolytic.
- S. milleri grp - deep tissue abscesses
- Species that cause subacute bacterial endocarditis - S. mutans (dental caries), S. mitis, S. salivarius. Detect w/blood cultures. Tx w/PCN for weeks
Strep Abiotrophia sp
Nutritionally-deficient Strep.
- Will not grown on ordinary blood agar -> needs spec vitamin or nutrient. Colony resembles viridans or non-hemolytic strep species
- Causes bacterial endocarditis -> sometimes difficult to detect by culture unless lab thinks to add “feeder colony” or special nutrients to media
Enterococcus
Naturally in gut. Non-hemolytic strep. Grp D. Strep
E. faecalis and E. faecium
- IS SUSCEPTIBLE (to ampicillin). Most common clinical isolate.
- UM (ultra mean) - resistant to ampicillin. More likely to be resistant to vancomycin than E. faecalis (VRE). Ctrl w/std precautions and reduced use of vancomycin
Enterococcus dzs
- Opportunistic infxns (wound and soft tissue, bacteremia related to indwelling lines).
- Endocarditis
- UTIs
- Wound infxns in intensive care units “Me too”
Opportunistic Corynebacterium pathogens
- Corynebacterium ulcerans - skin infxns
- Corynebacterum jeikeium - nosocomial bloodstream and wound infxns (automatically resistant to ampicillins)
Erysipelothrix rhusiopathiae
Coryneform. Gram positive diphtheroid-like rod. Found in animals, meat, and seafood
Disease: Erysipeloid – Painful slowly spreading skin infection.
• Follows traumatic inoculation of skin –Fishermen, butchers, veterinarians
Clostridium perfringens features
Gram positive spore forming rod. No spores in tissue stains.
– Fast growing anaerobic fermenter - generates large amounts of H2 & CO2
– Found in colon and soil.
– Encapbsulated and non-motile.
Culture characteristics: 1) double zone of hemolysis on blood agar. 2) Litmus milk stormy fermentation

Clostridium perfringens toxins
- Alpha - main pathogenic factor!!! Diffuses through tissue, killing cells and producing more necrotic growth
- Theta toxin - toxic for heart mm and caps. Similar to Streptolysin O in beta strep
- Enterotoxin - causes food poisoning
Clostridium perfringens - other destructive mechs
- Fermentation of mm carbs -> crepitation, palpable gas -> gas gangrene. Contam w/dirt, feces. Rapidly life-threatening! -> can’t wait for cultures -> clinical dx needed! Remove infected tissues immediately, surgical debridement, drain wound. Hyperbaric O2 chamber, tx w/PCN. Culture and gram stain -> boxcar.
- Destructive EC enzs - collagenase, DNAse, hyaluronidase, protease
- Anaerobic cellulitis -> mixed anaerobic flora including Clostridium
Lactobacillus
Resemble alpha strep. Nml vaginal flora. If replaced with Mobiluncus, vaginitis results. Can cause blood infxn in big doses
Actinomyces
Pathogenic anaerobe! Long, Gram pos rods. Often BRANCHING. No spores, not acid-fast
Can cause serious chronic infxn. IUDs, aspiration pneumonia, abscesses in neck or head. May see pus w/granules in infxn (sulphur granules)
- A. israelii - most common pathogen in serious infxn. “Molar tooth” colony morphology. (A. naeslundii, A. meyeri)
Propionibacterium
Anaerobic, “coryneform,” Gram pos, non-sporeforming rod. Nml skin flora -> opportunistic pathogen, common blood culture contam.
Infxns - acne, opportunistic infection of prosthetic devices. Part of mixed anaerobic infxns
Bacteroides fragilis
Most common Gram neg anaerobic infxn. PCN RESISTANT.
#1 member - B. fragilis - capsule w/antiphagocytic fxn #2 - Fusobacterium
Rickettsia
Gram neg bacilli. Fevers w/a rash. Infect vascular endothelium -> RBCs leak from breaks in BVs -> rash and petechial lesions. Systemic sx’s.
Gen sx’s: fever, HA, external rash and internal focus lesions, endotoxin-like shock may occur
Difficult to culture (not routine testing!), need PH labs.
Rickettsia rickettsii
D/t bite from Dermacentor variabilis. Sim dz as R. conorii.
Rash is main feature -> wrists, ankles, trunk. RASH ON PALMS AND SOLES IS KEY
- Need clinical dx -> tx w/abx immediately!
Rickettsia akari
Rickettsialpox. Transmit via house mouse mite bite. Benign, self-limiting illness. Papulovesicle -> fever w/rash
Rickettsia tsutsugamushi
Scrub typhus. Rodent mites
Rickettsia prowazekii
Pediculus humanus (louse, defecates when it feeds -> ctrl pops!)
Typhus fever sx’s: fever, HA, malaise, myalgia. Rash on trunk to extremities (can get gangrene). Complications: CNS and heart
Rickettsia prowazekii relapse
Brill’s Dz. Relapse of louse-borne typhus. 10-40 years after first infxn.
Rickettsiae remain dormant in reticuloendothelial cells. Decreased immunity of old age enables attack
Borrelia burgdorferi
Large spirochète. Stains weakly w/ordinary stains -> culture is difficult -> use EIA for AB plus Wetern blot for confirmation. Long doubling time: 8-24 hours. Has toxic LPS. Transmitted by Ixodes tick. Deer, white-footed mouse.
Dz stages: - Primary lesion -> erythema chronicum migrans (ECM rash). Slowly expanding red ring, biopsy of leading edge -> organism in leading edge
- Secondary stage -> Spirochetemia and systemic sx’s - fever, mm and jt pains, meningeal irritation
- Late stage -> few organisms in diverse organs w/immunological-mediated dmg