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77 Cards in this Set
- Front
- Back
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What is the stratum corneum?
What are Langerhan's cells? |
SC: dead layer of cells, barrier. Important protective layer
Langer: tissue macrophages |
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What is contained within the dermis?
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Collagen and elastin
Rich blood supply: good healing. Lymphatics Appendages |
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What are the appendages found in the dermis?
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Hair follicles
Sebaceous glands Sweat glands |
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Function of the superficial fascia?
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Separates skin from muscles
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Chemical host defenses?
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Low pH due to sebum and resident bacteria.
NaCl due to sweat production discourages some (but not all) bacteria. Good for S. epidermidis. Skin lipids may offer some protection. |
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How does normal flora serve as host defense?
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Saturation of host binding sites.
Competes for food. Production of bacteriocides. Mostly Gram +. More Gram - and anaerobes in wet and warm places. |
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Why do skin normal flora not cause infection usually? When might they?
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Have low virulence.
Need proper circumstances to cause trouble. Can be resident or transient. Transient more likely to cause skin disease. |
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5 organisms that tend to be resident normal skin flora?
2 organisms that tend to be transient skin flora? |
Resident:
- Diptheroids - S. epidermidis - Propionibacterium acnes. - Micrococci - Streps. Transient: - S. aureus - S. pyogenes |
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What is meant by exogenous infection?
Endogenous infection? Toxin induced skin changes? |
Exogenous: from outside.
Endogenous: from underlying tissue or hematogenous spread. Toxin-induced skin changes: toxins produced at distant site (ex. skin changes related to bacteremia). |
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4 causes of exogenous infections?
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Trauma (any breach: hang nail, crush injury, surgery, iatrogenic - IV, decub).
Excessive moisture (occlusive dressings, diapers,, immersion infections) Compromised blood flow (trauma, vasc disorders - DM, PVD) Debris/ foreign body (necrotic tissue at deeper site, post surg) |
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Is toxin-induced skin changes a true skin infection?
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No. It is just cutaneous changes related to a disseminated infection.
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In a wound infection, what does the risk of disseminated infection (bacteremia, sepsis) directly depend upon?
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Number of microbes in the wound.
>/= 10^5th CFU equals infection (in most cases) |
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6 major skin pathogens?
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S. aureus
S. pyogenes (Strep group A) Pseudomonas aeruginosa Clostridium perfringens Pasteurella multocida Bacteroides fragilis |
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What is the most common PYOGENIC bacteria?
Second most common? |
Staph aureus.
(responsible for more infections in bvarious places in the body than any other organism) 2nd: Strep pyogenes (grp A) |
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How does Staph aureus produce abscesses?
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Produces enzymes which degrade skin lipids.
Surface proteins assist in colonization. Specific proteins for binding to fibrin and collagen. Fibrinogen: protective clot. Also produces exotoxins. |
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At what point would S. aureus cause a skin infection?
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Barrier damage.
Need a fairly large inoculum. |
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What is MRSA?
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Mutant form of S. aureus.
Multi-drug resistant (gene cassettes through plasmids). Found in hospital and community. Inhabits nares. |
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6 risk factors for MRSA?
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- Playing contact sports.
- Sharing towels/ personal items. - Immunosuppression. - Unsanitary/ crowded living conditions - dormitories or military barracks. - Health care worker - Very young, very old. |
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What is the hallmark of a hospital acquired MRSA? (skin infection in a patient hospitalized in past year).
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Abscess formation.
Panton-Valentine leukociding (cytotoxin). |
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What constitutes a community acquired MRSA infection?
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Not recently (w/in past year) hospitalized.
No medical procedures (dialysis, surgery, catheters) |
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What should you consider any infection w/ crustin, pus or abscess?
What should you do about it? |
Community acquired MRSA.
Culture and sensitivity. *Community acquired MRSA may cause more than half of all community acquired staph infections. |
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What do you often see in an infection with Strep pyogenes (Group A beta hemolytic strep)?
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Abscess formation.
Usually related to break in barrier. |
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What are the virulence factors of Strep pyogenes?
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Protein M binding to skin.
Aggressive strains use spreading factors (Hyaluronidase, DNAse, streptokinase which degrades fibrin). Streptolysin S & O: pore formers. Hyaluronic capsule. Exotoxins. |
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What is Pasteurella multocida?
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Gram negative non-sporeulating coccobacilus. Facultative.
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How might one acquire an infection with Pasteurella multocida?
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Animal bite. P. mult is a normal flora of URT of animals.
Depth of puncture matters (cats worse than dogs). |
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What are 3 virulence factors of Pasteurella multocida?
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Capsule
Hyaluronidase Exotoxin |
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What is Eikenella corrodens?
3 virulence factors? |
Facultative, gram negative, pleomorphic rod.
Endotoxin Capsule Adhesion factors |
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How might one acquire an infection with Eikenelle corrodens?
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Human bite (normal flora of human mouth)
"fight bite" Also found in animal mouths. |
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What is Streptococcus viridans?
Virulence factors? |
Aerobic, gram positive cocci, alpha hemolytic.
Used to be called S. mutans. Not very virulent. |
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How might one acquire an infection with Streptococcus viridans?
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Human bite. Normal flora of human mouth.
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What is Pseudomonas aeruginosa?
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Gram negative, aerobic rod.
Opportunistic. Ubiquitous and can cause infection almost anywhere, but is only opportunistic. |
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What are the virulence factors of P. aeruginosa?
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Many, but none particularly potent.
Endotoxin/ exotoxin. Adhesins/ Invasins Risk related to breach in integument. Can be acquired in burns, hot tubs. |
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What is Bacteroides fragilis?
Virulence? |
Anaerobic, nonsporulating gram negative rod.
Normal flora in large bowel - can form infection in decub ulcers. Capsule protects organism. Causes host activation of cytokines --> inflammation! |
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Risks of acquiring an infection with Bacteroides fragilis
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Surgery.
DM. Neutropenia. Concomitant infection w/ other microbes. "plays well with others" |
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What is Clostridium perfringens?
Virulence factors? |
Anaerobic sporulating gram positive rod.
Toxins. Spreading factors melt tissues: - Collagenase - Hyaluronidase. Bacterial spores produce gas (in ischemia) which further damages tissue. |
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Risks of acquiring an infection with C. perfringens?
Prevalence of gas gangrene? |
Risks: vascular compromise, foreign body, polymicrobial infections ("plays well w/ others")
Only small # of pts exposed will develop gangrene. |
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3 skin reactions to microbial invasion?
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Spreading infection.
Abscess formation. Necrotizing infections. |
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3 examples of spreading skin infections? Which layers of skin do they involve?
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Impetigo: epidermis only.
Erysipelas: dermis/ lymphatics. Cellulitis: subcutaneous layer. |
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Causes of impetigo?
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Normal flora of nose or mouth.
S. pyogenes. S. aureus. |
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Treatments for impetigo?
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Topical mupirocin (Bactroban) for single lesions.
Cephalosporin PO (Cephalexin) 7 days Erythromycin PO for 10 days in pen allergic patients. |
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What is Erysipelas?
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Infection of lymphatics, dermis. May move to involve subcu.
Painful, fiery red, indurated, confluent. Fever, cills. Lymphadenopathy. Usually caused by S. pyogenes. |
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What should you be sure not to confuse Erysipelas with?
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Rosacea
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Treatment for Erysipelas?
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Elevation (if extremity), saline dressings.
Penicillin PO for 2 weeks. Cephalexin PO for 10 days. Erythromycin PO for 10 days if pen allergic. Never treat this topically. |
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What are some circumstances in which you would want to treat Erysipelas more aggressively and how would you do that?
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Rapidly spreading, elderly, young children, immunocompromised.
Treat with IV pen or ceph. Erythromycin for pen allergic. |
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What is cellulitis?
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Acute inflammation to and including subcu.
Spreads rapidly. +/- lymphangitis. Pathogens: S. aureus, S. pyogenes. |
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In cellulitis, what causes the marked inflammatory response even if only few organisms are present?
What are the spreading factors of cellulits? |
Toxins.
Spreading factors: S. pyo: hyaluronidase. |
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What is a common cause of cellulitis? Organisms?
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Bites.
Cats & dogs: pasteurella multocida Humans: S. viridans, pyogenes. S. aureus Eikenella corrodens anaerobes. |
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Empiric treatment of cellulitis?
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PO abx coverage for S pyo, S. aureus for 7-14 days (Dicloxacillin, Cephalexin).
E-mycin for pen allergic. Broader coverage for bites: amox/ clavulonic acid. 14 days |
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Under what conditions would you treat cellulitis more aggressively?
How would you? |
periorbital, very old/ young, immunocompromised, failure of PO abx.
IV: cefazolin (ancef), Ampicillin and sulbsactam. |
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In cellulitis due to a bite, what other things would you consider/ do for treatment besides abx?
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Look for and treat underlying tissue damage (tendon bone).
Consider xray. Copious irrigation. Debridement if nec. Hep B prophylaxis (human bite). HIV risk assessment. Tetanus. |
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In a human bite, specifically how would you treat cellulitis?
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Amox and clavulanic acid (Augmentin).
Doxy PO in pen allergic. Ampicillin sodium and Sulbactam (Unasyn). |
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In an animal bite, specifically how would you treat cellulitis?
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Same abx as human.
Assess for abscess in cat bites! Debride! |
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If Hosp acquired MRSA is suspected in cellulitis, how should you treat?
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Vanco
+/- Linezolid +/- Rifampin |
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If comm acquired MRSA is suspected in cellulitis, how should you treat?
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Bactrim.
if Bactrim resistant: Rifampin. |
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What are skin abscesses usually caused by?
Names of types of abscess? |
Hair follicle blockage. Or trauma.
If hair follicle: - Folliculitis - Furuncles - Carbuncles |
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What is the pathological process of abscess formation?
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Exaggerated WBC reaction.
Walling off of infected site. In S. aureus, coagulase fibrin clot formation. |
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2 primary pathogens of abscess formation?
3 secondary? |
Primary:
- S. aureus - S. pyo Secondary: - P. aeruginosa. - S. pyogenes - B. frag |
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Basics of abscess treatment?
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Incision and drainage.
Removal of hair. DO NOT CLOSE!! Add appropriate abx. |
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Abx treatment for abscess?
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Topical for folliculitis (self-limiting).
PO for follicle related: Dicloxacillin, Cephalexin or E-mycin (in pen allergic). other: broad spectrum amox/ clavulonic acid. |
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IV treatment for abscess?
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Cefazolin
Vanco if MRSA suspected. |
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If P. aeurginosa causes abscess from hot tubs (hot water, high pH, low chlorine), how should you treat?
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Cipro, levofloxacin.
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What is a Pilonidal cyst?
Primary pathogen? Treatment? |
Cyst/ abscess at the site of the tailbone (right above gluteal cleft)
Anaerobes: B. frag. Tx: Incision and drainage. |
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What is the most common pathogen in paronychia/ abscess?
Treatment? |
Staph aureus.
I&D. Oral Cephalexin. |
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2 presentations of necrotizing fasciitis?
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Gas gangrene
Myonecrosis |
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Pathogens that cause necrotizing fasciitis?
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Rare.
S. pyogenes, S. aureus. Mixed aerobic and anaerobic microbes (B. grag). C. perfringens. |
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Host factors that may lead to necrotizing fasciitis?
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Hypoxia, recent trauma, immunocompomized.
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Bacterial factors that cause infection in necrotizing fasciitis?
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Hydrogen, nitrogen, H2S, methane produced from auerobic and anaerobic bacteria.
Gas accumulates in soft tissue. Exotoxin and spreading factors involved. |
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Patient presentation of necrotizing fasciitis?
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4 hrs-4 days after initial wound.
- IM infection, IVDU, trauma, bug mite. Adults more often on extremities, kids more often on trunk Higher mortality rate when head, neck, chest or abdomen involved. |
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What does the site look like and how does it progress (in necrotizing fasciitis)?
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Erythema, warm to touch. May look like cellulitis but disproportionate pain!!
Moves to bluish-black tissue. Subcu emphyzema. +/- desquamation. Bullae form. (days to weeks later) Brown, foul smelling discharge. Organisms disseminated hematogenously. |
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What is the mortality rate of necrotizing fasciitis?
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100% if untreated!!
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Testing for diagnosis of necrotizing fasciitis?
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CBC/Diff.
Blood culture. Wound culture/ gram stain. ABG (met acidosis). CRP. Xray (air in soft tissue - gas). CT/ MRI |
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What is the scoring profile used to assess risk for necrotizing fasciitis?
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LRINEC score.
Laboratory Risk Indicator for Necrotizing Fasciitis |
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Treatment for Necrotizing fasciitis?
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Airway management.
Hemodynamic support. O2. (hyperbaric) Debridement: surgical. "finger test" IVIG (IV immunoglobulin) for gas. Abx. |
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What Abx would you give for necrotizing fasciitis?
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Broad spectrum (cover gram +/- and anerobes).
Clindamycin and gentamycin. Piperacillin/ tazobactam. Imipenem. Vanco if MRSA suspected. |
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What are some special considerations to be made in regards to the diabetic patient and risk of wound?
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Vascular compromise.
Infection often polymicrobial. - most common path: S. aureus. - the more chronic, the more polymicrobial. May quickly spread to bone and joints due to immunocompromised and poor blood supply. |
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Treatment of diabetic wound?
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Debride necrotic tissue! Vital!
Explore to assess depth. Broad spectrum abx: poor blood supply to area so, topical? Nutrition and glycemic control! Correlate tx w/ deep wound culture. |
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Prognosis of diabetic foot ulcer?
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Cause of 85% of surgical lower extremity amputations.
Compared to pts w/ DM w/out ulcer: - 2.4x relative risk of death. |
