Soft tissue, bone and joint infections

• bacteria/viruses cannot penetrate intact skin
• nonspecific defenses:
  • exfoliation- sloughing off of stratum corneum dislodges adherent bacteria
  • dryness- more infection in moist areas (groin etc)
  • acidic pH -pH 5.5 due to hydrolisis of sebum acids by skin flora
    • free fatty acids inhibit group A strep
  • low temperature
  • sweat glands- saltiness inhibits bacteria
  • normal flora- compete with pathogens for colonisation sites and nutrients
    • S. epidermidis (90% of peopole)
    • S. aureus (80% of people)
    • Micrococci
    • Diphtheroids

ADD EPIDERMAL LAYERS DIAGRAM

• Staphylococcus aureus
  • Gram postitive cocci
  • coagulase positive
  • form distinctive  "golden colonies" on agar
• Streptococcus pyogenes
  • AKA group A strep
  • gram positive cocci
  • beta haemolysis on agar

• Skin
  • epidermis>dermis
    • impetigo
    • folliculitis
    • furunculosis
    • carbunculosis
    • erysipelas
    • (cellulitis)
• subcutaneous tissues
  • superficial fascia>subcut fat, nvs, art, vns>deep fascia
    • (cellulitis)
    • necrotising fascitis
• muscle
  • myonecrosis

• excessive moisture (induces breakdown of stratum corneum)
  • occlusive dressings
  • obesity-  intertriginous folds (NB intertriginous=where 2 areas of skin rub together)
• minor abrasions
• surgery
• crush injuries (e.g. RTA)
• burns
• iatrogenic (hosiptal admission)
• percutaneous (e.g. IV catheters)
• bed sores
• any condition that compromises blood supply
  • e.g. diabetics

• superficial infection
  • usually Staphylococcal
  • sometimes also S. pyogenes
• friable golden crusts over erythematous skin
• more common in children
• highly infective
• Rx
  • topical fucidin or mupirocin
  • oral flucloxacillin if widespread or unresponsive

• folliculitis
  • infection of hair follicles
    • follicle centred pustules
    • common sites:
      • scalp, groin, beard/moustache (moist areas w/ hair removal)
  • mostly (95%) S. aureus
• furunculosis
  • deep inflammatory lesion progressing from follicultitis 
• carbuncle
  • extends into subcut layer
  • multiple abcesses, seperated by CT
• acute paronchia
  • skin infection arising form nail

Treatment for all: oral flucloxacillin

• acute, spreading infection of lower dermis and associated subcut layers
• diffuse inflammation without necrosis or localisation of pus "red halo"
  • skin is hot, red and painful
• causative organisms:
  • commonly S. aureus (CA-MRSA= community associated MRSA - NB less resistant)
  • less commonly S. pyogenes, C. perfringens
• most commonly affects lower extremities
• diagnosis
  • acute, tender, eythematous, swollen area of skin
  • fever and malaise
  • WCC and CRP
  • NB blood cultures not useful unless pt septic
• treatment
  • rest and elevation, mark area of cellultits
  • oral penicilllin V & flucloxacillin (IV if severe)

• well demarcated cellulitis with fever and malaise
• lesions raised above surrounding skin + clear line of demarcation
  • diagnosis through clinical appearance
• S. pyogenes most common cause
• legs or face most common sites
• treatment: penicillin

• infants, young children and the immunocompromised
• mediated by production of exfoliative toxins A or B carried by ~3% S. aureus
  • released into blood stream from localised infection
• causes widespread superficial exfoliation
• treatment: flucloxacillin

• caused by either single (eg Gp A) or multiple organisms
• bacteria enter fascial plane (via trauma/surgery/occult bacteraemia) and spread rapidly
  • inflammatory response- vessel thrombosis- compromises blood supply and nerves to skin
    • skin over infected area: red/dusky red/grey and painless
• 3 stages of symptoms
  • early (<24hr)
    • presence of skin trauma w/ pain disproportionate to injury
    • flu like symptoms and thirst
  • advanced
    • swelling of painful area
    • large violet blotches
    • mottled, flaky appearance at trauma site
  • critical symptoms
    • toxic shock, severe fall in BP, unconsciousness
• Treatment: IV antibiotics and surgery

• Clostridium perfringens is most common cause
• common in past wars with devitalised wounds contaminated by soil
• can occur in synergistic infections
  • e.g. wound infected by coliforms which use up oxygen crfeating conditions for anaerobes
• more common in pt w/ underlying blood vessel disease, DM or colon ca
• treatment: urgenct surgery to remove dead tissue

• "infections that affect the surgical wound or deeper tissues handled during the procedure resulting in local signs and clinical symtpoms" (within 30 days of surgery or 1 year if implant)
  • classified as incisional or organ/space infection
• up to 20% of all healthcare associated infectioins- 5% of all surgeries
• typical features of SSI:
  • incr exudate/swelling/erythema/pain/local temp,
  • change in granulation tissue- discolouration, prone to bleed, highly friable
• factors that impact on SSI
  • pt- extremes of age, poor nutritional state, obesity, immunocompromised,smoking
  • procedural- scrub, pre-op shaving & skin prep, skin anti-sepsis, length of op, thearte ventilation, instrument sterilisation, foreign material in surgical site
  • microbial- level of contamination
• prevention
  • pre-op: patient prep, hair removal, antibiotic prophylaxis, staff prep
  • intra-op: team prep, pt skin prep, pt homeostasis, wound dressings
  • post-op: dressing and wound cleaning, ab Rx, debridement, wound care services

• infection of joint space
• S. aureus, Streptococci, Gram negatives
• esp if Hx of RA or trauma
• routes of bacterial entry:
  • haematogenous (most important)
  • direct inoculation via trauma
  • arthritis with assoc tendonitis
• bacteria enter joint space>inflammatory response>neutrophil invasion

• S. aureus, H. influenzae, E. coli, P. aeruginosa, Proteus mirabilis
  • via direct inoculation (trauma/surgery) or haematogenous route
• pathology
  • bacteria in metaphysis results in: oedema, incr vascularity, influx polymononuclear L
  • blood supply to area decr: necrosis of infected bone- formation of sequestrium
  • residual dead bone acts as foreign body- hard to eradicate bacteria (chronic progresion)
• acute clinical features:
  • adults- severe pain, decr mvmt, fever/malaise, backache, history of UTI or uro surg
  • infant- failure to thrive, drowsy, irritable, metaphyseal tenderness, decr ROM
• acute osteomyelitis diagnosis:
  • Hx and exam
  • FBC, ESR, blood culture,aspiration (NB risk of introducing more infection)
  • XR (normal in first 10-14 days), USS, bone scan, MRI
• treatment: flucloxacillin (clindamycin if allergic) or vancomycin if MRSA (+ fusidic acid, linezolid or rifampicin if prothesis present or life threatening condition) for 4-6/12 wk (ac/chr)

• cellultis > deep soft tissue infection > osteomyelitis
• organisms
  • skin organisms: S. aureus, Gp A strep, diphtheroids
  • gram -ve bacilli: E. coli, K. pneumoniae, Pseudomonos spp
  • anaerobes
• RFs
  • vascualr disease
  • peripheral neuropathy
  • poor foot care
• Treatment:
  • mild
    • flucloxacillin (if MRSA- doxacycline/if pen allergy- clindamycin)
  • moderate
    • co-amoxiclav (if MRSA- add vancomycin/pen allergy- clindamycin)
  • severe
    • Tazosin (add vancomycin if MRSA/pen allergy- meropenem)

• viruses
  • HSV and VZV produce vesicular lesions
    • HSV normally only gentital/oral regions
    • both can persist in DRG- can reactive w/ dermatomal distribution
  • other V have characteristic skin rashes
    • rubella, measles, parvovirus, HSV6
• dermatophyte infcetion (ringworm)
  • fungi that invade dead tissues or its appendages (nails/hair)
  • most common are Trichophton, Epidermophyton, MIcrosporum
    • hard to distinguish clinically
  • spread person-person or animal-person
  • diagnosis clinically acording to site:
    • tinea pedis (athletes foot)
    • tinea barbae (Barbers itch)
  • treatment: topical imidazoles/oral triazone if resistant or widespread