Skin and soft tissue infections

• • Infections of the skin is usually treated empirically.

  • Swab and culture whenever possible.

  • Rising incidence of community-associated MRSA (CA-MRSA) and nosocomial MRSA, severe infections in which S. aureus is the likely primary pathogen should be treated empirically with vancomycin, 1 g IV q12h, until susceptibilites are available. Therapy should then be switched to oxacillin or cefazolin if the strain proves susceptible. Linezolid and daptomycin should be reserved for severe infections that have not responded to treatment.

  • CA-MRSA has emerged in Pts with no risk factors. Can cause necrotizing skin infections (often associated with the Panton-Valentine leukocidin virulence factor).

• Panton-Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. It is present in the majority of community-associated Methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. PVL creates pores in the membranes of infected cells. PVL is produced from the genetic material of a bacteriophage that infects Staphylococcus aureus, making it more virulent.

• Recurrent boils, or indurated skin lesions.

• CA-MRSA is sensitive to vancomycin and usually to TMP/SMX and clindamycin. Surgical drainage is necessary for most lesions.

Cellulitis involves skin and underyling soft tissue superficial to fascia. It has less distinct margins than erysipelas.

GABHS and S. aureus are the usual pathogens and are clinically indistinguishable.

Tx:

• • Oxacillin, 1-2 g IV q4h or cefazolin, 1-2 g IV q8h; consider vancomycin, 1 g IV q12h in sick patients.

  • If PCN allergy, alternatives are macrolides or clindamycin.

  • Mild disease is treated with PO meds.

  • Coexisting T. pedis is treated with topical antifungals to prevent recurrence of LE cellulitis.

  • Diabetic patients with cellulitis often require broader-spectrum coverage.

  • Water-borne pathogens: Severe cellulitis is sometimes seen after exposure to fresh (Aeromonas hydrophila) or salt water (Vibrio vulnificus). Initial therapy include ceftazidime, 2 g IV q8h; cefepime, 2 g IV q8h; or ciprofloxacin, 759 mg PO bid. Doxycycline, 100 mg IV/PO q12h should be added for Vibrio infections, which have a strong prediliction for patients with cirrhosis.

Erysipelas. Painful, superficial, erythematous, sharply demarcated lesions that is usually found on lower extremities and is caused by GABHS in the normal host.

Tx:

• • PCN-V, 250-1000 mg PO qid or PCN-G, 1-2 million units IV q6h depending on the severity of illness.

  • In patients who are PCN allergic, macrolides or clindamycin are alternatives.

Necrotizing Fasciitis

• • An infectious disease emergency with high mortality due to extensive soft-tissue infection and thrombosis of the microcirculation with resulting necrosis.

  • Infection spreads quickly along fascial planes and may be associated with sepsis or TSS.

  • Fournier's gangrene is necrotizing fasciitis of the perineum.

Dx:

• Clinical. High suspicion prompting immediate surgical exploration where lack of resistance to probing is diagnostic.

• Bacterial etiology is either mixed (aerobic and anaerobic organisms) or monomicrobial (GABHS or S. aureus, including CA-MRSA).

• May present initially like simple cellulitis, with rapid progression to necrosis with dusky, hypoesthetic skin and bulla formation in association with severe pain.

Dxtic testing:

• Cultures of operative specimens and blood should be obtained.

• Imaging done early in disease process, CT scans and plain films may demonstrate gas and fascial edema.

Tx:

• Aggressive surgical debridement is critical, along with IV ABx and volume support.

• Initial empiric ABx therapy should be broad spectrum and include a carbapenem or beta-lactam/beta-lactamase inhibitor or high-dose PCN, or clindamycin with a FQ. Vancomycin should be added until MRSA can be excluded.

• Adjunctive hyperbaric oxygen may be useful.

Infected Decubitus Ulcers and Limb-Threatening Diabetic Foot Ulcers

• Polymicrobial infection; superficial swab cultures are not reliable.

• OM is a frequent expected complication and should be excluded.

Tx:

• Wound care and debridement is the primary therapy.

• Moderately severe infections require systemic ABx covering S. aureus, anaerobes, and enteric gram-negative organisms. Options include clindamycin, 450-900 mg IV q8h plus either a 3G cephalosporin or ciprofloxacin, 500-750 mg PO bid; a beta-lactam/beta-lactamase inhibitor combination, or a carbapenem (ertapenem, or meropenem) depending upon severity of illness.

• Less severe diabetic foot infections are usually due to S. aureus and Streptococci and can be treated with cephalexin, dicloxacillin, or clindamycin, unless MRSA is isolated, in which case vancomycin may be necessary.

Osteomyelitis: It is an inflammatory process caused by infecting organism that can lead to bone destruction. It should be considered first when skin or soft-tissue infections overlie bone and when localized bone pain accompanies fever or sepsis.

Etiology:

• • Acute hematogenous OM is caused most frequently by S. aureus.

  • Vertebral OM may be due to S. aureus, GNB, or Mycobacterium TB.

  • OM assoc w a contiguous focus of inf may be due to S. aureus, GNB, coagulase-neg staph (surgical-site inf), or anaerobes (inf sacral decub ulcers)

  • OM in presence of ortho devices is most often caused by S. aureus or coagulase-negative Staph. species.

  • OM assoc w/ Hb-pathies is most often caused by S. aureus or Salmonella species.

  • Chronic OM is usually assoc w/ a sequestrum of necrotic bone and may involve gram-negative pathogens as well as S. aureus.

Dx:

• Dx is made by detection of bone exposed through the skin ulcer or by imaging with plain films, bone scintigraphy, or MRI.

• Bx and cultures of the affected bone should be performed (before initiation of antimicrobials, if possible) for pathogen-directed therapy.

• ESR and CRP are usually markedly elevated and can be used to monitor the response to therapy.

Tx:

• If causative organism is not identified, empiric therapy should be selected to cover S. aureus (oxacillin or vancomycin) and any other likely pathogens

• Cure typically requires at least 4-6 weeks of high-dose antimicrobial therapy. Parenteral therapy should be given initially; oral regimens may be considered after 2 - 3 weeks only if the pathogen is susceptible and adequate bactericidal levels can be achieved.

• Acute hematogenous OM. In the absence of vascular insufficiency or a FB, this disease can be treated with antimicrobial therapy alone.

• OM associated with vascular insufficiency (e.g., DM patients) is seldom cured by drug tx alone; revascularization, debridement, or amputation is often needed. Inf are generally polymicrobial, including anaerobes.

• OM in the presence of orthopedic devices is rarely eradicated by antimicrobials alone. Cure typically requires removal of the device. When removal is impossible, the addition of rifampin, 300 mg PO tid, is recommended. Long-term, suppression antimicrobial therapy may be needed.

• Salmonella OM may require surgical tx and administration of a 3G cephalosporin or ciprofloxacin.

• Chronic OM. Eradication requires a combination of medical and surgical treatment to remove the persistent nidus of infection. Long-term, suppressive antimicrobial therapy can be used if surgery is not feasible. Hyperbaric oxygen may be a useful adjunctive therapy.

Anaerobic Myonecrosis (Gas gangrene)

• • C. perfingens, C. septicum, S. aureus, GABHS, or other anaerobes.

  • Distinguish these condition from necrotizing fasciitis requires gross inspection of the involved muscle at the time of surgery.

Tx:

• • Needs prompt surgical debridement and combination antimicrobial therapy with IV PCN and clindamycin. A 3G cephalosporin, ciprofloxacin, or an aminoglycoside should be added untial the GS excludes gram-negative involvement.