INFECTIOUS DISEASES
SOFT TISSUE AND BONE INFECTIONS
CELLULITIS
Infection of superficial and deep dermis and subcutaneous fat
Microbiology & clinical (NEJM 2004;350:904; CID 2005;41:1373)
• Primarily strep and staph, including MRSA; may include GNRs in diabetics/immunosupp.
• Community-acquired MRSA (CA-MRSA) (NEJM 2005;352:1485 & 2006;355:666)
Up to 75% of purulent skin/soft tissue infxns, depending on local epi (rapidly increasing)
Clinically indistinguishable from MSSA, often assoc. w/ purulent drainage or exudate
High-risk groups: athletes, military, prison, MSM, communities w/ high prevalence
Often TMP-SMX sensitive; variably clindamycin sensitive (may falsely appear susceptible on lab testing, requires confirmation w/ D-test; NEJM 2007;357:380)
• Erythema, edema, warmth, pain (rubor, tumor, calor, dolor)
• Lymphangitis (proximal red streaking) and regional lymphadenopathy
• Toxic shock syndrome can occur w/ staph or strep infxn. Fever, HA, N/V, diarrhea, myalgias, pharyngitis, diffuse rash w/ desquamation, HoTN, shock. BCx may be 
.
• Bites: skin and oral flora (incl anaerobes) + special exposures:
Diagnosis
• Largely clinical diagnosis; BCx low yield (Se <5% in simple cellulitis) but useful if 
• Aspirate of bulla or pus from furuncle or pustule may provide microbiologic dx
Treatment
• Limb elevation; erythema may worsen after starting abx b/c bacterial killing → inflam.
• I&D if abscess is present in addition to cellulitis
• Worse outcomes if vasc. insuff., edema, immunosupp., resistant orgs. or deeper infxn
• In obese Pts, adequate drug dosing important to avoid treatment failure (J Infect 2012;2:128)
OTHER CUTANEOUS INFECTIONS
“DIABETIC FOOT” = INFECTED NEUROPATHIC FOOT ULCER
Leading cause of DM-related hosp. days & nontrauma amputations
Microbiology
• Mild (superficial, no bone or joint involvement): usually S. aureus or aerobic streptococci
• Limb- or life-threatening = deep, bone/joint involvement, systemic tox., limb ischemia
• Mono- or polymicrobial with aerobes + anaerobes
aerobes = S. aureus, strep, enterococci and GNR (including Pseudomonas)
anaerobes = anaerobic streptococci, Bacteroides, Clostridium (rare)
Clinical manifestations
• Clinical dx: ≥2 classic s/s of inflammation (erythema, warmth, tenderness [may be absent in neuropathy], pain or induration) or purulent secretions ± crepitus (indicating gas and ∴mixed infection w/ GNR & anaerobes or Clostridium)
• Complications: osteomyelitis, systemic toxicity (fever, chills, leukocytosis, hyperglycemia)
Diagnostic studies
• Avoid superficial swabs (only helpful if for S. aureus and suspect infxn); wound cx (eg, deep tissue sample or curettage at ulcer base after débridement) has ↑ Se
• Blood cx should be obtained in all Pts, in 10–15%
• Osteomyelitis should always be ruled out: probe to bone test for all open wounds in a diabetic foot (high Sp but low Se); imaging (see below); bone biopsy best
Treatment (CID 2012;54:e132)
• Elevation, non–weight-bearing status, wound care, glycemic control, antibiotics
• Evaluation and treatment for venous insufficiency and arterial ischemia
• Many require surgery: early, aggressive and repeated débridement; revascularization or amputation may be necessary
• Management by multidisciplinary team improves outcomes (Circulation 2006;113:e463)
NECROTIZING FASCIITIS
Definition
• Infection and necrosis of superficial fascia, subcutaneous fat and deep fascia (necrosis of arteries and nerves in subcutaneous fat → gangrene)
• Fournier’s gangrene: necrotizing fasciitis of the male genitalia or female perineum
Epidemiology
• Affects healthy individuals but ↑ risk: DM, PVD, EtOH abuse, IDU, immunosupp., cirrhosis
Microbiology
• Type I (after abd/perineal surgery or trauma; in DM, PVD): polymicrobial (w/ anaerobes)
• Type II (usually extremities): Strep pyogenes ± CA-MRSA, often healthy w/o obvious portal of entry; up to 1/2 have toxic shock syndrome (TSS)
Clinical manifestations
• Need high degree of clinical suspicion because of nonspecific physical exam
• Most common sites: extremities, abdominal wall and perineum, but can occur anywhere
• Cellulitic skin Ds with poorly defined margins + rapid spread + systemic toxicity
• Pain out of proportion to apparent cellulitis; skin hyperesthetic and later anesthetic
• Bullae, darkening of skin to bluish-gray ± crepitus or radiographically visible gas
Diagnostic signs
• Clinical dx sufficient to initiate urgent surgical exploration
• Aspiration of necrotic center; BCx; Gram stain; ✓ CK for tissue necrosis
• Imaging: non-contrast CT, but do not delay therapy (Arch Surg 2010;145:452)
• Microbiologic dx from Gram stain and culture of surgical specimens
Treatment
• Definitive treatment is surgical débridement of necrotic tissue and fasciotomy
• Type I: breadth of GNR coverage determined by host, prev hosp, prev Rx and initial
Gram stain; eg, carbapenem or (3rd-gen ceph + amp + [clinda or metronidazole])
• Type II: PCN + clinda. If ↑ risk of CA-MRSA, + vanco. If concern for strep, IVIG.
Prognosis
• Generally fatal if untreated; reported mortality 20–50%
CLOSTRIDIAL MYONECROSIS (GAS GANGRENE)
Definition
• Life-threatening, fulminant clostridial infection of skeletal muscle
• Wound contamination w/ clostridial spores after trauma (penetrating or crush injury)
• Most commonly C. perfringens; C. septicum assoc w/ cancer (GI, heme), even w/o trauma
Clinical manifestations
• Incubation period 6 h to 2–3 d
• Sense of heaviness/pain, often at site of trauma; rapid worsening; marked systemic toxicity
• Bronze skin discoloration, tense bullae, serosanguineous or dark fluid and necrotic areas
• Crepitus present but not prominent (gas is in muscle), may be obscured by edema
Diagnostic studies
• Gram stain: lg, Gram bacilli w/ blunt ends (can be Gram-variable), few polys
• Bacteremia in ~15%
• Plain radiographs: gas dissecting into muscle
Treatment
• Surgical exploration with débridement, fasciotomies and amputation if necessary
• Antibiotics: high-dose penicillin G 24 MU IV divided q2–3h + clinda 900 mg IV q8h
OSTEOMYELITIS
Infection of bone due to hematogenous seeding or direct spread from contiguous focus
Microbiology (NEJM 1997;336:999; Lancet 2004;364:369)
• Hematogenous: S. aureus; mycobacterial infection of vertebral body = Pott’s disease
• Contiguous focus (may be acute or chronic)
open fracture, orthopedic surgery, etc.: S. aureus and S. epi
skin breakdown + vasc. insuffic. (eg, diabetic foot): polymicrobial (aerobic + anaerobic GPC & GNR)
Clinical manifestations
• Surrounding soft-tissue compromise ± fistula to superficial skin
• ± Fever, malaise and night sweats (more common in hematogenous than contiguous)
• Vertebral osteomyelitis (seen in Pts >50 y): unremitting, focal back pain, usually fever (NEJM 2010;362:1022)
Diagnostic studies (JAMA 2008;299:806)
• Identification of the causative organism is key
• Culture from tissue (surgical sampling/needle bx), not swabs of ulcers or fistulae drainage
• High suspicion in diabetic foot (see above) if can probe ulcer to bone or ulcer >2 cm2
• Blood cultures (more often with acute hematogenous osteomyelitis)
• ESR >70 greatly increases likelihood of osteo (JAMA 2008;299:806)
• Imaging
Plain radiographs: normal early in disease; lytic lesions seen after 2–6 wk
MRI: can detect very early changes (overall Se 90%, Sp 82%; Archives 2007;167:125)
CT: can demonstrate periosteal reaction and cortical and medullary destruction
CT & MRI very Se but ↓ Sp; false if contig focus w/ periosteal reaction, Charcot Ds
Radionuclide imaging: very Se but non-Sp (false if soft tissue inflammation)
Treatment
• Antibiotics (based on cx data) × 4–8 wk
• Surgery should be considered for any of the following: acute osteo that fails to respond to medical Rx, chronic osteo, complications of pyogenic vertebral osteo (eg, early signs of cord compression, spinal instability, epidural abscess) or infected prosthesis
EPIDURAL ABSCESS
Etiology
• Hematogenous spread (2/3): skin infection, soft tissue (dental abscess) or endocarditis
• Direct extension (1/3): vertebral osteo, sacral ulcer, spinal anesthesia or surgery, LP
• Risk factors: diabetes, renal failure, alcoholism, IVDU, immunosupp.
• S. aureus most common pathogen, increasing incidence of MRSA
Clinical manifestations
• Back pain (unremitting including midline) + often fever ± nerve root or cord signs
Diagnostic studies
• MRI
• Aspiration of abscess fluid for Gram stain & cx or operative Gram stain & cx
• Blood cx (frequently )
Treatment
• Antibiotics ± surgery (decompressive laminectomy and débridement) for failure to improve on medical Rx or early s/s of cord compression (w/ vertebral osteo and epidural abscess, may see paraplegia 48–72 h after first signs)