Infectious Diseases in Critical Care Medicine

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both (140). Characteristics of CA-MRSA include a lack of hospital-associated risk factors,
susceptibility to many non-b-lactam antibiotics, distinct genotypes, and distinct genetic
determinants of virulence. Numerous reports have suggested the easy transmission CA-MRSA
in settings where people are in close contact. These settings include household, day care
centers, military installation and jails. Other groups reported to be at increased risk for
CA-MRSA infection includes, athletes, Native Americans, Pacific Islanders and men who have
sex with men (139,141).
This organism has prompted many clinicians to add vancomycin, linezolid, daptomycin,
tigeycycline, or other agents effective against MRSA in the empiric treatment of severe skin
and soft tissue infections. On November 19, 2008, the FDA advisory board recommended
telavancin to be approved for the treatment of skin and soft tissue infections caused by
S. aureusincluding MRSA. Telavancin is a lipoglycopeptide (10 mg/kg/day), which is
bactericidal against MRSA (142). In phase 3 studies in patients with skin and soft tissue
infection it showed noninferiority compared with vancomycin (90% vs. 85%). Most strains of
MRSA in this study were MRSA and SCC mec type IV and PVL positive (139,143).
With CA-MRSA there has been increasing use of trimethoprim/sulfamethoxazole,
clindamycin, and long-acting tetracyclines. In a randomized control trial for efficacy of
trimethoprim/sulfamethoxazole or vancomycin, all patients withS. aureusskin infection were
cured (95). Clindamycin and linezolid have the ability to inhibit protein synthesis and to turn
off toxin production in MRSA. Inducible resistance to clindamycin can be detected by a D-zone
test, which some investigators feel should be performed on all isolates of CA-MRSA.
Dalbavancin, oritavancin, ceftobiprole, ceftaroline, and iclaprim are investigational drugs
effective against MRSA. Dalbavancin is a semisynthetic bactericidal lipoglycopeptide with a
long half-life compatible with weekly doses (1000 mg on day 1 followed by 500 mg on day 8).
Oritavancin (1.5–3 mg/kg/day) is a bacteriocidal glycopeptide. In one study cure rates were
74% versus 80% for oritavancin and vancomycin. Ceftobiprole is a broad-spectrum third-
generation cephalosporin. In phase 3 study comparing with vancomycin cure rates were 91.8%
for ceftobiprole and 90% for vancomycin (144). Iclaprim, a selective dihydrofolate inhibitor,
and ceftaroline, a new cephalosporin, are other investigational drugs effective in vitro against
MRSA. Surgical drainage is crucial for abscess, and debridement or fasciotomy for necrotizing
infections needs to be considered.


SUMMARY
A wide variety of skin and soft tissue infections can occur in the critical care settings. The rise
in immunocompromized patients such as those with AIDS, transplant recipients, and those
receiving chemotherapy or prolonged corticosteroid therapy have led to diverse etiologies,
clinical manifestations, and severity.S. aureusremains the most common pathogen causing
infections from minor skin lesions to severe life-threatening illness such as purpura fulminans.
CA-MRSA has become increasingly prevalent in many parts of the world. However, a variety
of other pathogens may be identified and need to be considered with certain epidemiological
clues. Important considerations when evaluating patients include underlying medical
conditions; exposure history; presenting signs, symptoms, and radiographic patterns. It is
important to discriminate between infectious and noninfectious etiology of skin and soft tissue
inflammation. The key to treating serious skin and soft tissue infections successfully is prompt
recognition, followed by appropriate antibiotic and surgical intervention as needed to decrease
the morbidity and mortality.


REFERENCES



  1. Roth RR, James WD. Microbiology of the skin: resident flora, ecology, infection. J Am Acad Dermatol
    1989; 20:367–390.

  2. Roth RR, James WD. Microbial ecology of the skin. Annu Rev Microbiol 1988; 42:441–464.

  3. Greene JN. The microbiology of colonization, including techniques for assessing and measuring
    colonization. Infect Control Hosp Epidemiol 1996; 17:114–118.

  4. Granto PA. Pathogenesis and indigenous microorganisms of humans. In: Murray PR, Baron EJ,
    Jorgensen JH,et al., eds. Manual of Clinical Microbiology. Vol 1, 8th ed. Washington, D.C.: ASM
    Press, 2003:44–54.


316 Sharma and Saravolatz

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