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Further Advances in the Treatment of Methicillin-resistant Staphylococcus aureus
Some new ESCs are available only in intravenous forms. It appears as though The Special Issue of Nosocomial Infections Due to
the novel cephalosporins are equivalent to vancomycin for therapy of SSTIs Community-acquired MRSA
with fewer adverse effects. Clinicians also have a general familiarity and a In the last decade, CA-MRSA has migrated to hospitals, causing various
high comfort level with cephalosporins. In addition, with favourable data nosocomial infections, including post-partum endometritis, prosthetic
from more studies, the drugs could gain rapid acceptance. Plus, with their joint infections, bloodstream infections and pneumonia.
3–5
As a result,
activity against Gram-negative bacteria, they may prove useful in new types of empirical therapy need to be considered, and proactive
complicated soft-tissue infections from which multiple organisms are planning for changing prophylaxis is indicated. Leading physicians,
isolated, such as those in patients with diabetes. The novel together with the infection control team, should take the time now to
diaminopyrimidine iclaprim is a second-generation dihydrofolate reductase develop guidelines for the prevention and control of nosocomial CA-
inhibitor that has similarities to trimethoprim. It has shown synergy with MRSA infections. In the absence of clinical trials, each institution will need
sulphonamides and it appears to have good oral bioavailability. to monitor the efficacy of the antibiotics selected and all adverse events.
Community-acquired Pneumonia Empirical Therapy of Hospital-acquired Pneumonia and
S. aureus pneumonia following influenza was described classically during Hospital-acquired Bloodstream Infections
the 1918–1919 pandemic
26
and again noted in the 1957 Asian influenza As with community-acquired pneumonia caused by CA-MRSA, the key
pandemic.
27
More recently, small studies of CA-MRSA have been described point is that in the case of CA-MRSA nosocomial pneumonia, it may be
after annual epidemics of influenza.
28
With greater virulence compared with worth using at least one drug that inhibits protein synthesis, and IVIG may
both HA-MRSA and methicillin-susceptible S. aureus, CA-MRSA can cause be useful. However, the utility of either suggestion is based on some biology
severe necrotising lung disease and death even in young patients. No and uncontrolled series, but has not been proved to be efficacious in large,
carefully controlled clinical trials have been performed to suggest optimal double-blind, placebo-controlled trials.
therapy. Some small case series have ascribed some benefit to adding
antibiotics that inhibit protein synthesis, with the authors postulating that an Peri-operative Prophylaxis in Hospitals with
inhibition of PVL production is beneficial.
29
In addition, there may be utility Community-acquired MRSA Incisional Wound Infections
shown in the future with intravenous immunoglobulin (IVIG), which has As the proportion of CA-MRSA isolates among all S. aureus surgical-site
been found to contain antibodies to PVL.
30
In 1932, Panton and Valentine infections increases, there should be some consideration given to altering
described the therapeutic value of serum containing high levels of antibody drugs that are currently used for peri-operative prophylaxis. No studies have
to the leukocidin for treating ‘pyemic’ cases of severe S. aureus infection in been completed to provide information with regard to the best choices and
people.
8
Currently, several authors, including ourselves, recommend it. now more institutions than previously are using vancomycin. Standard uses
Linezolid – with or without vancomycin – has been used to treat CA-MRSA of available first-, second- or third-generation cephalosporins are not
pneumonia. It is reasonable to initiate therapy with both drugs. However, appropriate whenever MRSA surgical site infections are common.
no study has shown clearly an advantage of one over the other or with both
drugs combined. Daptomycin is not recommended because surfactants bind Summary
to and neutralise the activity of the drug in the lung. Currently, there are S. aureus are virulent organisms that are part of the normal flora of people,
insufficient clinical data to recommend tigecycline or any of the newer drugs and are capable of rapidly exchanging genes that code for antibiotic
shown in Table 1 for treating CA-MRSA pneumonia. resistance. As a result, they continue to pose serious challenges for clinicians
faced with too few clinical trials to be informed of the best therapy.
Community-acquired Bloodstream Infections Currently, there is also a limited understanding of the biology of these
It is rare for bloodstream infections caused by CA-MRSA to be described, versatile organisms. To date, no effective vaccines exist to prevent S. aureus
but they can occur after furuncles and even cause endocarditis.
31
infections, but some pharmaceutical companies are exploring this approach.
Complications are severe and include suppurative infections in the lung and Although new drugs have been developed, in the last decade only linezolid
brain. In general, the same approach to CA-MRSA-related pneumonia is and daptomycin represent those targeting novel sites in the bacteria.
32
reasonable for bloodstream infections. In the latter, however, daptomycin Nevertheless, the advantages of the new derivative glycopeptides, ESCs and
might be considered, whereas it should not be used when pneumonia is dihydrofolate reductase inhibitors include better safety profiles compared
present. No clinical trials have defined best therapy for CA-MRSA with vancomycin and an improved comfort level for prescribing physicians
bloodstream infections. familiar with the classes of drugs in general. ■
1. Robinson, DA, Kearns AM, Holmes A, et al., Lancet, 10. Goldstein BP, Draghi DC, Sheehan DJ, et al., AAC, 21. Noel GJ, Bush K, Bagchi P, et al, Clin Infect Dis, 2008;46:647–55.
2005;365:1256–8. 2007;51:1150–54. 22. Parish D, Scheinfeld N, Curr Opin Investig Drugs, 2008;9:201–9.
2. Moran GJ, Krishnadasan A, Gorwitz RJ, et al., N Engl J Med, 11. Bennett JW, Lewis JS, Ellis MW, Ther Clin Risk Manag, 2008;4:31–40. 23. Talbot GH, Thye D, Das A, et al, AAC, 2007;51:3612–16.
2006;355:666–74. 12. Anderson VR, Keating GM, Drugs, 2008;68:639–49. 24. Korbila I, Falagan ME, Curr Opinion Investig Drugs, 2008;9:871–8.
3. Saiman L, O’Keefe M, Graham III PL, et al., Clin Infect Dis, 13. Roecker AM, Pope SD, Expert Opin Pharmacother, 2008;9:1745–54. 25. Micek ST, Clin Infect Dis, 2007;45(Suppl. 3):S184–90.
2003;37:1313–19. 14. Dunbar LM, Tang DM, Manasa RM, Ther Clin Risk Manag, 26. Chickering HT, Park JH, JAMA, 1919;72:617–26.
4. Kourbatova EV, H Alvosa JS, King MD, et al., Am J Infect Control, 2008;4:235–44. 27. Louria DB, Blummenfeld HL, Ellis JT, et al., J Clin Invest,
2005;33:385–9. 15. Stryjewski ME, Graham DR, Wilson SE, et al, Clin Infect Dis, 1959;38:213–65.
5. Seybold U, Kourbatova EV, Johnson JG, et al., Clin Infect Dis, 2008;46:1683–93. 28. Hageman JC, Uyeki TM, Francis J S, et al., Emerg Infect Dis,
2006;42:647–56. 16. Nannini EC, Stryjewski ME, Expert Opin Pharmacother, 2006;12:894–9.
6. McDougal LK, Steward CD, Killgore GE, et al., J Clin Microbiol, 2008;9:2197–2207. 29. Micek ST, Dunne M, Kollef MH, Chest, 2005;128:2932–8.
2003;41:5113–20. 17. Poulakou G, Giamarellou H, Expert Opin Investig Drugs, 30. Gauduchon V, Cozon G, Vandenesch F, et al., in vitro, J Infect Dis,
7. Zafar U, Johnson LB, Hanna M, et al., Infect Control Hosp Epidemiol, 2008;17:225–43. 2004;189;346–53.
2007;28:966–9. 18. Crandon J, Nicolau DP, Future Microbiol, 2008;3:251–63. 31. Bahrain M, Vasiliades M, Wolff M, et al, Scand J Infect Dis,
8. Panton PN, Valentine MB, Lancet, 1932;1:506–8. 19. Novel GJ, Strauss RS, Amsler K, et al., AAC, 2008;52:37–44. 2006;38:702–7.
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EUROPEAN INFECTIOUS DISEASE 89
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