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Understanding Staph Infections Is Key to Combating Them

Jeannette Yeznach Wick, RPh, MBA, FASCP
Published Online: Wednesday, August 1, 2007   [ Request Print ]

In the mid-1800s, Louis Pasteur and Robert Koch first observed and cultured staphylococci, the bacterial ?bad boys,? causing numerous life-threatening infections. Staphylococci?gram-positive nonmobile cocci that divide in irregular grape-like clusters?are facultative anaerobes, but they prefer aerobic conditions. Two are common: Staphylococcus epidermidis, which normally colonizes skin and mucous membranes, and S aureus (so called because of its yellow-to-orange colony pigment1), which normally colonizes human nares and perineum and can cause disease.2 Less common causes of foreign-body infections, bacteremia, endocarditis, bone infections, and organ abscesses are S epidermidis, S saprophyticus, S lugdunensis, and S schleiferi. S aureus? invasive character is partially the result of a loose-fitting polysaccharide capsule that may impede phagocytosis.

In 1946, penicillin became a viable weapon against S aureus, but resistance developed rapidly because of this organism?s ability to produce beta-lactamase. In the early 1960s, discovery of methicillin gave new hope.3 Subsequently, other semisynthetic penicillins and better infection-control measures slowed S aureus? epidemic spread. Soon, however, methicillin-resistant S aureus (MRSA) appeared.

Where Infection Starts
Neonates are susceptible to S epidermidis and S aureus colonization. S aureus may start in the umbilical area and move into the nose.4,5 With age, some people become permanent carriers. S aureus may spread to close contacts, but established nasal flora usually prevents acquisition of new strains.6 Unfortunately, antibiotic treatment may eliminate that protection and allow other strains to colonize.

Up to 40% of community-dwelling people carry S aureus in their nares. Hospital patients and personnel have higher carriage rates. Carriers who are dispersers spread staphylococci on clothes and bedding and by airborne transmission. Dust particles containing staphylococci may travel considerable distances.

Hemodialysis patients, diabetics, drug addicts, and patients with various dermatologic conditions are at highest risk.7,8 Postsurgically, carriers develop more infections than noncarriers.9

Prescribers controlled early MRSA epidemics with aminoglycosides. In the late 1970s, however, gentamicin resistance developed, and a new wave of hospital outbreaks started.10 Since then, MRSA strains have been reported globally,11 in both hospitals and communities.12 Today, nearly 40% of S aureus in the United States is MRSA. Globally, incidence varies widely.13 Patients at highest risk are described in Table 1. Person-to-person transmission of MRSA usually occurs via health care workers? hands.8

Table 1

Staphylococcal infections often are intensely purulent. The infected area tends to encapsulate, leading to abscess formation.14 Table 2 describes several specific staphylococcal infections.15

Managing Infection
Simple drainage usually is sufficient to address uncomplicated superficial and chronic staphylococcal lesions. Acute serious staphylococcal infections (eg, pneumonia or bacteremia) require immediate antibiotic therapy after antibiotic-susceptibility testing. Pending culture results, empiric treatment with a penicillinase-resistant penicillin or a cephalosporin is acceptable. Cell-wall-active antibiotics and aminoglycosides are synergistic when the organism is susceptible to both. Combinations of a beta-lactamase-stable semisynthetic penicillin and an aminoglycoside often are used for severe systemic infections, particularly in immunocompromised hosts. Clindamycin and rifampin possess good anti-staphylococcal activity. Some chronic or recurrent infections can be controlled with an oral penicillinase-resistant penicillin over months or years.

Table 2

References

1. Rosenbach FJ. Mikro-organismen bei den Wund-Infektions-Krankheiten des Menschen. Wiesbaden: JF Bergmanns Verlag; 1884.

2. Hart D. Operation room infections. Arch Surg (Chicago). 1937; 34:874-896.

3. Rolinson GN, Stevens S. Microbiological studies on a new broad-spectrum penicillin, "Penbritin." Br Med J. 1961; 2:191-196.

4. Mevissen-Verhage EAE, Marcelis JH, Harmsen-van Amerongen WCM, de Vos NM, Berkel J, Verhoef J. Effect of iron on neonatal gut flora during the first week of life. Eur J Clin Microbiol. 1985;4:14-18.

5. Kauffman CA, Bradley SF. Epidemiology of community acquired infection. In: Crossley KB, Archer GL, eds. The Staphylococci in Human Disease. New York, NY: Churchill Livingstone; 1997:287-308.

6. Hollis RJ, Barr JL, Doebbeling BN, Pfaller MA, Wenzel RP. Familial carriage of methicillin-resistant Staphylococcus aureus and subsequent infection in a premature neonate. Clin Infect Dis. 1995;21:328-332.

7. Fr?nay HME, Vandenbroucke-Grauls CMJE, Molkenboer MJCH, Verhoef J. Long-term carriage, and transmission of methicillin-resistant Staphylococcus aureus after discharge from hospital. J Hosp Infect. 1992;22:207-215.

8. Boyce JM. Epidemiology and prevention of nosocomial infections. In: Crossley KB, Archer GL, eds. The Staphylococci in Human Disease. New York, NY: Churchill Livingstone; 1997:309-329.

9. Kluytmans JA, Mouton JW, Ijzerman EP, et al. Nasal carriage of Staphylococcus aureus as a major risk factor in wound infections after cardiac surgery. J Infect Dis. 1995;171:216-219.

10. Speller DCE, Raghunath D, Stephens M, et al. Epidemic infection by a gentamicin resistant Staphylococcus aureus in three hospitals. Lancet. 1976;1:464-466.

11. Townsend DE, Ashdown N, Bolton S, et al. The international spread of methicillin-resistant Staphylococcus aureus. J Hosp Infect. 1987;9:60-71.

12. Fr?nay HME, Van Leeuwen WJ, De Neeling AJ, et al. Surveillance of methicillin-resistant Staphylococcus aureus (1989?1992). Br Med J. 1994;308:58-64.

13. Diekema DJ, Pfaller MA, Schmitz FJ, et al. Survey of infections due to Staphylococcus species: frequency of occurrence and antimicrobial susceptibility of isolates collected in the United States, Canada, Latin America, Europe, and the Western Pacific region for the SENTRY Antimicrobial Surveillance Program, 1997-1999. Clin Infect Dis. 2001;32(suppl 2):S114-S132.

14. Easmon CSF. Staphylococcal diseases. In: Smith GR, Easmon CSF, eds. Topley & Wilson's Principles of Bacteriology, Virology and Immunity. Vol 3. London: Edward Arnold; 1990:215-238.

15. Verhoef J, Fluit AC, Schmitz FJ. Staphylococci and other micrococcaceae. In: Choen J, Powderly WG, Berkeley SF, et al, eds. Cohen & Powderly: Infectious Diseases. 2nd ed. London: Harcourt Publishers Limited; 1999:2004.

16. Benoit R, Suchard JR. Necrotic skin lesions: spider bite-or something else? Consultant. 2006;46:1386-1394.

17. Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant S aureus infections among patients in the emergency department. N Engl J Med. 2006;355:666-674.

18. Berger-B?chi B. Resistance not mediated by ?-lactamase (methicillin resistance). In: Crossley KB, Archer GL, eds. The Staphylococci in Human Disease. New York, NY: Churchill Livingstone; 1997:158-174.

19. Nobel WC, Virani Z, Cree RGA. Co-transfer of vancomycin and other resistance genes from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus. FEMS Microbiol Lett. 1992; 93:195-198.

20. Cookson BD. MRSA: major problem or minor threat? (Editorial). J Med Microbiol. 1993; 38:309-310.

21. Ferrara AM. Treatment of hospital-acquired pneumonia caused by methicillin-resistant Staphylococcus aureus. Int J Antimicrob Agents. 2007;30:19-24.

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