Staphylococcus epidermidis

False-color electron micrograph of Staphylococcus epidermidis. Source: CDC/Segrid McAllister.

Other Names

• Staph
• Staph epi
• S. epidermidis
• Coagulase negative staphylococci (CoNS)

Effect on Humans

Role in disease

While at one time the appearance of S. epidermidis in clinical material could be dismissed as contamination, it is now one of the most important agents of nosocomial infections especially in individuals with weakened immune systems, newborn children, and people with implanted medical devices. It is often difficult for the clinical microbiologist and treating doctor to distinguish between strains of S. epidermidis that are causing illness and strains that are simply contaminants.^[3]

These bacteria are responsible for a growing number of infections among hospital patients whose immune systems are weakened.^[4] Such infections often occur because the bacterium is carried from the surface of the skin to deeper tissues and the blood stream by insertion of venous catheters or peritoneal dialysis catheters.

Little is known about how S. epidermidis causes disease in humans. A characteristic of many strains of this microbe is the production of a capsule or slime resulting in the formation of a biofilm.^[5] In a biofilm, S. epidermidis is protected against attacks from the immune system and against antibiotic treatment, making S. epidermidis infections difficult to stop.

S. epidermidis is also responsible for many cases of late-onset sepsis in newborns. ^[6]

A related bacteria Staphylococcus aureus causes food poisoning, skin infections and can often be resistant to many antibiotics.

Clinical Conditions

When S. epidermidis causes illness in humans, it most commonly results in the following clinical conditions:

• Blood stream infection, usually as a result of a catheter in the vein, in people with healthy immune systems.

• Blood stream infection in people with weakened immune systems^[7] (although outcome of such infections may not be serious^[8]).

• Endocarditis, or infection of both native heart valves (heart valves we were born with) or prosthetic (artificial) heart valves.

• Cerebrospinal fluid (CSF) shunt infection.

• Peritoneal dialysis catheter infection.

• Urinary Tract Infection, particularly with indwelling urinary catheters or urinary tract complications.

• Infection in prosthetic joints.

• Infection of vascular grafts (tubes inserted into blood vessels to bypass areas of blockage or damage).

• Infection in newborn children.^[6]

• Eye infection, particularly after eye surgery.

• Infection of heart pacemakers or or implantable cardioverter-defibrillators^[9]

• Infection of breast implants.^[10]

Microbiology

• S. epidermidis are small (~ 1 µm in diameter), gram-positive bacteria that appear as individual cocci (round organisms) under the microscope. They occur singly, in pairs, or in short chains and have a strong tendency to form clusters, hence the name Staphylococcus—from the Greek staphyl (bunch of grapes) and coccos (granule).

• They grow rapidly on blood agar and other nonselective laboratory media and, unlike Staphylococcus aureus, are not hemolytic on blood-agar plates. On slants or solid culture the bacterial colonies are often white or cream colored. In addition, S. epidermidis does not produce an enzyme (coagulase) that congeals blood, hence they are called coagulase-negative staphylococci compared with the coagulase-positive Staphylococcus_aureus|Staphylococcus aureus.

• In 1884, Rosenbach described the two pigmented colony types of staphylococci and proposed the appropriate nomenclature: Staphylococcus aureus (yellow) and Staphylococcus albus (white). The latter species is now named Staphylococcus epidermidis. Kloos and Schleifer later devised a scheme in which coagulase-negative staphylococci could be easily differentiated into species using biochemical characteristics.^[11]

Treatment

S. epidermidis bacteria are usually resistant to many antibiotics.^{[12] [13]} Most infections require treatment with antibiotics that are effective, such as vancomycin, rifampin, and newer quinolones such as gatifloxacin and moxifloxacin. In addition, effective treatment usually requires removal of any implanted medical device that is infected with S. epidermidis, such as indwelling venous catheters, and prosthetic (artificial) heart valves and joints.

Cases of S. epidermidis resistant to vancomycin are now appearing and other antibiotics such as linezolid^[14] and quinupristin/dalfopristin^[15] may need to be used.

References

1. ↑ Goldmann DA, Pier GB. Pathogenesis of infections related to intravascular catheterization. Clin Microbiol Rev.1993 Apr;6(2):176-92. Abstract | PDF
2. ↑ von Eiff C, Peters G, Heilmann C. Pathogenesis of infections due to coagulase-negative staphylococci. Lancet Infect Dis. 2002 Nov;2(11):677-85. Abstract
3. ↑ Kirchhoff LV, Sheagren JN. Epidemiology and clinical significance of blood cultures positive for coagulase-negative staphylococcus. Infect Control. 1985 Dec;6(12):479-86. Abstract
4. ↑ von Eiff C, Proctor RA, Peters G. Coagulase-negative staphylococci. Pathogens have major role in nosocomial infections. Postgrad Med. 2001 Oct;110(4):63-4, 69-70, 73-6. Abstract
5. ↑ Fitzpatrick F, Humphreys H, O'Gara JP. The genetics of staphylococcal biofilm formation--will a greater understanding of pathogenesis lead to better management of device-related infection? Clin Microbiol Infect. 2005 Dec;11(12):967-73. Abstract | Full Text | PDF
6. ↑ ^{6.0 6.1} Isaacs D, Australasian Study Group For Neonatal Infections. A ten year, multicentre study of coagulase negative staphylococcal infections in Australasian neonatal units. Arch Dis Child Fetal Neonatal Ed. 2003 Mar;88(2):F89-93. Abstract | PDF
7. ↑ Winston DJ, Dudnick DV, Chapin M, Ho WG, Gale RP, Martin WJ. Coagulase-negative staphylococcal bacteremia in patients receiving immunosuppressive therapy. Arch Intern Med. 1983 Jan;143(1):32-6. Abstract
8. ↑ Engelhard D, Elishoov H, Strauss N, et al. Nosocomial coagulase-negative staphylococcal infections in bone marrow transplantation recipients with central vein catheter. A 5-year prospective study. Transplantation. 1996 Feb 15;61(3):430-4. Abstract
9. ↑ Sohail MR, Uslan DZ, Khan AH, et al. Management and outcome of permanent pacemaker and implantable cardioverter-defibrillator infections. J Am Coll Cardiol. 2007 May 8;49(18):1851-9. Abstract
10. ↑ Ahn CY, Ko CY, Wagar EA, Wong RS, Shaw WW. Microbial evaluation: 139 implants removed from symptomatic patients. Plast Reconstr Surg. 1996 Dec;98(7):1225-9. Abstract
11. ↑ Kloos WE, Schleifer KH. Simplified scheme for routine identification of human Staphylococcus species. J Clin Microbiol. 1975 Jan;1(1):82-8. Abstract | PDF
12. ↑ Archer GL, Climo MW. Antimicrobial susceptibility of coagulase-negative staphylococci. Antimicrob Agents Chemother. 1994 Oct;38(10):2231-7. PDF
13. ↑ Santos Sanches I, Mato R, de Lencastre H, Tomasz A; CEM/NET Collaborators and the International Collaborators. Patterns of multidrug resistance among methicillin-resistant hospital isolates of coagulase-positive and coagulase-negative staphylococci collected in the international multicenter study RESIST in 1997 and 1998. Microb Drug Resist. 2000 Fall;6(3):199-211. Abstract
14. ↑ Draghi DC, Sheehan DJ, Hogan P, Sahm DF. In vitro activity of linezolid against key gram-positive organisms isolated in the united states: results of the LEADER 2004 surveillance program. Antimicrob Agents Chemother. 2005 Dec;49(12):5024-32. Abstract | Full Text | PDF
15. ↑ John MA, Pletch C, Hussain Z. In vitro activity of quinupristin/dalfopristin, linezolid, telithromycin and comparator antimicrobial agents against 13 species of coagulase-negative staphylococci. J Antimicrob Chemother. 2002 Dec;50(6):933-8. Abstract | Full Text | PDF

External Links

Microbiology Bytes: Staphylococcus

Textbook of Bacteriology: Staphylococcus