Public Health Agency of Canada
Symbol of the Government of Canada

Share this page

STAPHYLOCOCCUS AUREUS

PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

SECTION I - INFECTIOUS AGENT

NAME: Staphylococcus aureus

SYNONYM OR CROSS REFERENCE: MRSA (methicillin-resistant Staphylococcus aureus), MSSA (methicillin-susceptive (or sensitive) Staphylococcus aureus), VISA (vancomycin-intermediate Staphylococcus aureus), hVISA (heteroresistant vancomycin-intermediate Staphylococcus aureus), VRSA (vancomycin-resistant Staphylococcus aureus), staph infection, staphylococcus infection, impetigo, toxic shock syndrome.

CHARACTERISTICS: Staphylococcus aureus are Gram-positive, catalase positive cocci belonging to the Staphylococcaceae family Footnote 1, Footnote 2. They are approximately 0.5-1.5 µm in diameter, nonmotile, non-spore-forming, facultative anaerobes (with the exception of S. aureus anaerobius) that usually form in clusters. Many strains produce staphylococcal enterotoxins, the superantigen toxic shock syndrome toxin (TSST-1), and exfoliative toxins. Staphylococcus aureus are part of human flora, and are primarily found in the nose and skin Footnote 3.

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Staphylococcus aureus is an opportunistic pathogen that can cause a variety of self-limiting to life-threatening diseases in humans Footnote 2. The bacteria are a leading cause of food poisoning, resulting from the consumption of food contaminated with enterotoxins Footnote 4. Staphylococcal food intoxication involves rapid onset of nausea, vomiting, abdominal pain, cramps, and diarrhea Footnote 2, Footnote 4. Symptoms usually resolve after 24 hours Footnote 4. Animal bites can result in local infections, cellulitis, erythema, tenderness, mild fever, adenopathy, and lymphangitis (rarely) Footnote 5. Scalded skin syndrome is caused by exfoliative toxins secreted on the epidermis and mostly affects neonates and young children Footnote 2. Other skin conditions caused by Staphylococcal exfoliative toxins include blisters, skin loss, pimples, furuncles, impetigo, folliculitis, abscesses, poor temperature control, fluid loss, and secondary infection Footnote 2, Footnote 4, Footnote 6, Footnote 7. S. aureus can also cause necrotizing fasciitis in immunocompromised individuals, although this is very rare Footnote 8. Necrotizing fasciitis is life-threatening and causes severe morbidity.

Certain strains of S. aureus produce the superantigen TSST-1, which is responsible for 75% of toxic shock syndrome (TSS) cases Footnote 2. The clinical presentation of TSS is severe and acute symptoms include high fever, vascular collapse, vomiting, diarrhea, myalgia, hypotension, erythematous rash, desquamation, and involvement of at least 3 organs Footnote 2, Footnote 9, Footnote 10. Mortality is very high and death can occur within 2 hours Footnote 9. Toxic shock syndrome is associated with vaginal colonization with toxin-producing S. aureus during menstruation, complications with staphylococcal infection at other sites, or complications of surgical procedures Footnote 10. Deep infections include endocarditis, peritonitis, necrotizing pneumonia, bacteremia, meningitis, osteomyelitis, septic arthritis, and infections of bones, joints and organs Footnote 2, Footnote 6, Footnote 7.

EPIDEMIOLOGY: Worldwide distribution. Staphylococcus aureus is one of the most common causes of skin, soft-tissue, and nosocomial infection Footnote 7. Rates of infection in community settings are increasing Footnote 7, Footnote 11. Residents of nursing homes are also at an increased risk of acquiring MRSA Footnote 12. Around 20% of individuals are persistent carriers of Staphylococcus aureus, about 60% are intermittent carriers, and approximately 20% rarely carry it Footnote 3. Children are more likely to be persistent carriers of the bacteria Footnote 3. Young women are at a higher risk for toxic shock syndrome Footnote 10.

HOST RANGE: Humans, wild and domestic animals, including cows Footnote 13.

INFECTIOUS DOSE: At least 100,000 organisms in humans Footnote 14.

MODE OF TRANSMISSION: Ingestion of food containing enterotoxins Footnote 4. Vertical transmission during vaginal delivery is uncommon Footnote 15. Person-to-person transmission occurs through contact with a purulent lesion or with a carrier Footnote 3. Unsanitary conditions and crowded community settings increase exposure to S. aureus Footnote 16. Infection may be spread from person-to-person through health care workers or patients Footnote 3. Nasal colonization can lead to auto-infection Footnote 17.

INCUBATION PERIOD: Onset of symptoms after consuming contaminated food is usually 30 minutes to 8 hours Footnote 4. Colonies of S. aureus can be carried for an undetermined amount of time; some individuals may carry it chronically, and some may carry it intermittently Footnote 3.

COMMUNICABILITY: Communicable period is as long as a purulent lesion is present or carrier state persists.

SECTION III - DISSEMINATION

RESERVOIR: Staphylococcus aureus is found in humans in the nose, groin, axillae, perineal area (males), mucous membranes, the mouth, mammary glands, hair, and the intestinal, genitourinary and upper respiratory tracts Footnote 2, Footnote 4, Footnote 18. Many animals act as reservoirs, particularly cows with infected udders Footnote 13.

ZOONOSIS: Yes, through direct or indirect contact with an infected animal Footnote 5.

VECTORS: None.

SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Antibiotics such as cloxacillin and cephalexin are commonly used to treat staph infections Footnote 19. Vancomycin which is administered intravenously is used to treat MRSA Footnote 20.

DRUG RESISTANCE: Many strains of Staphylococcus aureus have increasing resistance to multiple antibiotic classes Footnote 6. Methicillin resistant strains are common causes of nosocomial infection Footnote 21. Increasing resistance to vancomycin is being documented in many hospitals Footnote 6.

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 70% ethanol, clorhexidine, 1% sodium hypochlorite, 2% glutaraldehyde, 0.25% benzalkonium chloride, and formaldehyde Footnote 12, Footnote 22, Footnote 23.

PHYSICAL INACTIVATION: Staphylococcus aureus can grow in a pH of 4.2 to 9.3 and in salt concentrations of up to 15% Footnote 4. Enterotoxins are resistant to temperatures that would destroy the bacilli Footnote 4. Sensitive to dry heat treatment of 160-170oC for at least an hour, but not to moist heat treatment Footnote 24.

SURVIVAL OUTSIDE HOST: Survives on carcasses and organs (up to 42 days), floors (less than 7 days), glass (46 hours), sunlight (17 hours), UV (7 hours), meat products (60 days), coins (up to 7 days), skin (30 minutes to 38 days) (citation needed). Depending on colony size, S. aureus can survive on fabrics from days to months Footnote 25.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. In outbreak settings, food poisoning can be diagnosed on clinical grounds with food cultured for S. aureus Footnote 2. Toxic shock syndrome can be indicated with a clinical diagnosis and isolation of S. aureus strain, TSST-1, or enterotoxins B or C. This can be achieved using ELISA, reverse passive latex agglutination, or PCR. Scalded skin syndrome can be diagnosed clinically, with presence of Nikolsky’s sign and identification of S. aureus retrieved from the infection site. Bacteremia and deep site infections are confirmed with direct microscopic examination of clinical specimen.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Treatment of abscesses usually does not need antibiotic therapy; appropriate drainage is usually sufficient Footnote 6. Proper antibiotic therapy is required for more serious infections.

IMMUNIZATION: None Footnote 2.

PROPHYLAXIS: Elimination of nasal carriage by using topical mupirocin also eliminates hand carriage Footnote 3.

SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: 29 reported cases as of 1973, with 1 death Footnote 26.

SOURCE/SPECIMENS: Infective stages may be present in CSF, joint aspirates, blood, abscesses, aerosols, faeces, and urine Footnote 2, Footnote 4, Footnote 6, Footnote 18.

PRIMARY HAZARDS: Trauma of cutaneous barrier, parenteral inoculation, direct implantation of medical devices (i.e. indwelling catheters and IVs), ingestion of infected material, and contact with aerosols Footnote 2, Footnote 4, Footnote 18.

SPECIAL HAZARDS: Contaminated request forms that have been wrapped around specimen containers Footnote 21. Direct contact with open cuts and lesions of skin.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 Footnote 27.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes Footnote 28.

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities Footnote 28.

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled.

SECTION IX - REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: December 2011

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright ©
Public Health Agency of Canada, 2011
Canada

REFERENCES:

Footnote 1
Becker, K., Harmsen, D., Mellmann, A., Meier, C., Schumann, P., Peters, G., & von Eiff, C. (2004). Development and evaluation of a quality-controlled ribosomal sequence database for 16S ribosomal DNA-based identification of Staphylococcus species. Journal of Clinical Microbiology, 42(11), 4988-4995. doi:10.1128/JCM.42.11.4988-4995.2004
Footnote 2
Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., Pfaller, M. A., & Yolken, R. H. (Eds.). (2003). Manual of Clinical Microbiology (8th ed.). Herdon, VA, United States of America: American Society for Microbiology.
Footnote 3
Kluytmans, J., van Belkum, A., & Verbrugh, H. (1997). Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks. Clinical Microbiology Reviews, 10(3), 505-520.
Footnote 4
Le Loir, Y., Baron, F., & Gautier, M. (2003). Staphylococcus aureus and food poisoning. Genetics and Molecular Research : GMR, 2(1), 63-76.
Footnote 5
Goldstein, E. J., Citron, D. M., Wield, B., Blachman, U., Sutter, V. L., Miller, T. A., & Finegold, S. M. (1978). Bacteriology of human and animal bite wounds. Journal of Clinical Microbiology, 8(6), 667.
Footnote 6
Eisenstein, B. I. (2008). Treatment challenges in the management of complicated skin and soft-tissue infections. Clinical Microbiology and Infection : The Official Publication of the European Society of Clinical Microbiology and Infectious Diseases, 14 Suppl 2, 17-25. doi:10.1111/j.1469-0691.2008.01922.x
Footnote 7
Fridkin, S. K., Hageman, J. C., Morrison, M., Sanza, L. T., Como-Sabetti, K., Jernigan, J. A., Harriman, K., Harrison, L. H., Lynfield, R., & Farley, M. M. (2005). Methicillin-resistant Staphylococcus aureus disease in three communities. The New England Journal of Medicine, 352(14), 1436.
Footnote 8
Miller, L. G., Perdreau-Remington, F., Rieg, G., Mehdi, S., Perlroth, J., Bayer, A. S., Tang, A. W., Phung, T. O., & Spellberg, B. (2005). Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. The New England Journal of Medicine, 352(14), 1445.
Footnote 9
Chen, C., Tang, J., Dong, W., Wang, C., Feng, Y., Wang, J., Zheng, F., Pan, X., Liu, D., Li, M., Song, Y., Zhu, X., Sun, H., Feng, T., Guo, Z., Ju, A., Ge, J., Dong, Y., Sun, W., Jiang, Y., Wang, J., Yan, J., Yang, H., Wang, X., Gao, G. F., Yang, R., Wang, J., & Yu, J. (2007). A glimpse of streptococcal toxic shock syndrome from comparative genomics of S. suis 2 Chinese isolates. PloS One, 2(3), e315. doi:10.1371/journal.pone.0000315
Footnote 10
Parsonnet, J., Hansmann, M. A., Delaney, M. L., Modern, P. A., DuBois, A. M., Wieland-Alter, W., Wissemann, K. W., Wild, J. E., Jones, M. B., & Seymour, J. L. (2005). Prevalence of toxic shock syndrome toxin 1-producing Staphylococcus aureus and the presence of antibodies to this superantigen in menstruating women. Journal of Clinical Microbiology, 43(9), 4628.
Footnote 11
David, M. D., Kearns, A. M., Gossain, S., Ganner, M., & Holmes, A. (2006). Community-associated meticillin-resistant Staphylococcus aureus: nosocomial transmission in a neonatal unit. The Journal of Hospital Infection, 64(3), 244-250. doi:10.1016/j.jhin.2006.06.022
Footnote 12
Hughes, C. M., Smith, M. B., & Tunney, M. M. (2008). Infection control strategies for preventing the transmission of meticillin-resistant Staphylococcus aureus (MRSA) in nursing homes for older people. Cochrane Database of Systematic Reviews (Online), (1)(1), CD006354. doi:10.1002/14651858.CD006354.pub2
Footnote 13
Fitzgerald, J. R., Sturdevant, D. E., Mackie, S. M., Gill, S. R., & Musser, J. M. (2001). Evolutionary genomics of Staphylococcus aureus: insights into the origin of methicillin-resistant strains and the toxic shock syndrome epidemic. Proceedings of the National Academy of Sciences of the United States of America, 98(15), 8821-8826. doi:10.1073/pnas.161098098
Footnote 14
Schmid-Hempel, P., & Frank, S. A. (2007). Pathogenesis, virulence, and infective dose. PLoS Pathogens, 3(10)
Footnote 15
Reusch, M., Ghosh, P., Ham, C., Klotchko, A., Singapuri, S., & Everett, G. (2008). Prevalence of MRSA colonization in peripartum mothers and their newborn infants. Scandinavian Journal of Infectious Diseases, 40(8), 667-671.
Footnote 16
Stevens, A. M., Hennessy, T., Baggett, H. C., Bruden, D., Parks, D., & Klejka, J. (2010). Methicillin-Resistant Staphylococcus aureus Carriage and Risk Factors for Skin Infections, Southwestern Alaska, USA. Emerging Infectious Diseases, 16(5), 797.
Footnote 17
van Belkum, A., Emonts, M., Wertheim, H., de Jongh, C., Nouwen, J., Bartels, H., Cole, A., Cole, A., Hermans, P., Boelens, H., Toom, N. L., Snijders, S., Verbrugh, H., & van Leeuwen, W. (2007). The role of human innate immune factors in nasal colonization by Staphylococcus aureus. Microbes and Infection / Institut Pasteur, 9(12-13), 1471-1477. doi:10.1016/j.micinf.2007.08.003
Footnote 18
Spendlove, J. C., & Fannin, K. F. (1983). Source, significance, and control of indoor microbial aerosols: human health aspects. Public Health Reports, 98(3), 229.
Footnote 19
Sharma, S., & Verma, K. K. (2001). Skin and soft tissue infection. Indian Journal of Pediatrics, 68 Suppl 3, S46-50.
Footnote 20
Hansra, N. K., & Shinkai, K. (2011). Cutaneous community-acquired and hospital-acquired methicillin-resistant Staphylococcus aureus. Dermatologic Therapy, 24(2), 263-272. doi:10.1111/j.1529-8019.2011.01402.x; 10.1111/j.1529-8019.2011.01402.x
Footnote 21
Collins, C. H., & Kennedy, D. A. (1999). Laboratory-acquired infections. Laboratory-acquired Infections: History, incidence, causes and prevention. (4th ed., pp. 234). Oxford, UK: Butterworth Heinemann.
Footnote 22
Sinha, B., François, P. P., Nüße, O., Foti, M., Hartford, O. M., Vaudaux, P., Foster, T. J., Lew, D. P., Herrmann, M., & Krause, K. H. (1999). Fibronectin-binding protein acts as Staphylococcus aureus invasin via fibronectin bridging to integrin α5β1. Cellular Microbiology, 1(2), 101-117.
Footnote 23
Egusa, H., Watamoto, T., Matsumoto, T., Abe, K., Kobayashi, M., Akashi, Y., & Yatani, H. (2008). Clinical evaluation of the efficacy of removing microorganisms to disinfect patient-derived dental impressions. The International Journal of Prosthodontics, 21(6), 531-538.
Footnote 24
Moesby, L., Hansen, E. W., Christensen, J. D., Hoyer, C. H., Juhl, G. L., & Olsen, H. B. (2005). Dry and moist heat sterilisation cannot inactivate pyrogenicity of Gram positive microorganisms. European Journal of Pharmaceutical Sciences : Official Journal of the European Federation for Pharmaceutical Sciences, 26(3-4), 318-323. doi:10.1016/j.ejps.2005.07.003
Footnote 25
Neely, A. N., & Maley, M. P. (2000). Survival of enterococci and staphylococci on hospital fabrics and plastic. Journal of Clinical Microbiology, 38(2), 724-726.
Footnote 26
Pike, R. M. (1976). Laboratory-associated infections: summary and analysis of 3921 cases. Health Laboratory Science, 13(2), 105-114.
Footnote 27
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
Footnote 28
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.