Background. Black people in the USA is afflicted with a higher rate of methicillin-resistant Staphylococcus aureus (MRSA) infection. This study determined the prevalence of MRSA carriage among black college students at a university setting. Methods. Hand and nasal swabs were collected and screened for MRSA by mannitol fermentation, coagulase, and DNase activities and their resistance to oxacillin. MRSA isolates were analyzed for antimicrobial resistance pattern, genetic profile for staphylococcal cassette chromosome mec (SCCmec) type, pulsed-field type, multilocus sequence type (ST), and the presence of Panton-Valentine leukocidin (PVL) gene. Results. MRSA was isolated from 1 of the 312 (0.3%) hand swabs and 2 of the 310 (0.65%) nasal swabs, respectively. All isolates lack multidrug resistance and have type IV SCCmec, characteristic of community-associated MRSA. These isolates were a ST8-MRSA-IVa-PVL(+) (USA300 strain), a ST8-MRSA-IVb-PVL(？), and a new MLST, ST2562-MRSA-IV-PVL(？), identified in this study. These isolates were thus not transmitted among students. Conclusion. We found a low rate of MRSA carriage among students in a black university. Our finding highlights the need of future study which involves multiinstitutions and other ethnic group to assess the association of black race with MRSA carriage. 1. Introduction Staphylococcus aureus, a bacterium commonly isolated from humans, is an important causative agent for skin and soft tissue infections, pneumonia, septic arthritis, endocarditis, osteomyelitis, and sepsis [1]. Methicillin-resistant Staphylococcus aureus (MRSA) strains resistant to β-lactam antimicrobial agents have caused increased S. aureus infection and mortality [2, 3]. Black people in the USA is afflicted with a higher rate of MRSA infection as indicated by studies of pediatric patients, community-onset skin and soft tissue infections, right-sided endocarditis patients, and hospital patients [4–10]. A report by Klevens et al. [11] described significant race disparity through a surveillance program in 2004-2005: incidence rates of invasive MRSA infection were consistently higher among blacks than whites in all age groups. Overall, infection rate was more than twice as high, and mortality rate was 80% higher for blacks than for whites. The reason for these racial disparities is not known. It is well known that S. aureus carriage is a major risk factor for infection, and MRSA colonization as opposed to MSSA colonization is associated with an increased risk of infection [1–3]. A question needs to be answered is whether a higher rate
References
[1]
F. D. Lowy, “Medical progress: Staphylococcus aureus infections,” The New England Journal of Medicine, vol. 339, no. 8, pp. 520–532, 1998.
[2]
J. Kluytmans, A. van Belkum, and H. Verbrugh, “Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated risks,” Clinical Microbiology Reviews, vol. 10, no. 3, pp. 505–520, 1997.
[3]
M. Z. David and R. S. Daum, “Community-associated methicillin-resistant Staphylococcus aureus: epidemiology and clinical consequences of an emerging epidemic,” Clinical Microbiology Reviews, vol. 23, no. 3, pp. 616–687, 2010.
[4]
S. K. Fridkin, J. C. Hageman, M. Morrison et al., “Methicillin-resistant Staphylococcus aureus disease in three communities,” The New England Journal of Medicine, vol. 352, no. 14, pp. 1436–1444, 2005.
[5]
T. J. Ochoa, J. Mohr, A. Wanger, J. R. Murphy, and G. P. Heresi, “Community-associated methicillin-resistant Staphylococcus aureus in pediatric patients,” Emerging Infectious Diseases, vol. 11, no. 6, pp. 966–968, 2005.
[6]
S. Bratu, D. Landman, J. Gupta, M. Trehan, M. Panwar, and J. Quale, “A population-based study examining the emergence of community-associated methicillin-resistant Staphylococcus aureus USA300 in New York City,” Annals of Clinical Microbiology and Antimicrobials, vol. 5, article 29, 2006.
[7]
A. E. Chen, M. Goldstein, K. Carroll, X. Song, T. M. Perl, and G. K. Siberry, “Evolving epidemiology of pediatric Staphylococcus aureus cutaneous infections in a Baltimore hospital,” Pediatric Emergency Care, vol. 22, no. 10, pp. 717–723, 2006.
[8]
M. D. King, B. J. Humphrey, Y. F. Wang, E. V. Kourbatova, S. M. Ray, and H. M. Blumberg, “Emergence of community-acquired methicillin-resistant Staphylococcus aureus USA 300 clone as the predominant cause of skin and soft-tissue infections,” Annals of Internal Medicine, vol. 144, no. 5, pp. 309–317, 2006.
[9]
B. Hota, C. Ellenbogenn, M. K. Hayden, A. Aroutcheva, T. W. Rice, and R. A. Weinstein, “Community associated methicillin-resistant Staphylococcus aureus skin and soft infections at a public hospital: do public housing and incarceration amplify transmission?” Archives of Internal Medicine, vol. 167, pp. 1026–1033, 2007.
[10]
T. Lalani, J. J. Federspiel, H. W. Boucher et al., “Associations between the genotypes of Staphylococcus aureus bloodstream isolates and clinical characteristics and outcomes of bacteremic patients,” Journal of Clinical Microbiology, vol. 46, no. 9, pp. 2890–2896, 2008.
[11]
R. M. Klevens, M. A. Morrison, J. Nadle et al., “Invasive methicillin-resistant Staphylococcus aureus infections in the United States,” Journal of the American Medical Association, vol. 298, no. 15, pp. 1763–1771, 2007.
[12]
P. L. Graham, S. X. Lin, and E. L. Larson, “A U.S. population-based survey of Staphylococcus aureus colonization,” Annals of Internal Medicine, vol. 144, no. 5, pp. 318–325, 2006.
[13]
M. J. Kuehnert, D. Kruszon-Moran, H. A. Hill et al., “Prevalence of Staphylococcus aureus nasal colonization in the United States, 2001-2002,” Journal of Infectious Diseases, vol. 193, no. 2, pp. 172–179, 2006.
[14]
R. J. Gorwitz, D. Kruszon-Moran, S. K. McAllister et al., “Changes in the prevalence of nasal colonization with Staphylococcus aureus in the United States, 2001–2004,” Journal of Infectious Diseases, vol. 197, no. 9, pp. 1226–1234, 2008.
[15]
Clinical and Laboratory Standards Institute, Performance Standards for Antimicrobial Disk Susceptibility Tests; Approved Standard, Clinical and Laboratory Standards Institute, Wayne, Pa, USA, 9th edition, 2006, Document M2-A9.
[16]
K. Zhang, J. A. McClure, S. Elsayed, T. Louie, and J. M. Conly, “Novel multiplex PCR assay for characterization and concomitant subtyping of staphylococcal cassette chromosome mec types I to V in methicillin-resistant Staphylococcus aureus,” Journal of Clinical Microbiology, vol. 43, no. 10, pp. 5026–5033, 2005.
[17]
M. R. Mulvey, L. Chui, J. Ismail et al., “Development of a Canadian standardized protocol for subtyping methicillin-resistant Staphylococcus aureus using pulsed-field gel electrophoresis,” Journal of Clinical Microbiology, vol. 39, no. 10, pp. 3481–3485, 2001.
[18]
F. C. Tenover, R. D. Arbeit, R. V. Goering et al., “Interpreting chromosomal DNA restriction patterns produced by pulsed- field gel electrophoresis: criteria for bacterial strain typing,” Journal of Clinical Microbiology, vol. 33, no. 9, pp. 2233–2239, 1995.
[19]
M. C. Enright, N. P. J. Day, C. E. Davies, S. J. Peacock, and B. G. Spratt, “Multilocus sequence typing for characterization of methicillin-resistant and methicillin-susceptible clones of Staphylococcus aureus,” Journal of Clinical Microbiology, vol. 38, no. 3, pp. 1008–1015, 2000.
[20]
G. Lina, Y. Piémont, F. Godail-Gamot et al., “Involvement of Panton-Valentine leukocidin-producing Staphylococcus aureus in primary skin infections and pneumonia,” Clinical Infectious Diseases, vol. 29, no. 5, pp. 1128–1132, 1999.
[21]
T. P. Levin, B. Suh, P. Axelrod, A. L. Truant, and T. Fekete, “Potential clindamycin resistance in clindamycin-susceptible, erythromycin-resistant Staphylococcus aureus: report of a clinical failure,” Antimicrobial Agents and Chemotherapy, vol. 49, no. 3, pp. 1222–1224, 2005.
[22]
International Working Group on the Classification of Staphylococcal Cassette Chromosome Elements (IWG-SCC), “Classification of staphylococcal cassette chromosome mec (SCCmec): guidelines for reporting novel SCCmec elements,” Antimicrobial Agents and Chemotherapy, vol. 53, no. 12, pp. 4961–4967, 2009.
[23]
A. M. Stevens, T. Hennessy, H. C. Baggett, D. Bruden, D. Parks, and J. Klejka, “Methicillin-resistant Staphylococcus aureus carriage and risk factors for skin infections, Southwestern Alaska, USA,” Emerging Infectious Diseases, vol. 16, no. 5, pp. 797–803, 2010.
[24]
A. ？sterlund, G. Kahlmeter, L. Bieber, A. Runehagen, and J. M. Breider, “Intrafamilial spread of highly virulent Staphylococcus aureus strains carrying the gene for Panton-Valentine leukocidin,” Scandinavian Journal of Infectious Diseases, vol. 34, no. 10, pp. 763–787, 2002.
[25]
K. Boubaker, P. Diebold, D. S. Blanc et al., “Panton-valentine leukocidin and staphyloccoccal skin infections in schoolchildren,” Emerging Infectious Diseases, vol. 10, no. 1, pp. 121–124, 2004.
[26]
L. G. Miller, S. J. Eells, A. R. Taylor, et al., “Staphylococcus aureus colonization among household contacts of patients with skin infections: risk factors, strain discordance, and complex ecology,” Clinical Infectious Diseases, vol. 54, no. 11, pp. 1523–1535, 2012.
[27]
J. E. Morita, R. S. Fujioka, A. D. Tice et al., “Survey of methicillin-resistant Staphylococcus aureus (MRSA) carriage in healthy college students, Hawai'i,” Hawaii Medical Journal, vol. 66, no. 8, pp. 213–215, 2007.
[28]
R. E. Rohde, R. Denham, and A. Brannon, “Methicillin resistant Staphylococcus aureus: carriage rates and characterization of students in a Texas university,” Clinical Laboratory Science, vol. 22, no. 3, pp. 176–184, 2009.
[29]
D. Rackham, S. Ray, A. Franks, K. Bielak, and T. Pinn, “Community-associated methicillin-resistant Staphylococcus aureus nasal carriage in a college student athlete population,” Clinical Journal of Sport Medicine, vol. 20, no. 3, pp. 185–188, 2010.
[30]
S. J. . Millian, J. N. Baldwin, M. S. Rheins, and H. H. Weiser, “Studies on the incidence of coagulase-positive staphylococci in a normal unconfined population,” American Journal of Public Health, vol. 50, pp. 791–798, 1960.
[31]
W. C. Noble, “Carriage of Staphylococcus aureus and beta haemolytic streptococci in relation to race,” Acta Dermato-Venereologica, vol. 54, no. 5, pp. 403–405, 1974.
[32]
A. Lamikanra, B. D. Paul, O. B. Akinwole, and M. O. Paul, “Nasal carriage of Staphylococcus aureus in a population of healthy Nigerian students,” Journal of Medical Microbiology, vol. 19, no. 2, pp. 211–216, 1985.
[33]
W. C. Noble, R. E. O. Williams, M. P. Jevons, and R. A. Shooter, “Some aspects of nasal carriage of staphylococci,” Journal of Clinical Pathology, vol. 17, pp. 79–83, 1964.
[34]
E. S. Yang, J. Tan, S. Eells, G. Rieg, G. Tagudar, and L. G. Miller, “Body site colonization in patients with community-associated methicillin-resistant Staphylococcus aureus and other types of S. aureus skin infections,” Clinical Microbiology and Infection, vol. 16, no. 5, pp. 425–431, 2010.
[35]
D. Mertz, R. Frei, N. Periat et al., “Exclusive Staphylococcus aureus throat carriage at-risk populations,” Archives of Internal Medicine, vol. 169, no. 2, pp. 172–178, 2009.
[36]
K. T. Chen, H. Campbell, L. N. Borrell, R. C. Huard, L. Saiman, and P. Della-Latta, “Predictors and outcomes for pregnant women with vaginal-rectal carriage of community-associated methicillin-resistant Staphylococcus aureus,” American Journal of Perinatology, vol. 24, no. 4, pp. 235–240, 2007.
[37]
H. A. Cook, E. Y. Furuya, E. Larson, G. Vasquez, and F. D. Lowy, “Heterosexual transmission of community-associated methicillin-resistant Staphylococcus aureus,” Clinical Infectious Diseases, vol. 44, no. 3, pp. 410–413, 2007.
