Volume 22, Number 9—September 2016
Multidrug-Resistant Staphylococcus aureus, India, 2013–2015
To the Editor: Methicillin-resistant Staphylococcus aureus (MRSA) is a versatile pathogen capable of causing a wide variety of human diseases. Increased frequency of S. aureus infections imposes a high and increasing burden on healthcare resources. In many countries, MRSA infections in hospitals are common. Data from the National Nosocomial Infections Surveillance system suggest that, in the United States, incidence of nosocomial MRSA infections is steadily increasing and that these infections account for >60% of intensive care unit admissions (1,2).S. aureus has developed resistance to several antimicrobial drugs, including second- and third-line drugs. Only a few drugs, such as vancomycin (a glycopeptide), daptomycin (a lipopeptide), and linezolid (an oxazolidinone), have been approved for the treatment of serious infections caused by MRSA. Another drug, tigecycline (a glycylcycline), has shown good activity against MRSA strains in vitro (3). The epidemiology of MRSA is constantly changing, which results in variation in its drug-resistance patterns throughout regions and countries (4). Therefore, to support clinicians in preventing and treating infection, epidemiologic surveillance is essential. We report resistance patterns of S. aureus collected over 2 years (December 2013–November 2015) from blood samples of patients admitted to 1 hospital in Odisha, eastern India.
A total of 47 S. aureus isolates were collected; only 1 isolate per patient was included in the study. Susceptibility of the isolates was tested against antimicrobial agents according to the Clinical and Laboratory Standards Institute broth microdilution procedure and interpretation criteria (http://clsi.org/). MICs for the isolates were confirmed by using a Vitek 2 Compact automated system (bioMérieux, Marcy l’Étoile, France). S. aureus ATCC 25923 was used as a control strain. S. aureusidentification was confirmed by using a Vitek 2 system, by hemolytic activity on blood agar, and by positive catalase activity test results. Clinical MRSA isolates were analyzed by using PCR with specific primers: mecA (5), cfr (6), and VanA (7).
Among the 47 S. aureus isolates, 28 (60%) were resistant to oxacillin (MICs 4–64 mg/L) and cefoxitin (MICs 8–64 mg/L). All MRSA isolates were able to grow in selective medium containing either aztreonam (75 mg/L) or colistin (10 mg/L). Screening of MRSA isolates showed that 2 isolates were highly resistant to vancomycin (MIC >100 mg/L) (Figure). Further screening showed that both vancomycin-resistant isolates were also resistant to linezolid (MIC >100 mg/L) (Figure). PCR amplification of both isolates indicated presence of all 3 genetic determinants:mecA (methicillin resistance), cfr (linzolid resistance), and VanA (vancomycin resistance). Among the 3 isolates that showed resistance to tigecycline (MIC >50 mg/L), 1 isolate was susceptible to vanocmycin and linezolid (Figure). Unlike previously reported isolates, these 2 MRSA isolates showed resistant phenotypes to linezolid, tigecycline, and vancomycin.
MICs observed in this study were higher than those previously reported. Vancomycin-resistant S. aureus has been identified in many other countries. Most linezolid-resistant S. aureus has been isolated from patients in North America and Europe (8). The tigecycline-resistant S. aureus isolate (MIC >0.5 mg/L) reported from Brazil was also susceptible to linezolid, teicoplanin, and vancomycin (9).
This study indicates the emergence of multidrug-resistant S. aureus with co-resistance to methicillin, vancomycin, linezolid, and tigecycline. Although the clinical significance of these findings is unknown, the decline in drug effectiveness against S. aureus infections represents a looming threat to patient health and highlights the possibility of a return to illness and death rates similar to those before antimicrobial drugs were available.
I thank Enketeswara Subudhi and Dinesh Goyal for kindly providing the bacteria samples and related information.
This research was partly supported by the Science and Engineering Research Board, Department of Science and Technology, New Delhi, India.
- Klevens RM, Edwards JR, Tenover FC, McDonald LC, Horan T, Gaynes R. Changes in the epidemiology of methicillin-resistant Staphylococcus aureusin intensive care units in US hospitals, 1992–2003. Clin Infect Dis. 2006;42:389–91.
- Centers for Disease Control and Prevention. National Nosocomial Infections Surveillance (NNIS) system report, data summary from January 1992 through June 2004, issued October 2004. Am J Infect Control. 2004;32:470–85.
- Brandon M, Dowzicky MJ. Antimicrobial susceptibility among Gram-positive organisms collected from pediatric patients globally between 2004 and 2011: results from the tigecycline evaluation and surveillance trial. J Clin Microbiol. 2013;51:2371–8.
- Rodríguez-Noriega E, Seas C, Guzmán-Blanco M, Mejía C, Alvarez C, Bavestrello L, Evolution of methicillin-resistant Staphylococcus aureus clones in Latin America. Int J Infect Dis. 2010;14:e560–6.
- Wielders CLC, Fluit AC, Verhoef BJS, Schmitz FJ. mecA gene is widely disseminated in Staphylococcus aureus population. J Clin Microbiol.2002;40:3970–5.
- Kehrenberg C, Schwarz LJ, Hansen LH, Vester B. A new mechanism for chloramphenicol, florfenicol and clindamycin resistance: methylation of 23S ribosomal RNA at A2503. Mol Microbiol. 2005;57:1064–73.
- Miele A, Bandera M, Goldstein BP. Use of primers selective for vancomycin resistance genes to determine van genotype in enterococci and to study gene organization in VanA isolates. Antimicrob Agents Chemother. 1995;39:1772–8.
- Gu B, Kelesidis T, Tsiodras S, Hindler J, Humphries RM. The emerging problem of linezolid-resistant Staphylococcus. J Antimicrob Chemother.2013;68:4–11.
- Dabul AN, Camargo IL. Molecular characterization of methicillin-resistant Staphylococcus aureus resistant to tigecycline and daptomycin isolated in a hospital in Brazil. Epidemiol Infect. 2014;142:479–83 .
Suggested citation for this article: Kumar M. Multidrug-resistant Staphylococcus aureus, India, 2013–2015 [letter]. Emerg Infect Dis. 2016 Sep [date cited]. http://dx.doi.org/10.3201/eid2209.160044