Dr. Hiramatsu's most memorable career achievement was the discovery of MRSA strain Mu50 with reduced vancomycin susceptibility, called vancomycin-intermediate S. aureus (VISA), and its precursor strain Mu3. Mu3 is known as heterogeneously vancomycin-resistant S. aureus (hetero-VISA or hVISA).
Dr. Hiramatsu and his lab identified the mobile genetic element that confers methicillin resistance upon Staphylococcus aureus. They named it staphylococcal cassette chromosome mec (SCCmec). The PCR-based SCCmec typing has become an indispensable method for the epidemiological study of MRSA in the world. Applying the SCCmec sequence typing, Dr. Hiramatsu could prove that the community-acquired MRSA (CA-MRSA) that were ascendant in the turn of the 21st century were distinct MRSA clones from the healthcare-associated MRSA (HA-MRSA) which had been prevailing in the hospitals of the world for the last half century. He showed that most of the CA-MRSA strains on the rise carried novel SCCmec (types IV and V), whereas authentic HA-MRSA strains carried SCCmec types I~III (2002~2004).
Dr. hiramatsu and his lab completed the first S. aureus whole genome sequencing using the representative HA-MRSA strain N315 and VISA strain Mu50 and also determined the genome sequence of the highly virulent CA-MRSA strain MW2 (2002). They sequenced the genomes of S. haemolyticus and Macrococcus caseolyticus to explore the origin of SCCmec.
Understanding the mechanism of vancomycin resistance in VISA clinical strains has long been a major interest for Dr. Hiramatsu. He proposed a novel mechanism, clogging of peptidoglycan mesh by the affinity-trapped vancomycin molecules, as the cause of vancomycin resistance in VISA. Dr. Hiramatsu's efforts now are directed towards the understanding of the genetic mechanism for the vancomycin resistance.