In methicillin-resistant Staphylococcus aureus (S. aureus) (MRSA), resistance to β-lactams is due to alteration of penicillin-binding proteins (PBPs). This resistance mechanism arises from the acquisition of the mecA gene, encoding a PBP2a with low affinity for β-lactams.1,2 In 2011, a new resistance gene was described, the mecC gene that encodes PBP2c. Its presence has spread3 and for this reason its identification is essential to establish adequate antibiotic therapy.
We present the case of a patient with mecC MRSA bacteraemia.
This was a 70-year-old man with multiple pathologies, who attended the accident and emergency department due to poor pain control after a fall. He was diagnosed with dorsal fractures and presented with hyperbilirubinaemia with jaundice, and it was decided to admit him. His condition worsened and blood and urine cultures were taken. Empirical treatment with piperacillin-tazobactam was started and he was admitted to the Intensive Care Unit (ICU) with suspicion of septic shock.
In the Gram stain of the blood culture, Gram-positive cocci were observed in clusters that were identified by PCR (Xpert® MRSA/SA BC, Cepheid) as methicillin-susceptible S. aureus (MSSA), so cloxacillin was added. After performing culture and antibiogram following the EUCAST breakpoints,4 resistance to β-lactams was observed. Immunochromatography was performed (CLEARVIEW™ PBP2a SA Culture Colony Test, Abbott) with a negative result for PBP2a. With suspicion of infection by mecC MRSA, a second commercial PCR was performed (FilmArray® Blood Culture Identification Panel, bioMérieux) with a positive result for the targets mecA/C and MREJ. Furthermore, by microdilution (MicroScan Pos Combo Panel Type 33, Beckman Coulter), MIC values for oxacillin and cefoxitin were 2 mg/l and >4 mg/l, respectively, and the rest of the families of antibiotics were interpreted as susceptible. The presence of the mecC gene was confirmed by "home PCR" with specific molecular targets and sequencing. Antibiotic therapy was changed to daptomycin and levofloxacin but the patient died 14 days after admission.
Recent publications suggest that the appearance of mecC MRSA predates the use of antibiotics,5 and that transmission to humans can occur through contact with animals.3,6,7 In addition, colonisation, advanced age and underlying disease have also been associated with infection.8 In our case, the patient confirmed contact with livestock and in the nasal sample for the study of resistant bacteria collected on his admission to the ICU, mecC MRSA was also isolated, so the patient was colonised and the infection developed.
In microbiological diagnosis, the discovery of the mecC gene with 70% nucleotide homology to the mecAgene, and PBP2c encoding with 62% amino acid sequence similarity to PBP2a means tests targeting the detection of the mecA gene and PBP2a misidentify a mecC MRSA isolate as MSSA.2,9 Therefore, performing an antibiogram and using specific techniques is essential.2mecC MRSA accounts for less than 1% of all MRSA, and the majority belong to the clonal complex (CC) CC130. In Spain, within this CC, the most common sequence type and spa type are ST1945 and t843, respectively.5,8 In our patient, the initial PCR and the immunochromatographic technique that detects the presence of PBP2a identified the isolate as MSSA. However, after carrying out the antibiogram, resistance was confirmed by specific PCR and sequencing, also demonstrating the presence of the mecC gene integrated into the SCCmec XI cassette chromosome. Furthermore, through multilocus sequence typing (MLST), it was catalogued within CC130, and through molecular typing by PCR and subsequent sequencing of the spa type, a new spa type registered as t20888, within ST1945, was detected.
In conclusion, this was a case of invasive infection by mecC MRSA with a new spa type and with a fatal outcome in which the patient met the risk factors for infection by this microorganism: close contact with livestock, underlying disease, advanced age and nasal colonisation. In microbiology laboratories, it is important to carry out a manual antibiogram along with the use of rapid molecular techniques, since mechanisms not included in the molecular targets of commercial PCRs may be identified. This is essential for choosing the most appropriate antibiotic therapy.
We would like to thank Carmen Torres and her working group from the Universidad de La Rioja [University of La Rioja] for helping to characterise the strain of S. aureus carrying the mecC gene.
