Significantly reduced identification and antibiogram times
Sensitivity and specificity
Minimal training required
Case 1:A 31-year old male on the haematology unit with acute myeloid leukaemia had a recent Clostridium difficile infection and a central line enterococcal infection. He was on prophylactic posaconazole and the lines were removed. From rectal swabs he had been found to be colonised with a multidrug-resistant (MDR) Pseudomonas, suspected to be a carbapenemase producer. He deteriorated rapidly over the course of a few hours with shortness of breath, fevers, and clinical signs of sepsis. He was empirically started on piperacillin-tazobactam, with an aminoglycoside (amikacin). We took blood cultures at 11.00; his white cell count at this point was 0.3, so he was still essentially neutropaenic, with platelets of 38 and haemoglobin of 9.
The blood culture signal on the machine was positive at 16.31 with a Gram-negative organism on gram film. We processed the blood culture according to our normal standard of care, and also on the Accelerate Pheno™ system. The ID came through at 19.11 as Pseudomonas aeruginosa, which worried us because of what he was colonised with. We were already in the middle of an outbreak investigation, as the haematology unit had recently had a patient with MDR Pseudomonas, a GES-5 carbapenemase producer resistant to meropenem, ciprofloxacin, ceftazidime, gentamicin, sensitive to amikacin and colistin. The patient was stable, and we decided to keep him on the piperacillin-tazobactam and amikacin for the time being, but we asked to be called immediately if he deteriorated. We ensured we had colistin on the unit so that if he deteriorated we could give him that.
Six hours later we had the full antibiogram. It was an MDR organism that fitted with what he was colonised with. This allowed us to rationalise the antibiotic choice. We phoned the haematology doctors at 02.00 and changed the antibiotics to colistin and amikacin, with the information given. Using the Accelerate PhenoTest™ BC gave us clarity—we knew what we were dealing with, and it helped us to manage the patient as appropriately as possible with very targeted antibiotics. On review we realised he had a perineal tear. The patient recovered from his neutropaenia, and antibiotics were stopped at 2 weeks after the positive blood culture. With our standard system we would have had to wait for at least another 24-48 hours to identify the organism. In a very immunocompromised patient, it could have been extremely detrimental if we had not got this right.
Case 2:A 26-year-old female came in to the emergency department, after a collapse at home, with a queried septic arthritis. We were called in by the orthopaedic ward who said she was profoundly septic. On review, she was in respiratory failure with low blood pressure and acute kidney injury on a background of Noonan’s syndrome. She was quite a complex patient with cardiac issues, secondary to her Noonan’s. She was seen by the orthopaedic team at 11.00, and started on empirical treatment: intravenous meropenem. She had a background of penicillin allergy with a rash, so although meropenem is very broad-spectrum, that seemed reasonable at the time. The blood culture was signal positive at 11.00. The lab informed me at 11.15 that there was a Gram-negative bacillus coming through in the blood culture. They put this straight on to the Accelerate Pheno™ system. The patient was picked up by the high-dependency outreach team and transferred to intensive care. At 12.30, we got an ID and it was a Serratia marcescens, which we know to be a carrier of an AmpC resistance mechanism and therefore highly likely to be MDR. The antibiotic susceptibility testing (AST) then came through at 17.30, and it confirmed that we were doing the right thing with meropenem, but we felt we could also give gentamicin as she was on dialysis filtration, and still deteriorating. We isolated her in a side room for optimal infection control, as this was a MDR organism, and she was subsequently found to have influenza A. She was subsequently found to have pneumonia, possibly secondary to having influenza A in the community. We were able to optimise her treatment over and above what we would normally do with our standard of care and have surety that we were using the right antibiotics. This knowledge also helped greatly with infection control actions. The patient made a recovery after a time in intensive care and the high-dependency unit (HDU).
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