RESUMO
We report a case of acute disseminated encephalomyelitis (ADEM) secondary to Mycoplasma pneumoniae infection that failed to improve with methylprednisolone and intravenous immunoglobulin (IVIG); who responded with plasmapheresis. A 21- year- old female with an unremarkable medical history, initially presented to an outside hospital with fever and an influenza-like illness and was subsequently intubated for worsening sensorium. Brain magnetic resonance imaging was suggestive of ADEM or vasculitis for which she received five days of pulse steroids and IVIG. She showed no signs of improvement and was transferred to our hospital for plasmapheresis. Her work up revealed an elevated IgM antibody and positive sputum for Mycoplasma pneumonia by polymerase chain reaction, suggesting the pathogen as the culprit for her ADEM. Intravenous azithromycin and daily plasmapheresis were initiated for seven consecutive days. Following commencement of her treatment, the patient experienced good recovery and was subsequently extubated. She continued to improve with physical therapy and gained mobility, with the help of a walker. Patients commonly present with ADEM following viral infection or vaccination and less frequently post bacterial infection. The current treatment of ADEM due to Mycoplasma pneumoniae is based on limited case reports. Our patient poorly responded to pulse steroids and IVIG, while she markedly improved on azithromycin and plasmapheresis. In patients presenting with encephalopathic signs and neurological manifestations following pneumonia; Mycoplasma pneumoniae infection and subsequent immune-mediated demyelination should be considered.
RESUMO
OBJECTIVE: This study compared the activity of ceftolozane-tazobactam and ceftazidime-avibactam against 120 bacterial strains, including extended-spectrum beta-lactamase (ESBL) producers, carbapenem-resistant Enterobacteriaceae (CRE), and Pseudomonas aeruginosa, isolated from patients admitted to Cleveland Clinic Abu Dhabi, United Arab Emirates. METHODS: In vitro susceptibility was tested using the Etest strip minimum inhibitory concentration (MIC) method, and PCR was used to characterize the carbapenemase enzymes produced by CRE strains. RESULTS: All 29 ESBL isolates were susceptible to ceftazidime-avibactam (MIC50 0.125µg/ml), whereas all but one were susceptible to ceftolozane-tazobactam (MIC50 0.38µg/ml). Twenty-seven (45%) CRE isolates were susceptible to ceftazidime-avibactam (MIC50 ≥256µg/ml), whereas only six (10%) isolates were susceptible to ceftolozane-tazobactam (MIC50 ≥256µg/ml). Very few NDM-1 isolates were susceptible to ceftazidime-avibactam, whereas the majority of OXA-48 isolates were susceptible. Twenty-nine (94%) P. aeruginosa isolates were susceptible to ceftazidime-avibactam (MIC50 1.5µg/ml), whereas 30 (97%) isolates were susceptible to ceftolozane-tazobactam (MIC50 0.75µg/ml). CONCLUSIONS: Ceftolozane-tazobactam and ceftazidime-avibactam showed comparable activity against ESBL and P. aeruginosa, with ceftazidime-avibactam having lower MICs against ESBL isolates and ceftolozane-tazobactam having lower MICs against P. aeruginosa. Ceftazidime-avibactam showed better activity against all CRE isolates except for those carrying the NDM-1 enzyme.
