Patient Presenting with Abscess Unresponsive to Treatment and Progressive to Osteomyelitis: A Rare Cause Burkholderia mallei.

Glanders is a rare zoonotic disease caused by Burkholderia mallei (B. mallei). B. mallei can cause pneumonia, abscesses, osteomyelitis in severe cases, sepsis, and even death in humans. In this report, we present a 15-year-old male patient living in a rural area who was diagnosed with glanders. The patient, who did not have any previous disease, was followed up with a diagnosis of pneumonia in the hospital, where he was admitted with complaints of cough and abdominal pain and presented to us with pain, redness, and swelling in his leg. Magnetic resonance imaging of the lower extremity revealed osteomyelitis in the fourth and fifth metatarsals of the right foot. B. mallei growth was detected in the abscess culture. Meropenem treatment was started. The patient's symptoms regressed with treatment. The patient was discharged with oral ciprofloxacin for B. mallei eradication. Glanders are usually transmitted through direct contact with infected animals, especially single-hoofed animals such as horses, or through inhalation of aerosols containing B. mallei. It is a rare disease-causing pneumonia and abscesses and can be life-threatening in severe cases. Diagnosis of glanders is difficult because the initial symptoms are non-specific. Isolation of B. mallei in culture is the gold standard for diagnosing the disease. There is no clear recommendation for treating glanders and imipenem; meropenem ceftazidime can be used based on antibiotic susceptibility tests.

Comparison of in vitro activities of plazomicin and other aminoglycosides against clinical isolates of Klebsiella pneumoniae and Escherichia coli.

OBJECTIVES: To compare the in vitro activity of plazomicin and two older aminoglycosides (gentamicin and amikacin) against 180 isolates of Escherichia coli and Klebsiella pneumoniae, including subsets of 60 non-ESBL-producing, 60 ESBL-producing and 60 carbapenem-resistant (46 carrying blaOXA-48, 11 carrying blaNDM and 3 carrying blaOXA-48 and blaNDM) strains. METHODS: MICs of plazomicin, gentamicin and amikacin were determined by a gradient diffusion method. Gentamicin and amikacin MICs were interpreted according to CLSI criteria and EUCAST breakpoint tables. Plazomicin MICs were interpreted using FDA-defined breakpoints. RESULTS: All non-ESBL-producing and ESBL-producing isolates were susceptible to plazomicin. The plazomicin susceptibility rate (71.7%) in carbapenem-resistant isolates was significantly higher than those observed for gentamicin (45%) and amikacin (56.7% and 51.7% according to CLSI and EUCAST breakpoints, respectively). Gentamicin, amikacin and plazomicin susceptibility rates (35.6% for gentamicin; 44.4% and 37.8% for amikacin according to CLSI and EUCAST breakpoints, respectively; 64.4% for plazomicin) in carbapenem-resistant K. pneumoniae were significantly lower than those observed for carbapenem-resistant E. coli isolates (73.3% for gentamicin; 93.3% for amikacin and plazomicin). Gentamicin, amikacin and plazomicin susceptibility rates for blaNDM-positive isolates were lower than those observed for blaOXA-48-positive isolates, but differences were not statistically significant. Among the isolates that were non-susceptible to both gentamicin and amikacin, the plazomicin susceptibility rate was less than 30%. CONCLUSIONS: Although plazomicin showed excellent in vitro activity against carbapenem-susceptible isolates, the plazomicin resistance rate increased to 35.6% among carbapenem-resistant K. pneumoniae and further increased to 45.5% among blaNDM-positive isolates.