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INTRODUCTION: Tedizolid phosphate 200 mg, once daily for 6 days, has recently been approved for the treatment of patients with acute bacterial skin and skin structure infections (ABSSSIs) in several countries; however, clinical experience in real-life settings is currently limited. Here, we report on the use of tedizolid with an extended treatment duration for complex and severe ABSSSIs in real-world clinical settings. METHODS: Two patients with cellulitis and two patients with surgical site infection (SSI), aged 26-60 years, were treated with tedizolid phosphate 200 mg, intravenous/oral (IV/PO) or IV only, once daily at four different institutions. RESULTS: Two morbidly obese patients had non-necrotizing, non-purulent severe cellulitis, which were complicated by sepsis or systemic inflammatory response syndrome plus myositis. One female patient failed on first-line empiric therapy with IV cefalotin, clindamycin and imipenem (3-4 days), and was switched to IV/PO tedizolid (7 + 5 days). One male patient received IV clindamycin plus IV/PO tedizolid (5 + 5 days), but clindamycin was discontinued on Day 3 due to an adverse event. For both patients, clinical signs and symptoms improved within 72 h, and laboratory results were normalized by Days 7 and 8, respectively. Two other patients (one obese, diabetic female with chronic hepatitis and chronic obstructive pulmonary disease) had complicated SSIs occurring 10 days after hernia repair with mesh or 3 months after spinal fusion surgery with metal implant. First patient with previous methicillin-resistant Staphylococcus aureus (MRSA) bacteremia received a 7-day tedizolid IV course empirically. The second patient with culture-confirmed MRSA infection received a 14-day IV course. Both patients responded within 72 h, and local and systemic signs normalized by end of treatment. There were no reports of thrombocytopenia. CONCLUSION: Tedizolid phosphate 200 mg for 7-14 days was a favored treatment option for patients with severe/complex ABSSSIs, and was effective following previous treatment failure or in late-onset infections. FUNDING: Editorial assistance and the article processing charges were funded by Bayer AG, Berlin, Germany.
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Traveler's diarrhea (TD) is a crucial area for research, as it affects millions of tourists each year and creates a large economic burden. More than 60% of TD cases are caused by a variety of bacterial enteropathogens: diarrhea-producing Escherichia coli, Shigella, Campylobacter, Salmonella, Aeromonas, Plesiomonas, and noncholera Vibrios. Noroviruses are also an important cause of morbidity among travelers. Recent studies have identified host genetic risk factors associated with susceptibility to pathogen-specific TD. Prevention strategies should be emphasized, as all individuals with TD experience approximately 24 hours of disability and 5-10% experience chronic functional bowel disease. Poorly absorbed rifaximin provides protection for trips lasting 2 weeks or less. TD vaccines are also currently in development. All individuals planning trips to developing regions should be armed with 1 of the 3 agents that have shown efficacy for self-treatment of TD: ciprofloxacin (or levofloxacin), rifaximin, or azithromycin, depending upon the location of the trip. Although global epidemiologic changes in etiologic agents as well as antibiotic resistance patterns have been better understood recently, changes should be expected during the next decade due to new prevention and treatment approaches.