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Abstract The treatment of patients with infection secondary to carbapenem-resistant Acinetobacter baumannii with emerging cefiderocol resistance remains challenging and unclear. We present a case of in vivo emergence of pandrug-resistant A baumannii that was successfully treated with the compassionate use of investigational sulbactam-durlobactam–based antibiotic regimen. We also performed a longitudinal genomic analysis of the bacterial isolates and showed the development of resistance and genetic mutations over time.

Silent Sinus Syndrome (SSS) is known to be a rare clinical condition, characterized by spontaneous and progressive enophthalmos and hypoglobus associated with atelectasis of the maxillary sinus and alteration of the orbital floor. Most of the patients with this syndrome present with ophthalmological complaints without any nasal sinus symptoms, and it typically has a painless course and slow development, ergo the term “silent.” Here we present a case report of a patient with occasional coughing spells as the presenting symptom of Silent Sinus Syndrome, which has not been previously described in the literature. The CT scan findings suggested chronic rhinosinusitis. The radiological findings were suggestive of maxillary sinus hypoplasia, with evidence of maxillary sinus atelectasis. Awareness of this syndrome is important for specialists who work with nasal sinus disease, since its management is different than chronic rhinosinusits.

Cough and angioedema are well-known adverse reactions of ACE inhibitors. However, other adverse effects of upper airways such as postnasal drainage, rhinitis and nasal blockage, are less frequently recognised. These might share the same pathophysiological mechanism: bradykinin accumulation. We present two patients with ACE inhibitor-induced upper respiratory symptoms that improved after the discontinuation of ACE-inhibitors and substitution with angiotensin II receptor blockers. The incidence of these adverse events is not accurately known, since these are not required to be reported, but it is estimated to be low. This presents challenges to the physician and demonstrates the importance of keeping it as a differential diagnosis. Most physicians are aware of ACE inhibitor-induced cough but not of ACE inhibitor-induced nasal blockage, rhinitis or postnasal drainage. Identifying these can avoid unnecessary diagnostic tests and inappropriate treatment.

Ceftolozane–tazobactam and ceftazidime–avibactam are preferred treatment options for multidrug-resistant Pseudomonas aeruginosa infections; however, real-world comparative effectiveness studies are scarce. Pharmacokinetic and pharmacodynamic differences between the agents might affect clinical response rates. We aimed to compare the effectiveness of ceftolozane–tazobactam and ceftazidime–avibactam for treatment of invasive multidrug-resistant P aeruginosa infections. This multicentre, retrospective, observational study was conducted at 28 hospitals in the USA between Jan 1, 2016, and Dec 31, 2023. Eligible patients were adults (age ≥18 years old) with microbiologically confirmed multidrug-resistant P aeruginosa pneumonia or bacteraemia treated with ceftolozane–tazobactam or ceftazidime–avibactam for more than 48 h. Patients were matched (1:1) by study site, severity of illness, time to treatment initiation (≤72 h or >72 h), and infection type. The primary outcome was clinical success at day 30, which was defined as survival, resolution of signs and symptoms of infection with the intended treatment course, and the absence of recurrent infection due to P aeruginosa. Secondary outcomes included all-cause mortality and development of resistance to study drug. 420 eligible patients were included (210 in each treatment group), of whom 350 (83%) had pneumonia and 70 (17%) had bacteraemia. Baseline demographics, comorbidities, and severity of illness indicators were similar between groups. On treatment initiation, 336 (80%) patients were in the intensive care unit, 296 (70%) were receiving mechanical ventilation, and 168 (40%) required vasopressor support. Clinical success was observed in 128 (61%) of 210 patients treated with ceftolozane–tazobactam and 109 (52%) of 210 patients treated with ceftazidime–avibactam. By conditional logistic regression analysis, the adjusted odds ratio (aOR) of success after treatment with ceftolozane–tazobactam compared with ceftazidime–avibactam was 2·07 (95% CI 1·16–3·70). For patients with pneumonia, clinical success was observed in 110 (63%) of 175 patients in the ceftolozane–tazobactam group and 89 (51%) of 175 patients in the ceftazidime–avibactam group (aOR 2·34 [95% CI 1·22–4·47]). Among patients with bacteraemia, rates of clinical success were 51% (18 of 35 patients) for patients treated with ceftolozane–tazobactam and 57% (20 of 35 patients) for those treated with ceftazidime–avibactam (0·76 [0·23–2·57]). There were no significant differences between groups in 30-day or 90-day mortality. Among patients whose baseline isolates were tested for susceptibility, resistance developed in 22% (38 of 173) of patients treated with ceftolozane–tazobactam and 23% (40 of 177) of patients treated with ceftazidime–avibactam. Treatment with ceftolozane–tazobactam resulted in higher rates of clinical success compared with ceftazidime–avibactam for invasive infections due to multidrug-resistant P aeruginosa. Differences were driven by improved response rates for patients with pneumonia who were treated with ceftolozane–tazobactam. There were no significant differences between study groups with respect to all-cause mortality; treatment-emergent resistance was common with both agents. Merck Sharp & Dohme.