ABSTRACT
OBJECTIVES: The use of cephalosporins combined with clavulanate for the treatment of ESBL-harbouring Enterobacteriaceae has been scarcely described. We aimed to describe the effect of different concentrations of clavulanate in the MIC of cefixime and ceftibuten of ESBL-producing Escherichia coli and Klebsiella pneumoniae. METHODS: ESBL-producing E. coli and K. pneumoniae isolates were studied. Fixed concentrations of cefixime and ceftibuten (ranges of 32-0.25 and 64-0.5 ng/ml, respectively) were used. Combinations of cefixime/clavulanate and ceftibuten/clavulanate in different ratios (1:0, 1:1, 2:1, 4:1, 8:1, 16:1, 32:1) were tested. MIC were determined by broth microdilution. RESULTS: A total of 6 ESBL-producing E. coli, 6 ESBL-producing K. pneumoniae and 2 control E. coli were tested. When different quantities of clavulanate were added to cefixime and ceftibuten, greater than two-fold decreases in the MIC were observed. When testing the 1:1 cefixime/clavulanate ratio, 10/12 isolates were susceptible. When the ratios 2:1, 4:1, 8:1 and 16:1 were tested, susceptibility was noted for 9/12, 8/12, 4/12 and 5/12 isolates, respectively. Only 2/12 K. pneumoniae isolates were susceptible when the ratio 32:1 was tested. When testing ceftibuten/clavulanate, all isolates remained susceptible across all experiments. CONCLUSIONS: Clavulanic acid has a favourable effect in reducing the MIC of cefixime and ceftibuten in isolates of ESBL-producing E. coli and K. pneumoniae. Combining clavulanate with ceftibuten or cefixime could be a useful treatment strategy.
ABSTRACT
The incidence and distribution of coccidioidomycosis are increasing. Information scarcity is evident in Mexico, particularly in non-endemic zones and specific populations. We compared the treatment and outcomes for patients with isolated pulmonary infections and those with disseminated coccidioidomycosis, including mortality rates within six weeks of diagnosis. Of 31 CM cases, 71% were male and 55% were disseminated. For 42% of patients, there was no evidence of having lived in or visited an endemic region. All patients had at least one comorbidity, and 58% had pharmacologic immunosuppressants. The general mortality rate was 30%; without differences between disseminated and localized disease. In our research, we describe a CM with a high frequency of disseminated disease without specific risk factors and non-significant mortality. Exposure to endemic regions was not found in a considerable number of subjects. We consider diverse reasons for why this may be, such as climate change or migration.
ABSTRACT
Spontaneous mediastinal emphysema (ME) is a rare clinical entity often associated with sudden changes in intrathoracic pressures. The presumed pathophysiological mechanism is diffuse alveolar injury leading to alveolar rupture and air leak. Inflammatory alterations installed over the airway following SARS-CoV-2 infection may reduce its distensibility and compliance conferring an increased risk of developing the complication, even in the absence of mechanical ventilation. However, the exact mechanism by which ME occurs in SARS-CoV-2 pneumonia is unknown. We report a case of a 58-year-old man that presented to the emergency department with dyspnea, subcutaneous emphysema of the neck and high clinical suspicion of COVID-19 infection. There was no smoking history and no lung comorbidities. The patient was admitted into a monitored unit and received management accordingly (having never required mechanical intubation). During chest radiological evaluation ME was found and ultimately resolved with noninvasive maneuvers. We want to emphasize the importance of this adverse event despite their non-smoking history and the exclusion of positive pressure ventilation. Given the recent increase in the number of patients with COVID-19 related pneumonia, the presence of pneumomediastinum in patients with COVID-19 infection should alert the clinician to monitor the patients carefully for possible worsening of disease, especially when lung lesions are severe.
