Veterinarians should protect themselves against tick bites, and should use masks to prevent transmission by inhalation of zoonotic infections in endemic countries.
Mucormycosis is increasingly common in patients with risk factors such as diabetes mellitus, neutropenia, and corticosteroid therapy. However, mucormycosis seems to be less common in patients with human immunodeficiency virus (HIV) infection compared to patients with other risk factors. Despite their lower virulence, Lichtheimia species should be regarded as emerging pathogens among Mucoralean fungi. We report a fatal case of pulmonary mucormycosis due to Lichtheimia ramosa in a 52-year-old man with an end-stage HIV infection. He had a cachectic appearance and his CD4 count was 8 cells/mm(3). The fungal infection was diagnosed based on a positive sputum culture with histopathologic confirmation. The fungus was resistant to caspofungin, anidulafungin, and voriconazole [minimum inhibitory concentration (MCI) >32 µg/ml], whereas the E test MIC values of itraconazole, posaconazole, and amphotericin B were 0.38, 0.38, and 0.5 µg/ml, respectively. Although intravenous drug use is the main risk factor for the development of mucormycosis in HIV-infected patients, it may also develop in patients with low CD4 count, opportunistic infections and/or additional diseases, such as Kaposi's sarcoma or severe immunodeficiency, as in our case.
IntroductionUrinary tract infections (UTIs) are the most common community-onset infections in the adult population in many parts of the world. Clinical manifestations of community-onset UTIs range from asymptomatic bacteriuria to acute pyelonephritis with sepsis [1,2]. The major UTI pathogen is Escherichia coli, and there is increasing multidrug resistance in the isolates from community-onset infections. Multidrug resistance of these isolates is frequently associated with the presence of extended-spectrum β-lactamase (ESBL) genes [3,4]. ESBL-producing isolates are resistant to all penicillins, cephalosporins, and aztreonam, combined with high resistance rates to fluoroquinolones and trimethoprim/ sulfamethoxazole (TMP-SMX) [5]. Multidrug resistance of ESBL-positive E. coli makes it more difficult to decide the antibiotic treatment in community-onset UTI and increases the risk of treatment failure. Early initiation of appropriate empirical therapy reduces mortality, especially in life-threatening UTIs [6]. Therefore, a better understanding of the risk factors for community-onset UTIs caused by ESBL-positive E. coli will guide clinicians in choosing appropriate empirical therapy. Also, it will ensure that measures are taken to reduce risk factors for these resistant infections.For this reason, we aimed to determine the prevalence and risk factors for community-onset UTI caused by ESBL-producing E. coli.
Materials and methods
Study population and data collectionThis prospective cohort study was conducted between January 2012 and March 2014 in cases of communityonset UTI caused by E. coli. Demographic characteristics, Background/aim: Community-onset urinary tract infections (UTIs) caused by extended-spectrum β-lactamase (ESBL)-producing Escherichia coli have increased in many parts of the world. This study aimed to determine the prevalence and risk factors for communityonset UTI caused by ESBL-producing E. coli.
Materials and methods:This prospective cohort study was conducted between January 2012 and March 2014 in cases of communityonset UTI caused by E. coli. Patients with UTI due to ESBL-producing E. coli and patients with UTI due to non-ESBL-producing E. coli were compared to identify risk factors for ESBL-producing E. coli in the community.Results: A total of 305 patients (116 males [46.4%]; mean age: 57.76 ± 18.06 years) were included in the study. Among these patients, 154 (50.5%) were infected with ESBL-producing E. coli. In multivariate analysis, the healthcare-associated UTI (odds ratio [OR]: 1.80; 95% confidence interval [
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