Acute respiratory distress syndrome is a common complication of severe viral pneumonia, such as influenza and COVID‐19, that requires critical care including ventilatory support, use of corticosteroids and other adjunctive therapies to arrest the attendant massive airways inflammation. Although recommended for the treatment of viral pneumonia, steroid therapy appears to be a double‐edged sword, predisposing patients to secondary bacterial and invasive fungal infections (IFIs) whereby impacting morbidity and mortality. Mucormycosis is a fungal emergency with a highly aggressive tendency for contiguous spread, associated with a poor prognosis if not promptly diagnosed and managed. Classically, uncontrolled diabetes mellitus (DM) and other immunosuppressive conditions including corticosteroid therapy are known risk factors for mucormycosis. Upon the background lung pathology, immune dysfunction and corticosteroid therapy, patients with severe viral pneumonia are likely to develop IFIs like aspergillosis and mucormycosis. Notably, the combination of steroid therapy and DM can augment immunosuppression and hyperglycaemia, increasing the risk of mucormycosis in a susceptible individual. Here, we report a case of sinonasal mucormycosis in a 44‐year‐old woman with hyperglycaemia secondary to poorly controlled diabetes following dexamethasone therapy on a background of influenza pneumonia and review 15 available literatures on reported cases of influenza and COVID‐19 associated mucormycosis.

As an opportunistic pathogen, Escherichia coli (E. coli) is widely recognized as the main cause of nosocomial infections as well as some disorders especially those associated with urinary tract infections (UTIs). This study, therefore, sets out to determine the extent of antibiotic resistance to quinolones and to measure the frequency of qnr genes (A, B, and S) within extended-spectrum beta-lactamase (ESBL) and non-ESBL-producing strains of E. coli isolated from UTI-diagnosed patients as well as to investigate their antimicrobial susceptibility patterns for some selected antibiotics in southwest Iran. Two hundred E. coli strains were isolated from UTI-diagnosed patients, hospitalized in nine different wards of Ahvaz Golestan Hospital between November 2015 and March 2016. The isolates were confirmed through well-practiced phenotypical methods. Moreover, the antimicrobial susceptibility test was successfully performed using a disk diffusion method. ESBL production among the isolates was screened by double disk synergism test (DDST), and the qnr genes were identified using a multiplex PCR. Out of the 200 samples collected, 167 isolates were confirmed to be E. coli strains. Maximum and minimum resistance were reported against nalidixic acid and chloramphenicol with 65.3% and 17.4%, respectively. Most of the isolates were resistant to all three types of quinolones studied in this research. Using multiplex PCR, the qnr genes were found in 100 (59.88%) strains (qnrA = 10, qnrB = 21, qnrS = 41, qnrB-S = 21, qnrB-A = 1, qnrA-S = 3, qnrA-B-S = 3), 58% of which was found among ESBL-producing isolates. Resistance to quinolones antibiotics was highest among ESBL-producing isolates harboring, especially qnrS among other determinants of the qnr gene. There is a need for sensitive antibiotic stewardship especially in hospitals of Ahvaz, Khuzestan province. Further research is needed to ascertain the gravity of quinolones resistance in Iran and to quickly act against its spread among other nosocomial pathogens.

Two major hospitals in Kano, North West Nigeria have recorded increasing resistance of clinical pathogens to broad spectrum β lactams, mediated by extended spectrum β- lactamase (ESβL) and non ESBLs. A study was therefore undertaken to determine the occurrence and prevalence of plasmid and chromosomal mediated AmpC βL and carbapenemase in addition to already known ESBL due to increasing resistance of pathogens from the two hospitals to carbapenems, cephamycins and flouroquinolones. Antibiogram tests and ESBL, AmpC and carbapenemase production tests were performed on all the isolates. AmpC and carbapenemase producers were further screened for AmpC inducibility and metallo beta lactamase production respectively. Majority of the isolates (> 80%) were resistant to both β-lactam and non β-lactam antibiotics. Reduced susceptibility to levofloxacin, nitrofurantoin, nalidixic acid and ofloxacin among the isolates were observed with the exception of P. aeruginosa which is totally resistant to imipenem and levofloxacin. An overall prevalence of 14.4%, 11.9% and 11.9.3% for ESβL, AmpC and carbapenemase was observed respectively. About 7.9% of the AmpC producers can over expressed the chromosomally mediated AmpC and 85.8% of the carbapenemase producers require metal for their action. Co-production of either of two and/or all of the enzymes was observed in E. coli, P. mirabilis and P. aeruginosa. Antibiotic resistance among isolates from the two hospitals is increasing and the major cause of this resistance in the pathogens studied are production of AmpC, carbapenemase (especially Metallo β- lactamase) in addition to already known ESBL enzymes by the pathogens. Some of the isolates also possess the capacity to elaborate two or more of the enzymes concurrently, which would renders them resistant to a multitude of antibiotics.