الفهرس 
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Abstract
This study illustrated that a high level of resistance of P. aeruginosa isolated from patients with different types of HCAIs admitted at different departments at Sohag University Hospital to multiple classes of antibiotics and the resistance rate towards colistin, which is the last-resort treatment in clinic for infections with MDR Gram-negative bacteria, is in continuous increase. This has become a great worldwide clinical problem. In order to prevent transmission of these resistant strains, accurate and rapid monitoring techniques should be administered with the wise use of antibiotics and avoidance of unnecessary treatment with broad spectrum antibiotics for P. aeruginosa without antibiotic sensitivity testing to avoid treatment failure and development of resistance due to unnecessary use of this class of antibiotics.
PCR assays allows faster establishment of effective antibiotic therapies, and will lead to improved therapeutic success and reduced empirical treatments with broad-spectrum antibiotics, which are costly and have high toxicities, and eventually slow potential development of antibiotic resistant organisms. In terms of infection control programs, such rapid detection of resistance could be used to prevent nosocomial spread of resistant strains in advance.
It’s important to reduce the spread of HCAIs by strict infection control measures as hand hygiene practice, proper cleaning, disinfection and sterilization of equipments and hospital environment to prevent cross transmission and regular surveillance for resistant strains of P. aeruginosa with isolation of infected patients to prevent transmission of infection.
It is important to control development of antibiotic resistance by monitoring potential developing of new resistant genes that may be produced within Gram negative bacteria including P. aeruginosa. This will help to establish effective antibiotic therapies and prevent nosocomial infection as well as environmental spread of resistant strains.
Summary
Nosocomial infections (NIs) caused by P. aeruginosa represent a widespread problem in today’s healthcare environment with between 7% and 10% of hospitalized patients acquiring an infection annually. This microorganism is regarded as one of the human opportunistic pathogens, which may lead to widespread diseases such as septicemia, pneumonia, wound, respiratory and urinary tract infections. Also, NIs have a significant burden to patients, they affect the general health of patients, cause functional disability, emotional stress and may lead to conditions that reduce quality of life.
In addition, the widespread use of antibiotics has fostered the development of resistance in a variety of pathogenic bacteria. Unfortunately, the emergence of bacterial strains that exhibit resistance to a variety of antibiotics (multi-drug resistant strains) are becoming the major causes of treatment failure of infections worldwide.
P. aeruginosa infections are clinical problem; it’s difficult to treat because of high resistance to many antibiotics (Multi-drug resistant) and a high risk of emergence of resistance during therapy. In patients infected by strains resistant to carbapenems, fluoroquinolones, and aminoglycosides, it is very difficult to select an appropriate antibiotic for treatment. Therefore, the medical community has inevitably reintroduced older antibiotics such as colistin which has great antibacterial activity, especially against Gram-negative bacteria such as P. aeruginosa, it targets lipopolysaccharide in the outer membrane.
Unfortunately, it has been observed in recent years that colistin-resistant P. aeruginosa strains are also being increased. Resistance to colistin is mediated mainly through lipid A structural adjustments, resulting from the addition of phosphoethanolamine (Pet) and 4-amino-4-deoxy-L-arabinose (L-Ara-N) to the lipid A moiety on the surface membrane; these additions make lipid A less cationic such that the anionic colistin is unable to bind and initiate membrane lysis.
The plasmid mediated colistin resistance genes (mcr genes) diminish bacterial affinity toward colistin by encoding phosphoryl-ethanolamine transferase, which reduces the negative charge of the microbial outer membrane, resulting in the development of microbial resistance.
Our study was carried out in Sohag University Hospital in the period between May 2020 and May 2022. We collected 225 samples from different hospital departments to detect P. aureginosa strains isolated from patients with different types of infections.
Samples were taken from infected patients, cultured on selective media (cetrimide agar). Seventy five P. aeruginosa strains were isolated all were subjected to antibiotic sensitivity testing (disc diffusion method). According to CLSI 2016 the antibiotic susceptibility profile of the isolated P. aeruginosa strains was as follows:
Twenty eight percent (28%) were susceptible to Piperacillin, (12%) to Ceftazidime, (12%) to Cefepime, (24%) to Aztreonam, (60%) to Imipenem, (64%) to Meropenem, (76%) to Colistin, (56%) to Polymyxin B, (52%) to Gentamicin, (40%) to Tobramycin, (40%) to Amikacin, (32%) to Netilmycin, (36%) to Ciprofloxacin, (36%) to Levofloxacin, (24%) to Lomefloxacin, (36%) to Norfloxacin, (28%) to Ofloxacin and (24%) to Gatifloxacin.
Colistin resistance rate among P. aeruginosa isolates was determined by disc diffusion method and confirmed by Epsilometer method. According to these test results, 24% of isolates were Colistin resistant. Then the isolates were tested for mcr genes by PCR; mcr-1 gene was found in (44.44%) of colistin resistant strains while the percentage of mcr-2 gene was (16.67%).