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Abstract Pe. ”erug.inosa has been considered to be one of the causes of serious diseases in man and it infrequently is the cause of infection in normal individuals unless they have suffered from ma~~r trauma or burns. It is involved in respiratory. cutaneous and disseminated infections in individuals who have defective host de f,mses of cutaneous batTLers, granulocytes or a mmuno-: Several plasmids encoding resistance to one or more. antibioti.; could be identified from cl a n i ce l isolates Ps. aeruginosd. The present investigation was carried out in order to clarify the <Jenetic basis of Ps. aeruginosd ani:ibiotic resistdnce. Five Ps. aeruginosa isolates were used. two isolates; 1 & 2 we re isolated from the urine of two patients with chronic urinary tract infection and three lsolaLes. 3. 4, and 5, were isolated from patients with cance, bladder. The results obt.ei no.t ,,:howedt.het all five: isolates were equally sensitive to amikacin and were sensitive to tobr-<lmycinwith d i f f crerrt degrees. The most resist- ant isolate to tobramycl,-’W<l~J no. 1. The most resistant isolate to kanarr~cin was isolate no. 1 followed by isolate; 4,”3 and 5 res.:-,ectivelywhile isolate nc , 2 was sensitive. Also isolate no. 1 was highly resistant to st,’eptomycin followed by isolates; 4. 5 and 3. respectIvely. while isolate no. 2 was sensitive. The four Isolates; 1, 2. 4 and 5 were resistant to gentamicin. Isolate no. 1 was the most resistant one to gentamicin followed by isolate no. 4, while the isolates 2 and 5 were equal in their resistance to gentamicin and less than isolate no. 4. Isolate no. 3 was sensitive on the border line. Isolate no. 1 which was resistant to the four antibiotics had the lowe,,’::MIC of amikacin which reached 50 ~g/ml followed by Tm and Gm which reached for’ e it ner 400 ~g1m!. .•·.•hile those for Km and Sm more than 400 ~g/rnl. MIC for isolate no. 2 to Am. Tm , Km , Sm and Gm were; 25. 50. 100. 200 and 100 ug/ml respectIvely. Also MIC for isolate no. 3 to these antibiotics wen:, 12.5, 10C, 400. >400 and 50 ~g/ml respectively. for isolate no. 4 they were 25. 100. >400. >400. and 50 Ug/ml respectively and for isolate no 5 were; 12.5, 25. 100, 200 and 100 ~g/ml respectively. Single colonies of isolate no. 1 c;howed great variations in their levels of resistance to the different antibiotics indicating that the resistant genes are located in different plasmids. Isolate no. 2 single colonies were similar in their resistance to gentamicin levels indicating chromosomal mode of inheritance. In isolate no. 3. Km and Sm resistant genes were encoded by the same plasmids. Isolates no. 4 and 5 single colonies showed different levels of resistance to. Km. SOl and Gm with great agreement for resistance levels indicating the existence of the genes in the same plasmids. The percentages of E. coli k12 transformants which resist 10 ~g/ml of each antibiotics ranged from 1 1.75 when plasmid DNA was used as donor. The highest levels of resistance appeared for E. coli. k12 transformants to streptomycin followed by those; Km. Gm and Tm respectively. Transformation of the Gram positive S. aureus and B. eubt il is with plasmid DNA isolated from Ps. aeruginosa was unsuccessful. E. coli k12 ~ransformants indicated that the resistance to fun which can be acquired with a plasmid is probably 10 ~g Km/ml medium. The of 50 ~g Km resistance can be obtained from dose of plas~id as no. 20. 30 or 40 ~g Km/ml lowest single level double r”,o,isLance could be ”btained. This increase in the double dose had been attributed to gene interactions and c;~n~ regulatory mechanisms. Tree plasmids were respo”sible for the level of kanamycin resistance reclched 100 I1g/ml, 4 plasmids for the level of 200 I1g/ml. One plasmids tively. Each plasmid gave a resistance level of I1g medium. The possibility of gene interactions can be eXIsted. the same c.lppeClredfor tobramycin. Positive correlation between bilharzia. plasmid was estimated to give 50 I1g Sm/ml levels, 2 for the level of 100 I1g, 3 and 4 for the levels of 150 and 200 I1g/ml res~ecl:~ esistance Gm/ml also cancer high bacterial counts and high phage contents and no clear correlation was noticed between phage contents and the resistance of any of the antibiotics studied. In conclusion plasmids play an essential role in antibiotics resistance. To solve this problem it is essential to look for plasmid curing. Curing can occur spontaneously during growth and cell divisions or following treatments with some agents such as elevated temperatures. acridine hydrochloride. ascorbic acid and the bes~ ~herapeutic tz”eatnents might be through safe va cci net ioris. |