ABSTRACT
Background: There are somehow conflicting data in the literature on whether Treg cells in human SLE are impaired
Aim of the work: to quantify CD4+ CD25+ Foxp3[+] T cells [Treg] in Egyptian children with SLE and to correlate these findings with their disease activity scores and drug therapy
Methods: We enrolled 37 Egyptian children with active SLE. The disease activity was assessed by measuring serum levels of anti-ds DNA antibody and by using scores of SLEDAL Twenty healthy children were also enrolled as normal controls
Results: The CD4[+]CD25[+] CD4[+]CD25[bright] and CD4[=]CD25[dim] cells in patients were significantly increased in comparison to controls. There was no significant difference in the Fax% gated on CD4+CD25[bright], CD4[+]CD25[dim] but on the other hand there was a significant increase when gated on CD4 CD25 and whole CD4[+] cells in patients than controls. There was no significant difference between different grades of activity, different lines of treatments and patients outcomes as regards all studied values. There was no significant correlation between any of studied parameters with SLED AI score except gated lymphocytes which showed significant negative correlation
Conclusions: There is increase in the expression of FoxpS in CD4 T cells mostly CD25 in Egyptian pediatric patients with active SLE under corticosteroid treatment without correlation with SLED AI score
ABSTRACT
Background: Catheter-associated urinary tract infections [CAUTI] are commonly caused by Gram-negative bacteria which have a steady increase in their resistance to commonly used antimicrobial drugs, including fluoroquinolones
Objectives: The aim of this study was to identify the causative bacteria of CAUTIs, to assess resistance of Gram-negative bacilli to common fluoroquinolones, and to detect mutant gyrA gene responsible for fluoroquinolone resistance
Methods: 100 catheterized male patients, admitted to the Urology Department of Assiut University Hospital, were investigated for the causative organisms of CAUTI. Antimicrobial susceptibility testing of 123 isolates was performed by agar disc diffusion and minimum inhibitory concentration [MIC] test to ciprofloxaciri was performed to ftuoroquinolone-resistant Gram-negative isolates. Fluoroquinolone-resistant strains of E.coli, Klebsiella spp and Pseudomonas spp were investigated to detect the presence of quinolone resistance gyrA gene by PCR method
Results and conclusions: The isolates were E. coll [45.5%], Pseudomonas aeruginosa [19.6%] and Klebsiella spp [17.9%]. 28% of patients had quinolone-resistant isolates. Fluroquinolones resistance was detected in 36.6% of the total isolates [45/123] and in 37.5% of Gram negative isolates [39/104]. The highest quinolone resistance rate of the Gram negative isolates was observed to norfloxacin [33.7%]followed by levofloxacin [32.7%], and ofloxacin and lomefloxacin [30.8%]. The highest resistance rates were observed by Klebsiella spp to norfloxacin [45.4%, P<0.001], by Ps. aeruginosa to norfloxacin and levofloxacin [41.7% P<0.04], and by E. coll to lomefioxacin and levofloxacin [30.4%, P<0.04]. MIC values >32 microg/ml "were obtained by 66.7 % of Klebsiella spp, 72.7% of E. coli and 100% of Ps. aeruginosa resistant isolates. The high rate of quinolone resistance and the high MICs are alarming and the wide use of quinolones on empirical basis needs to be restricted. Twenty eight strains [85%] were positive for mutant gyrA gene by PCR. Not all quinolone-resistant isolates tested by PCR were positive for mutant gyrA gene suggesting that other causes for quinolone resistance may be involved?