ABSTRACT
Background: Typhoid fever is endemic in developing countries including Egypt, producing major public health problems with high mortality and morbidity.The emergence of resistant serovarTyphi [S. typhi] to commonly recommended antimicrobials is alarming in developing countries. Fluoroquinolones have been the empirical drug of choice for multidrug-resistant MDR typhoid. However, there have been several alarming reports of fluoroquinolones therapeutic failure in typhoid patients. Resistance of S. typhi to fluoroquinolones commonly results from target site mutation
Objectives:Determination of antimicrobial resistance pattern of S. typhi isolated from Egyptian patients with typhoid fever admitted to or attended Mansoura UniversityHospitals [MUHs] and Mansoura Fever Hospital, detection of quinolones resistant strains and using PCR-RFLP and sequencing techniques for testing mutation at QRDR of gyrA gene in the isolated strains
Methodology: Blood andStool samples from clinically suspected typhoid patients were screened by culture on suitable media and were identified biochemically. The identified S. typhi isolates were tested for susceptibility to antimicrobials using the Kirby Bauer disk diffusion method. Minimum inhibitory concentrations of ciprofloxacin were determined by E test. Interpretation of all results was done according to the CLSI guidelines 2015. Mutations in gyrA gene were detected by PCR-RFLP and sequencing methods
Results: Out of 500 blood and stool samples, 57 isolates were S. typhi [96.6%] and only two were S. paratyphi A [3.4%]. Of the 57 S. typhi, 80.7% were resistant to nalidixic acid,50.9% had ciprofloxacin MIC 0.125-0.5 µg/ml and 19.3% had ciprofloxacin MIC >1 microg/ml. Ser 83 mutation in gyrA was detected in 63.1% of the isolates
Conclusion: Increasedemergence of fluoroquinolones -resistant typhoidal Salmonella in Egypt which is caused mainly by point mutation at codon 83 [Ser83-Phe substitution TCC-TTC] in QRDR of gyrA gene
ABSTRACT
Background: chronic periodontitis is probably one of the most common bacterial infections in humans. Microorganisms within the gingival crevice and the periodontal pocket play a significant role in its initiation and progression. The traditional diagnosis of chronic periodontitis requires massive tissue destruction. Therefore, knowledge of disease progression prior to influential destruction will allow for treatment to achieve the best results. MMP-8 is a good biomarker that can be used for this purpose and also is its activator MMP-3
Aim of the work: assessment of MMP-8 and MMP-3 as biomarkers and indicators in the diagnosis of chronic adult periodontitis
Methods: immunologic screening of MMP-8 levels in GCF by ELISA. MMP-3 was immunohistochemically localized and its cellular origin in inflamed human gingival tissue was detected the study included thirty-two patients divided into two groups: A study group: included twenty four patients with chronic periodontitis and was subdivided into three subgroups: Subgroup [A]: Included eight patients treated only by scaling and root planning [SRP]. Subgroup [B]: Included eight patients treated with oral Doxycycline 20 mg twice a day in addition to [SRP]. Subgroup [C]: included eight patients surgically treated to remove the periodontal pockets in addition to [SRP]. A group including eight clinically normal individuals was used as a control group
Results: the results showed a statistically significant change in the level of MMP-8 in subgroups A, B, C after treatment compared to day 0 [p<0.000l] and to the control group. On clinical examination there was also a statistically significant improvement in patients of both subgroups [B] and [C] compared to group [A] after three months of treatment. The results of examining gum tissue samples from subgroup [C] patients showed the presence of positive MMP-3 immunoreaction in all cases in the basal and suprabasal layers as well as in lymphocytes and macrophages. Weak positive MMP-3 immunoreaction was detected in three out of the eight control samples [37.5%]
Conclusion: it was concluded that MMP- 8 levels in GCF in periodontitis patients decreased with different treatment modalities and this was associated with improvement in the clinical periodontal parameters. GCF MMP-8 concentrations differentiate periodontally healthy subjects from diseased ones. In addition to this comes MMP-3 that activates pro MMP-8. MMP-3 expression in chronic periodontitis was found to originate from residual gingival fibroblasts epithelial cells and macrophages. Improvement in biochemical and clinical outcomes was move pronounced in patients receiving a subantimicrobial dose of Doxycycline 20 mg twice a day
Abbreviations: MMPs, matrix mefalloproteinases; GCF, gingival crevicular fluid; PI, plaque index; GI, gingival index; PD, probe or periodontal pocket depths; AL, periodontal attachment level; SRP, scaling and root planning
ABSTRACT
Extra intestinal isolates of Escherichia coli associated with disease often express high molecular weight acidic polysaccharide capsules, or K antigens, on their cell surface. Over 80 such K antigens have been identified, and these have been divided into four principal groups based on serological, biochemical, and genetic data. The K5 polysaccharide is commonly associated with strains causing urinary tract infections and belongs to Group 2. These capsules resemble those possessed by Neisseria meningitides and hemophilic influenza. The K5 capsule gene cluster is composed of three principal regions, [1-3] and their transcription is driven by two convergent temperature-regulated promoters located upstream of regions 1 and 3. In this paper, working on the region 1 promoter evidence is presented of a role for two transcriptional regulators in the regulation of transcription of the Escherichia coli K5 capsule gene cluster and demonstrate, using a combination of reporter gene fusions, random transposon mutagenesis, P-Galactosidase assays, PCR and Southern blotting that mutations in any of these two genes markedly reduced transcription from region 1 promoter. Sequencing of these two mutated genes is required for full characterization
ABSTRACT
Background: implementation of MRSA decolonization programs is increasing and the emergence of mupirocin resistance among MRSA isolates has been a well-defined phenomenon in many parts of the world two mupirocin resistance phenotypes; low-level [LR-Mup] and high-level [HR-Mup] mupirocin resistance. Are defined in staphylococci. High-level mupirocin resistance cannot be eradicated with mupirocin
Aim of the Work: to assess the prevalence of the Mup A [ileS-2] gene encoding high-level mupirocin resistance among MRSA isolates and to study risk factors and predictors of mupirocin resistance in Mansoura University Hospitals [MUHs] supporting an efficient control of MRSA colonization
Materials and Methods: This study was carried out on 1200 nasal swab, MRSA isolates were detected by growth on Mueller-Hinton agar supplemented with 4% NaCl and oxacillin [6mglml] and confirmed by cefoxitin disc 'diffusion test [DDT]. Mupirocin resistance was detected by DDT and agar dilution test [ADT]. The presence of mup A [ileS-2] gene was tested by PCR for all mupirocin resistant MRSA isolates
Results: out of the 396 MRSA isolates, 76 mupirocin resistant strains were detected. Of them 59 [77.6%] were LR-Mup and 17 isolates [22.4%] were HR-Mup Significant risk factors included; previous ICU stay, previous treatment with mupirocin, other antibiotics and previous pseudomonas infection
Conclusion: mupirocin resistance is an emerging problem in MUHs. In our study HR- Mup mupirocin resistance was detected in 22.4% of MRSA isolates. The finding that the ileS2 gene was detected in all HR-Mup MRSA represents an alarming sign as this gene allow the fast spread of resistance among both MRSA, methicillin sensitive S. aureus [MSSA] and coagulase negative staphylococci [CoNS]. Thus we recommend a strict policy on mupirocin use. in MUHs including proper dose and duratio:1 as prolonged use has led to the development of a rapidly transmissible resistance
ABSTRACT
Background: Occult hepatitis C virus [HCV] infection is a type of recently identified chronic infections that is evidenced only by detection of HCV- RNA in patients' liver tissue with consistently negative serum tests for antibodies to HCV and HCV-RNA
Aim: To study the prevalence of occult HCV infection among Egyptian patients with abnormal liver function tests and compare the characteristics of those patients with other patients with overt chronic hepatitis C infection
Methods: The presence of HCV-RNA was tested by reverse-transcription polymerase chain reaction [RT-PCR] in both liver tissue and peripheralblood mononuclear cells [PBMCs] for forty five patients with abnormal liver function tests. Clinical features of 27 patients with occult HCV infection [ 27 out of 45 patients who were negative for anti-HCV and serum HCV-RNA] were compared to 50 untreated patients with chronic HCV [anti-HCV antibodies and serum HCV-RNA positive], matched for age, gender, duration of abnormal liver function tests and body mass index
Results: HCV-RNA was detected in liver tissue of 27 [59.4%] out of 45 patients with abnormal liver function tests who were negative for both anti-HCV antibodies and serum HCV-RNA with abnormal liver function tests [i.e., who had occult HCV infection]. Twenty patients out of the 27 [74%] having intrahepatic HCV-RNA, had also viral RNA in their PBMCs. Regarding the biochemical characteristics there was significant impairment in classic HCV infection; serum bilirubin [P < 0.001], ALT [P = 0.009], AST [P = 0.013], alpha fetoprotein [P < 0.001], and fasting blood glucose [P < 0.008], but serum albumin, cholesterol, triglycerides and prothrombin time were significantly higher in occult HCV than chronic HCV [P <0.001]. No significant difference regarding Gamma-glutamyl transpeptidase [P< 0.10] was found. Necroinflammatory reactions, fibrosis, [P<0.0001] and cirrhosis [P = 0.03] were significantly higher in chronic HCV than occult HCV, but there was no significant difference regarding steatosis [P = 0.41]
Conclusion: Patients with abnormal liver functions may have intrahepatic HCVRNA in the absence of anti-HCV antibodies and serum HCV-RNA. Occult HCV infection is a milder disease than chronic HCV. Screening of those patients with persistently abnormal liver function for occult HCV-RNA can be firstly done by examining PBMCs