This study was designed to determine the efficacy and safety of 1-week triple therapy regime consisting of pantoprazole, amoxicillin and clarithromycin in the cure of Helicobacter pylori infection leading to duodenal ulcer disease and/or gastritis. Sixty-one patients (47 males, 14 females with a mean age of 34 years) belonging to different ethnic groups suffering from H. pylori-associated duodenal ulcer and/or gastritis for an average of 2.46 years were recruited. Having satisfied primary selection criteria, patients received pantoprazole 40 mg b.i.d., clarithromycin 500 mg b.i.d. and amoxicillin 1,000 mg b.i.d. for 7 days. All medications were stopped there after H. pylori eradication was determined 4–6 weeks after treatment by a repeat endoscopy, a rapid urease test, H. pylori culture and histology assessment as indicators of cure. All three tests must be negative to consider the infection to have been successfully eradicated. Fifty-seven patients completed the efficacy analysis per protocol. Dramatic symptomatic improvement was noted in most patients immediately after stopping treatment and it was sustained at 6 weeks. At the end of the study, the healing rate of duodenal ulcers (complete re-epithelialization) following 1-week treatment only, as indicated above, and without any maintenance therapy was 66.7%, that of gastritis was 55.7%, and that of erosions was 64.3%. The overall eradication rate for H. pylori, however, was 93% (95% CI 83.0–98.1%). Furthermore, histologic evaluation revealed a remarkable resolution in the activity of gastritis in all the patients who had successful eradication of the infection.

This open-label study was designed to determine the extent of histological resolution of gastritis induced by Helicobacter pylori infection 4–5 weeks after successful eradication of the infection. Eradication was achieved using a triple therapy regimen consisting of a twice daily dose of pantoprazole 40 mg, clarithromycin 500 mg, and amoxicillin 1,000 mg taken for 1 week only. No other medications were given thereafter. Four biopsies were processed for histological examination of each patient, two from the antral and two from the corporeal mucosa, first at the start of the study and then again 4 weeks after cessation of the medication trial. Scoring for H. pylori colonization and the severity of gastritis was determined for each patient according to the Sydney system. 53 of 57 patients in this study had their H. pylori infection successfully eradicated by the regimen mentioned and could be histologically evaluated. According to the severity of gastritis in the antral mucosa, patients were studied in 3 groups: mild, moderate and severe gastritis. 17 of 19 cases with mild gastritis showed complete resolution of the inflammation, with residual inflammatory changes persisting in 2 cases only. 22 of the 26 cases with moderate gastritis showed almost complete recovery except for minor residual inflammatory changes as judged by irregularity of intracytoplasmic mucine storage. Persistent residual inflammatory changes in the lamina propria were detected in 4 cases. Of the 8 cases with severe gastritis 5 showed subsidence of the inflammatory changes, but the mucosa in these cases revealed some scarring, distortion of the glandular epithelium and atrophy. In 3 cases residual inflammation persisted. Conclusion: One-week therapy with a twice daily dose of pantoprazole 40 mg, clarithromycin 500 mg and amoxicillin 1,000 mg, used to eradicate H. pylori causing active inflammation of the gastric mucosa, has led to subsidence of the acute inflammatory changes in all the cases with residual inflammation persisting in 17%. Severe gastritis may cause irreparable damage to the gastric mucosa. The density of H. pylori colonization does not appear to be related to the severity of gastritis, nor to the successful eradication achieved.

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Background: Fungal infections have been on the rise during the last few decades. Immunnocompromised patients are at risk for developing deep mycotic infections of which invasive candidiasis (IC) is particularly serious. Although Candida albicans is the most common cause of IC, other species such as C. krusei, C. tropicalis, and C. parapsilosis have also been recovered with variable virulence factors. Objectives: We compared between albicans and non-albicans Candida infections among immunnocompromised patients admitted to the National Liver Institute (NLI) and Menoufia University Hospitals (MUH) as regards the incidence and type of infection, ability of biofilm formation as well as the virulence genetic profile. Methodology: 42 Candida isolates were collected from different types of infections and classified as C.albicans and C. non-albicans according to their characteristic reactions on Brilliance™ Candida Chromogenic Agar. The biofilm-forming ability of the isolated species was demonstrated phenotypically by the microtitre plate method (MTP) and multiplex PCR assay verified the existence of the contributing virulence genes. Results:Out of 42 Candida isolates, 9 (21.4%), 26 (61.9%) and 7 isolates (16.6%) were recovered from superficial, invasive and device associated infections respectively. The number of non-albicans spp. exceeded that of C.albicans [25/42(59.52%): 17/42(40.48%)] and the highest frequency was for C. parapsilosis (14/25:56%) followed by C. tropicalis (8/25:32%) and finally C. krusei (3/25:12%).The percentage of biofilmforming isolates was 94.1% for C. albicans and 72% for non-albicans Candida spp. with no significant statistical difference (P> 0.05). The expression of HWP1 gene was significantly higher in biofilm-forming Candida spp. (P= 0.02). Conclusion: Infections due to non-albicans species are rising especially in immunosuppressed patients. HWP1, ALS1, SAP5 and PLB1 genes were all detected in both C. albicans and non-albicans and the majority of isolated Candida spp. were biofilm producers.

Background: Acinetobacter baumannii became one of the emerging life-threatening hospital acquired infection pathogens with marked antibiotic resistance due to multiple resistance mechanisms. One of these mechanisms is production of carbapenemase enzymes like Ambler Class B and Class D enzymes that hydrolyze carbapenems the last resort antimicrobial drug for treating multidrug resistant organisms. Objectives: To study the antimicrobial resistance of A. baumannii with detection of bla OXA carbapenemase genes responsible for resistance to carbapenems. Also to evaluate effectiveness of newly issued commercial Rapidec Carba NP kit test for detection of carbapenemases production and to assess the effect of implementing infection prevention and control (IPC) practices in decreasing rate of ICU blood stream infections. Methodology: This study was conducted from May 2017 to September 2018 by collecting blood cultures from ICU patients. A. baumannii species were identified and antibiotic susceptibility was run by VITEK 2Compact automated ID/AST instrument. Carbapenemase production was tested phenotypically by using Rapidec Carba NP kit test. A. baumannii species were tested for carbapenemase genes bla OXA-51 , bla OXA-23, bla OXA-24 and bla OXA-58 by multiplex PCR. Results: there was a significant decrease in number of ICU blood stream infections after implementing IPC practices. Isolated A. baumannii species were 100 % resistant to Ampicillin/Sulbactam, Cefipime, Ceftriaxone, Imipenem and Trimethoprim/Sulphamethoxazole, while highest sensitivity was to Amikacin (27.4 %). All isolates A. baumannii species gave positive results with Rapidec Carba NP kit test. Only bla andbla OXA-51 (88.2 %) were detected in isolated A. baumannii species but bla OXA-24 andbla OXA-58 were not detected. Conclusion: A. baumannii is a great life-threatening hospital acquired pathogen with marked drug resistant and easy spread. Rapidec Carba NP kit test is an easy, non-labor phenotypic test for carbapenemases production detection which can replace old cumbersome, difficult and labor Carba NP test.