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Background and Objectives: Pneumocystis jiroveci is an important causative agent of Pneumocystis pneumonia. During childhood, exposure to Pneumocystis occurs and antibody was built in early childhood. The aim of this study was to describe the molecular epidemiology of P. jiroveci in children without any respiratory syndrome and survey the distribution of different mitochondrial large subunit, ribosomal ribonucleic acid (mtLSU- rRNA) genotypes. Materials and Methods: Mini-bronchoalveolar lavage (mini-BAL) fluids from pediatric patients with no history of lung disorders were obtained during a 14-month period. P. jiroveci colonization was confirmed by immunofluorescence staining, nested PCR and sequencing. Genotypic characterization at the mitochondrial large subunit rRNA gene was performed by direct sequencing. Results: Of 172 BAL specimens from patients, with mean age of 4.9 years, the prevalence of P. jiroveci colonization was 3.5% (6 samples). The results of sequencing revealed the two polymorphisms; 85/A; 248/C in 3 cases, and 85/T; 248/C in other cases. One sample also showed a mutation replacement at position 258 (T-to-C change), which was not reported previously. Conclusion: Colonized person as an environmental reservoir might play an important role in the progression of infection in immunocompromised patients. Diagnosis of the reservoir and genotyping can be essential for the prevention of nosocomial infections. [ABSTRACT FROM AUTHOR]

Background: Spontaneous bacterial peritonitis (SBP) is a fatal complication of ascites fluid infection. The causes of SBP in children differ from those in adults, and these bacteria are frequently resistant to antibiotics. Therefore, this study investigated the clinical findings, bacterial etiology, and antimicrobial resistance in children with SBP. Methods: This study was conducted on all new pediatric ascites patients, who were admitted to the Department of Pediatric Gastroenterology, Namazi Hospital, affiliated with Shiraz University of Medical Sciences (Shiraz, Iran) from 2021 to 2022. Required data such as demographic information, and clinical information such as complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Gram staining, blood culture by Automated Blood Culture System (BACTEC), and antibiogram of ascites fluids by disc diffusion method were all collected. Finally, the data were statistically analyzed using SPSS Software (version 26). Besides, the t test, Fisher's exact, Mann- Whitney, and Chi square tests were used for data analysis. In all tests, P≤0.05 was considered statistically significant. Results: The present study examined 62 children with ascites of which 18 (29%) had SBP. The median (IQR) age was 2.5 (8.1) years. Thirty-four (54.8%) of the participants were girls. Abdominal pain was the most common clinical manifestation in patients (54%), and there was a significant association between abdominal pain and SBP (P=0.02). In 12 positive ascites fluid cultures, coagulase-negative staphylococci had the highest frequency (25%), followed by Escherichia coli (16.7%). Thirdgeneration cephalosporins had a 25% sensitivity in the total positive cultures. This sensitivity was 33.3% for Gram-negative cultures and 16.6% for Gram-positive cultures. Conclusion: Although third-generation cephalosporins are recommended as the primary antibiotic for the empirical treatment of SBP, the present study found high bacterial resistance. Finally, empirical therapy should be tailored to each region's bacterial resistance features. [ABSTRACT FROM AUTHOR]

To evaluate the association of virulence genes CagA, VacA and UreAB of H. pylori with the development of different gastric disorders, polymerase chain reaction was performed on H. pylori organisms isolated from biopsy samples of stomach of patients with ulcerative disease and nonulcerative disease. The difference between the groups was statistically significant (p < 0.05) only for VacA gene. We detected 8 phenotypes, characterized as CagA(+)-VacA(-)-UreAB(+) (phe 1), CagA(-)-VacA(-)-UreAB(-) (phe 2), CagA(+)-VacA(+)-UreAB(-) (phe 3), CagA(+)-VacA(-)-UreAB(+) (phe 4), CagA(-)-VacA(+)-UreAB(+) (phe 5), CagA(+)-VacA(-)-UreAB(-) (phe 6), CagA(-)-VacA(+)-UreAB(-) (phe 7), CagA(-)VacA(-)-UreAB(+) (phe 8). The prevalence of phenotype 1 was significantly higher in the patients with UD than that in the patients with NUD (p < 0.05). These results suggest that in the population under our study, being infected by a H. pylori strain with the genotype CagA(+)-VacA(+)-UreAB(+) may be associated with an increased risk of acquiring an ulcer disease.