Mobile phones and Wi-Fi radiofrequency radiation are among the main sources of the exposure of the general population to radiofrequency electromagnetic fields (RF-EMF). Previous studies have shown that exposure of microorganisms to RF-EMFs can be associated with a wide spectrum of changes ranged from the modified bacterial growth to the alterations of the pattern of antibiotic resistance. Our laboratory at the nonionizing department of the Ionizing and Non-ionizing Radiation Protection Research Center has performed experiments on the health effects of exposure to animal models and humans to different sources of electromagnetic fields such as cellular phones, mobile base stations, mobile phone jammers, laptop computers, radars, dentistry cavitrons, magnetic resonance imaging, and Helmholtz coils. On the other hand, we have previously studied different aspects of the challenging issue of the ionizing or nonionizing radiation-induced alterations in the susceptibility of microorganisms to antibiotics. In this study, we assessed if the exposure to 900 MHz GSM mobile phone radiation and 2.4 GHz radiofrequency radiation emitted from common Wi-Fi routers alters the susceptibility of microorganisms to different antibiotics. The pure cultures of Listeria monocytogenes and Escherichia coli were exposed to RF-EMFs generated either by a GSM 900 MHz mobile phone simulator and a common 2.4 GHz Wi-Fi router. It is also shown that exposure to RF-EMFs within a narrow level of irradiation (an exposure window) makes microorganisms resistant to antibiotics. This adaptive phenomenon and its potential threats to human health should be further investigated in future experiments. Altogether, the findings of this study showed that exposure to Wi-Fi and RF simulator radiation can significantly alter the inhibition zone diameters and growth rate for L monocytogenes and E coli. These findings may have implications for the management of serious infectious diseases.
This research was aimed to investigate the prevalence and clinical impact of occult HBV infection in thalassemic patients with chronic HCV infection. In this cross-sectional study we have totally examined 60 patients suffering HBV and HCV infections by PCR and RT-PCR methods, respectively, in Kerman province of Iran. ELISA technique (RADIM, Italy) was used to detect anti-HBc, anti-HBs and HBsAg. The serum level of liver enzymes (SGOT, SGPT, DB, TB and ALK) were analyzed in the HCV infected patients (MAN, IRAN). Statistical analyses performed using t-test and Chi-square. We found that 27 cases (out of 60) were infected by HCV but HBV-DNA was not seen in HCV infected patients. Present findings also showed that none of samples were HBsAg positive but 9 (33%) (out of 27) HCV-RNA positive patients were anti-HBc positive and 11 (40.7%) were positive for anti-HBs. We found that SGOT, SGPT, DB, TB and ALK are above normal in 27 (100%), 19(70.3%), 12(44.5%), 15 (55.5%) and 15 (55.5%) RNA-HCV positive patients, respectively. The prevalence of hepatitis C infection is very high in thalassemic patients and based on other studies our results showed that the prevalence of HCV infection in Kerman is more than other provinces of Iran. In contrast with other studies HBV-DNA in these patients could not be detected, hence, it seems that occult HBV infection isn't frequent in Iranian thalassemic patients who suffering from chronic HCV infection.
Shigella is one of the important causes of diarrhea worldwide. Shigella has several virulence factors contributing in colonization and invasion of epithelial cells and eventually death of host cells. The present study was performed in order to investigate the distribution of virulence factors genes in Shigella spp. isolated from patients with acute diarrhea in Kerman, Iran as well as the genetic relationship of these isolates. A total of 56 isolates including 31 S. flexneri, 18 S. sonnei and 7 S. boydii were evaluated by polymerase chain reaction (PCR) for the presence of 11 virulence genes (ipaH, ial, set1A, set1B, sen, virF, invE, sat, sigA, pic and sepA). Then, the clonal relationship of these strains was analyzed by multilocus variable-number tandem repeat analysis (MLVA) method. All isolates were positive for ipaH gene. The other genes include ial, invE and virF were found in 80.4%, 60.7% and 67.9% of the isolates, respectively. Both set1A and set1B were detected in 32.3% of S. flexneri isolates, whereas 66.1% of the isolates belonging to different serogroup carried sen gene. The sat gene was present in all S. flexneri isolates, but not in the S. sonnei and S. boydii isolates. The result showed, 30.4% of isolates were simultaneously positive and the rest of the isolates were negative for sepA and pic genes. The Shigella isolates were divided into 29 MLVA types. This study, for the first time, investigated distribution of 11 virulence genes in Shigella spp. Our results revealed heterogeneity of virulence genes in different Shigella serogroups. Furthermore, the strains belonging to the same species had little diversity.
Background: The present study was conducted to investigate the distribution of virulence factors, capsular serotypes and antibiotic resistance properties of classical Klebsiella pneumoniae (cKP) and hypermucoviscous/hypervirulent Klebsiella pneumoniae (hvKP) isolated from different clinical specimens in Kerman, south-east of Iran. Materials and Methods: A total of 146 K. pneumoniae isolates were obtained from different clinical specimens. HvKP isolates were identified using the string test. Genes of capsular serotypes K1, K2, K5, K20, K54 and K57 and virulence-associated genes, rmpA, kfu, fimH, mrkD, allS, iutA, magA, entB and ybtS were evaluated by PCR. Antimicrobial susceptibility was also determined using the disc diffusion method. Results: Out of 146 K. pneumoniae isolates, 22 (15.1%) were hvKP. More than half of the hvKP isolates, 13 (59.1%), belonged to non-K1, K2, K5, K20, K54, K57 serotypes. Out of 22 hvKP isolates, 3 and 3 had K1 and K2 serotypes respectively. Among all isolates, entB 140 (95.9%) and mrkD 138 (94.5%) were the most common virulence genes. RmpA, iutA and kfu were associated with hvKP isolates (P-value <0.05). However, no significant difference was found in fimH, allS, mrkD, entB and ybtS genes between hvKP and cKP strains. HvKP exhibited significantly lower resistance rates to all antimicrobial agents than cKP, except to trimethoprim-sulphamethoxazole and ampicillin (P-value <0.05). Conclusion:The frequency of hvKP was low, but overall, the prevalence of virulence-related genes was higher in hvKP than cKP. HvKP was not related to specific serotypes. Furthermore, hvKP isolates were more susceptible to antimicrobial agents compared to cKP isolates.
Differences have been suggested to occur in the composition of intestinal microflora from allergic and non-allergic children. In this study we used a semi-quantitative enzyme-linked immunosorbent assay (ELISA) for the measurement of Clostridium difficile-specific immunoglobulin G (IgG) (CDIgG). CDIgG was excellent in differentiating between adults with or without Cl. difficile colitis (absorbance levels, positive vs. negative controls: geometric mean (GM) 0.301, 95% CI: 0.289-0.314 vs. GM 0.167, 95% CI: 0.155-0.181; mean difference 1.8-fold, 95% CI: 1.65-1.95; p < 0.0001). We used this technique to investigate whether there are any differences between atopic wheezy infants and non-atopic non-wheezy controls. In a prospective cohort study (n = 390) 10 patients were identified at 1 year of age (atopic, history of recurrent wheeze) and matched (gender, month of birth, exposure to Der p 1, Fel d 1 and Can f 1) with a control group of infants (non-atopic, no history of wheeze). The patients had significantly higher Cl. difficile-specific IgG absorbance levels (GM 0.298, 95% CI: 0.249-0.358) compared with controls (GM 0.235, 95% CI: 0.201-0.274; mean difference 1.27-fold, 95% CI: 1.07-1.50; p = 0.01). These results suggest that there may be differences in the composition of intestinal microflora between allergic and non-allergic infants at 1 year of age, with allergic children having higher Cl. difficile IgG antibody levels.
Enzymatic alteration of aminoglycosides by aminoglycoside-modifying enzymes (AMEs) is the major mechanism of resistance to aminoglycosides. The purpose of this study was to determine the frequency of AME genes, staphylococcal chromosomal cassette mec (SCCmec) types, and molecular analysis of the coagulase (coa) gene in Staphylococcus aureus strains isolated from clinical specimens. Totally, 102 S. aureus were tested by disk diffusion and microbroth dilution methods for susceptibility to aminoglycosides. AMEs genes and SCCmec types were determined by multiplex polymerase chain reaction (PCR). For polymorphism analysis, the 3' end region of the coa gene was amplified by PCR and the products were then subjected to restriction digestion with HaeIII enzyme. Of the 102 S. aureus, 42 (41.2%) were methicillin-resistant S. aureus (MRSA). Thirty-five (83%) of MRSA strains were resistant to kanamycin, 32 (76.2%) to tobramycin, 30 (71.4%) to gentamicin, 25 (59.5%) to amikacin, and 10 (23.8%) to netilmicin. The aac(6')-Ie-aph(2″) was the most frequent gene among MRSA isolates 19 (45.2%), followed by aph(3')-IIIa 8 (19%), ant(4')-Ia 6 (14.3%), and aph(2″)-Id 2 (4.8%). SCCmec types included type I 10 (23.8%), II 1 (2.4%), III 21 (50%), and IV 7 (16.7%). Three (7.2%) isolates were nontypeable. Digestion of the PCR products of the coa gene yielded 19 distinct restriction fragment length polymorphism patterns. In conclusion, given the alarming rate of resistance to aminoglycosides among MRSA, the monitoring of aminoglycoside resistance and AME genes should be performed to limit the spread of aminoglycoside resistance among MRSA isolates. Several variants of the coa gene were found in the studied isolates, although the majority of the MRSA isolates belonged to a limited number of coagulase types.
Waterpipes are frequently contaminated with microorganisms. This study revealed potential microbial hazards in waterpipes that may contribute to respiratory tract colonisation.
Background and aims. Streptococcus mutans is the main pathogenic agent involved in dental caries, and may be eliminated using mouthwashes. The objective of this study was to compare the effects of fluoride, chlorhexidine, and fluoride-chlorhexidine mouthwashes on salivary S. mutans count after two weeks of use and determine the prevalence of their side effects on the oral mucosa.Materials and methods. In this clinical trial, 120 12-14 year-old students were selected and divided into three groups. Each group was given one of fluoride, chlorhexidine, or fluoride-chlorhexidine mouthwashes. They were asked to use it twice a day for two weeks. Salivary samples were collected at baseline and after two weeks. Data were analyzed by Wilcoxon and Kruskal-Wallis tests.Results. In all the study groups, there were statistically significant reductions in salivary S. mutans counts two weeks after using the mouthwashes (P < 0.05). In addition, fluoride-chlorhexidine mouthwash had a significant effect on the reduction of S. mutans count in comparison with fluoride alone. The prevalence of oral side effects in fluoride-chlorhexidine mouth-wash was more than 90%.Conclusion. Adding fluoride to chlorhexidine mouthwash can significantly decrease salivary S. mutans count after two weeks. Fluoride-chlorhexidine has the highest rate of oral side effects between the evaluated mouthwash compounds.
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