Oleuropein, a phenolic component of Olea europaea L. ameliorates CCl4-induced liver injury in rats through the regulation of oxidative stress and inflammation.

OBJECTIVE: This study aimed to assess the hepatoprotective role of oleuropein (Olp), a phenolic compound found in olive, against carbon tetrachloride (CCl4)-induced liver damage in rats. MATERIALS AND METHODS: The research involved male albino rats, which received intraperitoneal injections of 100 mg/kg b.w. of oleuropein for 8 consecutive weeks before being subjected to carbon tetrachloride (CCl4) at a dosage of 1.0 ml/kg b.w. Changes induced by CCl4 in antioxidant and inflammatory marker levels were assessed using ELISA assay kits. Moreover, CCl4-induced liver tissue architecture alteration, fibrosis, and expression pattern of protein were evaluated by performing H&E, Sirius red, Masson trichrome, and immunohistochemistry staining. RESULTS: Increased serum transaminases and massive hepatic damage were observed by this liver toxicant. The hepatic injury was further evidenced by a significant decrease in antioxidant enzyme activity [superoxide dismutase (SOD), glutathione peroxidase (GPx), Glutathione (GSH) and Total Antioxidant Capacity (T-AOC)]. The administration of CCl4 resulted in an increased inflammatory response, which was measured by C-reactive protein, interleukin-6, as well as tumor necrosis factor-alpha. Olp as a curative regimen led to significant attenuation in the inflammatory response and oxidative/nitrosative stress. This polyphenol treatment improved the hepatic tissue architecture and decreased fibrosis. In the CCl4 treatment group, the expression pattern of IL-6 protein was high, whereas expression was decreased after Olp, as evidenced by immunohistochemistry staining. CONCLUSIONS: The study suggests that oleuropein treatment has the potential to reduce liver damage caused by CCl4 induction by inhibiting oxidative stress and inflammation and maintaining liver tissue architecture. This could make it a promising treatment option for liver pathogenesis.

Staphylococcus aureus dry-surface biofilms are more resistant to heat treatment than traditional hydrated biofilms.

BACKGROUND: The importance of biofilms to clinical practice is being increasingly realized. Biofilm tolerance to antibiotics is well described but limited work has been conducted on the efficacy of heat disinfection and sterilization against biofilms. AIM: To test the susceptibility of planktonic, hydrated biofilm and dry-surface biofilm forms of Staphylococcus aureus, to dry-heat and wet-heat treatments. METHODS: S. aureus was grown as both hydrated biofilm and dry-surface biofilm in the CDC biofilm generator. Biofilm was subjected to a range of temperatures in a hot-air oven (dry heat), water bath or autoclave (wet heat). FINDINGS: Dry-surface biofilms remained culture positive even when treated with the harshest dry-heat condition of 100°C for 60min. Following autoclaving samples were culture negative but 62-74% of bacteria in dry-surface biofilms remained alive as demonstrated by live/dead staining and confocal microscopy. Dry-surface biofilms subjected to autoclaving at 121°C for up to 30min recovered and released planktonic cells. Recovery did not occur following autoclaving for longer or at 134°C, at least during the time-period tested. Hydrated biofilm recovered following dry-heat treatment up to 100°C for 10min but failed to recover following autoclaving despite the presence of 43-60% live cells as demonstrated by live/dead staining. CONCLUSION: S. aureus dry-surface biofilms are less susceptible to killing by dry heat and steam autoclaving than hydrated biofilms, which are less susceptible to heat treatment than planktonic suspensions.

Determination of bacterial species present in biofilm contaminating the channels of clinical endoscopes.

BACKGROUND: Outbreaks of endoscopy-related Carbapenem-resistant Enterobacteriaceae has highlighted failures in endoscope decontamination resulting in biofilm formation. Biofilms are tolerant to detergents and disinfectants. We evaluated decontaminated endoscope channels for residual bacterial contamination and biofilm presence. METHODS: 64 channels were collected from 12 gastroscopes and 11 colonoscopes. Aerobic bacteria were isolated from inside the endoscope tubing by scrapping, sonication, and aerobic plate culture. Total number of contaminating bacteria was determined by quantitative real-time PCR with 16s rRNA eubacterial universal primers. Microbial diversity was assessed using next generation DNA sequencing. Biofilm presence was visually confirmed by confocal laser scanning and scanning electron microscopy. RESULTS: 47% of channels were culture positive, with α-haemolytic Streptococci from gastroscopes and coliforms from colonoscopes the most frequently isolated species. Sphingomonas spp., Staphylococcus spp., Streptococcus spp., and Pseudomonas aeruginosa were also isolated. An average of 1.2 × 103 bacteria/cm contaminated air-water channels, 2.8 × 102 and 6.6 × 102 bacteria/cm contaminated gastroscope and colonoscope working channels, respectively. Biofilm was on all 39 channels examined and was principally composed of environmental bacteria, although all samples contained potential pathogens. CONCLUSION: Biofilm is present on many endoscope channels obtained from Australian hospitals. Any soil including biofilm can compromise disinfectant action.

Staphylococcus aureus dry-surface biofilms are not killed by sodium hypochlorite: implications for infection control.

BACKGROUND: Dry hospital environments are contaminated with pathogenic bacteria in biofilms, which suggests that current cleaning practices and disinfectants are failing. AIM: To test the efficacy of sodium hypochlorite solution against Staphylococcus aureus dry-surface biofilms. METHODS: The Centers for Disease Control and Prevention Biofilm Reactor was adapted to create a dry-surface biofilm, containing 1.36 × 10(7)S. aureus/coupon, by alternating cycles of growth and dehydration over 12 days. Biofilm was detected qualitatively using live/dead stain confocal laser scanning microscopy (CLSM), and quantitatively with sonicated viable plate counts and crystal violet assay. Sodium hypochlorite (1000-20,000parts per million) was applied to the dry-surface biofilm for 10min, coupons were rinsed three times, and residual biofilm viability was determined by CLSM, plate counts and prolonged culture up to 16 days. Isolates before and after exposure underwent minimum inhibitory concentration (MIC) and minimum eradication concentration (MEC) testing, and one pair underwent whole-genome sequencing. FINDINGS: Hypochlorite exposure reduced plate counts by a factor of 7 log10, and reduced biofilm biomass by a factor of 100; however, staining of residual biofilm showed that live S. aureus cells remained. On prolonged incubation, S. aureus regrew and formed biofilms. Post-exposure S. aureus isolates had MICs and MECs that were not significantly different from the parent strains. Whole-genome sequencing of one pre- and post-exposure pair found that they were virtually identical. CONCLUSIONS: Hypochlorite exposure led to a 7-log kill but the organisms regrew. No resistance mutations occurred, implying that hypochlorite resistance is an intrinsic property of S. aureus biofilms. The clinical significance of this warrants further study.

Intensive care unit environmental surfaces are contaminated by multidrug-resistant bacteria in biofilms: combined results of conventional culture, pyrosequencing, scanning electron microscopy, and confocal laser microscopy.

BACKGROUND: Hospital-associated infections cause considerable morbidity and mortality, and are expensive to treat. Organisms causing these infections can be sourced from the inanimate environment around a patient. Could the difficulty in eradicating these organisms from the environment be because they reside in dry surface biofilms? AIM: The intensive care unit (ICU) of a tertiary referral hospital was decommissioned and the opportunity to destructively sample clinical surfaces was taken in order to investigate whether multidrug-resistant organisms (MDROs) had survived the decommissioning process and whether they were present in biofilms. METHODS: The ICU had two 'terminal cleans' with 500 ppm free chlorine solution; items from bedding, surrounds, and furnishings were then sampled with cutting implements. Sections were sonicated in tryptone soya broth and inoculated on to chromogenic plates to demonstrate MDROs, which were confirmed with the Vitek2 system. Genomic DNA was extracted directly from ICU samples, and subjected to polymerase chain reaction (PCR) for femA to detect Staphylococcus aureus and the microbiome by bacterial tag-encoded FLX amplicon pyrosequencing. Confocal laser scanning microscopy (CLSM) and scanning electron microscopy (SEM) were performed on environmental samples. FINDINGS: Multidrug-resistant bacteria were cultured from 52% (23/44) of samples cultured. S. aureus PCR was positive in 50%. Biofilm was demonstrated in 93% (41/44) of samples by CLSM and/or SEM. Pyrosequencing demonstrated that the biofilms were polymicrobial and contained species that had multidrug-resistant strains. CONCLUSION: Dry surface biofilms containing MDROs are found on ICU surfaces despite terminal cleaning with chlorine solution. How these arise and how they might be removed requires further study.

Quantifying the risk of respiratory infection in healthcare workers performing high-risk procedures.

This study determined the risk of respiratory infection associated with high-risk procedures (HRPs) performed by healthcare workers (HCWs) in high-risk settings. We prospectively studied 481 hospital HCWs in China, documented risk factors for infection, including performing HRPs, measured new infections, and analysed whether HRPs predicted infection. Infection outcomes were clinical respiratory infection (CRI), laboratory-confirmed viral or bacterial infection, and an influenza infection. About 12% (56/481) of the study participants performed at least one HRP, the most common being airway suctioning (7·7%, 37/481). HCWs who performed a HRP were at significantly higher risk of developing CRI and laboratory-confirmed infection [adjusted relative risk 2·9, 95% confidence interval (CI) 1·42-5·87 and 2·9, 95% CI 1·37-6·22, respectively]. Performing a HRP resulted in a threefold increase in the risk of respiratory infections. This is the first time the risk has been prospectively quantified in HCWs, providing data to inform occupational health and safety policies.