Antibiotic and disinfectant resistance of Salmonella isolated from egg production chains.

To investigate the contamination of Salmonella and its drug resistance in egg production chains, 111 Salmonella strains of different serotypes isolated from egg production chains were used in the study. The minimum inhibitory concentrations (MICs) of antibiotics and disinfectants against Salmonella isolates were determined, meanwhile, antibiotic and disinfectant resistance genes were amplified. The results showed that the resistance frequency of trimethoprim (TMP, N=100, P=90.09%) was highest among Salmonella isolates and all isolates were sensitive to amoxicillin and clavulanate (AMC), ceftiofur sodium (CFS) and gentamicin (CN), respectively. There were six different antibiotic resistance profiles, and TMP profile was the most prevalent type (N=36, P=32.43%). 52.25% of Salmonella isolates appeared multi-drug resistance. The MICs of benzalkonium chloride (BC) and cetylpyridinium chloride (CPC) against Salmonella strains ranged from 8 to 128 µg/mL and 8 to 256 µg/mL, respectively. Compared to quality control strain Escherichia coli ATCC10536, 101 Salmonella isolates (P=90.99%) had dual resistances to BC and CPC. 109 Salmonella (P=98.20%) were co-resistant to antibiotic and disinfectant. Detection of drug resistance genes showed that blaTEM gene was dominant (N=49, P=44.14%). The qnrA, qnrB and qepA genes were not detected. Only qacEΔ1 gene (N=63, P=56.76%) was detected among the disinfectant resistance genes. There was a significant correlation between sul1 gene and qacEΔ1 gene (P < 0.01). S. Derby showed multi-resistances to TMP, oxytetracycline (OTC), amoxicillin (AML) and ciprofloxacin (CIP). Eleven antibiotic resistance genes were found in S. Derby, in which the prevalence of qacEΔ1 gene was 81.25% (N=52). Besides, the drug resistance frequency and the prevalence of drug resistance genes in internal farm environment were higher than those in external environment. High frequency of drug resistances and high prevalence of drug resistance genes were detected in all links of the egg production chains, including package, storage and sale. Our results showed that severe antibiotic and disinfectant resistances existed in egg production chains. Therefore, further hygiene supervision should be implemented to prevent and control Salmonella, and standardize the use of antibiotics and disinfectants.

Mechanism of Abnormal Coagulation Induced by Tigecycline in Cancer Patients.

Tigecycline is a broad-spectrum active intravenous antibiotic that is active against methicillin-resistant staphylococcus aureus. In Phase 3 and 4 clinical trials, increased all-cause mortality was observed in patients treated with tigecycline compared to patients in the control group. The reason for the increase is unclear. In this study, we found that tigecycline cause abnormal coagulation in tumor patients, especially in patients with hematological malignancies. The main manifestations were decreased fibrinogen and prolonged activated prothrombin time (APTT), thrombin time (TT), and D-dimer. In addition, through functional studies, we found that tigecycline inhibit platelet adhesion and aggregation, and the coagulation function of patients gradually recover after discontinuation. Gene sequencing results suggested that tigecycline significantly regulate the expression of genes related to platelet function pathways and increase the incidence of single nucleotide polymorphisms and the number of alternative splices in the Chinese hamster ovary (CHO) cells treated with tigecycline. An abnormal function and low numbers of platelets are common in patients with hematological malignancies. Our study can explain the mechanism of abnormal coagulation caused by tigecycline. Additionally, doctors who apply tigecycline to cure infections in tumor patients should be warned.

Effect of SP-A/B in lipoic acid on acute paraquat poisoning.

BACKGROUND: This study was undertaken to observe the concentration of SP-A/B and the pulmonary surfactant in the lung tissue of rats with acute lung injury/acute respiratory distress syndrome caused by paraquat poisoning after the treatment of metabolic antioxidant-lipoic acid and whether its influence was related to TNF-α. METHODS: Sixty-six male Sprage-Dawley rats were randomly divided into three groups: normal control group (NS group), 6 rats; paraquat poisoning group (PQ group), 30 rats; and paraquat+lipoic acid treatment group (LA group), 30 rats. The rats in the PQ and LA groups were subdivided into 3-, 6-, 12-, 24-, 48-hour subgroups, with 6 rats in each group. After the rats were sacrificed, lung tissue from the same part was taken from the rats. After HE staining, histological changes were observed in the tissue under a light microscope. Lung tissue was also taken to test the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). Whole blood (0.8 mL) without anticoagulant was drawn from the tail vein of rats for the determination of the TNF-α level. The total RNA of the lung tissue was collected, and the Rt-PCR method was used to measure the levels of SP-A and SP-B mRNA. RESULTS: HE staining showed that histopathological changes were milder in the LA group than in the PQ group. There were significant differences in MDA and SOD levels between different intervals both in intergroups and intragroups except the 3-hour subgroup (P<0.01). Likewise, the significant differences in the levels of TNF-α were also present between the three groups and between different intervals (P<0.01). The significant differences in SP-A mRNA and SP-B mRNA amplification ratio were seen between the three groups at the same intervals (P<0.01), but the differences between different intervals in the PQ group were statistically significant (P<0.05). The differences between different intervals in the LA group were statistically significant (P<0.01). CONCLUSION: Lipoic acid in acute paraquat poisoning could diminish lung tissue damage by regulating directly tumor necrosis factor and indirectly the content of pulmonary surfactant so as to reduce pulmonary edema, improve lung compliance, and finally protect lung tissues.

Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type II alveolar epithelial cells.

BACKGROUND: Edaravone (3-methyl-1-penyl-2-pyrazolin-5-one) is a potent free-radical scavenger and has the antioxidant ability to inhibit lipid peroxidation. The study aimed to examine the effect of edaravone on protecting the acute injury of human type II alveolar epithelial cells (A549 cells) induced by paraquat (PQ) and the change of production of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD). METHODS: A549 cells were cultured and divided into PQ group (group P), edaravone-treated group (group E) and normal control group (group C). The cells in group P were exposed to paraquat (600 µmol/L), and the cells in group E were treated with edaravone (100 µmol/L) additionally, and no drug intervention was given to the cells in group C. Real-time monitoring by LSCM was used to detect the cell response and the intracellular dynamic change of ROS level in A549 cells after administration of PQ and edaravone. And the levels of SOD and MDA were detected respectively by biochemistry colorimetry. Data were expressed as mean ± standard error of the mean. Statistical analysis was carried out with the soft SPSS 16.0. RESULTS: The concentration of intracellular ROS significantly increased when PQ was given to A549 cells. But after administration of edaravone, the concentration of intracellular ROS was decreased. Compared to the PQ group, the levels of SOD in the edaravone group were significantly increased while the levels of MDA were markedly decreased. CONCLUSIONS: Paraquat can increase the oxidative stress, and induce the lipid peroxidation of A549 cells. Edaravone has the effect to scavenge reactive oxygen species, and to protect against the PQ-induced lung toxicity.