Serotypes, virulence genes, and antimicrobial susceptibility of Escherichia coli isolates from pigs.

One hundred two pathogenic Escherichia coli isolates from diseased pigs were analyzed for serotypes, virulence genes, antimicrobial susceptibility, and the molecular basis of phenicol resistance. Of these 102 E. coli isolates, 101 were typeable and belonged to 27 different O serogroups. However, 69% of these isolates belonged to one of the following eight serogroups: O8, O54, O64, O65, O92, O108, O119, and O120. Serogroups O8 (23%) and O64 (10%) were the most prevalent among typeable isolates. High-resistance phenotypes were observed in all the isolates, with the majority displaying resistance to chloramphenicol (89%), streptomycin (83%), enrofloxacin (78%), and doxycycline (60%). The chloramphenicol resistance genes cat1, cat2, and cmlA were detected in 58%, 49%, and 65%, respectively, of the chloramphenicol-resistant isolates. The floR gene was detected in 57% of the florfenicol-resistant isolates and in 52% of chloramphenicol-resistant isolates. Pulsed-field gel electrophoresis showed that the 32 floR-positive isolates with florfenicol minimum inhibitory concentration ≥ 8 µg mL⁻¹ belonged to 25 different pulsed-field gel electrophoresis profiles, indicating the spread of floR among swine pathogenic E. coli isolates.

[A clinical analysis of 137 cases of influenza A(H1N1)].

OBJECTIVE: To analyze the epidemiology and clinical characteristics of influenza A (H1N1). METHODS: A retrospective analysis was performed on the clinical data of 137 cases of influenza A (H1N1) admitted into our hospital during May to August 2009. RESULTS: In the early stage, most cases were imported from the US, Australia, Canada and the UK. While in the later stage, most of them were secondary. The patients were mainly children and youngsters. And the most common clinical manifestations were fever (n = 108), cough (n = 93) and sore throat (n = 67) while the most common signs congestive throat (n = 99) and swelling tonsil (n = 46). The average fever period was 3.3 ± 1.5 days. The clinical symptoms vanished in 4.4 ± 1.9 days. And the average length of stay was 5.5 ± 2.1 days. Laboratory tests: the count of leukocytes declined while that of lymphocytes increased in 39 cases (39.5%). The test of influenza A (H1N1) nucleic acid was positive. The chest radiograph showed intensive pulmonary markings or patchy pneumonia-like signs. TREATMENTS: the groups of patients using Chinese herbs, western medicine plus Chinese herbs, symptomatic relief and placebo showed no significant difference in fever period, recovery time and the negative-converting period of influenza A (H1N1) nucleic acid tests became negative. CONCLUSION: Influenza A (H1N1) may be recessive or dominant. Despite a strong infectivity, the clinical symptoms are mild and the clinical course is self-limited, similar to the seasonal influenza.

Effects of Ergosterol, Isolated from Scleroderma Polyrhizum Pers., on Lipopolysaccharide-Induced Inflammatory Responses in Acute Lung Injury.

The present study aimed to investigate the protective role of ergosterol, isolated from Scleroderma polyrhizum Pers., in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by LPS (0.5 mg/kg), and ergosterol (25 and 50 mg/kg) was administrated orally 1 h prior to LPS administration. Ergosterol pretreatment at doses of 25 and 50 mg/kg decreased LPS-induced lung histopathological changes, lung wet-to-dry weight ratio. In addition, pretreatment with ergosterol inhibited inflammatory cells and proinflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Furthermore, we demonstrated that ergosterol blocked the activation of nuclear factor-kappaB (NF-κB), cyclooxygenase (COX)-2, and nitric oxide synthase (iNOS) pathways. The results presented here suggest that the protective mechanism of ergosterol may be attributed partly to the inhibition of NF-κB, COX-2, and iNOS pathways.