Characteristics and accurate identification of Pantoea dispersa with a case of spontaneous rupture of hepatocellular carcinoma in China: A case report.

INTRODUCTION: Pantoea dispersa belongs to the genus Pantoea, which is isolated from Enterobacteriaceae. It has been reported to cause some kinds of infections, but there are few detailed studies on it, especially its characteristics and identification methods, which has caused a lot of trouble in clinical work. PATIENT CONCERNS: A 51-year-old Chinese man was admitted to our hospital with a 7-hour history of progressive abdominal pain. He was previously diagnosed with liver cirrhosis secondary to chronic hepatitis B infection and hepatocellular carcinoma. An emergency hepatic artery embolization for hemostasis was performed under local anesthesia. Forty-eight hours later, the patient presented sudden onset of high fever up to 39.0 °C and chill. DIAGNOSIS: Morphological and phenotypic profiles were performed for preliminary identification for P dispersa. The biochemical features were obtained by VITEK 2 Test Kit. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis and 16S ribosomal RNA sequencing were performed to accurately identify P dispersa. INTERVENTION: Antibiotic therapy of intravenous ceftazidime was started empirically. The antibiotic treatment was switched to intravenous cefepime at the same time because of suspected ceftazidime treatment failure and microbiological sensitivity. OUTCOMES: The patient remained afebrile, and the second blood culture results were negative. Chest X-ray was normal as well. In order to control the progression of the hepatic lesion, transarterial chemoembolization was performed under local anesthesia. After completion of 14 days of antibiotic treatment, the patient was discharged with no signs of recurrence. CONCLUSION: P dispersa, a gram-negative bacterium rod, were facultative anaerobic, which displayed yellow pigmentation, round, raised, smooth on culture plates. Conventional analysis was difficult to complete its identification. With biochemical tests, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis and 16S ribosomal RNA sequencing, P dispersa can be accurately identified. It will help physicians understand the related clinical manifestations and make timely and effective treatment for patients.

Bloodstream infection caused by Bacteroides caccae in a patient with renal hypertension: a case report.

Bacteroides caccae is an anaerobic bacterium with a reportedly high isolation rate; however, it rarely causes bloodstream infections. Patients with hypertension are at increased risk of developing anaerobic bacterial infection. In this study, we report a case of bacteremia caused by B. caccae in a patient with renal hypertension and gastrointestinal hemorrhage. This study describes the clinical manifestations of bloodstream infection involving B. caccae to provide guidance for laboratory technicians and clinicians. A 42-year-old Chinese man was admitted for gastrointestinal hemorrhage and subsequently diagnosed with anaerobic blood infection. The pathogenic bacteria isolated from anaerobic blood culture bottles were identified as B. caccae by using an automatic bacterial identification instrument and mass spectrometry (MS). B. caccae is an intestinal opportunistic pathogen that can invade the intestinal mucosa and cause anaerobic bloodstream infection. Two or more sets of blood cultures and MS identification can greatly improve the positive detection rate of blood cultures of anaerobic bacteria. Furthermore, the increased drug resistance of anaerobic bacteria necessitates drug sensitivity tests for anaerobic bacteria in many hospitals. Thus, the early prevention and control of primary diseases with appropriate diagnoses and timely anti-infection therapies are necessary to reduce B. caccae bloodstream infection.

C16, a novel sinomenine derivatives, promoted macrophage reprogramming toward M2-like phenotype and protected mice from endotoxemia.

Macrophage plays a critical part in host defense, tissue repair, and anti-inflammation; Macrophage reprogramming is responsible for disease development or regression. We aimed to clarify the effect of sinomenine-4-hydroxy-palmitate (C16), on macrophage reprogramming and anti-inflammatory in endotoxemia model. According to a structure modification of SIN (Sinomenine), C16 was found. Then, based on the endotoxin model, the mice liver and kidney toxicity was evaluated and serum cytokines level of IL-6 (Interleukin-6), TNF-α (Tumor necrosis factor-α), and IL-1ß (Interleukin-1ß) were measured by ELISA (Enzyme linked immunosorbent assay). Then, we confirmed the effect of C16 on macrophages reprogramming, we used the flow cytometry to test the effect of C16 on macrophages apoptosis in vitro. Then, iNOS (Inducible nitric oxide synthase), M1-type related cytokines, such as IL-1ß, TNF-α, and M2-type related cytokines, such as Arg-1 (Arginase-1), CD206, Fizz1, and Ym1 was detected, which expressed in ANA-1 and primary peritoneal macrophages. To further explore the molecular mechanism of C16 in reprogramming of macrophages from M1 toward M2 phenotype, the expression of STAT1 (signal transducer and activator of Transcription 1), STAT3, ERK1/2 (extracellular signal regulated kinase1/2), AKT, p38, and its corresponding phosphorylation were determined by western blot. Our results demonstrated that C16 improved the survival rate of LPS- (lipopolysaccharide) challenged mice and decreased the inflammatory cytokines expression; After C16 treatment, the expression of M1 phenotype correlation factors decreased significantly, while the expression of M2 phenotype correlation factors increased significantly at different levels compared with normal group. It indicated that C16 reprogram macrophages phenotype from M1 toward M2 following LPS stimulus. Furthermore, the results also showed that C16 showed anti-inflammatory effect by inhibiting LPS-induced p38, AKT and STAT1 phosphorylation and contributing ERK1/2 activation. C16 promoted macrophage reprogramming toward M2-like phenotype via p-p38/p-AKT or STAT1 signals pathway and C16 might be a valid candidate for inflammatory disease.