Wohlfahrtiimonas chitiniclastica: current insights into an emerging human pathogen.

Since the first description of Wohlfahrtiimonas chitiniclastica in 2008, a number of well described case reports demonstrating its pathogenic role in humans have been published. Infections may be closely linked to flies, such as Wohlfahrtia magnifica, Lucilia sericata, Chrysomya megacephala or Musca domestica. These insects are potent vectors for the distribution of W. chitiniclastica causing local or systemic infections originating from wounds infested with fly larvae. However, other potential sources of transmission of W. chitiniclastica have been described such as soil or chicken meat. Infections in humans reported to date comprise wound infections, cellulitis, osteomyelitis and sepsis. This review summarizes all the literature available up to now and gives the current knowledge about this emerging human pathogen. Additionally, four patients with proven W. chitiniclastica infections treated at Dresden University Hospital between 2013 and 2015, are included. Special focus was placed on microbiological identification and antibiotic susceptibility testing of the pathogen.

Central adjudication of venous ultrasound in VTE screening trials: reasons for failure.

BACKGROUND: The accuracy of screening ultrasound for venous thrombosis in asymptomatic patients is still a matter of debate. The VENUS study evaluated the accuracy of centrally adjudicated venous ultrasound against venography in patients after major orthopedic surgery and found the sensitivity of ultrasound to be poor for both proximal and distal deep vein thrombus (DVT). OBJECTIVES: To evaluate whether thrombus characteristics such as location or size influence the diagnostic performance of centrally adjudicated venous ultrasound. METHODS: All false negative sonograms of the VENUS study were re-evaluated against the corresponding venograms. Discrepancies were categorized into types of diagnostic failures. Within these categories, thrombus characteristics such as location, length or size of thrombus were evaluated. RESULTS: One hundred and twelve pairs of discrepant ultrasound and venography documents were compared with 28 pairs with concordant results. Discrepancies were caused by local documentation failure (37.5%), failure of the ultrasound method (43.7%) and failure of the central adjudication process (18.7%). The overall size of thrombi was small, which caused about 40% of all sonographic failures with a detection threshold of five Marder points, a thrombus length of 9.5 cm and a number of 3.5 pathological compression manoeuvres. Proximal or distal location of DVT did not affect thrombus detection. CONCLUSION: If centrally adjudicated ultrasound is to be used in future VTE screening trials, training of local sonographers and central adjudicators needs to be intensified, because asymptomatic DVTs seem to be small and ultrasound sensitivity depends on the number of pathological compression manoeuvres documented in the ultrasound document. In contrast, distal or proximal thrombus location itself does not influence sensitivity.

Angiotensin II-induced superoxide anion generation in human vascular endothelial cells: role of membrane-bound NADH-/NADPH-oxidases.

BACKGROUND: Angiotensin II (ANG II) mediated hypertension accelerates atherosclerosis (AS) and thereby increases the incidence of myocardial infarction (MI). On the other hand, superoxide anion (O2-) is involved in the modification of low density lipoproteins, inhibition of prostacyclin (PGI2) formation and breakdown of nitric oxide. These events finally lead to rapid progression of AS and MI. In the present study, we investigate whether ANG II can induce O2- release from human vascular endothelial cells (HVECs) and the possible mechanisms involved. METHODS AND RESULTS: The expression of ANG receptors subtype-1 (AT-1) and subtype-2 (AT-2) were identified by using reverse transcription polymerase chain reaction and sequence analysis. The O2- production was dose-dependently increased in HVECs treated with ANG II (10(-7)-10(-9) M) and with a maximum rate after 1 h of incubation. This event was significantly inhibited by pretreatment of cells with the specific AT-1 blocker losartan (10(-7) M) and to a lesser extent by the specific AT-2 receptor blocker PD123319 (10(-7) M). The combined incubation of both receptor blockers was even more effective. In addition, our lucigenin-enhanced chemiluminescence assay showed that the activity of plasma membrane-bound NADH-/NADPH-oxidases derived from ANG II-treated cells was also significantly increased, this effect was reduced in cells pretreated with losartan or to lesser extent by PD123319. However, the activity of xanthine oxidase remained unchanged in response to ANG II. Furthermore, the basal O2- release from HVECs was inhibited in cells treated with angiotensin-converting enzyme (ACE) inhibitor, Lisinopril (10(-6) M), and this event could be reversed by ANG II. CONCLUSION: ANG II induces O2- release in HVECs via activation of membrane-bound NADH-/NADPH-oxidase, an effect, that is mediated by both AT-1 and AT-2 receptors. This suggests that acceleration of AS and MI in ANG II-mediated hypertension may at least be due to ANG II-induced O2- generation from vascular endothelial cells. In this case, the ACE inhibitors and the ANG receptor antagonists may act as causative "antioxidants".