Epizootic Emergence of Usutu Virus in Wild and Captive Birds in Germany

This study aimed to identify the causative agent of mass mortality in wild and captive birds in southwest Germany and to gather insights into the phylogenetic relationship and spatial distribution of the pathogen. Since June 2011, 223 dead birds were collected and tested for the presence of viral pathogens. Usutu virus (USUV) RNA was detected by real-time RT-PCR in 86 birds representing 6 species. The virus was isolated in cell culture from the heart of 18 Blackbirds (Turdus merula). USUV-specific antigen was demonstrated by immunohistochemistry in brain, heart, liver, and lung of infected Blackbirds. The complete polyprotein coding sequence was obtained by deep sequencing of liver and spleen samples of a dead Blackbird from Mannheim (BH65/11-02-03). Phylogenetic analysis of the German USUV strain BH65/11-02-03 revealed a close relationship with strain Vienna that caused mass mortality among birds in Austria in 2001. Wild birds from lowland river valleys in southwest Germany were mainly affected by USUV, but also birds kept in aviaries. Our data suggest that after the initial detection of USUV in German mosquitoes in 2010, the virus spread in 2011 and caused epizootics among wild and captive birds in southwest Germany. The data also indicate an increased risk of USUV infections in humans in Germany

Cell-specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain

BACKGROUND: The complement cascade not only provides protection from infection but can also mediate destructive inflammation. Complement is also involved in elimination of neuronal synapses which is essential for proper development, but can be detrimental during aging and disease. C1q, required for several of these complement-mediated activities, is present in the neuropil, microglia, and a subset of interneurons in the brain. METHODS: To identify the source(s) of C1q in the brain, the C1qa gene was selectively inactivated in the microglia or Thy-1(+) neurons in both wild type mice and a mouse model of Alzheimer’s disease (AD), and C1q synthesis assessed by immunohistochemistry, QPCR, and western blot analysis. RESULTS: While C1q expression in the brain was unaffected after inactivation of C1qa in Thy-1(+) neurons, the brains of C1qa (FL/FL) :Cx3cr1 (CreERT2) mice in which C1qa was ablated in microglia were devoid of C1q with the exception of limited C1q in subsets of interneurons. Surprisingly, this loss of C1q occurred even in the absence of tamoxifen by 1 month of age, demonstrating that Cre activity is tamoxifen-independent in microglia in Cx3cr1 (CreERT2/WganJ) mice. C1q expression in C1qa (FL/FL) : Cx3cr1 (CreERT2/WganJ) mice continued to decline and remained almost completely absent through aging and in AD model mice. No difference in C1q was detected in the liver or kidney from C1qa (FL/FL) : Cx3cr1 (CreERT2/WganJ) mice relative to controls, and C1qa (FL/FL) : Cx3cr1 (CreERT2/WganJ) mice had minimal, if any, reduction in plasma C1q. CONCLUSIONS: Thus, microglia, but not neurons or peripheral sources, are the dominant source of C1q in the brain. While demonstrating that the Cx3cr1 (CreERT2/WganJ) deleter cannot be used for adult-induced deletion of genes in microglia, the model described here enables further investigation of physiological roles of C1q in the brain and identification of therapeutic targets for the selective control of complement-mediated activities contributing to neurodegenerative disorders. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12974-017-0814-9) contains supplementary material, which is available to authorized users

Placement of Ommaya Reservoirs Using Electromagnetic Neuronavigation and Neuroendoscopy: A Retrospective Study with Cost-Benefit Analysis

BACKGROUND: Placement of intraventricular catheters in oncology patients is associated with high complication rates. Placing Ommaya reservoirs with the zero-error precision protocol (ZEPP), a combination of neuronavigation (AxiEM stereotactic navigation) and direct verification of catheter tip placement with a flexible neuroendoscope, is associated with decreased complication rates as a result of increased catheter placement accuracy. However, the ZEPP costs more than traditional methods of catheter placement, and the question of whether this increased accuracy with the ZEPP is cost-effective is unknown. METHODS: We performed a single-center retrospective chart review of 50 consecutive ommaya reservoir patient placements between 2010 and 2017. Twenty-five ventricular catheters were placed using the ZEPP protocol, and 25 ventricular catheters were placed using only AxiEM stealth navigation. Postoperative catheter accuracy and complication rates were assessed. A cost-benefit analysis was then conducted to determine if the overall cost for placing Ommaya reservoirs with the ZEPP was effective compared with the alternative method of using neuronavigation alone. RESULTS: In the non-ZEPP cohort, 10 of 25 catheters were placed within the optimal location compared with 25 of 25 catheters placed in the ZEPP cohort. Three complications occurred in the non-ZEPP cohort: 2 malpositioned catheters required surgical revision and 1 catheter-related hemorrhage resulted in a prolonged stay in the intensive care unit. No complications occurred in the ZEPP cohort. A cost-benefit analysis showed $4784 savings per patient with ZEPP utilization because of the high complication-associated costs. CONCLUSIONS: Implementation of the ZEPP for verifying ventricular catheter placement in Ommaya reservoirs improved catheter tip accuracy, resulted in lower complication rates, and was more cost-effective when compared with the non-ZEPP cohort, which used only neuronavigation. The ZEPP can be used for ventricular shunt catheter placement to decrease complications and verify catheter tip accuracy in Ommaya or standard ventriculoperitoneal shunts

Intracranial ectopic pituitary adenoma Case report

✓ The authors report a unique case of ectopic intracranial pituitary adenoma, associated clinically with generalized seizures and aggressive behavior. The lesion presumably arose from cells in the pars tuberalis and did not involve the sella turcica