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Introduction Occlusion of cerebral arteries account for 40–50% of neurological complications of infective endocarditis with the emboli most commonly lodging in the middle cerebral artery. The management of these occlusions with the use of thrombolytic therapies are associated with intracranial hemorrhage whereas outcomes with endovascular thrombectomy, while still under investigation, appear to be more favorable. In this case report, we present a HIV patient with persistent staphylococcus lugdunenesis bacteremia of unknown origin and acute left middle cerebral artery occlusion, who underwent endovascular thrombectomy. Methods Case Report Results A 66‐year‐old male past medical history of HIV on Elvitegravir/Cobicistat/Emtricitabine/ Tenofovir, pancytopenia and treated hepatitis C who presented for malaise, back pain, and urinary symptoms for 1 week. Initial labs remarkable for pancytopenia, CD4 count 44 and positive urinalysis. Ceftriaxone was started for UTI and Trimethoprim/Sulfamethoxazole for PJP prophylaxis. Urine and multiple blood cultures were positive for staphylococcus lugdunensis. Vancomycin was added to antibiotic therapy. On day two of hospitalization, patient developed new onset aphasia, right facial droop, and right hemiparesis. Upon evaluation, NIHSS was 14. CT head was negative. CTA head and neck showed left M1 occlusion. CT perfusion showed an infarct core of 20cc and 144cc of penumbra. Due to concern for possible infective endocarditis, thrombolytics were not administered but he was taken for thrombectomy. Emboli retrieval was successful with mTICI‐2c reperfusion. During thrombectomy, clot noted to have septic emboli appearance. Post thrombectomy, patient had complete resolution of neurological deficits. MRI brain showed multiple punctate foci of restricted diffusion in the left middle cerebral artery distribution consistent with embolic process. TTE was inconclusive. Intraoperative cultures of the clot resulted positive for staphylococcus lugdunensis and pathology examination detailed clot with bacterial colonization. TEE was performed and negative for valvular vegetations, mass, thrombus, or endocarditis but there was an intrapulmonary shunt. Patient later developed a small acute left parietal lobe parenchymal hematoma and basal ganglia infarct. His neurological status remained unchanged. He completed 6 weeks of IV antibiotic therapy upon discharge. Conclusions This case illustrates the importance of timely endovascular thrombectomy in suspected cerebral septic emboli as outcomes are favorable. It supports prompt recognition of septic emboli bacterial species for targeted antibiotic therapy along with further investigation into staphylococcus lugdunensis and its relation with cerebral septic emboli. This case urges additional exploration into the relationship between HIV patients and cerebrovascular disease including cerebral septic emboli.

As the most prevalent bacterial cause of human gastroenteritis, food-borne Campylobacter infections pose a serious threat to public health. Whole Genome Sequencing (WGS) is a tool providing quick and inexpensive approaches for analysis of food-borne pathogen epidemics. Here we report the WGS and annotation of a Campylobacter coli strain, FNW20G12, which was isolated from milk in the United States in 1997 and carries multidrug resistance. The draft genome of FNW20G12 (DDBJ/ENA/GenBank accession number LWIH00000000) contains 1, 855,435 bp (GC content 31.4%) with 1902 annotated coding regions, 48 RNAs and resistance to aminoglycoside, beta-lactams, tetracycline, as well as fluoroquinolones. There are very few genome reports of C. coli from dairy products with multidrug resistance. Here the draft genome of FNW20G12, a C. coli strain isolated from raw milk, is presented to aid in the epidemiology study of C. coli antimicrobial resistance and role in foodborne outbreak.

Campylobacter jejuni is a leading bacterial cause of human gastroenteritis. The goal of this study was to analyze the C. jejuni F38011 strain, recovered from an individual with severe enteritis, at a genomic and proteomic level to gain insight into microbial processes. The C. jejuni F38011 genome is comprised of 1,691,939 bp, with a mol.% (G+C) content of 30.5%. PacBio sequencing coupled with REBASE analysis was used to predict C. jejuni F38011 genomic sites and enzymes that may be involved in DNA restriction-modification. A total of five putative methylation motifs were identified as well as the C. jejuni enzymes that could be responsible for the modifications. Peptides corresponding to the deduced amino acid sequence of the C. jejuni enzymes were identified using proteomics. This work sets the stage for studies to dissect the precise functions of the C. jejuni putative restriction-modification enzymes. Taken together, the data generated in this study contributes to our knowledge of the genomic content, methylation profile, and encoding capacity of C. jejuni.

Periventricular heterotopias is a malformation of cortical development, characterized by ectopic neuronal nodules around ventricle lining and caused by an initial migration defect during early brain development. Human mutations in the Filamin A (FLNA) and ADP-ribosylation factor guanine exchange factor 2 [ARFGEF2; encoding brefeldin-A-inhibited guanine exchange factor-2 (BIG2)] genes give rise to this disorder. Previously, we have reported that Big2 inhibition impairs neuronal migration and binds to FlnA, and its loss promotes FlnA phosphorylation. FlnA phosphorylation dictates FlnA-actin binding affinity and consequently alters focal adhesion size and number to effect neuronal migration. Here we show that FlnA loss similarly impairs migration, reciprocally enhances Big2 expression, but also alters Big2 subcellular localization in both null and conditional FlnA mice. FlnA phosphorylation promotes relocalization of Big2 from the Golgi toward the lipid ruffles, thereby activating Big2-dependent Arf1 at the cell membrane. Loss of FlnA phosphorylation or Big2 function impairs Arf1-dependent vesicle trafficking at the periphery, and Arf1 is required for maintenance of cell- cell junction connectivity and focal adhesion assembly. Loss of Arf1 activity disrupts neuronal migration and cell adhesion. Collectively, these studies demonstrate a potential mechanism whereby coordinated interactions between actin (through FlnA) and vesicle trafficking (through Big2-Arf) direct the assembly and disassembly of membrane protein complexes required for neuronal migration and neuroependymal integrity. [ABSTRACT FROM AUTHOR]