Molecular genetic diversity and characterization of conjugation genes in the fish parasite Ichthyophthirius multifiliis.

Ichthyophthirius multifiliis is the etiologic agent of "white spot", a commercially important disease of freshwater fish. As a parasitic ciliate, I. multifiliis infects numerous host species across a broad geographic range. Although Ichthyophthirius outbreaks are difficult to control, recent sequencing of the I. multifiliis genome has revealed a number of potential metabolic pathways for therapeutic intervention, along with likely vaccine targets for disease prevention. Nonetheless, major gaps exist in our understanding of both the life cycle and population structure of I. multifiliis in the wild. For example, conjugation has never been described in this species, and it is unclear whether I. multifiliis undergoes sexual reproduction, despite the presence of a germline micronucleus. In addition, no good methods exist to distinguish strains, leaving phylogenetic relationships between geographic isolates completely unresolved. Here, we compared nucleotide sequences of SSUrDNA, mitochondrial NADH dehydrogenase subunit I and cox-1 genes, and 14 somatic SNP sites from nine I. multifiliis isolates obtained from four different states in the US since 1995. The mitochondrial sequences effectively distinguished the isolates from one another and divided them into at least two genetically distinct groups. Furthermore, none of the nine isolates shared the same composition of the 14 somatic SNP sites, suggesting that I. multifiliis undergoes sexual reproduction at some point in its life cycle. Finally, compared to the well-studied free-living ciliates Tetrahymena thermophila and Paramecium tetraurelia, I. multifiliis has lost 38% and 29%, respectively, of 16 experimentally confirmed conjugation-related genes, indicating that mechanistic differences in sexual reproduction are likely to exist between I. multifiliis and other ciliate species.

Endoscopic resection of GI stromal tumor using full-thickness resection device: tips and tricks.

Video 1R0 endoscopic resection of gastric GI stromal tumor using a dedicated gastroduodenal full-thickness resection device.

The misclassification of gastric antral vascular ectasia.

Background: Gastric antral vascular ectasia (GAVE) is characterized by angiodysplastic lesions and is a rare form of gastrointestinal bleeding. Given the multiple patterns, GAVE can be misclassified. Aim: We analyzed the misclassification of GAVE among patients undergoing esophagogastroduodenoscopy (EGD). Methods: We performed a retrospective review of 941 EGDs between 2017 and 2019. Inclusion criteria included findings of GAVE on EGD±biopsy. Correct classification was based on visual EGD findings. Outcome variables included misclassification rate, endoscopist's background, and concordance between EGD and pathology. Cohen's Kappa test was used for concordance analysis. Results: A total of 110 patients had EGD findings of GAVE with a corresponding 184 EGDs. The misclassification rate among EGDs was 74/184 (40%). Furthermore, 81/110 patients were correctly classified with their first workup, whereas 29/110 patients needed repeat testing. In cases of misclassification, GAVE was mostly referred to as erythema (43%), with ulceration, gastritis, or polyps. Sixty-six (60%) patients had biopsies with a concordance of 76% between EGD and biopsy (κ=0.35). Conclusions: Our findings indicate GAVE was misclassified up to 40% on EGDs with hepatologists and gastroenterologists having similar misclassification rates. Proper identification is crucial given susceptibility to upper gastrointestinal bleeding. Relevance for Patients: This study emphasizes the importance of accurate classification of GAVE to ensure proper treatment of these lesions which can improve clinical outcomes.

Prevalence of metabolic syndrome in cirrhotics with gastric antral vascular ectasia.

BACKGROUND AND AIMS: Gastric antral vascular ectasia (GAVE) is characterized by angliodysplastic lesions that can cause upper gastrointestinal bleeding (UGIB). The mechanism behind GAVE and its association with other diseases remains unknown. We investigated the association of metabolic syndrome in cirrhotic GAVE patients when compared to esophageal variceal hemorrhage (EVH) patients. METHODS: We performed a retrospective review of 941 consecutive esophagogastroduodenoscopies (EGDs) for UGIB at a medical center between 2017 and 2019. The GAVE group consisted of EGD or biopsy diagnosed cirrhotic GAVE patients, and the EVH group consisted of EVH patients with active bleeding or stigmata of recent hemorrhage on EGD. Baseline variables including co-morbidities and cirrhotic etiology were recorded. Continuous variables were compared using Wilcoxon test and categorical variables were compared using Chi-square or Fisher's exact test. Multiple logistic regression analysis evaluated the association between GAVE and covariates. RESULTS: The final cohort had 96 GAVE and 104 EVH patients. Mean BMI was significantly higher in the GAVE cohort (32.6 vs 27.9, p < 0.0001) in addition to diabetes, hypertension, and hyperlipidemia (53.1% vs 37.5%; 76% vs 47.1%; 38.5% vs 14.4%; respectively, all p < 0.05). Non-alcoholic steatohepatitis (NASH) cirrhosis was more prevalent in GAVE than EVH patients (50% vs 24%, p = 0.0001). Multiple logistics regression revealed female sex, increased BMI, hypertension, and hyperlipidemia all having significantly higher risk of GAVE (all p < 0.05). CONCLUSION: Our data indicates that when compared to cirrhotics patients with EVH, cirrhotics with GAVE have increased risk of metabolic syndrome. This may play a role in the underlying pathophysiology of GAVE.

An Unexpected Association: Might GAVE Pave the Way to How the Metabolic Syndrome Behaves.

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Utility of Surface and Blood Polymerase Chain Reaction Assays in Identifying Infants With Neonatal Herpes Simplex Virus Infection.

Of 27 neonates with herpes simplex virus, DNAemia was observed in 100% with disseminated disease, 57% with central nervous system disease and 28% with skin, eye, mouth disease, suggesting DNAemia occurs frequently in these infants. Herpes simplex virus culture and polymerase chain reaction were performed on surface specimens from 13/27 infants, and ~50% tested positive only by polymerase chain reaction, suggesting the superiority of this technique.

Methicillin-resistant Staphylococcus aureus as a Cause of Lemierre's Syndrome.

Lemierre's syndrome (LS) or jugular vein suppurative thrombophlebitis is well described in literature. The organisms most often responsible are Fusobacterium necrophorum or anaerobic flora. We present a case of LS with an atypical microbiologic cause, methicillin-resistant Staphylococcus aureus. We also present retrospective review of all LS cases from our institution and identified 2 additional children with LS caused by methicillin-resistant S. aureus.

Skeletal Muscle TRIB3 Mediates Glucose Toxicity in Diabetes and High- Fat Diet-Induced Insulin Resistance.

In the current study, we used muscle-specific TRIB3 overexpressing (MOE) and knockout (MKO) mice to determine whether TRIB3 mediates glucose-induced insulin resistance in diabetes and whether alterations in TRIB3 expression as a function of nutrient availability have a regulatory role in metabolism. In streptozotocin diabetic mice, TRIB3 MOE exacerbated, whereas MKO prevented, glucose-induced insulin resistance and impaired glucose oxidation and defects in insulin signal transduction compared with wild-type (WT) mice, indicating that glucose-induced insulin resistance was dependent on TRIB3. In response to a high-fat diet, TRIB3 MOE mice exhibited greater weight gain and worse insulin resistance in vivo compared with WT mice, coupled with decreased AKT phosphorylation, increased inflammation and oxidative stress, and upregulation of lipid metabolic genes coupled with downregulation of glucose metabolic genes in skeletal muscle. These effects were prevented in the TRIB3 MKO mice relative to WT mice. In conclusion, TRIB3 has a pathophysiological role in diabetes and a physiological role in metabolism. Glucose-induced insulin resistance and insulin resistance due to diet-induced obesity both depend on muscle TRIB3. Under physiological conditions, muscle TRIB3 also influences energy expenditure and substrate metabolism, indicating that the decrease and increase in muscle TRIB3 under fasting and nutrient excess, respectively, are critical for metabolic homeostasis.