Urban-associated changes can have immediate or long-term consequences on animal populations. Such changes may be assessed through parasite prevalence and abundance in wildlife hosts, as urbanization can influence parasitism and disease transmission in wildlife. Snakes are widespread and diverse vertebrates that often persist in urban environments; however, parasitism of snakes in urban environments has yet to be studied, leaving the roles of snakes in parasite transmission uncharacterized. Field ecology, microscopy, molecular techniques, and geographic information science (GIS) were integrated to characterize parasitism of snakes in an urban old-growth forest park. The species, sex, mass, length, location, and prevalence of ecto-, hemo-, and fecal parasites were determined for 34 snakes of 6 species. Ectoparasites (mite), hemoparasites (Hepatozoon spp.), and fecal parasites (Entamoeba spp., Trichomonas spp., Strongloides spp., and an unidentified helminth) were detected in snakes and 64.7 % of snakes were infected by at least one of these parasites. Parasite infections were generally not related to the sex, age, or body condition of snakes. The locations of infected snakes were used to produce risk maps indicating where parasite prevalence is predicted to be greatest. The analysis of these maps indicated that snakes with fecal parasites were closer than non-infected snakes to the edge of the forest. This study confirms that snakes may be important parasite hosts or reservoirs in parasite transmission pathways in urban environments and it provides an integrative multidisciplinary approach that may be used to monitor parasitism dynamics in other urban wildlife areas.

Severe hypertriglyceridemia (HTG) is a known metabolic cause of acute pancreatitis (AP) in pediatric patients. The incidence of hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is less well established in pediatric compared to adult patients. Studies in adults suggest that higher risk of AP occurs when triglyceride levels (TG) are >1,000 mg/dL. Most common etiologies for severe HTG in pediatric patients are either from primary hypertriglyceridemia, underlying genetic disorders of lipid and TG metabolism, or secondary hypertriglyceridemia, separate disease or exposure which affects TG metabolism. Most common theories for the pathophysiology of HTG-AP include hydrolysis of TG by pancreatic lipase to free fatty acids leading to endothelial and acinar cell damage and ischemia, as well as hyperviscosity related to increased chylomicrons. Though there are varying reports of HTG-AP severity compared to other causes of AP, a steadily growing body of evidence suggests that HTG-AP can be associated with more severe course and complications. Therapeutic interventions for HTG-AP typically involve inpatient management with dietary restriction, intravenous fluids, and insulin; select patients may require plasmapheresis. Long term interventions generally include dietary modification, weight management, control of secondary causes, and/or antihyperlipidemic medications. Though some therapeutic approaches and algorithms exist for adult patients, evidence-based management guidelines have not been well established for pediatric patients.