MULTISPECIES SHIGELLA FLEXNERI OUTBREAK IN A ZOOLOGICAL COLLECTION COINCIDING WITH A CLUSTER IN THE LOCAL HUMAN POPULATION.

Shigella flexneri is a nonmotile gram-negative bacillus that affects humans and nonhuman primates. In August 2021, 15 primates at the ABQ BioPark demonstrated clinical signs of Shigella infection: 3 out of 4 Sumatran and hybrid orangutans (Pongo abelii), 6 out of 8 gorillas (Gorilla gorilla), 2 out of 9 chimpanzees (Pan troglodytes), and 4 out of 4 siamangs (Hylobates syndactylus). Three siamangs and one gorilla succumbed to complications of shigellosis during the initial outbreak and a chimpanzee died 10 mon later. Although it is well documented that Shigella may cause morbidity and mortality in nonhuman primates, the rapid and devastating nature of the outbreak, the difference from previous reports in zoological collections (enzootic vs outbreak), and the chronological overlap with the increase in human cases in the region makes discussion of this Shigella outbreak of significance. The cases presented here are significantly different than previous reports, because these were part of an outbreak that arose and subsided, versus other reports where the authors describe an enzootic disease with persistently infected animals. Close communication with the New Mexico Department of Health allowed for the investigation into possible sources of the outbreak, recommendations regarding biosecurity protocols, and staff education.

Interaction of voltage-gated sodium channel Nav1.6 (SCN8A) with microtubule-associated protein Map1b.

The mechanism by which voltage-gated sodium channels are trafficked to the surface of neurons is not well understood. Our previous work implicated the cytoplasmic N terminus of the sodium channel Na(v)1.6 in this process. We report that the N terminus plus the first transmembrane segment (residues 1-153) is sufficient to direct a reporter to the cell surface. To identify proteins that interact with the 117-residue N-terminal domain, we carried out a yeast two-hybrid screen of a mouse brain cDNA library. Three clones containing overlapping portions of the light chain of microtubule-associated protein Map1b (Mtap1b) were recovered from the screen. Interaction between endogenous Na(v)1.6 channels and Map1b in mouse brain was confirmed by co-immunoprecipitation. Map1b did not interact with the N terminus of the related channel Na(v)1.1. Alanine-scanning mutagenesis of the Na(v)1.6 N terminus demonstrated that residues 77-80 (VAVP) contribute to interaction with Map1b. Co-expression of Na(v)1.6 with Map1b in neuronal cell line ND7/23 resulted in a 50% increase in current density, demonstrating a functional role for this interaction. Mutation of the Map1b binding site of Na(v)1.6 prevented generation of sodium current in transfected cells. The data indicate that Map1b facilitates trafficking of Na(v)1.6 to the neuronal cell surface.

Transvenous occlusion of patent ductus arteriosus in 56 consecutive dogs.

OBJECTIVE: Document safety and efficacy of transvenous catheter occlusion of patent ductus arteriosus (PDA) over a wide range of ductal and patient sizes. ANIMALS, MATERIALS AND METHODS: Retrospective study of fifty-six consecutive dogs referred to Colorado State University with diagnosis of PDA. All cases utilized the transvenous approach, via the femoral vein. Occlusion was achieved using a coil (Flipper) in dogs with PDA minimal dimension of 4 mm, or if a coil was unstable following deployment. RESULTS: Ductal occlusion was achieved using the transvenous route alone in 54/56 dogs (96.4%). Occlusion was achieved using detachable Flipper coils in 39/42 dogs (92.9%) in which coil occlusion was attempted, with 38/39 dogs (97.4%) requiring only a single coil. In 16 dogs, occlusion was achieved using an Amplatzer duct occluder or vascular plug. Post-procedure residual ductal flow was absent or only mild in 36/39 (92.3%) dogs in which it was assessed. Procedural mortality rate was 1.7%, and major complication rate 7.0%. CONCLUSION: Transcatheter occlusion via a transvenous approach is a safe and effective method for treating PDA in dogs and is useful for small dogs (<2.5 kg).