Lethal acute hemorrhage from an aortoesophageal fistula following endoscopy-assisted esophageal foreign body removal in a dog.

OBJECTIVE: To describe the clinical presentation of a dog with fatal hemorrhage from an aortoesophageal fistula (AEF) immediately following endoscopic removal of an osseous esophageal foreign body. CASE SUMMARY: A 12-year-old, male mixed-breed dog presented to a university hospital with a 6-day history of gagging, hematemesis, and anorexia. Physical examination upon arrival was unremarkable. Blood work revealed leukocytosis without anemia. Thoracic radiographs from the referring veterinarian demonstrated the presence of an osseous esophageal foreign body at the level of the heart base. Subsequently, esophagoscopy was performed under general anesthesia. A triangular-shaped, osseous esophageal foreign body was visualized at the level of the heart base and successfully removed. Following its removal, a deep, nonbleeding, presumably nonperforated, esophageal ulcer was revealed. While recovering from anesthesia, the dog's condition acutely deteriorated, with absence of spontaneous respiration, severe tachycardia, hypotension, white-pale mucous membranes, and hypothermia. Severe anemia was present, with hypovolemic shock likely secondary to acute, postprocedural bleeding. Medical management included rapid packed red blood cell transfusion, crystalloid fluid therapy, and tranexamic acid. Despite initial stabilization, several hours later, the dog suffered cardiac arrest and cardiopulmonary resuscitation (CPR) was unsuccessful. At postmortem examination, a 1-mm AEF was identified on the ventral aspect of the aorta that communicated with the overlying esophagus. NEW OR UNIQUE INFORMATION PROVIDED: Aortoesophageal fistulas should be considered in any patient with severe bleeding following esophagoscopy. A history of hematemesis in a dog with an esophageal foreign body should raise suspicion of an AEF and dictate case management accordingly.

Acute mesenteric ischemia-like syndrome associated with suspected Spirocerca lupi aberrant migration in dogs.

OBJECTIVE: To describe acute mesenteric infarction due to suspected Spirocerca lupi aberrant migration in 5 dogs. CASE SERIES SUMMARY: All dogs were large breed, none of which exhibited typical clinical signs associated with spirocercosis. All dogs were eventually diagnosed with septic peritonitis. On exploratory laparotomy, thickening of the jejunal arteries, surrounding mesojejunum, and segmental necrosis were identified. Similar thickening and hematoma formation were found in other regions of the mesentery. In 4 of the cases, the necrotic segment was located in the distal jejunum. Histology revealed thrombotic mesenteric vessels with intralesional S. lupi nematode larvae. Resection and anastomosis of the necrosed section was performed and all but 1 dog survived and were discharged within 1-6 days. NEW OR UNIQUE INFORMATION PROVIDED: Spirocerca lupi is a potential cause of mesenteric infarction in endemic areas when no other obvious etiology is identified.

Semaphorin3A accelerates neuronal polarity in vitro and in its absence the orientation of DRG neuronal polarity in vivo is distorted.

Axon guidance cues are critical for neuronal circuitry formation. Guidance molecules may repel or attract axons directly by effecting growth cone motility, or by impinging on neuronal polarity. In Semaphorin3A null mice, many axonal errors are detected, most prominently in DRG neurons. It has been generally assumed the repellent properties of Semaphorin3A are the cause of these erroneous axonal projections. Here we show that, in semaphorin3A-null mice, the initial trajectory of neurons in the DRG is abnormal, suggesting that Semaphorin3A may instruct neuronal polarity. In corroboration, in vitro Semaphorin3A dramatically increases neuronal polarization, as indicated by GSK3beta and Rac1 sub-cellular localization in DRG neurons. Polarization effects of Semaphorin3A are regulated by activated MAPK, as indicated by p-MAPK 42/44 polarization and the need for its activity for Rac1 and GSK3beta polarization. Taken together, our findings suggest that Semaphorin3A plays a role in the formation of neuronal polarity, in addition to its classic repellent role.

Semaphorin 3A and neurotrophins: a balance between apoptosis and survival signaling in embryonic DRG neurons.

Large numbers of neurons are eliminated by apoptosis during nervous system development. For instance, in the mouse dorsal root ganglion (DRG), the highest incidence of cell death occurs between embryonic days 12 and 14 (E12-E14). While the cause of cell death and its biological significance in the nervous system is not entirely understood, it is generally believed that limiting quantities of neurotrophins are responsible for neuronal death. Between E12 and E14, developing DRG neurons pass through tissues expressing high levels of axonal guidance molecules such as Semaphorin 3A (Sema3A) while navigating to their targets. Here, we demonstrate that Sema3A acts as a death-inducing molecule in neurotrophin-3 (NT-3)-, brain-derived neurotrophic factor (BDNF)- and nerve growth factor (NGF)-dependent E12 and E13 cultured DRG neurons. We show that Sema3A most probably induces cell death through activation of the c-Jun N-terminal kinase (JNK)/c-Jun signaling pathway, and that this cell death is blocked by a moderate increase in NGF concentration. Interestingly, increasing concentrations of other neurotrophic factors, such as NT-3 or BDNF, do not elicit similar effects. Our data suggest that the number of DRG neurons is determined by a fine balance between neurotrophins and Semaphorin 3A, and not only by neurotrophin levels.