(roundworm) is the most common helminth infection globally and a cause of lifelong morbidity that may include allergic airway disease, an asthma phenotype. We hypothesize that larval migration through the lungs leads to persistent airway hyperresponsiveness (AHR) and type 2 inflammatory lung pathology despite resolution of infection that resembles allergic airway disease. Mice were infected with by oral gavage. Lung AHR was measured by plethysmography and histopathology with hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) stains, and cytokine concentrations were measured by using Luminex Magpix. -infected mice were compared to controls or mice with allergic airway disease induced by ovalbumin (OVA) sensitization and challenge (OVA/OVA).-infected mice developed profound AHR starting at day 8 postinfection (p.i.), peaking at day 12 p.i. and persisting through day 21 p.i., despite resolution of infection, which was significantly increased compared to controls and OVA/OVA mice. -infected mice had a robust type 2 cytokine response in both the bronchoalveolar lavage (BAL) fluid and lung tissue, similar to that of the OVA/OVA mice, including interleukin-4 (IL-4) ( < 0.01 and < 0.01, respectively), IL-5 ( < 0.001 and < 0.001), and IL-13 ( < 0.001 and < 0.01), compared to controls. By histopathology, -infected mice demonstrated early airway remodeling similar to, but more profound than, that in OVA/OVA mice. We found that larval migration causes significant pulmonary damage, including AHR and type 2 inflammatory lung pathology that resembles an extreme form of allergic airway disease. Our findings indicate that ascariasis may be an important cause of allergic airway disease in regions of endemicity.

Pyloric atresia with epidermolysis bullosa (EB) dystrophica is a rare entity that may not be immediately recognized. We describe the fourth confirmed case of pyloric atresia associated with the dystrophic subtype of EB diagnosed by standard pathologic measures, and discuss the clinical disease features and recent advances in the pathophysiology.

Colorectal malignancies may be stented to alleviate obstruction. The stent is a polarized and braided network of metallic wires. Pathology associated with colorectal stents is yet to be described. The authors reviewed 7 cases involving stented colorectal segments from patients lacking clinical suspicion of Crohn disease. In 4 cases, orientation of the specimens and stents matched the corresponding anatomic landmarks. In 3 cases, the specimens lacked helpful anatomic landmarks, and orientation was possible only after correlating with the intrinsic polarity of the stents. Stented areas showed artifacts resembling Crohn disease, including rounded cobblestones, pseudopolyps, and simple fissures, as well as unique artifacts including rhomboid cobblestones, complex fissures, oblique fissures with remarkably straight edges, and conical fragments of tissue that appeared to float. Crohn disease was misdiagnosed in 1 case in which the stent was removed intraoperatively and was never received. Colorectal stents help orient ambiguous specimens and induce patterned injury that can be confused with Crohn disease.

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