Gastric and enteric phytobezoars caused by ingestion of persimmon in equids

CASE DESCRIPTION-13 equids (10 horses, 2 donkeys, and 1 pony) were examined for signs of colic (n = 7), weight loss (6), anorexia (3), and diarrhea (2). Ten equids were evaluated in the fall (September to November). Seven equids had a history of persimmon ingestion. CLINICAL FINDINGS-A diagnosis of phytobezoar caused by persimmon ingestion was made for all equids. Eight equids had gastric persimmon phytobezoars; 5 had enteric persimmon phytobezoars. Gastroscopy or gastroduodenoscopy revealed evidence of persimmon ingestion in 8 of 10 equids in which these procedures were performed. TREATMENT AND OUTCOME-2 of 13 equids were euthanatized prior to treatment. Supportive care was instituted in 11 of 13 equids, including IV administration of fluids (n = 8) and treatment with antimicrobials (5), NSAIDs (5), and gastric acid suppressants (4). Persimmon phytobezoar-specific treatments included dietary modification to a pelleted feed (n = 8); oral or nasogastric administration of cola or diet cola (4), cellulase (2), or mineral oil (2); surgery (4); and intrapersimmon phytobezoar injections with acetylcysteine (1). Medical treatment in 5 of 7 equids resulted in resolution of gastric persimmon phytobezoars. Seven of 8 equids with gastric persimmon phytobezoars and 1 of 5 equids with enteric persimmon phytobezoars survived > 1 year after hospital discharge. CLINICAL RELEVANCE-Historical knowledge of persimmon ingestion in equids with gastrointestinal disease warrants gastroduodenoscopy for evaluation of the presence of persimmon phytobezoars. In equids with gastric persimmon phytobezoars, medical management (including administration of cola or diet cola and dietary modification to a pelleted feed) may allow for persimmon phytobezoar dissolution.     

Dough Strain Hardening Properties as Indicators of Baking Performance

Bread loaf volume is an important economic criterion. Breeders, millers, and bakers need measurements allowing them to evaluate dough performance during processing. Strain hardening is an important dough property. It describes the stability of the gas cell walls and the ability of cells to expand further; therefore, the higher the strain hardening index (n), the better the baking performance. Dough exhibits strain hardening during uniaxial extensibility tests. However, obtaining n from an extensibility test is time consuming. The objectives of this study were to identify the extensibility parameters that contribute to n. Three parameters were retained in the model (R² = 0.90): dough strength (R_max), extensional delay (E_Diff), and initial slope of the curve (E_i). R_max was the largest contributor and was proportional to the dough strain hardening properties. E_Diff and E_i had a detrimental effect on n. The appropriateness of the model was validated with two sample sets (19 genotypes, 12 environments). Significant correlations were found between loaf volume and n (r = 0.52–0.64) for 7 of the 12 environments. The strain hardening index was found to be a good predictor for baking performance as judged by loaf volume.     

Comparative pathophysiology and management of protein‐losing enteropathy

Protein‐losing enteropathy, or PLE, is not a disease but a syndrome that develops in numerous disease states of differing etiologies and often involving the lymphatic system, such as lymphangiectasia and lymphangitis in dogs. The pathophysiology of lymphatic disease is incompletely understood, and the disease is challenging to manage. Understanding of PLE mechanisms requires knowledge of lymphatic system structure and function, which are reviewed here. The mechanisms of enteric protein loss in PLE are identical in dogs and people, irrespective of the underlying cause. In people, PLE is usually associated with primary intestinal lymphangiectasia, suspected to arise from genetic susceptibility, or “idiopathic” lymphatic vascular obstruction. In dogs, PLE is most often a feature of inflammatory bowel disease (IBD), and less frequently intestinal lymphangiectasia, although it is not proven which process is the true driving defect. In cats, PLE is relatively rare. Review of the veterinary literature (1977‐2018) reveals that PLE was life‐ending in 54.2% of dogs compared to published disease‐associated deaths in IBD of <20%, implying that PLE is not merely a continuum of IBD spectrum pathophysiology. In people, diet is the cornerstone of management, whereas dogs are often treated with immunosuppression for causes of PLE including lymphangiectasia, lymphangitis, and crypt disease. Currently, however, there is no scientific, extrapolated, or evidence‐based support for an autoimmune or immune‐mediated mechanism. Moreover, people with PLE have disease‐associated loss of immune function, including lymphopenia, severe CD4+ T‐cell depletion, and negative vaccinal titers. Comparison of PLE in people and dogs is undertaken here, and theories in treatment of PLE are presented.