**3. Pathogenesis**

Neiger et al. [25] and Reed [26] opined that corticosteroids increased the secretion of free and total hydrochloric acid, diminished mucus secretion, and promoted bacterial colonization of peptic ulcers. Hinton et al. [8] reported that the common predisposing factors for gastroduodenal ulcer were nonsteroidal anti-inflammatory drug (NSAID) administration, corticosteroids, hepatic disease, major surgery, shock, decreased gastric circulation, gastric hyper secretions, and gastrointestinal neoplasia and predisposing factors for gastroduodenal perforation were IBD, nonneoplastic infiltrative gastrointestinal disease, *Dirofilaria immitis*, otitis externa, ulcerative dermatitis, dilated cardio myopathy, polycystic kidney, and thyroid illness. Various authors reported that nonsteroidal anti-inflammatory drug administration resulted in duodenal ulcer formation was primarily due to the inhibition of prostaglandin synthesis via inhibition of cyclooxygenase [26–29]. Roherer et al. [30] recorded that degenerative disk diseases along with corticosteroid administration induced ulceration.

Dossin and Henroteaux [12], Jergens [31], Pibot et al. [32], and Kobayashi et al. [33] described inflammatory bowel disease as a group of idiopathic, chronic, gastrointestinal tract disorders, characterized by infiltration of gastrointestinal tract mucosa by inflammatory cells like lymphocytes, plasma cells, and various forms of IBD including lymphocytic-plasmacytic, eosinophilic, and granulomatous enterocolitis.

Mucosal immune system might play an important role in the pathogenesis of small intestinal enteropathies like IBD and idiopathic SIBO. Increased numbers of CD4 T cells, IgA, IgG, and plasma cells were noticed in duodenal mucosa of dogs with IBD [34]. Cave [2] stated that heating the amino acid, lysine, reacted with reducing sugars to form Maillard compounds that cannot be digested or absorbed in a usable form and served as substrate for luminal bacteria in the small intestine, leading to quantitative or qualitative changes in the flora.

Dossin and Henroteaux [12] opined that gastroduodenal ulceration, erosion, delayed gastric emptying, and postprandial discomfort could lead to IBD. Sancho et al. [14] recorded significantly high serum gastrin in chronic lymphocytic-plasmacytic enteritis (LPE)due to duodenogastric reflux and further reported that refluxes of duodenal contents like bile, pancreatic juice, and other duodenal secretions in the stomach damaged the gastric mucosal barriers leading to an antral hypomotility and gastric acid hypersecretion.

Simpson et al. [35] reported that exocrine pancreatic insufficiency also caused small intestinal bacterial overgrowth in dogs. Small intestinal bacterial overgrowth was defined as proliferation of abnormal numbers of bacteria in the upper small intestine. Common bacteria noticed in the proximal small intestine of dog included *Streptococcus faecalis*, other *Streptococcus species*, *Staphylococcus aureus*, *Staphylococcus epidermidis*, *Staphylococcus xylosus*, other *Staphylococcus* spp., *Enterobacteriacea*, *Bacillus* sp., *Escherichia coli*, *Corynebacterium* sp., *Enterobacter cloacae*, *Pseudomonas* sp. and *Pasteurella multocida*, *Clostridium subterminale*, *Clostridium perfringens*, *Bifidobacterium* sp., *Eubacterium* sp., *Bacteroides fragilis*, *other Bacteroides* spp., *Peptostreptococcus tetradius*, *Peptostreptococcus* sp., *Propionibacterium acne*, and *Lactobacillus* sp. [60]. In small intestinal bacterial overgrowth, an increased numbers of luminal bacteria in the small intestine could damage the brush border of enterocytes directly or indirectly by attracting polymorphonucleocytes, deconjugating bile acids, producing hydroxylated fatty acid and alcohols, metabolizing dietary nutrients, and altering the absorptive function of the cells [36]. Rinkinen et al. [37] stated that IgA deficiency had been associated with increased susceptibility of small intestinal bacterial overgrowth and inflammatory bowel disease.

Intestinal lymphangiectasia was characterized by the abnormal dilatation of lymphatic vessels within the mucosa and submucosa, associated with exudation of protein-rich lymph, into the intestine resulting in lipid malabsorptions [32]. Primary or congenital lymphangiectasia was a result of insufficiency or aplasia of lymphatic vessels, and secondary or acquired lymphangiectasia was due to functional obstruction of the lymphatics, and it might be due to the right side heart failure, constrictive heart failure, or intestinal neoplasia and inflammation [37].

Bonfanti et al. [39] reported that adenocarcinoma, carcinoma, leiomyoma, leiomyosarcoma, fibrosarcoma, lymphoma, and extra medullary plasmacytoma were the most common gastrointestinal tumors in dogs.

German [40] reported that *Giardia* was a flagellate protozoon, transmitted by direct life cycle, and it predominantly inhabit the duodenum of dogs. *Giardia duodenalis* is the common cause of chronic diarrhea in dogs [41].

Richter [42] and Leib and Matz [43] recorded a variety of foreign bodies like fruit pits, rubber ball, cloth, metal objects, coins, sponges, hair ball, bottle caps, chew toys, marbles, and bones in duodenum.


#### **Table 1.**

*Common clinical signs of various duodenal disorders.*
