Chapter 14 IBD Flashcards

1
Q

What is Equine Chronic Inflammatory Bowel Disease (CIBD)?

A

A malabsorptive and maldigestive disorder characterized by dysfunction of the gastrointestinal tract due to infiltration of the mucosa and submucosa with eosinophils, lymphocytes, plasma cells, basophils, or macrophages.

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2
Q

What are the types of CIBD?

A

Eosinophilic enteritis, lymphocytic enteritis, plasmacytic enteritis, and granulomatous enteritis.

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3
Q

What age and breed are affected by CIBD?

A

CIBD can affect any age and breed, though it is often reported in younger horses.

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4
Q

What are common clinical signs of CIBD?

A

Severe weight loss, intermittent colic, malabsorption, hypoproteinemia, dependent edema, and recurrent colic.

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5
Q

What can cause acute and severe obstructive intestinal disease in horses with CIBD?

A

Focal eosinophilic enteritis causing severe segmental thickening of the gastrointestinal tract.

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6
Q

What are common clinical signs when the colon is involved in CIBD?

A

Soft feces or diarrhea.

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7
Q

What are some components of the gut immune system involved in CIBD?

A

Mucosal epithelium, enterocytes, goblet cells, antimicrobial peptides, gut-associated lymphoid tissue, Peyer’s patches, lymphoid follicles, and mesenteric lymph nodes.

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8
Q

What is the role of antigen-presenting cells in the gut immune system?

A

They continuously sample antigens from the intestinal lumen and determine the direction of the adaptive immune response.

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9
Q

What cytokines are associated with the Th1 pathway?

A

IFN-gamma.

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10
Q

What triggers the Th2 pathway in the gut immune system?

A

Parasite antigens such as Parascaris equorum and small strongyles.

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11
Q

What cytokines are associated with the Th2 pathway?

A

IL-4 and IL-5.

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12
Q

What type of response is triggered by bacteria such as Salmonella spp.?

A

A proinflammatory response characterized by Th17 and cytokines IL-17 and IL-23.

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13
Q

What is the role of T regulatory cells in the gut immune system?

A

They counteract any pro-inflammatory cytokines produced by Th17 cells.

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14
Q

What can defects in the gut immune system lead to?

A

Inappropriate and overacting responses resulting in intestinal inflammation, epithelial damage, and villous atrophy.

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15
Q

What is the primary immunoglobulin involved in the gastrointestinal immune response?

A

Mucosal secretory immunoglobulin A (IgA).

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16
Q

What is the role of IgA in the gastrointestinal tract?

A

It binds to pathogens and prevents them from crossing the mucosal epithelial barrier.

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17
Q

What technology has advanced the understanding of the equine gastrointestinal microbiome?

A

Next-generation sequencing of 16S ribosomal RNA (rRNA).

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18
Q

What is the core microbiome in healthy horses?

A

A relatively small set of microbiota, about 10-15% of the bacteria identified, shared among all horses irrespective of feed or geographical location.

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19
Q

What changes in the microbiome are observed in horses with colitis?

A

A shift towards less diversity.

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20
Q

What role do parasites play in CIBD?

A

The role is not fully understood, but horses may have an overzealous response to parasites due to deworming protocols or other factors.

21
Q

What dietary modification showed improvement in a group of warmblood horses with CIBD?

A

A gluten-restricted diet consisting of haylage, alfalfa, and black crushed oats.

22
Q

What genetic predisposition is suggested in horses with IBD?

A

Standardbred and Thoroughbred horses have been reported with IBD, though the small number of cases limits conclusions about genetic predisposition.

23
Q

What is MEEDS?

A

Multisystemic Epitheliotropic Eosinophilic Disease, involving the skin, gastrointestinal tract, liver, and pancreas without peripheral eosinophilia.

24
Q

What types of enteritis are associated with focal eosinophilic enteritis?

A

Idiopathic focal eosinophilic enteritis (IFEE) and colitis.

25
Q

What is the clinical presentation of lymphocytic and plasmacytic enteritis?

A

Moderate to severe infiltration of lymphocytes or plasma cells, villus blunting, fusion, atrophy, mucosal and/or submucosal edema.

26
Q

What can granulomatous enteritis in horses resemble in humans and cattle?

A

Crohn’s disease in humans and Johne’s disease in cattle.

27
Q

What are some etiological associations with granulomatous enteritis?

A

High levels of aluminum, hairy vetch ingestion, infections with Listeria monocytogenes, Salmonella typimurium, and cyathostomes.

28
Q

What is idiopathic systemic granulomatous disease also known as?

A

Sarcoidosis.

29
Q

What triggers inflammation in idiopathic systemic granulomatous disease?

A

Possibly associated with EHV-1, EHV-2, Borrelia spp., or immune stimulants like Bacillus Calmette-Guérin (BCG).

30
Q

What are common clinical signs of CIBD during physical examination?

A

Limb and ventral edema, moderate to poor body condition, thickened loops of intestine palpable on rectal examination.

31
Q

What diagnostic test confirms malabsorption in horses with CIBD?

A

A glucose absorption test.

32
Q

What is the primary method to obtain an intestinal biopsy for CIBD diagnosis?

A

Duodenal biopsy via gastroduodenoscopy or rectal mucosal biopsy.

33
Q

What is the typical histopathology finding in CIBD?

A

Inflammatory cell infiltrate within the mucosal epithelium and lamina propria of the small intestine.

34
Q

What is the treatment approach for CIBD?

A

Decreasing exposure to dietary, parasitic, or environmental allergens coupled with immunosuppression.

35
Q

What medications are used for immunosuppression in CIBD?

A

Corticosteroids and azathioprine.

36
Q

What antimicrobial has anti-inflammatory effects beneficial for CIBD treatment?

A

Metronidazole.

37
Q

What surgical intervention can be curative for focal eosinophilic enteritis?

A

Surgical resection.

38
Q

What is the prognosis for CIBD in horses?

A

Generally poor, with many cases ending in necropsy, though some horses show improvement or resolution of clinical signs.

39
Q

What type of dietary modification can benefit horses with suspected gluten sensitivity?

A

Avoiding wheat and mixed feeds, and feeding grasses, alfalfa, and oats.

40
Q

What is the recommended treatment for encysted small strongyles in horses with CIBD?

A

Fenbendazole (10 mg/kg PO SID for five days) or moxidectin (400 mcg/kg PO once).

41
Q

What additional care is necessary for horses with CIBD and poor body condition?

A

A highly digestible and well-balanced feed, with smaller amounts fed more frequently, and adding corn oil for fat.

42
Q

What are common histopathological standards for diagnosing gastrointestinal inflammation?

A

Evaluating surface epithelial injury, inflammation, villous stunting, crypt distension, lacteal dilation, mucosal fibrosis in the duodenum, and crypt hyperplasia, dilation/distortion, and fibrosis/atrophy in the colon.

43
Q

What are typical findings in rectal mucosal biopsies of healthy horses?

A

Scattered neutrophils in the lamina propria, slight to moderate lymphocyte and plasma cell cellularity, and varying degrees of eosinophil infiltration.

44
Q

What is the significance of eosinophil distribution in the gastrointestinal tract of horses?

A

Eosinophil distribution is independent of parasite challenge, with the highest numbers found in the cecum, ascending and transverse colon.

45
Q

What is the role of pre- and probiotics in CIBD treatment?

A

Unknown.

46
Q

What are common side effects of long-term corticosteroid therapy in horses?

A

Insulin resistance, laminitis, and a predisposition to secondary infections.

47
Q

What potential treatment shows local anti-inflammatory effects in the colon?

A

Olsalazine sodium, a prodrug split into two molecules of 5-aminosalicylic acid.

48
Q

What histological features distinguish normal from abnormal intestinal inflammation?

A

Normal intestinal histopathology includes a range of inflammatory cells, while severe inflammatory reactions with more than four cell layers thick are considered abnormal.

49
Q

What is the role of azathioprine in CIBD treatment?

A

To cause immunosuppression, though its use in CIBD has not been extensively evaluated.