1. With Ulceration Loss of blood and plasma protein through intestinal Ulcers (chronic histiocytic colitis;boxer colitis, Salmonellosis (mucosal damage)) 2. W/O Ulceration Increased mucosal permeability. Mucosa intact. (eg. IBD, Alimentary Lymphoma) 3. Deceased lymphatic drainage Lymphatic fluid lost to GI (eg. Lymphangectasia)

Intestine 1 Flashcards by Caleb Gwilliam

Define Protein-Losing Enteropathy (PLE)

Loss of protein via the GI Tract as a result of intestinal Pathology—>Hypoproteinemia

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Name 3 consequences for a Protein-Losing Enteropathy (PLE)

Weight Loss, Wasting, Edema

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Name 3 Types of PLE

With Ulceration
- Loss of blood and plasma protein through intestinal Ulcers (chronic histiocytic colitis;boxer colitis, Salmonellosis (mucosal damage))
W/O Ulceration
- Increased mucosal permeability. Mucosa intact. (eg. IBD, Alimentary Lymphoma)
Deceased lymphatic drainage Lymphatic
- fluid lost to GI (eg. Lymphangectasia)

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Small Intestinal Diarrhea is characterized by what?

LARGE volume; Small Increase in frequency Blood from small intestine will be partly digested–>BLACK, Tarry Feces Water absorption in the large intestine is normally very efficient; may compensate for small intestinal lesion (esp. Horse)

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Large Intestinal Diarrhea is characterized by what?

SMALL volume; Large Increase in Frequency Tenesmus is a prominent sign May contain A LOT mucus and fresh blood

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Water absorption by the Small intestine or Large intestine may be overwhelmed by what mechanisms?

Overwhelming quantity of ingesta
change in composition of ingesta
Decreased absorptive capacity
- Infiltrative diseases or inflammation
Reduced fecal transit time
- mechanical stimulation or inflammation–>strong propulsive contractions

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Define Osmotic Diarrhea

Molecules accumulate w/in the intestinal lumen due to problems with digestion and/or absorption–> elevation in intraluminal osmotic pressure–>fluid drawn into lumen Temporary feed withholding often helps alleviate clinical signs

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Name and Describe 2 mechanisms of osmotic diarrhea and give an example of each

Maldigestion- large molecules are not broken down–> Cannot be absorbed
- Poorly digestible feed (poorly digestible milk replacer
- Lactose intolerance
- Deficiencies in digestive factors (EPI; complete biliary obstruction)
Malabsorption: DECREASE in absorptive capacity
- loss of enterocytes
- villous atrophy
- shortened intestinal tract
- barrier to absorption-infiltrative diseases

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What are the 3 phases of intestinal digestion?

Intraluminal Phase, Mucosal Phase, Delivery Phase

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What phases of digestion are disrupted during osmotic diarrhea?

MUCOSAL Peptidase (Amino acids absorbed) Oligo-& saccharidases: Monosaccharides (absorbed)

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Which Phase(s) are disrupted during maldigestion?

Intraluminal Phase, Mucosal phase

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List three consequences of loss of enterocytes

Absorptive surface area of the mucosa is reduced–>OSMOTIC diarrhea Diminished breakdown of some molecules (maldigestion)–>OSMOTIC diarrhea Damage to protecive mucosal barrier–>EXUDATIVE diarrhea

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True or False Malabsorption is usually accompanied by some degree of maldigestion

TRUE Malabsorption results in a structural and/or functional mucosal abnormality that impairs absorptive capability–>loss of surface area or presence of barrier to absorption –>loss of digestive and absorptive functions

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What are 3 things that will decrease absorptive surface area?

Villous Atrophy Enterocyte Loss Short intestinal tract

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What is villous atrophy?

It is the shortening of the villi Usually follows enterocyte loss Can be chronic (IBD) or transient (rotavirus)

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What diseases are associated with villous atrophy?

Rotavirus, Coronavirus–>Loss of mature enterocytes Parvovirus, BVDV–>Loss of proliferative enterocytes (Mature cells continue to extrude but are not replaced) IBD, Lymphoma–>Chronic mucosal infiltration by inflammatory or neoplastic cells

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What cells does Coronavirus target?

MATURE enterocytes

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What can Crypt hyperplasia lead too? What is it a result of?

It can lead too villous atrophy It can be a result of chronic mucosal infiltration–>crypt hyperplasia–>immature enterocytes shed prematurely–>villous atrophy

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What is the general mechanism for Exudative Diarrhea?

Mucosal damage/infiltration–>increased mucosal Permeability–>passive transmucosal leakage of fluid, electrolytes, protein, and/or blood

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What are three mechanisms for exudative diarrhea?

Loss of mucosal epithelium->loss of barrier function Mucosal inflammation->inflammatory mediators->increased vessel permeability–>lamina proprial edema–>leakage of fluid and plasma proteins into lumen increased mucosal hydrostatic pressure/decreased plasma oncotic pressure–>fluid pushed or pulled into lumen

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What can cause decreased plasma oncotic pressure within the villus?

Hypoalbuminemia

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T or F The large intestine is more resistant to leakage as a result of increased hydrostatic pressure

TRUE

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What can cause intestinal hypermotility?

Stress, pharmaceuticals, hormonal dysfunction (hyperthroidism)

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What can cause intestinal hypomotility?

decreased latitudinal peristalsis with normal longitudinal peristalsis may contribute to decreased transit time

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Define Secretory Diarrhea

Excessive luminal secretions due to an imbalance between absorptive and secretory mechanisms Caused most commonly by bacterial toxins or inflammatory mediators

What is the MOST important cause of secretory diarrhea?

BACTERIAL EXOTOXINS they often affect absorption of Na+ and Cl- and therefore water

When do you normal see Cryptosporidium in Calves?

Between 1-3 Weeks

When do you normally see Coccidia in Calves?

Between 4-8 weeks

when do you normally see coronavirus in calves?

Between 0-3 weeks

When do you normally see rotavirus?

Between 0-2 Weeks

When do you normally see E.Coli in calves?

Between 0-1 Week

When do you normally see salmonella in a calf?

This can infect at any age, but it is usually between 0-4 weeks

What is a predisposing factor to ETEC in neonates?

FAILURE of passive transfer MOST common cause of diarrhea in neonatal calves

What are four clinical signs of ETEC?

Diarrhea (yellow scours) Dehydration Acidosis Electrolyte imbalances

How and where does ETEC cause infection?

They must adhere to the enterocytes through the use of PILI--\>proliferation They produce EXOTOXINS (heat labile, heat stabile) that affect Na+ and Cl- (and water) absorption/secretion (CL- in cryptes) in villi in the small intestine via increased intracellular cAMP Disrupt luminal pressure

What type of diarrhea does ETEC cause?

Secretory, SMALL intestinal Diarrhea

What is a result of ETEC infection?

PROFUSE diarrhea, and SEVERE dehydration Dilated, fluid-filled intestine

What histopathological features are there for ETEC?

Usually, NONE

Salmonellosis causes SEVERE mucosal damage in what tissues?

SMALL and LARGE intestine

T or F Salmonellosis causes severe ulceration and inflammation.

TRUE These two damages result in loss of mucosal barrier and increased mucosal permeability resulting in exudative diarrhea

T or F Some strains of salmonellosis release exotoxins

True These exotoxins can result in HYPERSECRETION

Salmonellosis is an important cause of colitis in what species?

HORSES (pigs, foals, calves, occasionally lambs)

What is a predisposing factor to Salmonellosis?

STRESS

T or F Salmonella infection can result in some animals to become carriers

TRUE, can shed bacteria in times of stress

Clostridia perfringens (types B & C) are what on gram stain?

GRAM +

T or F Clostridia perfringens do not produce exotoxins

FALSE They produce exotoxins that are highly cytotoxic--\>SEVERE mucosal damage--\>NECROHEMORRHAGIC diarrhea/sudden death

Who are more susceptible to C. Perfringens infection?

Neonates

What are your gross findings with C. Perfringens??

Segmental/diffuse, dark red Small intestine with dark red, liquid ingesta

Upon histopathology what do you see with C. Perfringens?

Diffuse/ segmental mucosal necrosis and hemorrhage Enteroadhered, G+ bacilli

What is a predisposing factor for salmonellosis?

STRESS

Give the Pathogenesis of Salmonellosis

Salmonella adheres to enterocytes/M cells--\> Transcellular pasage into lamina propria/peyer's patches--\>Phagocytosed by macrophages--\>toxin production--\> Neutrophil chemotaxis & Enterocyte apoptosis--\>enterocyte loss, vascular damage Some strains release exotoxins that cause CL- channel closure--\>hypersecretion also can cause a vascular thrombosis

Describe the pathogenesis for Samonellosis

Salmonella adheres to enterocytes/M cells--\> transcellular passage into lamina propria/peyer's patches--\> phagocytosed by macrophages--\>toxin production--\> neutrophil chemotaxis and enterocyte apoptosis--\> enterocyte loss and vascular damage Some strains can cause Cl- channel closures resulting in hypersecretion Also can cause vascular thrombosis

Write a Morphologic diagnosis for the following photo:

Enterocolitis (fibrinonecrotic), Acute, Multifocal to coalescing, severe (Acute salmonellosis)

When would you see salmonella in a calf?

0-4 Weeks Salmonella can present at any age and is also a very common cause of colitis in horses

What type of diarrhea do you see with salmonellosis?

Large & Small intestinal Diarrhea Exudative: mucosal damage and vascular damage Osmotic: Loss of surface area Secretory (some exotoxin producing strains): Closure of Cl- channels

What can you see as a result of Clostridia perfringens, types A-E?

They produce POTENT exotoxins (enterotoxemia)--\>severe mucosal damage--\>NECROHEMORRHAGIC diarrhea/SUDDEN death

T or F Clostria Perfringen types are Gram Negative bacteria

FALSE: They are Gram Positive RODS

Where can you find Clostridium perfringens?

They are normal GI Flora and are found in the soil as well, but can proliferate and produce BAD toxins under certain conditions

What will be your gross findings with Clostridia perfringens types B & C?

segmental/diffuse, dark red (transmural: existing or occuring across the entire wall of an organ or blood vessel) SMALL intestine -DARK red, liquid ingesta

What will you see microscopically with clostridia perfringens B and C?

segmental/ diffuse mucosal necrosis and hemorrhage with ENTEROADHERENT Gram+ bacilli

What type of diarrhea will you see with clostridial enteritis? (C. Perfringens B and C)

Acute, Small intestinal, exudative diarrhea (mucosal damage)

What is the difference between C. Difficile and C. perfringens?

C. Perfringens results in NECROHEMORRHAGIC diarrhea/sudden death, while C. Difficile results in Acute, necrotizing enterocolitis due to cytopathic bacterial exotoxins

What species is especially important with C. Difficile infection?

HORSES

What can cause an overgrowth of C. Difficile?

Stress, antibiotic therapy, surgery, GI stasis (these all result in a disruption in normal GI flora)

What is the causitive agent for Johne's Disease?

Mycobacterium avium subsp. paratuberculosis

When would you see infection of Johne's Disease or Mycobacterium avium supsp. paratuberculosis?

Animals are infected at onset of disease is delayed, affecting adult ruminants \>19 months THIS IS NOT A DISEASE OF YOUNG ANIMALS!!!!!!

What are clinical signs of Johne's Disease or Mycobacterium avium supsp. paratuberculosis?

- emactiaion - hypoproteinemia - intractable diarrhea (cattle only) - normal/increased appetite

What cell does mycobacterium avium supsp. paratuberulosis infect?

MACROPHAGES

Mycobacterium avium subsp. paratuberculosis attacks macrophages. How does this cause diarrhea?

SEVERE granulomatous inflammation of the ileum, cecum, proximal colon--\>mucosal thickening--\>malabsorption (infiltrative)

What is the morphologic Dx for this photo? What disease does this photo represent? Possible etiologic agent?

Diffuse, Severe, Chronic, Granulomatous enteritis (ileitis) Johne's disease Mycobacterium avium subsp. paratuberculosis

Johne's disease is characterized by thickening of the lamina propria and submucosa of the ileum, cecum, and proximal colon by macrophages. What 3 things are a result of this infiltrative bacteria?

- Barrier to absorption (inflammatory cell infiltration-macrophages): osmotic diarrhea - increased mucosal permeability - villous atrophy: osmotic diarrhea

Johne's disease causes diarrhea of where?

SMALL and Large intestine Mainly ileum

What are you gross findings with johne's disease?

moderately to severely thickened ileum, (cecum, proximal colon\_ Mucosa has corrugated appearance

What will you see for histopathology of johne's disease?

granulamatous inflammmation of the lamina propria and submucosa of affected segments -multinucleate GIANT cells Acid-Fast, intracellular bacteria