Diseases of the Gastrointestinal System

Question 1

Function of the digestive tract

Answer 1

Uptake, digestion, absorption of nutrients

Maintain protective barrier and prevent uncontrolled passage of macromolecules and infectious organisms

Question 2

Components of the Gastrointestinal barriers

Answer 2

Mucus
Epithelial Layer
Mucosa associated lymphoid system (MALT)
Indigenous microflora

Question 3

Role of mucin as a gastrointestinal barrier

Answer 3

Mucins when hydrated forms gel at mucosal surface to provided protective mucus blanket that lubricates mucosal surface.
Mechanically entraps macro and microorg and passes them along the intestine and contains Ig (A and M) that specifically bind pathogen as well as enz (lysozyme, complement, interferon

Question 4

Role of the epithelial layer as a gastrointestinal barrier

Answer 4

char by enterocytes connected by tight jxn, impermeable to large molecules

Question 5

Role of the MALT as a gastrointestinal barrier

Answer 5

A diffuse system of small concentrations of lymphoid tissue found in various submucosal membrane sites of the body

provides interaction b/w pathogen and lymphocytes; stimulates production of Ig to protect mucosa

GALT is a component of MALT
Peyers patches in the SI & lymphoglandular complexes in the LI is a component of GALT

Question 6

Role of the microflora as a gastrointestinal barrier

Answer 6

Microflora fxns in fermentation
Trophic effect on epithelium and causes a faster turnover rate;
Provides continuous stimulus to local lymphoid tissue; Protects vs pathogen spp by competition for binding site and nutrition

Question 7

Malformation of the oral cavity implications

Answer 7

Impede food uptake, starve to death

Question 8

Implications of erosions and ulcerations in the oral cavity

Answer 8

from systemic viral diseases

increase salivation and decrease food uptake

Question 9

How often are the pharynx and esophagus affected by diseases?

Answer 9

Infrequently because food doesn’t stay for too long in this place

Question 10

Which part of the stomach is more prone to ulcerations?

Answer 10

The esophageal part, because inappropriate diet, inadequate feeding pattern and abrupt change in food = disturb gastric function

Esophageal and cardiac glandular zone: pH5;
fundic and pyloric glandular zone: pH3.5

Question 11

Effect of feeding finely ground feed

Answer 11

Induce increase secretion of acid in stomach = esophageal part, forms ulceration

small particle size - young
larger particle size - adult

Question 12

Cause of bacterial overgrowth and multiplication in the stomach

Answer 12

Extremely bulky food given in large portion = distend stomach = fast release into duodenum, pH doesn’t drop sufficiently (no furthermixing of feed material and acid in the stomach) = chyme in the duodenum is less acidic (acid supposedly prevent bacterial overgrowth) = bacterial overgrowth

early weaning (normal - 21-28 days(5 wks, start of HCl prodn))
weaned at 10 days or less
Young pigs has no gastric acid yet, acquire thru lactobacillus (present in the milk of the dam), secrete lactic acid w/c inhibit multiplication of bacteria

Question 13

What is diarrhea

Answer 13

Passage of fluid and feces in an increased rate/frequency

Question 14

Mechanisms of diarrhea

Answer 14

Increased in permeability (inflammation-pore size increases in the epithelium; secretion exceeds absorption)
Overstimulation of crypt epithelial cells (bacterial toxin; LT toxin by E. coli)
Interference with digestion and absorption (viral diseases due to destruction of villi; electrolytes stay in the lumen, attracts water into the lumen = watery type of diarrhea)

Question 15

Malfunction in the Large Intestine

Answer 15

Diarrhea - increased secretion of water

Constipation - Increased absorption of water

Question 16

Differentiate SI and LI diarrhea in terms of frequency of defecation

Answer 16

SI - normal or slightly increased

LI - very frequent

Question 17

Differentiate SI and LI diarrhea in terms of fecal volume

Answer 17

SI - large quantity

LI - small quantity

Question 18

Differentiate SI and LI diarrhea in terms of urgency

Answer 18

SI - absent

LI - present

Question 19

Differentiate SI and LI diarrhea in terms of Tenesmus

Answer 19

SI - absent

LI - present

Question 20

Differentiate SI and LI diarrhea in terms of Mucus in feces

Answer 20

SI - absent

LI - present

Question 21

Differentiate SI and LI diarrhea in terms of Blood in feces

Answer 21

SI - dark black

LI - red

Question 22

Differentiate SI and LI diarrhea in terms of weight loss

Answer 22

SI - present

LI - rare

Question 23

Effect of ETEC on the elctrolytes

Answer 23

increased chloride ion secretion into the intestinal lumen, and decreased sodium and chloride absorption. also attract sodium, sodium attract water

Question 24

etiological agent of Clostridial enteritis

Answer 24

Clostridum perfringens Type C & A
C. difficile
C noyvi

anaerobic and practically present everywhere (feces and skin

Question 25

Epidemiology of Clostridial enteritis

Answer 25

Usually affecting piglets less than one week old (day 3)
Fatality rate is high and complete recovery is rare

Death due to enterotoxemia; typically a sudden and severe ds causing death w/in 12 hrs

Often affecting healthiest and biggest piglet

Question 26

Why are piglets less than 3 days old are prone to enterotoxemia?

Answer 26

Toxin is sensitive to trypsin w/c is absent in pigs less than 3 days old

Question 27

Pathogenesis of Clostridial enteritis

Answer 27

Infection is established in the jejunum

Attach and multiply in jejunal epith cell at apex > desquamation and destruction of mucosa > during multiplication, produce toxin that destroy tissue, dead tissue provide ideal environment that is o2 free > carried by blood and destroy other tissue

Lesions often with pieces of intestinal lining

Question 28

Three stages of clinical signs

Answer 28

Peracute: piglets nearly always have a hemorrhagic diarrhea

Acute: piglets with reddish brown liquid feces that contain necrotic debris

Chronic: intermittent or persistent diarrhea; perianal area is covered with dried feces

Question 29

Lesions of Clostridial enteritis

Answer 29

Jejunum is most consistently and severely affected, often filled with blood or blood tinged fluid; duodenum not usually affected

Emphysematous (result in gas formation due to infection), reddened segment of small intestine (acute), held together by acute peritonitis; mucosal necrosis also seen

Thick walled small intestine (chronic); mucosa is replaced by necrotic membrane

Question 30

Diagnosis of Clostridial enteritis

Answer 30

Clinical signs and gross necropsy findings

Isolation of the organism (anerobic media or aerobic in anaerobic incubator)

Question 31

Treatment and Prevention of Clostridial enteritis

Answer 31

Little can be done when clinical signs are evident
Sanitation and hygiene
Active immunization of sows

Management toward prophylaxis
Toxoid 5 and 2 weeks prior to farrowing

Question 32

Etiologic agent of Enteric Colibacillosis and strains

Answer 32

Escherichia coli (ETEC pathotype)

ETEC strains (fimbrial antigen) ((F4)K88, (F5)K99, (F6)987P, F41)

F4 and F6 assoc with swine; F4 in post weaning diarrhea in piglets

Question 33

Epidemiology of Enteric Colibacillosis

Answer 33

Frequently occurring in young piglets (as early as 2-3 hrs piglet); individual or whole litter may be affected; Primarily a disease of pigs up to 10 days
(age peaks at 1-4 days and extended 2-3 weeks post weaning)

Sows remain healthy, no manifestation in sows;
Spread of infection is slow
ROI: feco-oral, via the mouth (ingestion) or through the umbilical cord

Question 34

Pathogenicity of Enteric Collibacilosis

Answer 34

LT and ST toxin; causes damage

Can produce ds even without invading other tissue

Have the ability to adhere to intestinal lining and produce enterotoxin, leading to secretory diarrhea

Question 35

Clinical signs of Enteric Colibacillosis

Answer 35

Diarrhea and dehydration leading to death

Feces may be too clear and too fluid in consistency but may vary from clear (wet-butt) to whitish to varying shades of brown; pasty perineum

Abdominal musculature is flaccid and atonic

Anus and perineum may be inflamed from contact with alkaline fecal material (tail could necrose)

Question 36

Lesions of Enteric Colibacillosis

Answer 36

Distention of the small intestines
Loss of tone of intestinal wall
Dilation of the stomach which is often filled with undigested milk curd

Villous atrophy is not a common finding (no invasion  only toxin)
Lacteals prominent (lymphatic vessels extending into villous of SI, absorbs fats, alkaline materials can be found here) (presence of Chyle = alkaline milky materials found in lacteals)

Question 37

Diagnosis of Enteric Colibacillosis

Answer 37

Check pH of the feces (feces will be alkaline due to electrolytes not absorbed, bicarbonate and sodium = sodium bicarbonate (alkaline))
Isolation of the organism from the SI (e coli is normally present in LI)
Slide agglutination test (detection of O antigen)

Question 38

Treatment of Enteric Collibacilosis

Answer 38

Gut acting antibiotics - TPMS, Gentamicin

Antibiotic sensitivity is a must

Question 39

Prevention of Enteric Collibacilosis

Answer 39

Sound management practices
-Reducing challenge rate through hygiene

• Enhancing immunity (prevent mastitis thru autovaccination) Baby pigs starts to produce Ig and Ab at 10th day= prevent dam mastitis
• Maintaining an environment that places stresses on the piglets (Dry, warm envt = reduce moisture) (Low ambient temp can be detrimental as it may reduce peristalsis and increase time for bacteria to pass thru the intestine)