Diseases of the Gastrointestinal System Flashcards
Function of the digestive tract
Uptake, digestion, absorption of nutrients
Maintain protective barrier and prevent uncontrolled passage of macromolecules and infectious organisms
Components of the Gastrointestinal barriers
Mucus
Epithelial Layer
Mucosa associated lymphoid system (MALT)
Indigenous microflora
Role of mucin as a gastrointestinal barrier
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
Role of the epithelial layer as a gastrointestinal barrier
char by enterocytes connected by tight jxn, impermeable to large molecules
Role of the MALT as a gastrointestinal barrier
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
Role of the microflora as a gastrointestinal barrier
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
Malformation of the oral cavity implications
Impede food uptake, starve to death
Implications of erosions and ulcerations in the oral cavity
from systemic viral diseases
increase salivation and decrease food uptake
How often are the pharynx and esophagus affected by diseases?
Infrequently because food doesn’t stay for too long in this place
Which part of the stomach is more prone to ulcerations?
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
Effect of feeding finely ground feed
Induce increase secretion of acid in stomach = esophageal part, forms ulceration
small particle size - young
larger particle size - adult
Cause of bacterial overgrowth and multiplication in the stomach
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
What is diarrhea
Passage of fluid and feces in an increased rate/frequency
Mechanisms of diarrhea
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)
Malfunction in the Large Intestine
Diarrhea - increased secretion of water
Constipation - Increased absorption of water
Differentiate SI and LI diarrhea in terms of frequency of defecation
SI - normal or slightly increased
LI - very frequent
Differentiate SI and LI diarrhea in terms of fecal volume
SI - large quantity
LI - small quantity
Differentiate SI and LI diarrhea in terms of urgency
SI - absent
LI - present
Differentiate SI and LI diarrhea in terms of Tenesmus
SI - absent
LI - present
Differentiate SI and LI diarrhea in terms of Mucus in feces
SI - absent
LI - present
Differentiate SI and LI diarrhea in terms of Blood in feces
SI - dark black
LI - red
Differentiate SI and LI diarrhea in terms of weight loss
SI - present
LI - rare
Effect of ETEC on the elctrolytes
increased chloride ion secretion into the intestinal lumen, and decreased sodium and chloride absorption. also attract sodium, sodium attract water
etiological agent of Clostridial enteritis
Clostridum perfringens Type C & A
C. difficile
C noyvi
anaerobic and practically present everywhere (feces and skin
Epidemiology of Clostridial enteritis
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
Why are piglets less than 3 days old are prone to enterotoxemia?
Toxin is sensitive to trypsin w/c is absent in pigs less than 3 days old
Pathogenesis of Clostridial enteritis
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
Three stages of clinical signs
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
Lesions of Clostridial enteritis
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
Diagnosis of Clostridial enteritis
Clinical signs and gross necropsy findings
Isolation of the organism (anerobic media or aerobic in anaerobic incubator)
Treatment and Prevention of Clostridial enteritis
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
Etiologic agent of Enteric Colibacillosis and strains
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
Epidemiology of Enteric Colibacillosis
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
Pathogenicity of Enteric Collibacilosis
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
Clinical signs of Enteric Colibacillosis
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)
Lesions of Enteric Colibacillosis
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)
Diagnosis of Enteric Colibacillosis
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)
Treatment of Enteric Collibacilosis
Gut acting antibiotics - TPMS, Gentamicin
Antibiotic sensitivity is a must
Prevention of Enteric Collibacilosis
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)
