Intestinal Pathology of various animal species
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Transcript of Intestinal Pathology of various animal species
Intestinal Pathology
Villus Atrophy
A common Pathological change in intestineResults in malabsorption of nutrientsTwo categories
Intestine with apparently normal or hypertrophic crypts, associated with atrophy of villi to various degrees
Gut with some evidence of damage to the proliferative compartment and variable villus atrophy.
A. The first type occur in two formsPrimary increase in rate of loss of epithelium from
villus surface e.g. coronaviral and rotaviral infection, coccidia, some enteroinvasive bacteria, clostridial toxins, transient ischemia
Villus contract and become stubbyCompensatory expansion of the proliferative
compartment in crypts permits complete recoveryMicroscopic appearance vary depending upon
extent of cellular loss and regeneration Exfoliation into the gut, villi short/bluntSubsequently, the atrophic villi are covered by
poorly differentiated,low columnar, cuboidal or squamous cells.
Fusion of lateral surfaces of villi Erosion in sever cases,
Atrophy of villi and hypertrophy of crypts is also associated with chronic or persistent processes e.g. nematode parasitism, chronic coccidial infection, giardiasis, Johne's disease and histoplasmosis
T-cell activity(No, IL-12, TNF) seems to be associated with villus atrophy of this type in parasitisms
Immune reactions in the gut are associated with increased epithelial cell proliferation but cells not fully differentiated
Hypertrophy of crypts is the early and outstanding change in this lesion
B. Hypertrophy of crypts is the early and outstanding change in this lesion
Sequel to insults that cause necrosis of cells in crypts, or impair their mitotic capacity.
Agents causing this lesion has the capacity to damage dividing cells
These was also termed as Radi0mimetic as radian was the first known agent to cause this lesion
Other causes include cancer chemotherapeutic agents, T-2 mycotoxin, and pyrrolizidine alkaloids, BVD, Rinderpest
Microscopically: Damage e.g. apoptotic cells and neutrophils will be evident in the crypts before the villus atrophy
In severe necrosis, remaining cells become flattened to maintain integrity of crypt lining
The surface sloughing continues at normal rate though regenerative process is poor
Villi will eventually become atrophiedsquamous epithelial cells derived from
surviving crypts may cover the surface or surface will be eroded
Epithelial turnover in the cecum and colon is fundamentally similar to that in the small intestine, though villi are not present on the surface.
Lesions in the large bowel presumed to be associated with increased epithelial turnover include alterations in both surface and glandular epithelium.
E.g. number of goblet cells on the surface and in theupper portion of glands is often diminished, and
epithelium in these areas appears poorly differentiated
proliferative compartment in the gland may hypertrophy, causing glands to elongate and dilate.
Diarrhea
Presence of water in feces in relative excess in proportion to fecal dry matter
Severe electrolyte depletion, acid-base imbalance, and dehydration
Small-bowel diarrhea is classed as "secretory, malabsorptive,"or "effusive.
Secretory diarrhea result from derangement of normal secretory and absorptive mechanisms. Vibrio cholerae and Escherichia coli, Salmonella serotypes,
Yersinia enterocolitica, Shigella, and Campylobacter jejuniToxin-stimulate cAMP which shuts down sodium
chloride cotransport and stimulated chloride secretion
Resultantly more water flow from small bowel to colon
Malabsorptive diarrhea is exemplified by the osmotic retention of water in the gut lumen by poorly absorbed magnesium sulfate
Malabsorption commonly results from villus atrophy, no matter what the cause
Electrolyte and nutrient solute, malabsorbed along with osmotically associated water.
Increased permeability of the mucosa may contribute to diarrhea by permitting increased retrograde movement of solute and fluid from
the lateral intercellular space to the lumen, or by facilitating transudation of tissue fluid
Portal hypertension, right-sided heart failure, hypoalbuminemia , and expansion of plasma volume
Large-bowel diarrhea is due to a reduction in the innate capability of the colon to absorb the solute and fluid presented by the more proximal
bowel.Malabsorbed nutrients excess carbohydrate transfer from
small to large bowel result in colon osmotic overload and lead to diarrhea
Intestinal obstruction
Clinically acute obstruction involves the upper or middle small intestine
Chronic blockage usually involves the ileum and large bowel.
May be the sequel to a physical blockage of the lumen resulting from stenosis, obturation
(occlusion) by an intraluminal mass, or extrinsic compressionFailure of the intestinal circular smooth muscle
to contract blocks the peristaltic wave, causing functional obstruction, or pseudo-obstruction
Proximal to the point of obstruction there is accumulation of fluid and gas.
Intestinal distension associated with water and electrolyte sequestration into the lumen
Dehydration and circulatory collpase may occur
Stenosis and obturotion
Acquired stenosis occur due to intramural abscesses, intramural hematomas neoplasms and scarring following ulceration
Foreign bodies of all kinds are commonly foundMay act as a nucleus for enterolith Sharp impacted pointed foreign may cause pressure
necrosis with ulceration and possibly perforationEnteroliths were common in the colon of horses
(magnesium ammonium phosphate) Phytobezoars or phytotrichobezoars occur in colon
of horses
Foreign body obstruction
Small intestinal obstruction may be caused by parasites e.g. pigs and foals infested with large numbers of ascarids.
Impaction of the colon, by feces in dogs and cats, and by digesta, fibrous foreign material, sand, or feces in horses, is not uncommon
Impaction of the cecum or colon in horses may be precipitated by water deprivation, a change of diet from something soft and lush to hay or chaff, or poor dentition
Tumors, abscesses, peritonitis, and fibrous adhesions may cause extrinsic obstruction
Functional obstruction Paralytic ileus following rough handling during
surgery, or peritonitisIt is the result of neurogenic reflexes that
interfere with control of the inhibitory neurons of the myenteric plexus
Continual tonic discharge by these neurons inhibits contraction of circular smooth muscle and prevents
peristalsis.
The intestines are distended with a mixture of gas and fluid, and the wall is flaccid
Pseudo-obstruction, a clinical syndrome may result from segmental or diffuse neuromuscular dysfunction in the gut
Megacolon in Clydesdale foals, in association with hypoganglionosis of the myenteric plexus, has been reported
Gras, s sickness in horses common in those 3-6 years of age
In the acute disease, there is progressively severe tympany, swallowing is avoided, and saliva drools freely
The esophageal wall is sometimes edematous, and the mucosa may show longitudinal bands of congestion and ulceration
stomach is distended with alkaline mucinous fluidExcess fluid in the small intestine. Large intestine
is impacted with dry contents
Degenerative lesions e.g. subtle chromatolysis, nuclear eccentricity, and neuronal necrosis,
The formation of perineuronal eosinophilic axonal spheroids in many autonomic ganglia
Central neuropathy has also been reported
Idiopathic inflammatory bowel disease
mainly dogs, but less commonly cattle, cats, and horses
Associated with malabsorption and/or plasma loss into the gut
Also called as Lymphocyticplasmacytic enteritis, filled-villi syndrome, or eosinophilic gastroenteritis.
Difficult to diagnose as there is no landmark for histological lesions
Histologic abnormalities are grouped under three
broad headings: changes in mucosal architecture reflecting active or recent epithelial abnormality increased numbers of proprial leukocytes fibrosis within the lamina propria
Cardinal finding in small intestine is abnormally intense infiltrates of well-differentiated
lymphocytes and plasma cells, and sometimes eosinophils, in the lamina propria of villi, between crypts and perhaps in the submucosa
These cells are normally present in the intestine as well
A layer of plasma cells, lypmhocytes, eosinophils or neutrophils more than 4 cell thickness in deep mucosa is abnormal
Villi may be normal to severely atrophic Surface epithelium relatively normal, mucous
metaplastic or low columnar to cuboidalCrypts may be hypertrophic and lined by numerous
goblet cellsEdema of the lamina propria and dilation of lacteals
Idiopathic mucosal colitis
the colonic manifestation of chronic inflammatory bowel disease, and the commonest form of colitis
recognized in dogsEtiologically nonspecificChronic or chronic-active lymphocytic-plasmacytic or
eosinophilic mucosal inflammation.Mild acute mucosal colitis is characterized by
congestion of superficial capillaries and venules, and proprial edema
Neutrophils infiltrate the superficial lamina propria around vessels, lymphocytes and plasma cells relatively normal, but increase in mononuclear and eosinophils
Greater severity of the lesion is reflected in attenuation and exfoliation of surface epithelium, and the development of microerosions on
the mucosal surfaceEtiopathogenesis of idiopathic inflammatory
bowel disease is not understood in any animal species
However loss of tolerance to dietary antigen or antigens produced by the enteric microflora may be implicated.
Eosinophilic enteritis in cats and horses
Part of hypereosinophilic syndrome in middle to old aged cats
Diarrhea, sometimes bloody, vomition, loss of appetite, and loss of condition
Grossly: Intestinal thickening, hepato- and splenomegaly, and enlarged mesenteric lymph nodes and circulating eosinophilia, tan nodularities on the kidneys
Microscopically: well differentiated eosinophilic infiltration which may be transmural
Lymph nodes have hyperplastic follicles and many mature eosinophils in sinusoids
In horses, it is part of multisystemic epitheliotropic syndrome
Associated with eosinophilic granulomatous pancreatitis and eosinophilic dermatitis
Animals have weight loss, diarrhea hypoalbuminemia
Mucosal and sometimes transmural thickening may occur in any part of the alimentary tract
Esophageal and gastric squamous mucosa is hyperkeratotic
Folded mucosaMicroscopically: Diffuse infiltration of the mucosa,
submucosa, and deeper layers of the enteric wall by eosinophils, mast cells, macrophages, lymphocytes and some plasma cells.
Moderate to severe villus atrophy, fibroplasia in the lamina propria, and hypertrophy of the muscularis mucosae
Caseous foci in the mucosa and submucosa consist of central masses of eosinophils, sometimes surrounded by macrophages, giant cells, and occasionally fibrous tissue.
Villus atrophy
Eosinophilic interstitial infiltrates and granulomas in the biliary and pancreatic ducts, pancreas, salivary
glands, capsule, and outer cortex of enlarged firm mesenteric lymph nodes, and near portal tracts in the liver
Granulomatous enteritis
Chronic inflammatory infiltrates, including aggregates of histiocytes, and perhaps giant cells, in the lamina propria
submucosa is usually edematous, and lymphatics are prominent.
Affected lymph nodes are hyperplastic, usually with prominent sinus histiocytosis.
Johne's disease, other intestinal mycobacterioses, and Histoplasma enteritis are specific examples
Transmural granulomatous enteritis is occasionally seen in dogs and cats
Generally segmental and perhaps discontinuous
in distributionAffect lower ileum, colon, and draining lymph nodes.Marked necrosis in the centers of granulomas
and considerable fibrosis. Fibrosis
Idiopathic granulomatous enteritis as a cause of wasting and protein- losing enteropathy is most commonly seen as a sporadic problem in horses.
Usually small intestineCachectic animals with edema of depend partsMesenteric lymph nodes are usually enlarged, edematous,
with mottled firm gray areas, fibrotic nodules or caseous fociMicroscopic lesion may be patchy, regional, or diffuse, and it
may be mucosal, or transmural,Villi are mildly to markedly atrophic with hypertrophy of
cryptsEpithelium normal to low columnar/cuboidal, lamina propria
is edematous with histiocytes
Typhlocolitis in dogs
Diarrhea, frequent, small in volume, mucoid or bloody, and often accompanied by tenesmus.
Severe acute necrotizing colitis and typhlitis, leading to ulceration and perforation associated with Glucocorticoid therapy, functional adrenal cortical
tumors, and with trauma or surgery involving the spinal cord.
Uremia may also cause necrotic ulcerative colitis Trichuris vulpis, Entamoeba histolytica
Ulcerative, granulomatous transmural colitis by histoplasrnosis.
Leishmaniasis may also cause colitis with heavy mucosal macrophage infiltration
Canine coronavirus may also cause damage to colon
Campylobacter jejuni in some cases
Histiocytic ulcerative colitis is a distinctive histologic syndrome, recognized in Boxers and French Bulldog.
A chronic transmural ulcerative colitis characterized
by the presence of large numbers of macrophages
containingperiodic acid-Schiff-positive granules, in the deep mucosa and submucosa, and in lymph nodes
usually under 2 years of ageGrossly, the colon is variably thickened, folded,
and perhaps dilated and shortened
Patchy punctate red ulcers to more extensive irregular circular or linear lesions
Goblet cells disappear from the surface and glands.Microerosion of epithelium in the upper glands and
on the surface, neutrophilsMacrophages with phagocytic debris in mucosa and
with PAS positive material in deep lamina propriaCecum is also involved Exact cause unknown, various microbes postulatedDefect in lysosomal function in some boxer dogs
Colitis in cats
Colitis in cats is uncommon.Idiopathic mucosal colitis, similar to that described in
dogsTritrichomonas foetus, associated with persistent large
bowel diarrhea and idiopathic mucosal colitis in cats under 1 year age
Feline panleukopenia virus causes colonic lesions in about half the cases.
Mycotic colitis is occasionally seen in cats as a hemorrhagic ulcerative colitis by Candida,
zygomycetes, or AspergillusClostridium piliforme caused mild mucosal colitis in
several kittens
Transmural acute ulcerative colitis, with a heavy infiltrate of neutrophils, is the hallmark of Salmonella Typhimurium
AnaerobiospiriUum, associated with colitis in cats
Typhlocolitis in horses
Clostridial: animal is dehydrated, subcutaneous and serosal petechial hemorrhage
Dark blood with poor clottingLarge bowel, which is distended, with
abnormally fluid content.Serosa of the cecum and large colon may
appear cyanoticMucosa, submucosa edematousMucosa may appear brown and necrotic with
focal fibrinohemorrhagic exudate
Microscopically: superficial or full-thickness necrosis of the mucosa, dilation and perhaps thrombosis of small mucosal and submucosal venules
hemorrhage and edema in the mucosa, and the submucosa
Dilated lymphaticsSome neutrophilsClostridium pegringens type A, C. difficile Antibiotic therapy, stress, feed change
Subacute and chronic diarrhea in horses almost always involves the large intestine
Salmonella typhlocolitis must be suspected in such cases.
Potomac horse fever is associated with congestion and ulceration of the mucosa of the large bowel, and enlargement of mesenteric lymph nodes.
Diarrhea up to 10 daysRhodococcus equi in foals : Suppurative ulcers
involving lymphoid tissue in the typhlocolic mucosa, and cecal and colic lymphadenitis,
strongyles
Ischemic mucosal lesions due to arterial thromboembolism and slow flow lead to chronic diarrhea , cachexia due to persistent ulceration of the cecum or colon
NSAID’s has also been reported to cause cecum and colon ulceration
NSAID induced enterocolitis
Typhlocolitis in ruminants
Acute to subacute fibrinohemorrhagic typhlocolitis include salmonellosis, bovine viral diarrhea, Rinderpest coccidiosis adenoviral infection, winter dysentery (coronavirus).
Arsenic, other heavy metals, and oak or acorn poisoning may also cause hemorrhagic typhlocolitis and dysentery
Granulomatous typhlocolitis associated with chronic diarrhea and wasting may occur in Johne's disease
In sheep, hemorrhagic typhlocolitis may be present in animals with bluetongue and peste des petits ruminants
Salmonellosis may cause fibrinohemorrhagic enteritis in lambs and pregnant ewes
Coccidiosis may be implicated in hemorrhagic ileotyphlocolitis in lambs and kidsC. perfingens type D in goats