Villus atrophy is a common pathological change in the intestine that results in malabsorption of nutrients. There are two categories - intestine with normal or hypertrophic crypts and variable villus atrophy, or gut with evidence of damage to the proliferative compartment and crypts. The first type can be due to increased loss of epithelium from the villus surface by infections, toxins, or ischemia. The second type results from insults that damage dividing cells in the crypts like radiation or chemotherapy. Microscopically there may be damaged or apoptotic cells in crypts before villus atrophy develops.

1. Intestinal Pathology

4. Villus Atrophy
 A common Pathological change in intestine
 Results in malabsorption of nutrients
 Two 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 forms
 Primary increase in rate of loss of epithelium from
villus surface e.g. coronaviral and rotaviral infection,
coccidia, some enteroinvasive bacteria, clostridial
toxins, transient ischemia

5.  Villus contract and become stubby
 Compensatory expansion of the proliferative
compartment in crypts permits complete recovery
 Microscopic appearance vary depending upon extent of
cellular loss and regeneration
 Exfoliation into the gut, villi short/blunt
 Subsequently, the atrophic villi are covered by poorly
differentiated,low columnar, cuboidal or squamous cells.
 Fusion of lateral surfaces of villi
 Erosion in sever cases,

6.  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

7.  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

8.  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 atrophied
 squamous epithelial cells derived from surviving
crypts may cover the surface or surface will be
eroded

9.  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 the
 upper 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.

11. 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 jejuni
 Toxin-stimulate cAMP which shuts down sodium
chloride cotransport and stimulated chloride secretion

12.  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.

13.  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

14. 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
compression
 Failure of the intestinal circular smooth muscle to
contract blocks the peristaltic wave, causing functional
obstruction, or pseudo-obstruction

15.  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

17. Stenosis and obturotion
 Acquired stenosis occur due to intramural abscesses,
intramural hematomas neoplasms and scarring following
ulceration
 Foreign bodies of all kinds are commonly found
 May act as a nucleus for enterolith
 Sharp impacted pointed foreign may cause pressure
necrosis with ulceration and possibly perforation
 Enteroliths were common in the colon of horses
(magnesium ammonium phosphate)
 Phytobezoars or phytotrichobezoars occur in colon of
horses

18. Foreign body obstruction

19.  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

20.  Tumors, abscesses, peritonitis, and fibrous
adhesions may cause extrinsic obstruction
 Functional obstruction
 Paralytic ileus following rough handling during
surgery, or peritonitis
 It 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.

21.  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

22.  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 fluid
 Excess fluid in the small intestine. Large intestine is
impacted with dry contents

23.  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

24. 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

25.  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

26.  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 cuboidal
 Crypts may be hypertrophic and lined by numerous
goblet cells
 Edema of the lamina propria and dilation of lacteals

28. Idiopathic mucosal colitis
 the colonic manifestation of chronic inflammatory bowel
disease, and the commonest form of colitis
recognized in dogs
 Etiologically nonspecific
 Chronic 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

29.  Greater severity of the lesion is reflected in
attenuation and exfoliation of surface epithelium,
and the development of microerosions on
the mucosal surface
 Etiopathogenesis 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.

30. 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

31.  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

34.  Folded mucosa
 Microscopically: 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

35.  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

36. 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

38.  Transmural granulomatous enteritis is
occasionally seen in dogs and cats
 Generally segmental and perhaps discontinuous
in distribution
 Affect lower ileum, colon, and draining
lymph nodes.
 Marked necrosis in the centers of granulomas and
considerable fibrosis. Fibrosis

39.  Idiopathic granulomatous enteritis as a cause of wasting and
protein- losing enteropathy is most commonly seen as a
sporadic problem in horses.
 Usually small intestine
 Cachectic animals with edema of depend parts
 Mesenteric lymph nodes are usually enlarged, edematous,
with mottled firm gray areas, fibrotic nodules or caseous foci
 Microscopic lesion may be patchy, regional, or diffuse, and it
may be mucosal, or transmural,
 Villi are mildly to markedly atrophic with hypertrophy of
crypts
 Epithelium normal to low columnar/cuboidal, lamina propria
is edematous with histiocytes

40. 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.

41.  Leishmaniasis may also cause colitis with heavy
mucosal macrophage infiltration
 Canine coronavirus may also cause damage to
colon
 Campylobacter jejuni in some cases

42.  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 age
 Grossly, the colon is variably thickened, folded, and
perhaps dilated and shortened

43.  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, neutrophils
 Macrophages with phagocytic debris in mucosa and
with PAS positive material in deep lamina propria
 Cecum is also involved
 Exact cause unknown, various microbes postulated
 Defect in lysosomal function in some boxer dogs

44. Colitis in cats
 Colitis in cats is uncommon.
 Idiopathic mucosal colitis, similar to that described in
dogs
 Tritrichomonas 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 Aspergillus
 Clostridium piliforme caused mild mucosal colitis in
several kittens

45.  Transmural acute ulcerative colitis, with a heavy
infiltrate of neutrophils, is the hallmark of
Salmonella Typhimurium
 AnaerobiospiriUum, associated with colitis in cats

46. Typhlocolitis in horses
 Clostridial: animal is dehydrated, subcutaneous and
serosal petechial hemorrhage
 Dark blood with poor clotting
 Large bowel, which is distended, with abnormally
fluid content.
 Serosa of the cecum and large colon may appear
cyanotic
 Mucosa, submucosa edematous
 Mucosa may appear brown and necrotic with focal
fibrinohemorrhagic exudate

47.  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 lymphatics
 Some neutrophils
 Clostridium pegringens type A, C. difficile
 Antibiotic therapy, stress, feed change

49.  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 days
 Rhodococcus equi in foals : Suppurative ulcers involving
lymphoid tissue in the typhlocolic mucosa, and cecal and
colic lymphadenitis,
 strongyles

50.  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

51. NSAID induced enterocolitis

52. 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

53.  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 kids
C. perfingens type D in goats