Pathology of the intestines Flashcards
Enteritis
Inflammation of the intestines
Typhlitis or cecitis
Inflammation of the caecum
Colitis
Inflammation of the colon
Proctitis
Inflammation of the rectum
What effects does enteritis have?
Loss of fluid and electrolytes from body.
Malabsorption – due to effect on epithelial cells.
Osmotic effect - produces diarrhea;
Weight loss.
Types of enteritis
Catarrhal
Ulcerative
Haemorrhagic
Fibrinous
Necrotic
Proliferative
Lymphoplasmacytic
Eosinophilic
Catarrhal Enteritis
Initially hyperaemia of gut may be visible through the serosa.
Blood vessels obvious and whole bowel appears red looking, wet shiny and oedematous (no external damage).
Internally mucosa is oedematous, with mucoid appearance.
Initially contents are thin watery / serous.
As condition progresses exudate becomes more mucoid and cellular.
Mucous coats epithelial surface of gut.
Bowel contents may appear quite opaque as polymorphs enter it (i.e. may become mucopurulent).
In older cases of catarrhal enteritis villi become stubby due to loss of epithelial cells and mucosa may appear quite shiny.
Parasitic enteritis
Pre-patent period of 7-10 days then develops greenish diarrhoea.
In young animals can cause serious disease and die.
Gut filled with greenish soupy material.
Oedema and hyperaemia of mucosa.
Aetiology of viral enteritis
Coronavirus
Parvovirus
Rotavirus
Adenovirus
Herpesvirus
Calicivirus
Norovirus
Circovirus
Feline infectious enteritis / feline panleucopenia
Feline panleucopaenia virus (FPLV) (felids, mink, ferrets, raccon).
Uncommon now, as vaccine is available.
<6months old
Primarily in cat over last 10/15 years but now also seen in dog (canine parvovirosis).
Clinical signs of feline infectious enteritis
Seen in cats under 6 months age mostly and is common in groups of unvaccinated cats producing big outbreaks with vomiting and pyrexia.
Severe vomiting, severe thin watery foul smelling diarrhoea may be blood-tinged.
Usually die from dehydration despite treatment. May also die from other infections. Virus shed from urine and faeces for up to 6 weeks.
White blood cell count drops very low (almost non-existent from 10000 / mL to 1/ mL if lucky) - panleucopaenia.
Pathology of feline infectious enteritis
In cat thickened, turgid and swollen intestine, dull mottled appearance, pale.
Contents rather dry - gets worse lower down gut.
In upper small bowel see areas of depression in the mucosa due to destruction of tissue overlying Peyer’s patch (GALT).
Lower down see haemorrhagic enteritis (dog) or fibrinous (cat).
Inflammation sometimes doesn’t appear very severe.
Lesions may be very few and usually need histology for diagnosis.
If is a radiomimetic virus (has similar effect to radiation poisoning) as affects all rapidly dividing cells and destroys them - e.g. epithelium in the base of the crypts of small intestine are killed.
Histology of feline infectious enteritis
Complete necrosis of crypt lining cells with very little inflammation.
Collapse of villous architecture.
Submucosa not affected and lamina propria left intact.
If survives for more than a few days then see cyst-like structures histologically in deepest parts of glands of intestinal mucosa.
Flattened epithelial cells line these cystic glands and are enterocytes trying to repair the damage.
May see intranuclear inclusion bodies (but very hard to find).
May get lymphocyte invasion of mucosa.
Lymph nodes appear pale, oedematous, aplastic almost.
Bone marrow - pale and fatty looking, depleted of cells.
Canine parvovirosis
New disease but virus closely related to feline virus.
Canine parvovirus-2 (CPV-2).
DNA 98% homologous to virus of cat.
Canine virus does not cause disease in cats.
Clinical signs of canine parvovirosis
Virus shed only during clinical disease 7-10 days.
Enteritis in dogs > 6 weeks old, - myocarditis in puppies (uncommonly nowadays).
Rottweilers and Doberman pinschers at increased risk for parvovirus.
Vaccines very effective, but virus is hardy and survives in environment.
Microscopic lesions of canine parvovirosis
Villi atrophy
Crypt necosis
Submucosal oedema
Diagnosis of canine parvovirosis
Look for viral antigen in faeces by red cell agglutination test.
Immunoflurescence
ELISA
Serology - need caution.
Aetiology of bacterial enteritis
Colibacillosis
Clostridiosis
Salmonellosis
Colibacillosis
Only a few strains of this organism cause disease – identified by their serotypes.
Young animals are at highest risk for coliform diarrhoea.
Intrinsic and extrinsic factors act together to produce infection.
Shiga-toxin producing E. coli
- Verotoxin-IL-8
Pathogenesis of colibacillosis
Three mechanisms by which coliform organisms cause diarrhoea.
* Enterotoxigenic E. coli
* Enteroinvasive E. coli
* Enteropathogenic (attaching an effacing)
Can cause systemic infections
Enterotoxigenic E. coli
Calves: Enterotoxigenic E. coli (ETEC)- only seen in animals 4-5 days possibly up to 1 week. If older than 1 week not ETEC.
ETEC’s need two qualities -
○ adherence factors
○ heat stable toxins
Death is from dehydration and electrolyte loss.
Control of Enterotoxigenic E. coli
Management factors such as hygiene, good colostral intake, etc.
Enteroinvasive E. coli
These strains (O101) act like Shigella or Salmonella, penetrating enterocytes, invading lamina propria and spreading to lymph nodes and beyond.
Toxin damages enterocytes leading to villus blunting, elongation of crypts and sometimes mucosal ulceration.
Not common in animals.
Enteropathogenic E. coli (EPEC)
Organisms penetrate glycocalyx, adhere closely to mucosal cell surface and destroy microvilli.
Cause blunting of villi, crypt hypertrophy and inflammatory cells in lamina propria.
Colon often more severely affected than intestine.
Systemic colibacillosis infection
May have septicaemic coliform infections producing peracute death without diarrhoea, mainly in first 2 days of life, usually due to insufficient colostrum intake.
In this form lesions include endocarditis in cats, haemorrhagic pneumonia and bacteraemia in kenneled dogs.
Enterohaemorrhagic colibacillosis
EHEC and E. coli 0157:H7 produce similar type attachment-effacement lesions as AEPECE, leading to minimal inflammation.
Most common incriminated bacterial infections in dogs diarrhoea
Clostridium perfringens type E and Cl. difficile
Clostridium perfringens
Gram positive
Anaerobic bacillus (intestinal tract)
Excess growth leads to toxin production
Type E - canine haemorrhagic enteritis
Clinical signs of Clostridiosis
vary from mild to severe, with a self-limiting diarrhoea to a potential fatal haemorrhagic diarrhoea.
Pathogenesis of clostridial enterotoxaemia
Amount of quality of feed (CHO, proteins)
Change in the intestinal microbiome - toxins
Diarrhoea, anorexia, abdominal pain
Death
Two species of Salmonella
S. bongori
S. enterica
Pathogenesis of Salmonella
Organisms penetrate enterocytes, cross the mucosa, enter macrophages and may then either remain localised to the gut or are carried round the body and cause disease
Two main types of disease caused by Salmonella
Septicaemic
Enteric
Septicaemic salmonellosis
very dramatic produces death quite suddenly.
Diarrhoea often not seen before death.
Organism colonises bowel epithelium, affects Peyer’s patches (GALT) and invades across epithelium to submucosa by way of macrophages which it invades.
It may remain localised to submucosa of bowel or spread to lymph nodes and then on to become septicaemic.
Liver, lymph nodes and spleen are then mainly affected by this bacterium.
Animal may die at this stage (30%)
Unusual in very young.
Clinical signs of septicaemic salmonellosis
Pyrexia with little bit of diarrhoea occasionally.
Reddened skin, diffuse may be dark purplish red blotches like bruises.
Pathology of septicaemic salmonellosis
Excessive peritoneal fluid (blood tinged), mesenteric lymph nodes enlarged and haemorrhagic.
Ecchymotic and petechial haemorrhages on serosa and mucosa.
Lungs are collapsed and frothy.
Heart -often dilated with ecchymotic haemorrhages.
Viscera have half-cooked appearance - pale in colour.
Liver, kidneys - flabby and may see subcapsular haemorrhages.
Liver may contain small white foci of necrosis known as paratyphoid granuloma’s.
Guts may show mild catarrhal enteritis, may become fibrinous lower down.
Bowel generally flaccid, reddened and filled with fluid.
Diagnosis of septicaemic salmonellosis
by culture of blood and from mesenteric lymph nodes (which are oedematous and red).
Enteric Salmonellosis
Clinically differs between species.
Dogs have acute bouts of diarrhoea.
Cats febrile enterocolitis.
Clinical signs of enteric salmonellosis
Affected animals produce acute diarrhoea, watery and yellow, may be tinged with blood (not much blood).
May die from dehydration
Pathology of enteric salmonellosis
Enteritis throughout gut but gets worse along gut - catarrhal in duodenum and often fibrinous by ileocaecal junction and may see fibrinous inflammation with the formation of diptheretic membranes on the mucosal surface.
This necrotic and fibrinous change particularly affects Peyer’s patches (GALT) and caecal and colonic lymphoid nodules.
May lead to ulcers in terminal ileum and colon.
Very rarely do these ulcers rupture.
May also see focal necrosis particularly in liver, also in spleen.
Histologically these foci show a central zone of coagulation necrosis surrounded by macrophages and lymphocytes -i.e. paratyphoid granulomas.
What is the overlap of septicaemic and enteric salmonellosis
Septicaemic form may relocalise in gut and result in enteric disease.
Enteric cases of salmonella infection nearly always show some evidence of systemic spread.
What is a possible sequel to acute salmonellosis (especially in piglets)?
Stricture of the rectum
Lymphocytic-plasmacytic enteritis - signalment
Most commonly in dogs.
Basenji has a hereditary basis producing a severe protein losing enteropathy.
Pathology of lymphocytic-plasmacytic enteritis
Affects small intestine, sometimes quite extensively to produce chronic diarrhoea with lymphocytic or plasma cell infiltration of lamina propria rather than macrophages.
Sometimes eosinophilic infiltration is quite marked
Pathologenesis of lymphocytic-plasmacytic enteritis
Appears immune mediated.
Possibly food allergy.
Could try change of diet as often due to something present in the diet for some time not suddenly introduced.
Possibly caused by hypersensitivity to inhaled or ingested environmental allergens.
Histiocytic ulcerative colitis
(Granulomatous colitis)
Occurs in dog and cat.
In dog particularly in boxer and French bulldog.
In dogs less than two years with soft faeces containing mucous and blood.
Pathology of histiocytic ulcerative colitis
Raised ulcerative nodules in colon, which are due to an infiltration of mucosa and submucosa with of macrophages filled with PAS positive material.
Macrophages are filled with E. coli antigen as demonstrated by electron microscopy.
Accompanying lymphadenopathy.
Eosinophilic enteritis
Either focal or diffuse.
Focally as a disease of young dogs associated with Toxocara canis infection.
Diffuse has a predilection for GSDs but also other breeds and cats.
Focal eosinophilic enteritis
a disease of young dogs associated with Toxocara canis infection.
See pinhead sized white nodules in bowel under serosa. They consist of accumulations of eosinophils and occasionally macrophages and plasma cells.
Sometimes Toxocara larvae can be seen in the nodules.
Diffuse eosinophilic enteritis
has a predilection for German Shepherd but also in other breeds and cats.
Recurrent episodes of diarrhoea with tissue and circulatory eosinophilia.
Suggested that is type of hypersensitivity reaction.
Eosinophils heavily infiltrate all layers of stomach and intestines.
