Gastrointestinal Diseases in Farm Animals

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Gastrointestinal Diseases in Farm Animals Powered By Docstoc
					Gastrointestinal Diseases in
       Farm Animals



 Presented by Tim Morgan DVM,
              PhD
 Conditions Seen in All Species
• Developmental anomalies
  – Anal atresia – results when dorsal membrane
    separating anus and rectum fails to rupture, seen as
    retention of feces, seen in pigs, cattle, llamas and
    alpacas, horses, etc
  – Ileocolonic agangliosis – seen in white foals that are
    offspring of Overo horses
     • Foals appear normal at birth but develop colic and die by day
       2
     • Colon lacks myenteric plexus
  – Acquired megacolon – seen in pigs, cats, dogs, man
     • Fecal-filled colon secondary to trauma to colonic innervation
      Anal Atresia in Baby Pig




Marked abdominal distention   Fecal-filled spiral colon
      Overo Miniature Horse




• Normal Overo color
                   Megacolon
• The colon is chronically
  dilated (3-4 x normal) and
  filled with dry fecal
  material
• This leads to chronic
  constipation (infrequent
  or difficult evacuation of
  feces), tenesmus
  (straining to defecate)
  and dyschezia (painful
  defecation)
          Conditions in All Species
• Intestinal Obstruction
   – Foreign bodies in all species
• Enteroliths
   – Primarily see in horses, especially in Arabians older than 4 years
   – Vary in size and usually composed of ammonium magnesium
     phosphate crystals around a nidus (wire, stone, nail)
   – Usually lodge at pelvic flexure or transverse colon
• Impaction of Intestine
   – Occurs in all species but is especially common in horses
       • Cecal or colonic impaction with sand or fibrous ingesta
       • Ileal impaction with coarse roughage, hairballs, etc
       • Ascarid (Parascaris equorum) impaction in young horses following
         deworming
       • Rupture of impacted segment can occur – peritonitis – shock -
         death
          Impactions and Obstructions




                                              Sand impaction in colon of horse



Foreign body obstruction in
jejunum of a dog




                              Multiple hairball impaction in ileum of a cat
      Conditions in All Species
• Intestinal strictures
   – Can occur in any animal secondary to injury
   – Rectal stricture in pigs secondary to salmonellosis
     and damage to cranial hemorrhoidal artery
• Intussusception
   – Seen in dogs, cats, ferrets, horses, cattle, etc
   – One segment telescopes into immediately distal
     segment
      • Intussusceptum is trapped segment
      • Intussuscipiens is enveloping portion
   – Usually secondary to parasites, diarrhea, foreign
     body, etc
   – Clinically see as abdominal pain, vomiting, anorexia
   – Both segments eventually become necrotic
      Strictures and Intussusception




                                                               Intussusception in a
Rectal stricture in pig
                                                               dog




                          Intussusceptum and intussuscipiens
      Conditions in All Species
• Paralytic ileus
   – Nonmechanical hypomotility resulting in functional
     paralysis of bowel wall
   – Usually secondary to peritonitis, shock, toxemia,
     electrolyte imbalance, uremia
   – Seen as absence of bowel sounds, fluid and gas –
     filled gut loops
• Adynamic ileus
   – Sympathetic nerve inhibition secondary to
     manipulation and handling of bowel at surgery
   – Stomach and intestine fail to respond to presence of
     ingesta, but can respond to pharmacologic and
     electrical stimuli
   – Signs as for paralytic ileus
         Conditions in All Species
• Internal incarceration – entrapment of intestine in
  normal or pathologic openings in abdominal cavity –
  primarily see in horses
   – Mesenteric rents – defects in small intestine mesentery that
     probably develop as result of trauma
      • Segment of small intestine passes through defect, fills with fluid and
        gas, and becomes incarcerated
   – Through epiploic foramen – a natural opening bounded by
     caudate lobe of liver, portal vein, and inferior vena cava
      • Ileum most commonly incarcerated
• External incarcerations (hernias) – form when sac
  formed by pouch of parietal peritoneum penetrates
  outside abdominal cavity and loop of intestine becomes
  entrapped
   – Types include: umbilical, diaphragmatic, hiatal, inguinal,
     scrotal, and perineal
               External Hernias
• Inguinal hernia in young
  pig
   – One side involved
     (unilateral)
• Result of abdominal
  organs protruding through
  inguinal ring
• Seen clinically as skin-
  covered bulges in groin
• Also occur in puppies,
  and middle-aged female
  dogs
   – In older females may be
     due to stretching of
     abdominal tissue due to
     past pregnancies
          Conditions in All Species
• Volvulus – small intestine rotates on its mesenteric axis
  > 180 degrees
   – Thin-walled mesenteric veins are occluded while arterial blood
     continues to flow in resulting in severe organ congestion
   – Eventually segment of intestine obstructed and ischemic
     necrosis occurs
   – Clinically, animal becomes dehydrated and dies of endotoxic
     shock
   – In horse volvulus of left colon also occurs
       • Colon extends from cecum cranially on right, then transversely
         across ventral abdomen caudal to diaphragm to form left ventral
         colon which at its caudal end turns dorsally at pelvic flexure to form
         left dorsal colon
       • The left side loop of left ventral and dorsal colon undergoes volvulus
         of 180 degrees or more
       • Has same ischemic consequences as small bowel volvulus
       • Twist thought to be caused by overfilling of the left dorsal colon with
         feces or sand
       • Left dorsal colon displaced while left ventral colon is moved
         laterally causing clockwise twist of the axis
       • At necropsy, that portion of colon beyond twist is black and its wall
         filled with blood
                            Volvulus




Volvulus of small                                         Volvulus of portion
intestine in a dog                                        of small intestine in
                                                          a calf




                     Volvulus of large colon in a horse
       Conditions in All Species
• Torsion – rotation of tubular organ along its long axis
   – Most commonly seen in cecum of cattle and horses
   – Occasionally seen in abomasum of calves
   – Results in bowel obstruction and ischemic injury
• Pedunculated lipomas
   – Seen in horses >10 years-old
   – Benign fatty tumor that suspend from mesentery by a stalk which
     wraps around a segment of small intestine, occluding the lumen
     and interfering with blood supply
   – Clinical signs of colic
• Renosplenic entrapment
   – Left dorsal displacement of colon in horses
   – Right dorsal displacement of colon in horses
   – See later for details
         Pedunculated Lipoma
• Lipoma from 12 year-old
  thoroughbred mare.
• Lipoma has looped
  around segment of small
  intestine and caused
  obstruction of bowel –
  anterior segment
  becomes partially or
  completely obstructed
• The anterior bowel was
  distended with fluid and
  mesenteric blood vessels
  are prominent
             Miscellaneous Conditions
•   Intestinal rupture
     – Primarily seen as result of impaction or complication of anesthesia
     – In mares, may see following parturition
•   Diverticula (one = diverticulum)
     – Epithelium-lined cavities that are derived from mucosal epithelium that extend
       through muscularis mucosa and may reach serosa
     – May rupture and cause peritonitis
•   Muscular hypertrophy of distal ileum
     – Condition of unknown etiology in horses and pigs may represent work
       hypertrophy of ileum proximal to damaged ileocecal valve
     – Usually incidental but if severe can lead to impaction and rupture of the ileum
     – Hypereosinophilic syndrome of cats – associated with hypertrophy of tunica
       muscularis of ileum
          • Eosinophil infiltrates throughout intestine wall
•   Hemomelasma ilei
     – Pink to black plaques located on antimesenteric serosal surface of ileum and
       other regions of small intestine of horses
     – Result of tissue damage caused by strongyle larval migrations
•   Intestinal lipofuscinosis (brown dog gut)
     – Small intestine serosa is brown due to perinuclear Lysosomal accumulation of
       lipofuscin granules in smooth muscle cells
     – Seen with bile duct blockage, pancreatic insufficiency, chronic enteritis, Vitamin
       E deficiency or excess dietary lipids
         Miscellaneous Conditions




Hypertrophy of ileal smooth muscle in a   Diverticulum in calf duodenum that
pig                                       caused obstruction
       Gastrointestinal Intoxication
• Blister Beetle
   – Seen in horses consuming alfalfa hay infested with striped blister
     beetles
   – Toxic principle is cantharidin – highly irritating to mucous
     membranes causing acantholysis and vesicle formation
       • After ingestion is absorbed from GI tract and rapidly excreted in
         kidneys
       • Minimal lethal oral dose to horse has not been established but
         probably is <1 mg/kg BW
       • Also toxic to humans, cattle, sheep, goats, dogs, cats, rabbits and
         rats
   – Clinical signs in horses
       • Abdominal pain (colic), stiff hind legs, anorexia
   – Dx – submit urine to dx lab for cantharidin chemistry
       • Decreased serum calcium concentration
       • Hemorrhagic lesions in stomach and urinary bladder
       • Demonstration of striped blister beetles in hay
           Cantharidin Toxicity




Striped blister beetle   Hemorrhage in bladder mucosa
                 Cantharidin Toxicity




Acantholysis of squamous epithelium in   Hemorrhage in mucosa of glandular
glandular stomach                        stomach
  Diseases of Intestinal Epithelium
• Absorptive enterocyte
   – Rotavirus, coronavirus,
     bacteria (enterotoxigenic E.
     coli), cryptosporidia,
     coccidia
• Undifferentiated crypt
  cells
   – Parvovirus, BVD, FeLV,
     rinderpest, PPE, other
     bacteria
• Microvilli & glycocalyx
  abnormalities
   – Attaching E. coli, lactose
     intolerence
• Goblet cells
   – IBD
   Diseases of Lamina Propria
• Inflammation
  – HUC, Johne’s, IBD
• Necrotizing processes
  – BVD, R. equi
• Vascular changes
  – Bacterial endotoxins
• Lymphangiectasia
  – Johne’s, lymphoma,
    IBD
    Diseases caused by bacteria
• Escherichia coli (colibacillosis)
  – Enterotoxic E. coli – seen in 2 day to 3 week-old
    puppies, pigs, calves, lambs and humans
     • Bacteria colonize enterocytes via pili that anchor them
     • Produce toxin that causes cyclic AMP mediated increase in
       water and electrolyte secretion (secretory diarrhea) – profuse
       watery yellow
     • Small intestine is dilated and fluid-filled
     • Dx – culture bacteria, type toxin and/or pilus Ag,
       histopathology
  – Postweaning colibacillosis of pigs
     • Similar to above but E coli is hemolytic and a different strain
     • Bacteria produces verotoxin
  – Septicemic colibacillosis
     • Seen in newborn calves, lambs, foals that do not get
       colostrum
     • Bacteria have ability to penetrate gut mucosa, umbilicus, etc
       and get into blood – septicemia and multiple organ damage
       E. Coli diseases (cont’d)
– Edema disease (shigatoxigenic colibacillosis)
   • Seen in 6 to 14 week-old pigs that have had diet change
   • Hemolytic E. coli colonizes SI and produces heat-labile exotoxin
     (Shigatoxin 2e) that causes generalized endothelial damage
     resulting in edema in stomach, eyelids, spiral colon mesentery,
     gallbladder and brain
   • In brain, also see bilaterally symmetrical necrosis (malacia) - focal
     symmetrical encephalomalacia
   • Death is due to endotoxic shock
– Enteroinvasive colibacillosis
   • seen in humans, lab animals, cattle and pigs
   • E. coli invades colonic mucosa and produces verotoxin resulting in
     hemorrhagic colitis
   • Food-born illness in humans
– Attaching and effacing E. coli
   • Seen in rabbits, calves, pigs, lambs, dogs and humans
   • E. coli attach to enterocyte by cup and pedestal
   • Disrupt microvilli of enterocyte and cause fluid loss by unknown
     mechanism
           Enterotoxic Colibacillosis




Distended and fluid-filled SI in   Histologic section of E. coli attached to
baby pig                           enterocytes
                       E. Coli Diseases




                                            Edema in wall of stomach of young pig




Catarrhal enteritis in newborn calf
with E. coli enteritis (that progressed
to septicemia)
                                          Focal symmetrical encephalomalacia in pig
                        E coli Diseases




Red distended cecum and colon of            Hemorrhagic colitis due to verotoxin
rabbit with enteroinvasive colibacillosis
                      Salmonellosis
• More than 20 species recognized and all can be pathogenic
• Clinically, can present with acute diarrhea (can be bloody), fever and
  abdominal pain; may also see chronic diarrhea and weight loss
• Live in gallbladder, intestine, and mesenteric lymph node of carrier
  animals
• Produce disease invading gut mucosa and elaborating enterotoxins,
  cytotoxins (verotoxins) and endotoxins
• Colonize intestine – invade epithelial cells – taken up by
  macrophages in LP or PP – to regional lymph nodes or portal
  circulation of liver – systemic
• Toxins cause necrosis of enterocytes – neutrophilic inflammation of
  LP/fibrin on mucosal surface – vasculitis/thrombosis – enlargement
  of Lymph Nodes and Peyer’s Patches – necrosis and
  microgranulomas in liver – septicemia/bacteremia -
  meningoencephalitis, suppurative arthritis, and renal infarcts
• Forms recognized: peracute septicemia, acute enteric, and
  chronic enteric
                    Salmonellosis
• Peracute salmonella septicemia
   – Seen in calves, foals and young pigs
   – S. cholerasuis often involved
   – Diffuse fibrinoid necrosis of blood vessels – DIC – shock - death
• Acute enteric salmonellosis
   – seen in young and adult cattle, horses, pigs, dogs, cats, humans
   – Often caused by S. typhimurium
   – Diffuse catarrhal enteritis or fibrinonecrotic ileotyphlocolitis, with
     hepatocellular necrosis accompanied by inflammation,
     lymphadenopathy, cholecystitis
   – Chronic enteric salmonellosis
       • Seen in pigs, cattle sheep and horses primarily
       • Fibrinonecrotic colitis
       • Rectal stricture in swine – thrombosis of cranial hemorrhoidal artery
                        Salmonellosis




                                         Chronic enteric salmonellosis – pig colon
 Peracute salmonella septicemia-DIC




chronic enteric salmonellosis – cow SI Chronic enteric salmonellosis – sheep colon
                      Salmonella Colitis




Acute colitis in 18 year-old Quarterhorse   Acute colitis in 18 year-old human
mare – inflammation, loss of crypts         female (from NEJM, 2001)
            Clostridial Enteritis
• All can be normal gut inhabitants in low numbers and
  produce protein exotoxins (A - E) and some produce
  enterotoxin (A, C and D)
• Gram positive, spore-forming anaerobic bacilli
• Bacterial proliferate in SI – elaborate toxins that cause
  villous epithelial necrosis – leads to necrosis of LP –
  hemorrhage when blood vessels damaged
• Clostridium perfringens is main etiologic agent
• Exotoxin types: A = alpha; B = alpha, beta, epsilon; C =
  alpha, beta; D = epsilon; E = alpha, iota
                 Clostridial Enteritis
• C. perfringens Type A – produce necrotizing and lethal alpha toxin
   – Associated with necrotic and hemorrhagic enteritis in poultry and dogs,
     necrotic colitis in horses
   – In dogs, also associated with chronic intermittent diarrhea
• C. perfringens Types B and C (enterotoxic hemorrhagic enteritis) –
  produce necrotizing and lethal beta toxin
   – Types B and C seen in calves, lambs, foals, and piglets during first
     week of life
   – Type C seen in adult sheep, goats, and feedlot cattle
   – All can have hemorrhagic enteritis, mucosal ulceration,
     ascites/peritonitis
• C. perfringens Type D (pulpy kidney disease, overeating disease)
   – Seen in growing sheep, goats, horses and cattle – any age affected
   – Associated with overeating of grain or lush pasture that promotes
     sudden increase in bacteria numbers
   – Signs are of acute death that may be preceded by CNS signs (blind
     staggers)
   – Bacteria produce epsilon toxin which is vasotoxic – especially in
     capillaries of brain – leads to encephalomalacia that can be bilaterally
     symmetrical (as in edema disease of pigs)
   – In sheep, may see rapidly autolyzed kidneys
   – In goats, may see hemorrhagic or necrotic enterocolitis
        Clostridium perfringens Enteritis




  Baby pig SI – Type C enteritis




                                              Adult sheep SI – type C enteritis




Clostridial organisms around necrotic enterocytes
        Clostridium perfringens Colitis




5 day-old foal with                                   Opened colon with
red/white discoloration                               raised red areas, fibrin
of serosa of large colon                              and depressed areas




   Low-power micrograph of hemorrhage, necrosis and submucosal edema
            Clostridium Difficile
• Produces protein exotoxins A and B – bind to enterocyte
  receptors and affect tight junctions, also bind to
  endothelial cells and affect cell junctions
• Gram positive, spore-forming anaerobic bacillus
• Causes necrotizing enterocolitis in primates, humans
  (nosocomial) and foals; typhlocolitis in horses and
  enteritis in lab animals
• In nursing piglets, see typhlocolitis and mesocolonic
  edema
• Bacterial overgrowth and disease has followed
  intravenous or oral administration of antibiotics in variety
  of animals and humans
  Clostridium difficile enterocolitis




Ileum from two day-old foal with   Micrograph of necrotic “explosion” and
mucosal hemorrhage                 submucosal edema and inflammation
Clostridium difficile typhlocolitis




                   Baby pig spiral colon with
                   mesocolonic edema and
                   inflammation; mats of Clostridial
                   organisms are at mucosal surface
                 Clostridium Piliformis
•   Tyzzer’s disease
•   Seen in foals and laboratory animals (rabbits and rats) primarily; rarely seen
    in cats, dogs and calves
•   Filamentous, gram negative, spore-forming, intracellular bacteria
•   Spores may survive in soil or bedding for more than one year
•   Pathogenesis poorly understood – spores ingested – bacteria proliferates in
    lower GI tract – blood or lymphatics – liver (hepatocytes) and heart
    (myocytes)
•   In foals, seen in 1 to 6 week-olds
•   Animals usually have history of stress; sulfonamide administration may
    predispose rabbits
•   Signs may include fever, jaundice, diarrhea
•   Lesions are white to yellow 1-2 mm foci of necrosis in intestine, liver and
    myocardium
     – Also see hemorrhage on serosa of ileum, cecum and/or colon
     – Edema of wall of cecum
     – Hepatomegally
•   Microscopic lesions are foci of necrosis mixed with inflammatory cells.
    Viable cells at periphery of necrotic cells contain organisms (seen with silver
    stain)
              Tyzzer’s Disease
• Micrograph of liver from a
  2 week-old foal
• Viable hepatocytes
  adjacent to necrotic focus
  contain filamentous
  bacteria
• Silver staining is the way
  to Dx disease
• Organism can be grown
  only in tissue cultures
  (obligate intracellular
  bacteria) – difficult to do
  on routine basis
            Yersinia Enterocolitis
• Y. pseudotuberculosis,Y.
  enterocolitica
• Associated with acute
  inflammation and
  diarrhea in young sheep
  at pasture that are
  debilitated from factors
  such as starvation and
  cold weather
• Also seen in nonhuman
  primates and humans
• Lesion is necrotizing and
  suppurative enteritis with
  presence of cocobacilli
• Dx by culture and
  histopathology
             Mycobacterial Enteritis
•   Intestinal tuberculosis caused by M. tuberculosis (human, primates), M.
    bovis (bovine) and M. avium complex
•   All three types may produce infection in species other than their own
     – M. tuberculosis is most species specific but can produce disease in dogs, pigs
       and birds
     – M. bovis can cause disease in most warm-blooded animals, including humans
     – M. avium complex seen in birds, pigs, cattle, sheep, horses, deer, mink, dogs,
       cats and some reptiles
•   Inhalation of infective droplets is usual route – bacilli phagocytosed by
    alveolar macrophages – macrophages proliferate – granuloma with necrotic
    center – may calcify (tubercle)
•   Ingestion - M cells of tonsil and Peyer’s patches – granuloma – lymphatics
    – regional lymph nodes – granulomas
•   M cells are specialized epithelial cells that allow transport of antigens into
    lymphoid tissue
•   Dx is by culture of the organism from lesion, histopathology with acid-fast
    staining
                   Viral Enteric Diseases
•   Rotavirus – double strand RNA with protein spikes projecting from surface
    (spokes of a wheel)
     – Most animal species have their own virus and cross infection is not common
     – Cause profuse yellow diarrhea lasting 2-5 days in young animals
          • Calves during first week, nursing and post weaned pigs, foals, young children
     – Virus infects villous absorptive cells in SI – slough – blunting of villi, fusion of villi
       (intestine appears thin-walled)
     – Animals become dehydrated, combined enteric infections
     – Dx – fecal FA, electron microscopy, VI, histopathology
•   Coronavirus – single-stranded RNA with projecting peplomeres (resembles
    a crown)
     – Seen primarily in calves and pigs (TGE) and foals, FIP in cats, catarrhal enteritis
       in ferrets
     – Calves up to 21 days-old have profuse watery yellow diarrhea with blood and
       pigs of any age may vomit and have profuse watery yellow diarrhea
     – Virus infects absorptive villous cells of SI early and later infects both surface cells
       and crypt cells in colon and cecum- loss of villi in SI, and necrotic debris in
       crypts of LI
     – Dx fecal FA, electron microscopy, VI, histopathology
•   Adenovirus – DNA virus
     – Seen as inapparent infections in cattle, sheep, pigs and horses unless
       immunosuppression occurs as in CID of Arabian horses or Arabian crossbreds
     – See I/N inclusions in enterocytes – loss of enterocytes – villous blunting and
       fusion
Rotavirus Enteritis
Coronavirus Enteritis
Enteric Diseases of Pigs
                                 Nursing     Weaning     Growing Finishing or Breeding
                                0-21 days   3-10 weeks           10-26 weeks

      Bacterial Diseases
C. perfringens type C              ++           -                      -

Enteric colibacillosis            +++          +++                     -

Postweaning E. coli                 -          +++                     -

Edema disease                       -          +++                    ++

Proliferative enteritis             -           +                    +++

Salmonella enterocolitis           +            +                    +++

Swine dysentery                    +            +                    +++

         Viral Diseases
Porcine epidemic diarrhea          +           ++                    +++

Rotaviral enteritis               +++          +++                    +

Transmissible gastroenteritis     +++          +++                    ++

Adenovirus enteritis               +            +                      -

      Parasitic Diseases
Cryptosporidium sp                 +            +                      -

Isospora suis                     +++           +                      -

Strongyloides ransomi              +            +                     +

Trichuris suis                      -           -                     ++
      Porcine Proliferative Enteritis
• Seen in weaned, growing, finishing or breeding-aged animals
• Caused by Lawsonia intracellularis – curved gram negative
  organism that may be an obligate intracellular bacteria (can only be
  grown in cell culture)
• Organism invades crypt epithelial cells and induces proliferation of
  these cells – crypts elongate and mucosa becomes thick – villi
  become flat - chronic inflammation of LP – mucosal necrosis and
  hemorrhage
• Similar organism and lesions seen in horse, hamster, ostrich and
  macaques
• Clinically seen as acute hemorrhagic diarrhea or chronic
  fibrinonecrotic enterocolitis
• Ileum is affected first and infection spreads to jejunum and or
  cecum/colon
• Dx by histologic examination plus silver stain to visualize
  organisms, PCR also available
Porcine Proliferative Enteritis
Porcine Proliferative Enteritis
               Swine Dysentery
• Seen primarily in growing and adult swine
• Caused by Brachyspira (Serpulina) hyodysenteriae –
  anaerobic spirochete that produces a hemolysin
• The organism proliferates in the large intestine and
  causes degeneration of superficial mucosal epithelium,
  hemorrhage, inflammation and hypersecretion of mucus
• Organism does not invade cells or LP
• Damaged mucosa is unable to reabsorb fluid resulting in
  diarrhea
• Clinical signs are mucohemorrhagic diarrhea,
  dehydration and anorexia
• Lesions in cecum, spiral colon and rectum – blood, gray
  mucus and fibrin cover mucosa
• Dx by histopathology with silver stain and culture of
  organism
Swine Dysentery
      Pig Parasitic Diseases
• Coccidiosis – Isospora suis
  – Seen in pigs 6 days to 3 weeks old
  – Infection by sexual and asexual stages
    causes superficial mucosal necrosis, villous
    atrophy and exudation of fibrin onto mucosal
    surface
  – Heavy infections cause diarrhea, dehydration
    and anorexia
  – Dx by fecal float, mucosal impression smears
    stained with Giemsa stain or histopathology
Porcine Coccidiosis
              Parasitic Diseases
• Strongyloides ransomi
  (intestinal threadworm)
   – Nursing piglets get larvae
     via colostrum or from
     contaminated skin of sow
   – Piglets develop severe
     diarrhea when 10-14 days
     old with high mortality
   – DX by histopathology,
     mucosal scraping
        Pig Parasitic Diseases
• Trichuris suis –
  whipworms
  – Penetrate mucosa of
    cecum and colon and
    cause inflammation
    and goblet cell
    hyperplasia (excessive
    mucus)
  – Dx by fecal flotation for
    eggs or demo worms
    at necropsy
      Miscellaneous Pig Enteric
              Condition
• Intestinal emphysema
  – Lymphatics of small intestine serosa and
    mesentery are dilated and gas-filled
  – Etiology is undetermined
  – Not associated with clinical disease
  – Seen rarely in adult animals
Intestinal Emphysema
      Enteric Diseases of Ruminants
•   Bacterial Diseases
     –   Salmonellosis
     –   Johne’s disease
     –   E. coli (enterotoxigenic, enteropathogenic)
     –   Yersinia enterocolitica
     –   Clostridium perfringens types A,B,C.E
     –   Chlamydia spp
•   Viral Diseases
     –   Winter dysentery
     –   BVD
     –   Rotavirus, coronavirus
     –   Rinderpest
•   Parasitic diseases
     –   Coccidiosis
     –   Cryptosporidium
     –   Trichostrongylosis
•   Toxicities
     –   Arsenic
     –   Copper
•   Miscellaneous
     –   Peritonitis
     –   Intestinal adenocarcinoma – bracken fern
     –   Cecal dilatation/volvulus
     –   Intussusception
     Bacterial Enteric Diseases of
              Ruminants
• Johne’s disease (paratuberculosis)
   – Chronic disease characterized by diarrhea, hypoproteinemia,
     emaciation in cattle
   – Also seen in sheep and goats (no diarrhea), llamas, camels,
     farmed deer and other wild ruminants
   – Caused by Mycobacterium avium paratuberculosis
   – Calves infected intrauterine, at birth from colostrum or ingestion
     of contaminated feces
   – Clinical signs develop after two years
   – Bacteria infect macrophages in LP of SI and mesenteric lymph
     nodes
   – Lesions are thickened wall of distal SI with prominent transverse
     mucosal folds, mesenteric lymphadenopathy
   – Sheep, goats and deer may develop foci of caseous necrosis
     and mineralization in gut wall and LN
   – Dx by serology (ELISA), PCR, histopathology plus acid fast,
     culture (takes up to 3 months)
   – Rx = none known, test and cull
Johne’s Disease
    Enteric Bacterial Diseases
• Chlamydiosis (strains of Chlamydia psittaci)
  – Obligate, intracellular bacteria
  – Seen in calves, more severe in colostrum-deprived
    calves
  – Affected calves have diarrhea, fever and anorexia
  – Lesions are most severe in ileum but also see lesions
    in jejunum and colon – intestine wall and mesentery
    are edematous- lumen contains yellow fluid and fibrin
    – regional Lymph Nodes enlarged
  – Microscopically see organisms on brush border of
    epithelial cells – enter cells and multiply – into Lamina
    Propria – incite inflammation
  – Dx by fecal antigen test kit,
          Viral Enteric Diseases of
                 Ruminants
• Winter dysentery
   – Acute nonfatal disease of adult dairy cattle characterized by
     catarrhal inflammation of jejunum and ileum – see in Northern
     climates
   – Probably caused by a coronavirus
   – Acute onset of profuse dark green diarrhea that contains flecks
     of mucus and blood, anorexia and sudden drop in milk
     production
   – Will run through entire herd in a few days
   – Gross lesions are dark green fluid in SI, empty LI with linear
     hemorrhages along ridges of mucosal folds
   – Microscopically see necrosis of crypt epithelium with sloughing
     into crypt lumen
   – Dx by , clinical signs, histopathology, EM, FA
           Winter Dysentery
• Colon of dairy cow
  with linear
  hemorrhages over
  ridges of mucosal
  folds
BVD
    Enteric Parasitic Diseases of
             Ruminants
• Coccidiosis
  – Cattle – Eimeria sp infect cattle 1 month to 1 year-old
     • Severely infected develop diarrhea with blood, anorexia and
       dehydration
     • Damage mucosa of ileum, cecum and colon
  – Goats – host specific Eimeria sp in kids
     • Severely infected have diarrhea with mucus or blood,
       anorexia, dehydration
     • Lesions of mucosal necrosis usually in small intestine
  – Sheep – host specific Eimeria sp infect 1-6 month-old
     • Severely infected have diarrhea that may contain blood or
       mucus, anorexia, dehydration
     • Lesions in ileum, cecum, and colon – edema and
       inflammation of mucosa
               Cryptosporidiosis
• Non host-specific protozoan disease caused by C.
  parvum that causes enterocolitis in ruminants (especially
  calves), man, pigs and rarely in dogs, cats and horses
• Other cryptosporidia cause disease in birds and reptiles
• Organisms attach to epithelial cells in stomach, SI or
  colon – displace microvilli – enclosed by host cell
  membranes – undergo asexual/sexual cycle to produce
  oocysts
• Heavy infections can cause chronic watery diarrhea
  (may see blood), dehydration, electrolyte loss
• Disease is often self limiting in otherwise healthy
  animals, but can be fatal in immuno-compromised or
  with co-infections
• Dx by sucrose fecal flotation to see oocysts (4-5 micron
  in diameter), Giemsa-stained fecal smears (see dot,
  ringforms and banana-shaped), histopathology
Cryptosporidiosis
              Trichostrongylosis
• Small nematodes found in duodenum and jejunum of
  cattle, sheep, goats and other ruminants
• Three genera are significant: Nematodirus (2-3 cm long),
  Cooperia (1 cm long), Trichostrongylus (5-8 mm long) –
  all have direct life cycle
• Heavy infections in young animals can cause
  dehydration, diarrhea, anorexia, hypoalbuminemia,
  serous fat atrophy
• Adult parasites in shallow tunnels in mucosa – damage
  microvilli and epithelial cells – mild inflammatory
  infiltrates in LP
• Dx by fecal flotation, ID eggs
          Trichostrongylosis
• Trichostrongylus spp
  nematodes in tunnels
  within mucosa of a 6
  month-old calf
            Oesophagostomum
• Nodular worms of
  ruminants and pigs
• Ingested third stage
  larvae are ingested –
  penetrate mucosa of
  ileum, cecum and colon –
  fourth stage larvae
  penetrate gut wall and
  form granulomatous
  nodules on serosa
• Nodules composed of
  parasite fragments,
  central necrotic debris
  that may mineralize
• Can cause
  intussusceptions in young
  animals
           Cestodes (Tapeworms)

• Moniezia spp in ruminants
• Require two-three hosts to
  complete life cycle
• Attach to gut wall by anterior
  scolex (hooks and 4 suckers)
• Cause minimal damage at site
  of attachment – compete with
  host for nutrients which they
  absorb through their surface
• Flat, segmented and
  reproduce by addition of
  proglottids
• Usually of little clinical
  significance unless massive
  numbers cause functional GI
  obstruction
  Equine Small and Large Intestine
• Stomach and small intestine
  are unremarkable and similar
  to other monogastric species
• Large intestine is massive
  and complex in comparison to
  other animals
   – Cecum – SI empties ingesta
     into cecum through ileocecal
     orifice, contents flow into colon
     via cecocolic orifice
   – Ascending colon (great colon)
       • Right ventral colon (4
         bands)
       • Sternal flexure
       • Left ventral colon (4 bands)
       • Pelvic flexure
       • Left dorsal colon (I band)
       • Diaphragmatic flexure
       • Right dorsal colon (3
         bands)
   – Transverse colon (2 bands)
   – Small colon (descending
     colon) (2 bands)
   – Rectum
  Fermentation in Equine Intestine

• Digestive function in stomach and small intestine occurs
  as in any other monogastric animal
   – Dietary protein is digested and absorbed as amino acids much of
     soluble carbohydrate is absorbed as monosaccharides in small
     gut
• Large intestine is fermentation system analogous to
  rumen
   – Volatile fatty acids are produced in large quantities, absorbed
     through cecal and colonic epithelium, into blood, metabolized in
     liver, and distributed for use throughout body
   – Water is absorbed by ascending and descending colons (up to
     95% of luminal water)
   – Unlike ruminant, microbial protein is wasted because significant
     absorption does not occur in equine colon
•
         Intestinal Diseases of Horses
    Bacterial diseases
     –   Salmonella
     –   Equine intestinal clostridiosis
     –   Rhodococcus equi enteritis
     –   Potomac horse fever
•   Viral diseases
     –   Rotavirus
     –   Coronavirus
     –   Adenovirus (Arabian foals with CID)
•   Parasitic diseases
     –   Strongylosis
     –   Cyclostomiasis
•   Diseases associated with colic
     –   Ileal impaction
     –   Intra-abdominal adhesions
     –   Ascarid impaction
     –   Proximal enteritis jejunitis (anterior enteritis)
     –   Intussusception
     –   Volvulus of SI
     –   Pedunculated lipoma
     –   Internal incarcerations
     –   Inguinal hernia
     –   Impaction of cecum and large colon
     –   Enterolithiasis
     –   Left dorsal displacement
     –   Right dorsal displacement
     –   Volvulus of large colon
     –   Impaction and foreign body obstruction of descending colon
•   Miscellaneous
     –   Right dorsal colitis
     –   Equine granulomatous enteritis (IBD)
     –   Colitis X
     –   Foal Heat
         Intestinal Clostridiosis
• C. perfringens type A enterotoxin associated acute colitis
  in adult horses
• Organism in low numbers is normal inhabitant of colon
  and does not produce enterotoxin
• Some condition (antibiotic Rx, etc) allows for rapid
  growth of enterotoxin-producing strains
• Clinically similar to other forms of acute enterocolitis -
  may see fever, depression anorexia, acute colic with
  severe, dehydrating foul-smelling diarrhea, shock due to
  endotoxemia (hemorrhage in cortex of adrenal glands)
• Lesions are necrotizing to hemorrhagic typhlocolitis
• Diagnosis is by isolation of organism and detection of
  lethal type A toxin by PCR
                Intestinal Clostridiosis




Necrotizing hemorrhagic colitis   Hemorrhagic adrenal cortex
      Rhodococcus Equi Enteritis
• Bacteria is soil saprophyte that can grow in large
  numbers in cow manure, high summer temps – infection
  by inhaling dust or ingestion
• Gram positive aerobic pleomorphic rod that primarily
  affects foals 2-6 months old
• Can also cause abscesses in cattle, sheep, goats, cats
  and humans
• If inhaled, see bronchopneumonia that is
  pyogranulomatous with regional LN’s involved –
  coughing, fever
• If ingested, see pyogranulomatous, ulcerative enteritis of
  segments of SI, cecum, and/or colon
   – Secondary pyogranulomatous hepatitis
• Dx by transtracheal BAL culture, fecal culture of no value
  because can find organism in normal foals
                    Rhodococcus Equi




Pyogranulomatous bronchopneumonia   R equi in lung macrophage
                 Rhodococcus equi
• Small intestine of 3 month
  old foal
   – Mucosal surface has
     multiple, irregularly shaped
     depressed foci
   – These foci are ulcers and
     some have hemorrhage at
     the base
   – Other areas of mucosa
     have thickened, corrugated
     appearance
       • Macrophages full of
         bacteria are the cause of
         the thick mucosa
   – Mesenteric lymph nodes
     are enlarged and filled with
     macrophages full of
     bacteria
                 Rhodococcus equi




Pyogranulomatous hepatitis
                             Organisms in macrophages
              Potomac Horse Fever
• Acute diarrheal disease first described in horses in Maryland and
  Virginia along the Potomac river – now found in many states in USA
• Caused by Ehrlichia risticii (Neorickettsia risticii)
• Occurs sporadically, only one horse on a farm may be affected in
  summer or fall, can also infect dogs and cats
• Transmitted by trematodes that use snails as intermediate hosts –
  animal drinks from standing water and acquires trematode life
  stages along with organism
• Organism has tropism for mononuclear cells and enterocytes
• Clinical – fever, ileus (most consistent sign), colic, diarrhea,
  laminitis, leukopenia
• Mortality is 5-30%
• Dx by acute and convalescent serology (IFA) – four-fold rise in
  horse not vaccinated, therapeutic trial with oxytetracycline (dramatic
  response), definitive requires isolation of organism (difficult and
  expensive)
• Grossly see hyperemia mucosa of cecum and colon, may see
  petechial hemorrhages, intestinal contents are pale brown and fetid
• Microscopic – loss of surface epithelium, decreased crypts,
  pseudomembrane formation, macrophages in LP that contain
  clusters of organism (silver stains)
                          Strongylosis
• Strongyle infections in horses are caused by large and small
  strongyles
• Pathogenic large strongyles include S. vulgaris, S. edentatus and S.
  equinus
• S. vulgaris infection seen clinically as acute and chronic forms
    – Acute – sudden ingestion of large numbers of infective larvae leads to
      colic as 4th stage larvae migrate through mucosa, submucosa and into
      arterioles of intestine causing hemorrhage, edema and inflammation –
      may be fatal due to ischemia and infarction of LI
    – Chronic – ingestion of fewer infective larvae over longer period by older,
      more resistant, horses leads to weight loss, debilitation, chronic
      intermittent colic and diarrhea – seen as verminous arteritis (thrombi,
      lumen narrowing, fibrosis of wall) due to migration of larvae through
      intima of vessel
        • Embolization may occur – acute segmental infarction of large intestine and
          secondary sepsis/endotoxemia (thromboembolic colic, nonstrangulating
          infarction of large intestine)
• Dx based on clinical signs, neutrophilic leukocytosis, eosinophilia,
  fecal exam may reveal strongyle eggs but unreliable since disease
  caused by nonpatent larvae, peritoneal fluid analysis may reveal
  increased protein and eosinophilia, may see hypoalbuminemia
  especially with chronic form, therapeutic worming trial with
  ivermectin, etc.
Strongylosis
                 Cyathostomiasis

• Infection with small strongyles can be associated with
  chronic diarrhea and hypoalbuminemia
• 4th stage larvae migrate through mucosa of LI and may
  include period of hypobiosis were larvae remain
  encysted in mucosa
   – Hypobiotic larvae emerge in spring and may be cause of
     diarrhea and protein loss due to ulceration and hemorrhage of
     mucosa
   – Also see mucosal inflammation that can vary from eosinophilic to
     lymphocytic to granulomatous
• Clinically may see profuse watery diarrhea, ventral
  edema due to hypoproteinemia, intermittent mild colic,
  adequate deworming history
• Dx by biopsy of cecum or ascending colon mucosa, fecal
  usually unrewarding since infection not patent when
  clinical signs observed.
              Cyathostomiasis
• Hypobiotic larvae in colon
  of 8 year-old
  thoroughbred mare
• Marked architectural
  alteration of mucosa has
  occurred
• Mucosa also has diffuse
  lymphocytic inflammation
• Mare had marked weight
  loss, hypoproteinemia,
  and chronic intermittent
  diarrhea
 Ileal Impaction and Obstruction
• Associated with feeding of Bermuda grass hay in
  Southeastern USA, can also see with ileal
  hypertrophy
• Clinical findings are indicative of small intestinal
  obstruction without displacement or
  strangulation, mild to moderate abdominal pain,
  fluid-filled small intestine anterior to obstruction
• Dx by rectally palpable small intestine distention,
  nasogastric decompression, exploratory
  laparotomy
• In foals, may be secondary to abscesses in ileal
  wall or ileocecocolic lymph node
            Ileal Partial Obstruction

• Abscess in ileocecocolic lymph
  node of a 3 month-old foal
  caused by Rhodococcus equi.
• The enlarged node has
  resulted in partial obstruction
  of ileum (notice pale and
  dilated ileal mucosa anterior to
  mass)
• Notice red and congested ileal
  mucosa at level of and just
  posterior to abscess
• The abscess has a yellow,
  caseous center surrounded by
  a thick white capsule
• Microscopic – congestion and
  hemorrhage of submucosa at
  level of abscess
                  Anterior Enteritis
• Clinical syndrome of inflammation of duodenum and
  anterior jejunum that results in excessive fluid
  accumulation in lumen of SI that leads to marked small
  bowel distention as determined by rectal palpation
• Nasogastric decompression produces large volumes (6-
  20 L) of orange-brown colored fluid
   – Must be differentiated from distal small or large bowel
     obstruction
• Lesions always in duodenum, may see in pylorus of
  stomach and variably in jejunum
   – Red mucosa with edema of wall
   – Microscopy – degeneration and sloughing of villi, neutrophil
     infiltration into LP, fibrin on mucosal surface, hemorrhage in
     muscular layers
• Etiology is unknown (clostridium suspected but not
  proven experimentally)
• Rx is empirical – nasogastric tube, fluid and electrolyte
  replacement, antibiotics
Anterior Enteritis (proximal jejunitis)
• Pylorus of stomach
  and duodenum from
  adult horse
• Pylorus has raised,
  round to linear lesions
  and duodenum is
  diffusely hyperemic
  with prominent
  mucosal folds
  (edema)
       Maldigestion/Malabsorption
• Uncommon in horses
• Possible causes include
   – Following small bowel resection – not enough absorptive surface
     area
   – Infiltration of SI wall by inflammatory cells -noninfectious
     (granulomatous enteritis - IBD, eosinophilic gastroenteritis)
   – Infiltration of SI wall by inflammatory cells – infectious
     (Mycobacterium avium, fungi)
   – Enteric neoplasms
• Clinically see chronic weight loss, depression, lethargy,
  may or may not see diarrhea, may also have protein
  losing enteropathy (hypoproteinemia)
• Dx by glucose or xylose absorption test – abnormal test
  proves only inability to absorb sugars – presumed that
  this is reflective of inability to absorb proteins and lipid –
  primary cause may be difficult to determine without
  exploratory celiotomy and intestinal biopsies
       Protein-Losing Enteropathy
• Horses with maldigestive or malabsorptive conditions
  often develop hypoproteinemia
• Failure to absorb sufficient dietary protein
• Possible causes include;
   –   Inflammatory infiltrates into SI wall
   –   Mucosal ulceration
   –   Lymphangiectasia
   –   Neoplastic cells infiltrating SI wall
• If serum protein falls below 2 g/dL, not enough colloid
  osmotic pressure of plasma – fluid loss into interstitial
  space – edema of distal limbs, ventral midline, prepuce
• Dx is complex – must administer radio-labeled albumin
  parenterally and measure radioactivity in feces –
  presumptive dx made on ruling out other organ systems
  that could produce low serum protein (liver, renal, etc)
    Granulomatous Enteritis (IBD)
• Malabsorption and protein-losing enteropathic condition
  in horses, especially in young (1–5 year-old)
  Standardbreds
• Small intestine, LI and mesenteric lymph nodes usually
  involved
• Characterized by villous atrophy and infiltration of LP by
  lymphocytes, macrophages, plasma cells and
  multinucleate giant cells
• Must rule out infectious etiology prior to dx of IBD
• Recent work (Davidson et.al., Res Vet Sci, 2002)
  indicates that TNF-alpha may play pivotal role –
  therefore disease may represent abnormal immune
  response to normal gut flora or other dietary antigens
• Condition bears striking similarity to celiac disease of
  humans
• Dx is difficult, need exploratory abdominal surgery and
  biopsies for definitive
             Right Dorsal Colitis
• Toxicity resulting from NSAID administration (especially
  phenylbutazone)
• NSAID toxicity seen as renal disease (papillary necrosis)
  and gastric ulcers in humans and animals
• In horses see involvement of stomach and/or colon
• Margin of safety for “bute” is narrow in horses( lesions
  seen at 6.6 mg/kg/day but 4.4 mg/kg/day considered
  safe)
• NSAID’s inhibit prostaglandin synthesis – important in
  maintaining mucus barrier in colon and stomach
• Lesions are mucosal ulceration, edema and
  inflammation – in horse may only see colonic lesions
• May also see hypoproteinemia, low Na, low K, low
  chloride, metabolic acidosis
• May see laminitis as sequela
• Dx by history of NSAID administration, trans rectal
  palpation, exploratory abdominal surgery
                 Right Dorsal Colitis




                                 Mucosal necrosis, marked
Ulcers and edema of colon wall     inflammation and edema
                         Colitis X
• Syndrome of peracute rapidly fatal colitis and toxemia of
  unknown cause
• Resembles acute bacterial colitis with endotoxemia and
  endotoxic shock (Salmonella, Clostridiosis)
• In horse, LI is shock organ, so Colitis X may be marked
  type 1 hypersensitivity combined with endotoxemia
   – Implication is generalized anaphylaxis following exposure to
     some antigen at some body location, IgE on mast cells binds the
     antigen causing mast cell degranulation and release of
     proinflammatory mediators
   – Experimental evidence is lacking
• Clinically seen as in other forms of acute colitis with
  shock – dark red mucous membranes, lack of gut
  sounds, leukopenia, low Na, low K, low Ca, metabolic
  acidosis
• Dx usually done at necropsy and is based on exclusion
  of other identifiable diseases and conditions
• Bottom line – this syndrome needs clarification
• Diffuse eosinophil   • Marked edema and
  infiltration           hemorrhage
          Carbohydrate Overload
• Horses fed large amounts of grain, especially corn, are
  at risk if they are not accommodated to high grain diets
  may develop severe colitis, endotoxemia, metabolic
  acidosis and laminitis
• Sudden influx of CHO into LI is rapidly fermented by
  gram positive lactic acid – producing bacteria – marked
  increase in lactic acid production – decrease in pH of LI
  - causes osmotic diarrhea and mucosal damage -
  buffering capacity of mucosa overwhelmed – kills gram
  negative bacteria – large amounts of endotoxin released
  into circulation
• Clinical signs in mild cases – transient osmotic diarrhea,
  mild to moderate abdominal pain, dehydration, laminitis
• Severe cases may have depression (acidosis), intestinal
  tympany, red to brown mucous membranes (peripheral
  vasodilation of endotoxic shock) and laminitis
• Dx by history, grain in nasogastric decompression
 Nonstrangulating Displacement of
        Ascending Colon
• Ascending colon is freely movable except for right dorsal and ventral
  colons
• Feeding of large meals high in concentrates at irregular times
  promotes increased fermentation – gas and VFA’s rapidly produced
  – colonic displacement
    – Left dorsal displacement – ascending colon trapped in renosplenic
      space such that left ventral colon is situated in a dorsal position relative
      to left dorsal colon – Type I and Type II recognized
    – Right dorsal displacement – colon moves cranially, then either medial
      (medial flexion) or lateral (lateral flexion) to the cecum so that pelvic
      flexure ends up adjacent to diaphragm
    – Retroflexion – pelvic flexure moves cranially without movement of
      sternal or diaphragmatic flexures
• Any of the displacements cause partial obstruction of lumen –
  accumulation of gas or ingesta – distention
• Clinically see as intermittent mild to moderate abdominal pain, gas
  distention of colon (percussion), abdominal distention
• Dx by transrectal examination (consult with equine clinician for
  locations of displaced segments), exploratory surgery
           Left Dorsal Displacement
• Type I – large colon
  incarcerated in space bounded
  by suspensory ligament of
  spleen and dorsal body wall -
  sternal and diaphragmatic
  flexures of large colon located
  ventral to stomach which is not
  distended
    – Distended pelvic flexure is
      directed caudally and often
      rotated 180 degrees about
      long axis
• Key: 1=dorsal, 2=cranial, 3=left
  lateral view; A=spleen,
  B=stomach; C=liver,
  D=esophagus, E=left ventral
  colon, F=left dorsal colon,
  G=left kidney, H=base of
  cecum, J=right kidney,
  K=duodenum

                                     •   Livesey, Can Vet J, 1988
           Left Dorsal Displacement
• Type II – in addition to
  incarceration by suspensory
  ligament of spleen, large colon
  is displaced dorsally to lie
  between liver and stomach – in
  this position the stomach is
  distended and adds to the
  incarceration of the colon
    – Left dorsal colon and left
      ventral colon are often rotated
      180 degrees about long axis
• Key – a=dorsal, b=cranial,
  c=left lateral view; A=spleen,
  B=stomach, C=liver,
  D=esophagus, E=left ventral
  colon, F=left dorsal colon,
  G=left kidney, H=base of
  cecum, J=right kidney,
  K=duodenum

                                        •   Livesey, Can Vet J, 1988
 Strangulating Obstruction of LI
• Volvulus or torsion of ascending colon causes
  obstruction of blood flow leading to strangulation
   – Torsion occurs at sternal and diaphragmatic flexures
   – Volvulus usually occurs at mesenteric attachment and may
     include the cecum
   – Pregnant mares are at increased risk for torsion or volvulus of
     ascending colon
   – Torsion or volvulus greater than 270 degrees results in
     strangulation of the vasculature at site of twist
   – If greater than 360 degrees, indicates poor prognosis because
     vascular occlusion has caused marked ischemic necrosis of
     colon mucosa/wall
   – Clinically see as acute moderate to severe abdominal pain,
     decreased feces, gas distention of colon, metabolic acidosis,
     dehydration, endotoxic shock (secondary to devitalization of gut
     wall)
   – Dx transrectal palpation, exploratory surgery
                Impaction of LI
• Often occurs in ascending colon at pelvic flexure but can
  occur at other segments including cecum in all breeds of
  all ages
• Impaction of descending colon is more common in
  ponies and miniature breeds
• Potential causes are many – anything that affects motility
  (drugs, parasite migration), lack of exercise, poor
  dentition, coarse roughage, water restriction, foreign
  body, enteroliths, sand, etc
• Clinically see as mild to moderate, intermittent
  abdominal pain, partial to complete anorexia, reduced
  fecal production or dry hard, mucus-covered
• Dx by transrectal palpation, abdominal radiography may
  show foreign body in pony, foal or mini horse
   Intestinal Ischemia-Reperfusion
                 Injury
• Ischemia is reduction in gastrointestinal blood supply
  leads to mucosal injury
   – Can be caused by occlusion of arterial blood supply by
     thrombus, strangulation of intestinal vasculature, and decreased
     blood flow associated with shock
• Reperfusion injury is initiated during ischemia
   – Xanthine dehydrogenase is converted to xanthine oxidase when
     its substrate, hypoxanthine, accumulates because of ATP use
   – Little xanthine oxidase is produced during ischemia because
     oxygen is required as electron acceptor
   – During reperfusion, xanthine degrades hypoxanthine in presence
     of oxygen producing superoxide radical
   – Superoxide radical contributes to oxidative tissue damage and
     activates neutrophil chemoattractants
             Ischemia-Reperfusion




SI from foal with corrected   Blunted villous epithelium-
   volvulus                     neutrophils in LP
    Equine Gastrointestinal Neoplasia

•   Esophagus
     – Squamous cell carcinoma
•   Stomach
     – Squamous cell carcinoma
•   Small Intestine
     –   Lymphosarcoma
     –   Leiomyosarcoma
     –   Adenocarcinoma
     –   Melanoma
     –   Ganglioneuroma
     –   Intestinal carcinoid
     –   Plasma cell myeloma
•   Cecum, Colon, Rectum
     – Lymphosarcoma
     – Leiomyosarcoma
     – Neurofibroma
         Equine GI Neoplasia
• Primary and secondary tumors of GI tract are
  uncommon in horses
• Usually see in aged horses (>20 years old)
• Need to consider in horse with chronic weight
  loss, recurrent colic, hypoproteinemia, chronic
  diarrhea
• Dx workup should include complete physical,
  transrectal exam, CBC, serum chemistry panel,
  peritoneal fluid analysis and cytology (may see
  cancer cells), endoscopy (esophageal and
  gastric masses), laparotomy with biopsy
      Intestinal Lymphosarcoma

• Peritoneal fluid
  cytologic preparation
  from 20 year-old
  Arabian gelding with
  chronic weight loss
  and hypoproteinemia
• Smear contains
  neutrophils and
  atypical lymphocytes
  that contain red
  cytoplasmic granules
              Intestinal lymphosarcoma




View of SI from laparotomy – dark foci   Opened serosal nodule shows
   and nodules on serosal surface          central ulceration
                            Peritonitis
• Inflammation of mesothelial lining of peritoneal cavity characterized
  by desquamation of mesothelial cells, chemotaxis of neutrophils,
  release of inflammatory cytokines, and exudation of serum, fibrin
  and protein
• Occurs in all animals secondary to bacteria contamination, vascular
  insults of GI tract, trauma, neoplasia, chemical insult (urine, bile,
  chyle, pancreatic enzymes), or viral infections (feline coronavirus,
  equine viral arteritis, etc)
• Bacteria contamination can occur as result of hematogenous spread
  (Rhodococcus equi), perforation of bowel segment, devitalization of
  bowel secondary to strangulation or infarction or iatrogenic
  intervention (enterotomy, trocharization, etc)
• Clinically, may see colic, ileus, anorexia, fever, distended abdomen
  that is tense and painful on palpation; if rupture of bowel has
  occurred, animal will be have endotoxic shock, circulatory failure
• Dx by CBC (neutrophilic leukocytosis), peritoneal tap (collect in
  EDTA tube) look at color, turbidity, total protein, white blood cell
  count and differential, cytology
    – Normal is clear and straw colored, and does not coagulate
      spontaneously, has fewer than 5,000 wbc/microliter, protein is 1.5 g/dl-
      2.5 g/dl

				
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