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Module 16 > Pathology of Bacterial Infections Inflammatory in GI System > Flashcards

Pathology of Bacterial Infections Inflammatory in GI System Flashcards

1
Q

what is the main function of the GI system (4)

A
  1. selectively permeable barrier
  2. transit, digestion and absorption of nutrients, electrolytes and fluids
  3. prevent entry of pathogens and toxis
  4. immune function (extensively developed mucosal associated lymphoid tissue MALT)
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2
Q

what are the cell types in the intestine (6)

A
  1. globet cell
  2. enterocyte
  3. paneth cell
  4. M cell
  5. neuroendocrine cell
  6. stem cells
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3
Q

what are the functions of globlet cell

A

mucus layer production

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4
Q

what are the functions of enterocytes

A

absorption

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5
Q

what are the functions of paneth cell

A

antimicrobial proteins/peptides

  • lysozyme
  • phospholipase
  • DNAse
  • ribonuclease
  • alpha-defensins
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6
Q

what are the functions of M cells

A

microorganisms, particles and macromolecules uptake and transfer

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7
Q

what are the functions of neuroendocrine cell

A

serotonin

somatostatin

cholecystokinin

peptide UU

glucagon-like peptide

secretin regulation of: intestinal motility, secretions, visceral sensations, appetite

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8
Q

what are the functions of stem cells

A

intestinal epithelium renewal compartment reside in the lower half portion of the crypts

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9
Q

what are the mechanisms of diarrhea

A
  1. secretory
  2. osmotic/malabsorptive
  3. inflammatory
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10
Q

what is the mechanism of secretory diarrhea induced by bacterial toxins (11)

A
  1. ingestion of bacteria
  2. colonization of mucosa
  3. release of toxin
  4. heat labile or heat stable entertoxin
  5. pass through intestinal lumen through receptor
  6. causes increase in adenylyl or guanylate cyclase activity
  7. increase in cAMP or cGMP
  8. causes of activation of ion/H2O pumps
  9. causes water, K+, Cl-, Na+, HCO3- to pass through intestinal lumen
  10. causes severe dehydration/electrolyte imbalances
  11. leads to secretory diarrhea
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11
Q

what is the net effect of secretory diarrhea induced by bacterial toxins

A

net increase in electrolytes and water passing through small intestine to colon

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12
Q

what other factors stimulate secretory diarrhea (2)

A
  1. prostaglandins and other arachidonic acid derived inflammatory mediators
  2. histamine, kinins, cytokines
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13
Q

what factors cause increase in bacterial overgrowth (8)

A
  1. increased entry of bacteria
  2. abnormality of intestinal loops
  3. reduced clearance of bacteria
  4. reduced gastric acidity increased pH
  5. motility disturbance
  6. obstruction of intestine
  7. immunodeficiency
  8. cachexia (wasting syndrome)
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14
Q

what is the mechanism of malabsorption diarrhea due to bacterial overgrowth

A

multiple factors lead to bacterial overgrowth leading to:

  1. bile salt conjugation –> bile salt deficiency –> malabsorption
  2. toxins –> intestinal epithelial cell injury –> malabsorption
  3. consumption of nutrients –> malapsorbtion
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15
Q

what is the mechanism of inflammatory diarrhea (5)

A
  1. ingestion of bacteria
  2. cytotoxin release
  3. villous enterocytes release IL-8 –> activation of local macrophages which release histamine, serotonin, adenosine –> leukocytes recruitment
  4. these local factors cause increased intestinal Cl-, H2O secretion + inhibit absorption, promote secretory diarrhea
  5. acute inflammation –> prostaglandins/leukotrines, PAF, cytokines
  6. promote diarrhea
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16
Q

what are the consequences of diarrhea

A
  1. dehydration
  2. electrolyte depletion
  3. metabolic acidosis
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17
Q

what are the factors that influence gastroenteritis and diarrhea in domestic animals

A
  1. age
  2. immunity (colostrum?)
  3. environmental/seasonal factors
  4. management conditions
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18
Q

what are the issues that interfere with pathology diagnosis of diarrhea in swine and ruminants (2)

A
  1. causal agents can be transiently present
  2. causal agents produce lesions such as villus atrophy which are easily obscured by autolysis
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19
Q

how do you overcome the diagnostic issues in diarrhea in ruminants and swines

A
  1. evaluate one or more untreated animals representative of the herd problem
  2. preferably in the early phase of the disease and with symptoms (not in advanced condition if possible)
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20
Q

how would you collect samples in pathology diagnosis in ruminants and swine

A

euthanasia immediately followed by post mortem

PM procedure modified to prioritize collection of specimens from intestine

samples are formalin fixed within a few minutes of death and then timely collection of appropriate samples for additional testing (parasitology, bacterial culture, virology, PCR)

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21
Q

what are patterns of intestinal injury and some examples in horses, dogs, swine, calves, goats, bovine

A
  1. catarrheal enteritis and intestinal impaction: ascarids in horses
  2. hemorrhagic enteritis: dogs hookworms
  3. necrotizing colitis (‘swine dysentry’): pig brachyspira hydodysenteriae
  4. proliferative enteritis: goat coccidiosis
  5. granulomatous enteritis: bovine johne’s disease
  6. necrotizing-hemorrhagic enteritis: calf coccidiosis
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22
Q

what are the effects of bacterial virulence factors (5)

A
  1. production of bacterial toxins that kill phagocytes
  2. synthesis of bacterial proteins that prevent phagocytosis by blocking the interaction of opsonins with phagosomes
  3. bacterial capsule –> block contact with microbe –> prevent phagocytosis
  4. facilitate escape of the microbe into the cytoplasm before the microbe is killed in the phagolysomes
  5. production of bacterial antioxidants (ex. catalase) that block killing in phagolysosomes
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23
Q

what do E. coli (ETEC) adhere to

A

microvilli on intestinal epithelium

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24
Q

what effect do heat labile toxins from E. coli have

A

LT-I and LT-II

Cl- secretion from enterocytes which cause diarrhea

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25
Q

what effect do the heat stable toxins from E.coli have

A

inhibit Na+/Cl- cotransport in surface enterocytes which indice Cl- and water secretion from crypt enterocytes

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26
Q

what does verotoxin ETEC cause

A

porcine edema disease

shiga toxin –> systemic vascular endothelial damage –> leakage –> edema

brain and spinal cord vessels also affected –> neurological manifestations

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27
Q

what do enteropathogenic/attaching effacing E. coli (EPEC/AEEC) cause

A

attachment + translocation into enterocytes –> loss of microvillus brush border

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28
Q

what are enteroinvasive E. coli (EIC) cause

A

internalized by surface enterocytes –> disseminate through the body –> septicemic colibacillosis

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29
Q

what do the shiga toxin produce E.coli cause

A

protein synthesis inhibition + apoptosis

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30
Q

what are the gross signs of porcine edema disease

A

subcutaneous edema of snout, eyelids, angle of the mandible

edema of gastric wall

edema of mesocolon

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31
Q

what are the common serovars of salmonella

A

S. typhimurium

S. dublin

S choleraesuis

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32
Q

what type of bacteria is salmonella

A

gram negative

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33
Q

is salmonella an aerobe or anaerobic bacteria

A

aerobe/faculative anerobic

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34
Q

is salmonella motile or non motile

A

motile

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35
Q

how is salmonellosis transmitted

A

oro-fecal –> penetrate through M cells

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36
Q

what does salmonella invade

A

enterocytes

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37
Q

what is the virulence factor of salmonella

A

neutralization of macrophage nitric oxide (NO) production

bacteria survive within macrophage phagolysosomes

additional virulence factors: fimbriae (adhesions), lipopolysaccharide (LPS)

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38
Q

what affect do the salmonella toxins have (5)

A
  1. damage to the enterocytes –> interfere with closure of chloride channels –> secretory diarrhea
  2. interaction with toll like receptor (TLRs)
  3. cytokines/chemokines upregulation
  4. inflammation with neutrophil influx
  5. inflammatory cells-derived PGE-2–> further chloride hypersecretion

these all amplify inflammation that promote further chloride secretion and diarrhea

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39
Q

what is the pathogenesis of infection of salmonella

A
  1. salmonella invade M cells in intestinal epithelium
  2. macrophages in lamina propria and Peyer’s patches which are able to resist killing from macrophages
  3. transferred to mesenteric lymph nodes
  4. via portal circulation to liver
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40
Q

what is peracute septicemic salmonellosis

A

disease of calves, foals and pigs

younger animals most sensitive

usually fatal in animals 1-6 months of age

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41
Q

what is the pathogenesis of peracute septicemic salmonellosis

A

multisystemic vascular lesions with fibrinoid change, thrombosis and necrosis

  1. petechiation and blue discoloration (cyanosis) of ventral abdomen, extremities (ears commonly affected)
  2. death caused by disseminated intravascular coagulation (DIC)
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42
Q

how does salmonellosis classically present in swine

A

congestion/cyanosis of the ear pinna with ischemic necrosis of the tip

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43
Q

how does horse peracute salmonellosis present

A

colon have areas of hemorrhage and necrosis from vascular thrombosis and subsequent ischemia

hemorrhagic necrosis –> vascular thrombosis with subsequent ischemia

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44
Q

what bacteria causes acute enteric salmonellosis

A

salmonella typhimurium

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45
Q

how does acute enteric salmonellosis adhere

A

surface fimbrial antigens (pilus adhesion) mediate invasion

receptor mediated endocyte within enterocytes

membrane bound vacuoles –> translocate bacteria to lamina propria macrophages

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46
Q

what are the pathogenic affects of acute enteric salmonellosis

A
  1. interference with chloride channels –> secretory diarrhea
  2. induction of enterocyte apoptosis + recruitment of neutrophils
  3. endotoxins –> vascular thrombosis
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47
Q

what type of intestinal lesions does acute enteric salmonellosis cause

A

fibrino necrotic enterocolitis

malodourous intestinal contents with mucus, fibrin and occasionally blood

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48
Q

what extra intestinal lesions can be found with acute enteric salmonellosis (3)

A
  1. mesenteric lymph nodes: reactive lymphadenopathy
  2. liver: foci of hepatocellular necrosis
  3. gallbladder: fibrinous cholecystitis (distinctive sign in calves)
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49
Q

what lesion is shown here in a foal

A

acute salmonellosis, colitis with prominent fibrino necrotic membranes

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50
Q

what strain of salmonella causes chronic enteric salmonellosis

A

salmonella typhimurium

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51
Q

what species does chronic enteric salmonellosis occur in

A

pigs, cattle, horses

lesions most commonly observed in pigs

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52
Q

what lesions are seen in chronic enteric salmonellosis and where

A

multiple discrete areas of necrosis and ulceration mostly in the cecum and colon

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53
Q

what lesions are shown here in the horse

A

chronic enteric salmonellosis

colon, nodular ulcerative lesions

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54
Q

what type of bacteria is lawsonia intracellularis (gram - or +)

A

-ve

55
Q

what species are susceptible to Lawsonia intracellularis

A

swine, horses, hamster, rabbit, ferret, sheep, deer, fox

56
Q

what are the clinicopathological presentations of lawsonia intracellularis in swine

A

porcine intestinal adenomatosis (PIA)

necrotic enteritis

proliferative hemorrhagic enteropathy (PHE)

–> porcine proliferative enteropathy (PPE)

57
Q

what causes equine proliferative enteropathy (EPE)

A

lawsonia intracellularis

58
Q

when does equine proliferative enteropathy typically occur

A

in post weaning foals (2-8 months)

occasionally in adult animals

59
Q

what lesions are shown in this pig

A

lawsonia intracellularis infection

PPE intestinal adenomatosis

60
Q

what are the clinical signs in horses with Lawsonia intracellularis (8)

A
  1. rapidly deteriorating body condition
  2. anorexia
  3. hypoproteinemia (hypoalbuminemia)
  4. peripheral edema
  5. fever
  6. lethargy
  7. colic and diarrhea
  8. secondary bacteremia
61
Q

what do the virulence factors that lawsonia intracellularis produce cause

A

inhibition of enterocyte differentation –> impaired absorption –> osmotic/malabsorptive diarrhea

induction of enterocyte proliferation

62
Q

how is equine proliferative enteropathy (EPE) diagnosed

A
  1. ELISA (serum)
  2. PCR on feces
  3. distinctive gross PM findings
  4. immunohistochemistry
63
Q

what does Rhodococcus equi cause

A

enterocolitis in foals

64
Q

where Rhodococcus equi found

A

in the soil and as part of normal intestinal flora

65
Q

what does R. equi cause in foals

A

suppurative bronchopneumonia and about 50% of pneumonic foals also have ulcerative colitis

66
Q

where are the lesions associated with R. equi

A

in small and large intestine

most severe in peyer’s patches in SI, cecum, large colon, and related lymph nodes

67
Q

what are the ulcers covered in in R. equi infection

A

purulent/necrotic debris

68
Q

what occurs in the mesenteric LNs in R. equi

A

mesenteric LNs –> enlarged –> pyogranulomatous inflammation/abscesses

69
Q

what is shown here

A

foal with R. equi infection

ulcerative colititis

70
Q

what is shown here

A

suppurative/pyogranulomatous mesenteric lymphadenitis

R. equi infection

71
Q

is clostridia a gram negative or positive bacteria

A

gram + spore forming anaerobic bacillary bacteria

72
Q

what does clostridia perfringens cause

A

enterotoxemias

73
Q

what does clostridia difficile cause

A

entero-typhlo-colitis

74
Q

what does clostridia piliforme cause

A

tyzzer’s disease (necrotizing colitis, hepatitis and myocarditis)

75
Q

what changes in the enteric microenvironment favour expansion of enteric populations of clostridia (5)

A
  1. change in feed, abnormally nutrient rich digesta
  2. antibiotic therapy
  3. altered pancreatic exocrine function or trypsin inhibitors
  4. reduced intestinal motility
  5. primary infections (CPV-2 or coccidia in piglents and chickens)
76
Q

what are 3 mechanisms of clostridial disease (3)

A
  1. local effects of toxins on mucosa –> hemorrhage, fibrinous, or necrotic enteritis
  2. secretory effects of locally acting enterotoxin –> diarrhea and minor lesions
  3. systemic absorption of entero toxins –> effects at sites distant from gut
77
Q

what does Cl. perfringens type D enterotoxemia cause

A

focal symmetrical encephalomalacia

78
Q

what toxin does Cl. perfringens type D enterotoxemia produce

A

ε toxin which causes vascular endothelial damage –> vascular leakage

79
Q

what does ε toxin in Cl. perfringens cause

A

generalized brain edema

ischemia and degeneration/necrosis (malacia) in different areas of the brain

80
Q

what does clostridium perfringens type A cause in foals

A

necrotizing hemorrhagic enteritis

81
Q

what does clostridium perfringens type A cause in adult horses

A

enterocolitis

82
Q

what does what does clostridium perfringens type A cause in piglets

A

necrotizing enterocolitis

83
Q

what does clostridium perfringens type A cause in lambs and calves

A

enterotoxemia and hemorrhagic enteritis

84
Q

what does clostridium perfringens type A cause in chickens

A

necrotizing enteritis

85
Q

what does clostridium perfringens type A cause in canines

A

hemorrhagic canine gastroenteritis

bloody diarrhea

peracute syndrome with enteritis and colitis (occasionally hemorrhagic gastritis)

86
Q

what is the pathology of clostridial perfringens type C enterotoxemia in horses

A

serosal and mucosal congestion/hemorrhage

thickening with gelatinous clear transmural edema

mucosal necrosis/hemorrhage

brown to red foul smelling fluid intestinal contents

87
Q

what lesions can clostridium perfringens type C enterotoxemia in horses cause in the lungs (3)

A
  1. congestion
  2. hemorrhage
  3. thrombosis
88
Q

what lesions can clostridium perfringens type C enterotoxemia in horses cause in the heart

A

subepicardial and subendocardial hemorrhage

89
Q

what lesions can clostridium perfringens type C enterotoxemia in horses cause in the visceral organs and serosal surfaces (2)

A
  1. congestion
  2. hemorrhage
90
Q

what lesions can clostridium perfringens type C enterotoxemia in horses cause in the mesenteric lymph nodes (3)

A
  1. edema
  2. congestion
  3. hemorrhage
91
Q

what lesions can clostridium perfringens type C enterotoxemia in horses cause in the kidney (2)

A
  1. tubular degeneration
  2. necrosis
92
Q

where is clostridial difficile found

A

spores common in environment and intestinal tract of many mammals

93
Q

what does clostridium difficile cause in foals

A

hemorrhagic enterocolitis

94
Q

what does clostridium difficile cause in adult horses

A

necrotizing typhlocolitis

95
Q

what does clostridial difficile cause in suckling piglets

A

mesocolonic edema and typhlocolitis

96
Q

what do clostridium difficile exotoxins cause (3)

A
  1. damage to intestinal epithelium
  2. trigger inflammatory reaction
  3. stimulation of the enteric nervous system
97
Q

what are predisposing factors of clostridium difficile enteric infection in horses (8)

A
  1. antibiotic therapy
  2. hospitilization
  3. stress
  4. change of diet
  5. transportation
  6. starvation
  7. nasogastric intubation
  8. surgical or medical treatment
98
Q

what is the age related distribution of lesions in horses with clostridium difficile

A
  1. <1 mo: small intestine involvement
  2. 1mo- 1 y: colon (no small intestine or cecum)
  3. >1y: colon/cecum (no small intestines)
99
Q

what gross lesions can be found in horses with clostridium infections

A

left ventral colon: diffuse mucosal congestion/hemorrhage

large colon distended with abundant, turbid, green fluid (with grass particles and seeds in suspension)

large colon: transmural gelatinous edema

necrotizing or necro-hemorrhagic enteritis, colititis and/or typhlitis

100
Q

how is clostridium diagnosed

A

ELISA based detection of toxins

101
Q

what pathogen causes potomac horse fever (equine monocytic ehrlichiosis)

A

neorickettsia risticii

102
Q

where is neorickettsia risticii found

A

river valleys in NE usa but now throughout US and south america

103
Q

when is neorickettsia risticii disease most commonly observed in

A

summer

104
Q

what type of bacteria is neorickettsia risticii

A

obligate intracellular bacterial pathogen

105
Q

how is potomac horse fever transmitted

A

accidental ingestion of trematode larvae infected with N. risticii

106
Q

what disease does potomac horse fever cause (7)

A
  1. fever
  2. leukopenia
  3. depression
  4. inappetance
  5. diarrhea
  6. abortion in pregnant mares
  7. fibrino-necrotic to ulcerative colitis
107
Q

what is the disease expression of potomac horse fever cause

A
  1. colic
  2. subcutaneous edema
  3. laminitis
  4. shock
  5. mortality in up to 30% of untreated cases
108
Q

what are the differentials to the disease expression of potomac horse fever

A

salmonella

clostridium

109
Q

what is GCB

A

granulomatous colitis of boxer dogs

110
Q

what are the clinical signs of GCB (4)

A
  1. frequent bloody mucoid stools
  2. anemia
  3. hypoalbuminemia
  4. weight loss
111
Q

what is the gross pathology found with GCB (2)

A
  1. thickening and folding of the colon
  2. possible dilation and shortening with some segmental or focal areas of scarring and stricture
112
Q

what are the mucosal lesions of GCB (2)

A
  1. patchy punctate red ulcers
  2. more extensive irregular circular or linear lesions that may coalesce
113
Q

what disease are these lesions associated with

A

GCB of boxer dogs

114
Q

what histopathology changes can be seen here in GCB

A

lamina propria expanded by macrophages (containing PAS positive material)

115
Q

what histopathological changes can occur with GCB

A
  1. loss of colonic epithelium and goblet cells/microerosions
  2. neutrophilic infiltration and neutrophil efflux into the gut lumen
  3. glandular crypts displacement, with possible hyperplasia
116
Q

what can occur in the mucosa with GCB

A

E.coli isolates from GCB have an adherent/invasive phenotype similar to Crohn’s disease

there are clusters of bacteria within the mucosa

117
Q

what changes occur due to idiopathic inflammatory bowel disease (IBD) (4)

A
  1. villus blunting (and possible alteration of superficial epithelium)
  2. variable crypt dilation (filled with mucus and cellular debris)
  3. possible crypt epithelial hyperplasia
  4. inflammatory cell infiltration in lamina propria (and variably intraepithelial)

–> mostly small lymphocytes and plasmacells

–> variable numbers of neutrophils/eosinophils

118
Q

what is an important ddx with IBD

A

intestinal lymphoma because in IBD there can be small lymphocytes and plasma cells and variable number of neutrophils/eosinophils

119
Q

what are the genetic predispositions to IBD (4)

A
  1. Basenji
  2. german shepherds
  3. boxer (GCB)
  4. irish setter: enteritis associated with familial sensitivity to wheat protein
120
Q

what factors can contribute to IBD (4)

A
  1. perturbation of balance mucosal immunity/intestinal microbiota
  2. shifts in intestinal microbiome gram + –> gram - proteobacteria –> dysbiosis possible trigger and drive to persistent inflammation
  3. diet (food allergy/adverse food reaction)
  4. loss of tolerance to dietary and/or intestinal microflora antigens: innate immune response dysregulation as possible trigger
121
Q

what are the histological parameters in the stomach in IBD (3)

A
  1. fibrosis
  2. intraepithelial lymphocytes
  3. lamina propria inflammatory infiltrates
122
Q

what are the histological parameters in the duodenum and ileum in IBD (5)

A
  1. villus stunting
  2. crypt dilation
  3. lacteal dilation
  4. surface epithelial injury
  5. lamina propria inflammatory infiltrates
123
Q

what are the histological parameters of the colon in IBD (5)

A
  1. crypt dilation
  2. fibrosis
  3. goblet cell number
  4. surface epithelial injury
  5. lamina propria inflammatory infiltrates
124
Q

in calves <3 weeks what are the pathogens that can cause gastroenteritis (9)

A
  1. enterotoxigenic E.coli
  2. enterohemorrhagic E.coli (Shiga toxin)
  3. rotavirus
  4. cornnavirus
  5. bovine viral diarrhea (BVDV pestivirus)
  6. bvine herpesvirus
  7. clostridium perfringens type C
  8. GI parasites
  9. cryptosporidium
125
Q

in cattle >3 weeks what are the pathogens that can cause gastroenteritis

A
126
Q

in small ruminants <3 weeks what are the pathogens that can cause gastroenteritis

A
127
Q

in small ruminants >3 weeks what are the pathogens that can cause gastroenteritis

A
128
Q

in piglets <3 weeks what are the pathogens that can cause gastroenteritis

A
129
Q

in pigs >3 weeks what are the pathogens that can cause gastroenteritis

A
130
Q

in foals what are the pathogens that can cause gastroenteritis

A
131
Q

in adult horses what are the pathogens that can cause gastroenteritis

A
132
Q

in dogs what are the pathogens that can cause gastroenteritis

A
133
Q

in cats what are the pathogens that can cause gastroenteritis

A
134
Q

how do you differentiate lymphoma from IBD

A

histopathology, immunochemistry and PARR

  1. inraepithelial nests (>5 clustered lymphocytes) and intraepithelial plaques (lymphocytes obliterating >5 adjacent enterocytes) are both strong indicators for intestinal T-cell lymphoma

Module 16 (26 decks)

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