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MODULE 16 - Alimentary Tract Disease > PATHOLOGY - Gastrointestinal Bacterial Infections > Flashcards

PATHOLOGY - Gastrointestinal Bacterial Infections Flashcards

1
Q

What are the three mechanisms of diarrhoea?

A

Secretory diarrhoea
Malabsorptive diarrhoea
Inflammatory diarrhoea

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2
Q

What is the main cause of secretory diarrhoea?

A

Bacterial toxins

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3
Q

How do bacterial toxins cause secretory diarrhoea?

A

When bacteria are ingested and expose the small intestinal mucosa, they produce toxins which interact with receptors on the enterocyte surface resulting in a signalling cascade which activates ion/H20 pumps resulting in a net increase in lumenal electrolytes and water

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4
Q

List four additional causes of secretory diarrhoea

A

Prostaglandins
Histamine
Kinins
Cytokines

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5
Q

What is the main cause of malabsorptive diarrhoea?

A

Bacterial overgrowth

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6
Q

Which factors promote bacterial overgrowth in the gastrointestinal tract?

A

Increased entry of bacteria
Decreased gastric acid production which promotes bacteria survival
Abnormality of the intestinal loops
Decreased clearance of bacteria

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7
Q

What can cause a decreased clearance of bacteria?

A

Gastrointestinal motility abnormalities
Intestinal obstruction
Immunodeficiencies
Cachexia

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8
Q

How does bacterial overgrowth cause malabsorptive diarrhoea?

A

Bacterial overgrowth can cause deconjugation of bile salts, resulting in decreased bile salt production and decreased emulsification of lipids, causing malabsorption ot lipids and lipid soluble vitamins. Furthermore, bacterial toxins can cause intestinal epithelial damage resulting in malabsorption, and bacteria consume host nutrients resulting in malabsorption - all contributing to malabsorptive diarrhoea

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9
Q

How do bacteria cause inflammatory diarrhoea?

A

Ingestion of bacteria and release of bacterial toxins triggers enterocytes to release IL-8 which activates and recruits local macrophages which secrete histamine, serotonin and adenosine which increases chloride and water secretion and inhibits intestinal absorption. Macrophage activation also stimulates leukocyte recruitment and the release of proinflammatory mediators resulting in acute inflammation and diarrhoea

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10
Q

What are the three main consequences of diarrhoea?

A

Dehydration
Electrolyte imbalances and depletion
Metabolic acidosis

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11
Q

What are the main factors which intefere with pathological (post mortem) investigation of diarrhoea?

A

Causal agents are often present transiently
Causal agents can produce lesions that are easily obscured by autolysis

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12
Q

What should be done to overcome the limitations of pathological (post mortem) investigation of diarrhoea?

A
  1. Euthanasia immediately followed by post mortem which is modified to prioritise the collection of gastrointestinal specimens
  2. Evaluate one or more untreated animals that are representative of the herd
  3. Evaluate the post mortem in the early phase of disease
  4. Fix samples in formalin within minutes of death to prevent autolysis and to fix the tissue in an as life like state as possible
  5. Timely collection of appropriate samples for further investigation
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13
Q

Which investigative tests should be done when carrying out pathological (post mortem) investigation of diarrhoea?

A

Parasitology
Bacterial culture
Virology
PCR

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14
Q

What are the four main forms of escherichia coli (E.coli)?

A

Enterotoxic E.coli (ETEC)
Enteropathogenic E.coli (EPEC)
Enterohaemorrhagic E.coli (EHEC)
Enteroinvasive E.coli (EIEC)

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15
Q

What is the pathogenesis of enterotoxic E.coli (ETEC)?

A

Enterotoxic E.coli (ETEC) adheres to the microvilli on the intestinal epithelium and produces heat labile and heat stable toxins. Heat labile toxins stimulate Cl- secretion from the enterocytes resulting in secretory diarrhoea. Heat stable toxins inhibit Na+/Cl- co-transporters in surface enterocytes as well as induce Cl- and water secretion from crypt enterocytes, resulting in secretory diarrhoea

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16
Q

Which form of E.coli causes porcine oedema disease?

A

A strain of enterotoxic E.coli (ETEC) causes porcine oedema disease

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17
Q

What is the pathogenesis of enterotoxic E.coli (ETEC) which causes porcine oedema disease?

A

There is a strain of enterotoxic E.coli (ETEC) which produces Stx2 shiga toxin (also known as verotoxin) which causes systemic vascular endothelial cell damage resulting in leakage of fluid from the vessels and oedema

Oedema of the snout, mandibular area and ears
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18
Q

How can porcine oedema disease sometimes present with neurological signs?

A

Stx2 shiga toxin can even cause damage to the vascular endothelial cells in the brain and spinal cord resulting in oedema and neurological signs

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19
Q

What is the pathogenesis of enteropathogenic E.coli (EPEC)?

A

Enteropathogenic E.coli (EPEC) adheres to and translocates into the enterocytes, resulting in damage to and loss of the microvilli, compromising the absorbative capacity of the enterocytes, resulting in malabsorptive diarrhoea

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20
Q

What is the pathogenesis of enterohaemorrhagic E.coli (EHEC)?

A

Enterohaemorrhagic E.coli (EHEC) produces Stx1 and Stx2 of shiga toxin which causes inhibition of protein synthesis and enterocyte apoptosis, compromising the absorpative capacity of the small intestinal epithelium resulting in malabsorptive diarrhoea

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21
Q

What is the pathogenesis of enteroinvasive E.coli (EIEC)?

A

Enteroinvasive E.coli (EIEC) are internalised into the surface enterocytes and disseminate throughout the body which can progress to septicaemic colibacillosis

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22
Q

What are the most common forms of salmonella that cause disease in domestic animals?

A

Salmonella Typhimurium
Salmonella Dublin (most common in cows)
Salmonella Cholerasuis (most common in pigs)

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23
Q

What is the pathogenesis of salmonella?

A

Salmonella is transmitted via the faecal-oral route and adhere to and invade the intestinal epithelial cells, mediated by fimbrae. Salmonellae preferentially adhere to and invade M-cells however invasion enterocytes also occurs. Within the intestinal epithelium, endocytosis occurs which forms vacuoles which translocate the salmonella to the lamina propria macrophages. Salmonella neutralise the nitric oxide within macrophages and can then reside within phagolysosomes. Salmonella toxins trigger acute inflammation of the gastrointestinal tract as well as damage to enterocytes and inteferes within the closure of Cl- channels resulting in secretory diarrhoea. Salmonella toxins can also cause vascular thrombosis. The macrophages transport the salmonella to the mesenteric lymph nodes and then to the liver via the hepatic portal system.

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24
Q

What are M-cells?

A

M-cells are cells found in tne GALT and peyer’s patches of the gastrointestinal tract

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25
Q

What are the virulence factors of salmonella?

A

Fimbrae
Lipopolysaccharides (LPS)

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26
Q

What are the three clinical presentations of salmonella?

A

Acute enteric salmonellosis
Peracute septicaemic salmonellosis
Chronic enteric salmonellosis

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27
Q

Which form of salmonella most commonly causes acute enteric salmonellosis?

A

Salmonella Typhimurium

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28
Q

Which intestinal lesions result due to acute enteric salmonellosis?

A

Fibrino-necrotic entero-colitis due to localised intestinal wall thrombosis and inflammation

Foal, Acute Salmonellosis, colitis with prominent fibrino-necrotic membranes
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29
Q

Which extra-intestinal lesions result due to acute enteric salmonellosis?

A

Reactive lymphadenopathy of the mesenteric lymph nodes
Foci of hepatocellular necrosis
Fibrinous cholecystitis

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30
Q

Which extra-intestinal lesion is a distinctive sign of acute enteric salmonellosis in calves?

A

Fibrinous cholecystitis - patient will present with jaundice

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31
Q

Which signalement is prone to peracute septicaemic salmonellosis?

A

Young (less than six months) calves, foals and piglets however it can also be seem in adults

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32
Q

What is the prognosis for peracute septicaemic salmonellosis?

A

Usually fatal to animals less than 6 months old

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33
Q

What is the pathogenesis for peracute septicaemic salmonellosis?

A

Salmonella can travel into the bloodstream and cause multisystemic vascular lesions with thrombosis, ischaemia and necrosis resulting in petechiation and cyanosis of the ventral abdomen and extremities (most commonly the ears), progressing to disseminated intravascular coagulation (DIC) and shock which can cause death

Note the ear cyanosis and necrosis
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34
Q

Which form of salmonella most commonly causes chronic enteric salmonellosis?

A

Salmonella Typhimurium

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35
Q

Which intestinal lesions result due to chronic enteric salmonellosis?

A

Multifocal necrosis of the intestinal wall known as ‘button ulcers’

Equine button ulcers
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36
Q

Which species are most prone to ‘button ulcers’?

A

Pigs

Porcine button ulcers
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37
Q

(T/F) Lawsonia intracellularis is an faculative intracelluar bacteria

A

FALSE. Lawsonia intracellularis is an obligate intracellular bacteria

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38
Q

What is the pathogenesis of lawsonia intracellularis?

A

Lawsonia intracellularis virulence factors cause inhibition of enterocyte differetiation and induce enterocyte proliferation and mucosal thickening

Note the mucosal thickening
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39
Q

What are the three clinical presentations of lawsonia intracellularis in pigs?

A

Porcine intestinal adenomatosis (PIA)
Proliferative and necrotic enteritis
Proliferative haemorrhagic enteropathy (PHE)

Proliferative haemorrhagic enteropathy on the left and proliferative and necrotic enteritis on the right
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40
Q

What is the main clinical presentation of lawsonia intracellularis in horses?

A

Equine proliferative enteropathy

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41
Q

Which signalement are most prone to equine proliferative enteropathy?

A

Weaning foals (2 - 8 months old)

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42
Q

How do you diagnose lawsonia intracellularis?

A

Serum ELISA which detects L.intracellularis specific IgG
Faecal PCR which detects L.intracellularis DNA
Distinctive post mortem findings
Immunohistochemistry

Immunohistochemistry - the brown regions are lawsonia intracellularis bacteria
43
Q

Why is a faecal PCR preferential to a serum ELISA to diagnose lawsonia intracellularis?

A

A faecal PCR indicates there is an active infection however a serum ELISA only indicates exposure to the bacteria

44
Q

(T/F) Rhodococcus equi is an intracellular bacteria

A

TRUE.

45
Q

(T/F) Rhodococcus equi is a commensal bacteria in the horse intestinal tract

A

TRUE.

46
Q

Where is rhodococcus equi found within the environment?

A

Soil

47
Q

Which two disease processes are caused by rhodococcus equi in foals?

A

Suppurative bronchopneumonia
Ulcerative enterocolitis

48
Q

What is the pathogenesis of rhodococcus equi in foals?

A

Foals with suppurative bronchopneumonia can cough up rhodococcus equi bacteria which are then swallowed and establish infection within the gastrointestinal tract, causing ulcerative enterocolitis. However it is important to note foals can present with ulcerative enterocolitis even without suppurative bronchopneumonia. There can be ulcerative lesions covered in purulent and necrotic debris in the peyer’s patches in the small intestine, the caecum, the large colon and mesenteric lymph nodes. The mesenteric lymph nodes can become enlarged due to pyrogranulomatous inflammation and abscesses

49
Q

(T/F) Clostridia are commensal bacteria

A

TRUE.

50
Q

Which factors can result in expansion of clostridia within the intestinal tract?

A

Changes in diet resulting in abnormally nutrient rich ingesta
Antibiotic therapy
Altered pancreatic exocrine function
Trypsin inhibitors in the diet
Decreased intestinal motility
Primary infections

51
Q

Which infection can result in secondary clostridial expansion in dogs?

A

Canine parvovirus 2

52
Q

Which infection can result in secondary clostridial expansion in pigs and chickens?

A

Coccidiosis

53
Q

What are the three mechanisms of clostridial disease?

A
  1. Locally acting bacterial toxins can result in damage to the intestinal mucosa resulting in haemorrhagic, fibrinous or necrotic enteritis
  2. Locally acting bacterial toxins can cause secretory effects resulting in secretory diarrhoea and minor mucosal lesions
  3. Systemic absorption or bacterial toxins resulting in extra-intestinal sites affected
54
Q

What are the most common forms of clostridia that cause disease in domestic animals?

A

Clostridium perfringens
Clostridium difficile
Clostridium piliforme

55
Q

(T/F) All clostridia are Gram+ bacteria

A

FALSE. The majority of clostridia are Gram+ bacteria however clostridium piliforme is Gram -

56
Q

How is clostridium perfringens categorised?

A

Clostridium perfringens is categorised based on the exotoxins that they produce

i.e. there is type A, B, C, D, E, F and G

57
Q

What are the four main forms of exotoxin produced by clostridium perfringens?

A

α toxin
β toxin
ε toxin (epsilon)
ι toxin (lota)

58
Q

Which toxin do all serotypes of clostridium perfingens produce?

A

α toxin

59
Q

What are the affects of α toxin produced by clostridium perfringens?

A

α toxin is a lecinthase (a form of phospholipase) which acts on cell membranes resulting in haemolysis and/or necrosis of cells

60
Q

What are the affects of β toxin produced by clostridium perfringens?

A

β toxin is a pore forming toxin which results in intestinal cellular necrosis. β toxin also has neurological effects due to an unknown mechanism which has a paralysing affect on the intestine

61
Q

What are the affects of ε toxin produced by clostridium perfringens?

A

ε toxin is a protoxin which is activated by enzymatic digestion within the intestine. ε toxin can cause intestinal epithelial detachment and necrosis. ε toxin can also be absorbed systemically and cause pore formation within vascular endothelial cells resulting in leakage from the vessels and oedema

62
Q

What are the affects of ι toxin produced by clostridium perfringens?

A

ι toxin is a protoxin which is activated by proteolytic digestion within the intestine and increases local capillary permeability

63
Q

What can be used to diagnose clostridium perfringens serotype?

A

ELISA to type the exotoxins and bacteria
PCR to type the exotoxins

64
Q

Which intestinal lesions are most commonly associated with clostridium perfringens?

A

Haemorrhagic or necrotising enteritis/enterocolitis

Caused by type A, B, C, E, F and G clostridium perfringens

65
Q

Which exotoxins are produced by type A clostridium perfringens?

A

α toxin
NetF toxin

66
Q

What is NetF toxin?

A

NetF toxin is a β, pore-forming toxin resulting in intestinal necrosis as well as causes destruction of leukocytes and haemolysis

67
Q

Which intestinal lesions are caused by type A clostridium perfringens in foals?

A

Necrotising-haemorrhagic enteritis in foals

68
Q

Which intestinal lesions are caused by type A clostridium perfringens in adult horses?

A

Necrotising-haemorrhagic enterocolitis in adult horses

69
Q

Which intestinal lesions are caused by type A clostridium perfringens in dogs?

A

Haemorrhagic gastroenteritis in dogs

Characterised by bloody diarrhoea

70
Q

Which exotoxins are produced by type C clostridium perfringens?

A

α toxin
β toxin

71
Q

Which intestinal lesions result due to type C clostridium perfringens?

A
  • Intestinal serosal congestion and haemorrhage
  • Intestinal mucosal congestion, haemorrhage and necrosis
  • Intestinal mucosal thickening and transmural gelatinous oedema
  • Brown to red foul-smelling fluid intestinal contents
72
Q

Which extra-intestinal lesions result due to type C clostridium perfringens?

A
  • Pulmonary congestion, haemorrhage and thrombosis
  • Cardiac subepicardial and subendocardial haemorrhage
  • Congestion and haemorrhage of visceral organs
  • Oedema, congestion and haemorrhage of mesenteric lymph nodes
  • Kidney tubular degeneration and necrosis (due to the widespread haemorrhage and hypoperfusion)
73
Q

Which exotoxin mainly mediates the intestinal and systemic effects of type C clostridium perfringens?

A

β toxin

74
Q

Which exotoxins are produced by type D clostridium perfringens?

A

α toxin
ε toxin

75
Q

Which disease is caused by type D clostridium perfringens?

A

Clostridium perfringens type D enterotoxaemia

76
Q

What are the extra-intestinal lesions that result from clostridium perfringens type D enterotoxaemia?

A

Focal symmetrical encephalomalacia
Pulpy kidneys

77
Q

What is the pathogenesis of clostridium perfringens type D enterotoxaemia?

A

Type D clostridium perfringens produces ε toxin which can be absorbed systemically and cause pore formation in the vascular endothelial cells resulting in vascular leakage and generalised oedema of the brain and kidneys. In the brain, this can progress to ischaemia, necrosis and focal symmetrical encephalomalacia

78
Q

Which intestinal lesions result due to clostridium difficile?

A
  • Necrotising-haemorrhagic enteritis, colitis or typhlitis (inflammation of the caecum)
  • Intestinal mucosal thickening and transmural gelatinous oedema
  • Turbid, green fluid within the intestine
79
Q

Which differential diseases present very similarly to clostridium difficile?

A

Salmonella typhumirium
Type C clostridium perfringens
Potomac horse fever

Important to consider these as differentials and to do PCR or ELISA to determine diagnosis

80
Q

What are two key predisposing factors to clostridium difficile infection?

A

Antibiotic therapy
Hospitalisation

81
Q

Which disease is caused by clostridium piliforme?

A

Tyzzer disease

82
Q

Which is the tyzzer disease triad?

A

The tyzzer disease triad is a term used to describe the necrotising hepatitis, colitis and myocarditis due to clostridium piliforme infection

83
Q

Which histological staining techniques can be used to visualise clostridium piliforme?

A

Silver staining techniques

The brown areas are the clostridium piliforme
84
Q

Which bacteria causes potomac horse fever?

A

Neorickettsia risticii

85
Q

(T/F) Neorickettsia risticii is an obligate intracellular bacteria

A

TRUE.

86
Q

Where is potomac horse fever endemic?

A

United States (US)
South America

87
Q

When is potomac horse fevel most prevalent?

A

Potomac horse fever is most prevalent during the summer

88
Q

How is neorickettsia risticii transmitted to cause potomac horse fever?

A

Neorickettisia risticii is transmitted through accidental ingestion of trematode larvae containing neorickettsia risticii

89
Q

Which intestinal lesions are caused by neorickettsia risticii?

A

Fibrino-necrotic to ulcerative colitis

90
Q

What are the potential clinical signs of potomac horse fever?

A

Pyrexia
Leukopenia
Depression
Inappetence
Diarrhoea
Abortion in pregnant mares
Colic
Subcutaneous oedema
Laminitis
Shock

91
Q

Which differential diseases present very similarly to potomac horse fever?

A

Salmonellosis
Clostridial infection

Important to consider these as differential diagnoses

92
Q

Which dogs breeds are prone to granulomatous colitis?

A

Boxers
Bulldogs

93
Q

Which age-group is more prone to granulomatous colitis?

A

Young dogs (less than 4 years)

94
Q

Which bacteria is the most likely cause of granulomatous colitis?

A

Escherichia coli (E. coli)

95
Q

Which intestinal lesions present with granulomatous colitis?

A

Thickening and folding of the colon mucosa
Necrotising-haemorrhagic colitis
Shortening and dilatation of the colon
Segmental or focal areas of colon fibrosis and stricture
Patchy, punctate ulceration of the colon

96
Q

What is a key histological sign of granulomatous colitis?

A

Expansion of the laminal propria due to macrophage infiltration

97
Q

What are the clinical signs of granulomatous colitis of boxer dogs?

A

Large intestinal diarrhoea (haemorrhagic and mucoid)
Faecal tenesmus
Dyschezia
Anaemia
Hypoproteinaemia
Weight loss

98
Q

What is idiopathic inflammatory bowel disease (IBD)?

A

Idiopathic inflammatory bowel disease (IBD) is a general term used to describe inflammation of the gastrointestinal tract with the stomach always affected and the small and/or large intestine affected

99
Q

Which factors most likely contribute to the development of idiopathic inflammatory bowel disease (IBD)?

A

Genetics
Imbalance between GI immune system and GI microbiome
Dysbiosis
Diet

100
Q

Which dog breeds are prone to idiopathic inflammatory bower disease (IBD)?

A

German Shepherd
Irish Setter
Basenji

101
Q

Which disease can be misinterpreted as idiopathic inflammatory bowel disease (IBD)?

A

Gastrointestinal lymphoma

It is important to do the correct diagnostics to differentiate between

102
Q

How do you diagnose idiopathic inflammatory bowel disease (IBD)?

A

Diagnosis of exclusion along with endoscopy and endoscopic biopsies followed by histological assessment, immunohistochemistry and PCR for Antigen Receptor Rearrangement (PARR)

103
Q

How can PCR for Antigen Receptor Rearrangement (PARR) be used to differentiate between enteropathy-associated T-cell lymphoma and inflammatory bowel disease?

A

PCR for Antigen Receptor Rearrangement (PARR) is a clonality assay that helps to distinguish neoplastic lymphocytes from inflammatory lymphocytes. Neoplastic lymphocytes exhibit clonal expansion and thus all of their antibodies are the same and detect the same antigens, however, inflammatory lymphocytes are polyclonal and each antibody differs and detects a different antigen

104
Q

What is a defining histological feature of idiopathic inflammatory bowel disease (IBD)?

A

Lymphoplasmocytic inflammatory infiltration of the lamina propria

MODULE 16 - Alimentary Tract Disease (19 decks)

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