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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 emulsification of lipids, causing malabsorption of 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

Enterotoxigenic 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 enterotoxigenic E.coli (ETEC)?

A

Enterotoxigenic E.coli (ETEC) adheres to the microvilli on the intestinal epithelium, mediated by the K99 antigen which allows the bacteria to bind, 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 enterotoxigenic 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 enterocyte, 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 fimbriae. Salmonellae preferentially adhere to and invade M-cells however invasion via 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 with 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
What are the virulence factors of salmonella?
Fimbrae Lipopolysaccharides (LPS)
26
What are the three clinical presentations of salmonella?
Acute enteric salmonellosis Peracute septicaemic salmonellosis Chronic enteric salmonellosis
27
Which form of salmonella most commonly causes acute enteric salmonellosis?
Salmonella Typhimurium
28
Which intestinal lesions result due to acute enteric salmonellosis?
Fibrinonecrotic enterocolitis due to localised intestinal wall thrombosis and inflammation
29
Which extra-intestinal lesions result due to acute enteric salmonellosis?
Reactive lymphadenopathy of the mesenteric lymph nodes Foci of hepatocellular necrosis Fibrinous cholecystitis *(distinctive sign in calves)*
30
Which extra-intestinal lesion is a distinctive sign of acute enteric salmonellosis in calves?
Fibrinous cholecystitis - patient will present with jaundice
31
Which signalement is prone to peracute septicaemic salmonellosis?
Young calves, foals and piglets however it can also be seem in adults
32
What is the prognosis for peracute septicaemic salmonellosis?
Usually fatal to animals less than 6 months old
33
What is the pathogenesis for peracute septicaemic salmonellosis?
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
34
Which form of salmonella most commonly causes chronic enteric salmonellosis?
Salmonella Typhimurium
35
Which intestinal lesions result due to chronic enteric salmonellosis?
Multifocal necrosis and ulceration of the intestinal wall known as 'button ulcers'
36
Which species are most prone to 'button ulcers'?
Pigs
37
(T/F) Lawsonia intracellularis is an faculative intracellular bacteria
FALSE. Lawsonia intracellularis is an obligate intracellular bacteria
38
What is the pathogenesis of lawsonia intracellularis?
Lawsonia intracellularis virulence factors cause inhibition of enterocyte differetiation and induce enterocyte proliferation and mucosal thickening
39
What are the three clinical presentations of lawsonia intracellularis in pigs?
Porcine intestinal adenomatosis (PIA) Proliferative and necrotic enteritis Proliferative haemorrhagic enteropathy (PHE)
40
What is the main clinical presentation of lawsonia intracellularis in horses?
Equine proliferative enteropathy
41
Which signalement are most prone to equine proliferative enteropathy?
Weaning foals (2 - 8 months old)
42
How do you diagnose lawsonia intracellularis?
Serum ELISA which detects L.intracellularis specific IgG Faecal PCR which detects L.intracellularis DNA Distinctive post mortem findings Immunohistochemistry
43
Why is a faecal PCR preferential to a serum ELISA to diagnose lawsonia intracellularis?
A faecal PCR indicates there is an active infection however a serum ELISA only indicates exposure to the bacteria
44
(T/F) Rhodococcus equi is an intracellular bacteria
TRUE.
45
(T/F) Rhodococcus equi is a commensal bacteria in the horse intestinal tract
TRUE.
46
Where is rhodococcus equi found within the environment?
Soil
47
Which two disease processes are caused by rhodococcus equi in foals?
Suppurative bronchopneumonia Ulcerative enterocolitis
48
What is the pathogenesis of rhodococcus equi in foals?
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
49
Which intestinal lesions result due to rhodococcus equi infection?
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 Mesenteric lymph nodes can become enlarged due to pyrogranulomatous inflammation and abscesses
50
(T/F) Clostridia are commensal bacteria of the gastrointestinal tract
TRUE.
51
Which factors can result in expansion of clostridia within the intestinal tract?
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
52
What are the three mechanisms of clostridial disease?
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
53
What are the most common forms of clostridia that cause disease in domestic animals?
Clostridium perfringens Clostridium difficile Clostridium piliforme
54
(T/F) All clostridia are Gram+ bacteria
FALSE. The majority of clostridia are Gram+ bacteria however clostridium piliforme is Gram - | They are mostly gram+ anaerobes
55
How is clostridium perfringens categorised?
Clostridium perfringens is categorised based on the exotoxins that they produce | i.e. there is type A, B, C, D, E, F and G
56
What are the four main forms of exotoxin produced by clostridium perfringens?
α toxin β toxin ε toxin *(epsilon)* ι toxin *(lota)*
57
Which toxin do all serotypes of clostridium perfingens produce?
α toxin
58
What are the affects of α toxin produced by clostridium perfringens?
α toxin is a lecinthase *(a form of phospholipase)* which acts on cell membranes resulting in haemolysis and/or necrosis of cells
59
What are the affects of β toxin produced by clostridium perfringens?
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
60
What are the affects of ε toxin produced by clostridium perfringens?
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, haemorrhage and perivascular oedema
61
What are the affects of ι toxin produced by clostridium perfringens?
ι toxin is a protoxin which is activated by proteolytic digestion within the intestine and increases local capillary permeability
62
What can be used to diagnose clostridium perfringens serotype?
ELISA to type the exotoxins and bacteria PCR to type the exotoxins
63
Which intestinal lesions are most commonly associated with clostridium perfringens?
Haemorrhagic or necrotising Gastroenteritis/enteritis/enterocolitis | Caused by type A, B, C, E, F and G clostridium perfringens
64
Which exotoxins are produced by type A clostridium perfringens?
α toxin NetF toxin
65
What is NetF toxin?
NetF toxin is a β, pore-forming toxin resulting in intestinal necrosis as well as causes destruction of leukocytes and haemolysis
66
Which intestinal lesions are caused by type A clostridium perfringens in foals?
Necrotising-haemorrhagic enteritis in foals
67
Which intestinal lesions are caused by type A clostridium perfringens in adult horses?
Necrotising-haemorrhagic enterocolitis in adult horses
68
Which intestinal lesions are caused by type A clostridium perfringens in piglets?
Necrotising enterocolitis in piglets
69
Which intestinal lesions are caused by type A clostridium perfringens in lambs and calves ?
Haemorrhagic enteritis in lambs and calves
70
Which intestinal lesions are caused by type A clostridium perfringens in dogs?
Haemorrhagic **gastro**enteritis in dogs | Characterised by bloody diarrhoea
71
Which exotoxins are produced by type C clostridium perfringens?
α toxin β toxin
72
Which intestinal lesions result due to type C clostridium perfringens?
Serosal congestion and haemorrhage Mucosal congestion, haemorrhage, necrosis and thickening Transmural gelatinous oedema Brown to red foul-smelling fluid intestinal contents
73
Which extra-intestinal lesions result due to type C clostridium perfringens?
- 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)*
74
Which exotoxin mainly mediates the intestinal and systemic effects of type C clostridium perfringens?
β toxin
75
Which exotoxins are produced by type D clostridium perfringens?
α toxin ε toxin
76
What are the extra-intestinal lesions that result from clostridium perfringens type D?
Focal symmetrical encephalomalacia Pulpy kidneys
77
What is the pathogenesis of clostridium perfringens type D enterotoxaemia?
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
Which intestinal lesions result due to clostridium difficile?
Necrotising-haemorrhagic enteritis, colitis or typhlitis Mucosal thickening Transmural gelatinous oedema Turbid, green fluid within the intestine
79
Which differential diseases present very similarly to clostridium difficile?
Salmonella typhimirium Type C clostridium perfringens Potomac horse fever | Important to consider these as differentials and to do PCR or ELISA to determine diagnosis
80
What are two key predisposing factors to clostridium difficile infection?
Antibiotic therapy Hospitalisation
81
Which disease is caused by clostridium piliforme?
Tyzzer disease
82
Which is the tyzzer disease triad?
The tyzzer disease triad is a term used to describe the necrotising hepatitis, enteritis and myocarditis due to clostridium piliforme infection
83
Which histological staining techniques can be used to visualise clostridium piliforme?
Silver staining techniques (Warthin-Starry stain)
84
Which bacteria causes potomac horse fever?
Neorickettsia risticii
85
(T/F) Neorickettsia risticii is an obligate intracellular bacteria
TRUE.
86
Where is potomac horse fever endemic?
United States (US) South America
87
When is potomac horse fever most prevalent?
Potomac horse fever is most prevalent during the summer
88
How is neorickettsia risticii transmitted to cause potomac horse fever?
Neorickettisia risticii is transmitted through accidental ingestion of trematode larvae containing neorickettsia risticii
89
Which intestinal lesions are caused by neorickettsia risticii?
Fibrino-necrotic to ulcerative colitis
90
What are the potential clinical signs of potomac horse fever?
Pyrexia Leukopenia Depression Inappetence Diarrhoea Abortion in pregnant mares Colic Subcutaneous oedema Laminitis Shock
91
Which differential diseases present very similarly to potomac horse fever?
Salmonellosis Clostridial infection | Important to consider these as differential diagnoses
92
Which dogs breeds are prone to granulomatous colitis?
Boxers French bulldogs
93
Which age-group is more prone to granulomatous colitis?
Young dogs (less than 4 years)
94
Which bacteria is the most likely cause of granulomatous colitis?
Escherichia coli (E. coli)
95
Which intestinal lesions present with granulomatous colitis?
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
What is a key histological sign of granulomatous colitis?
Expansion of the laminal propria due to macrophage infiltration *(remember granulomatous = macrophages)*
97
What are the clinical signs of granulomatous colitis of boxer dogs?
Large intestinal diarrhoea *(haemorrhagic and mucoid)* Faecal tenesmus Dyschezia Anaemia Hypoproteinaemia Weight loss
98
What is idiopathic inflammatory bowel disease (IBD)?
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
What is a key histological feature of inflammatory bowel disease (IBD)?
Inflammatory infiltration of the lamina propria *(mostly lymphocytes and plasma cells)*
100
Which factors most likely contribute to the development of idiopathic inflammatory bowel disease (IBD)?
Genetics Imbalance between GI immune system and GI microbiome Dysbiosis Diet
101
Which dog breeds are prone to idiopathic inflammatory bowel disease (IBD)?
German Shepherd Irish Setter Basenji
102
Which disease can be misinterpreted as idiopathic inflammatory bowel disease (IBD)?
Gastrointestinal lymphoma | It is important to do the correct diagnostics to differentiate between
103
How do you diagnose idiopathic inflammatory bowel disease (IBD)?
Diagnosis of exclusion along with endoscopy and endoscopic biopsies followed by histological assessment, immunohistochemistry and PCR for Antigen Receptor Rearrangement (PARR)
104
How can PCR for Antigen Receptor Rearrangement (PARR) be used to differentiate between enteropathy-associated T-cell lymphoma and inflammatory bowel disease?
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

MODULE 16 - Alimentary Tract Disease (23 decks)

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