Pathology of bacterial infections in the GI system Flashcards

1
Q

Cell type in intestine responsible for Absorption

A

Enterocyte

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2
Q

Cell type in intestine responsible for Antimicrobial proteins

A

Paneth cell

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3
Q

Cell type in intestine responsible for Mucus production

A

Goblet cell

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4
Q

Cell type in intestine responsible for microorganisms, particles and macromolecules uptake and transfer

A

M cell

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5
Q

Cell type in intestine responsible for regulation of
intestinal motility, secretion, appetite etc

A

Neuroendocrine cell

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6
Q

3 Mechanisms of Diarrhoea

A
  1. Secretory
  2. Osmotic
  3. Inflammatory
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7
Q

Mechanisms of secretory diarrhoea induced by bacterial toxins

A

Secretory diarrhea from bacterial toxins involves adenylate cyclase activation, raising cAMP levels, stimulating ion secretion, and inhibiting absorption, resulting in watery diarrhea and electrolyte imbalance.

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8
Q

Mechanisms of malabsorption diarrhoea due to bacterial overgrowth

A

Excessive growth of bacteria in the small intestine, disrupting normal nutrient absorption. Mechanisms include bacterial fermentation of carbohydrates, bile acid deconjugation, mucosal damage, and competition for nutrients, leading to impaired absorption of nutrients and water, resulting in diarrhea with characteristic features such as steatorrhea (excess fat in stool) and nutrient deficiencies.

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9
Q

3 Consequences of diarrhoea

A

Dehydration
Electrolyte depletion and imbalance
Metabolic acidosis

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10
Q

What do endotoxins do

A

Stimulate macrophages and endothelial cells to secrete proinflammatory cytokines and nitric oxide.
Cause cell dysfunction and lysis.

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11
Q

What do exotoxins do

A

Inhibit biochemical pathways within a cell.

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12
Q

E.coli mechanism of action

A

Adhere to microvilli on intestinal epithelium
Cl- secretion from enterocytes causing Secretory diarrhoea

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13
Q

Salmonella mechanism of action

A

bacteria survive within macrophage phagolysosomes
Toxins interfere with closure of Chloride channels  secretory diarrhoea

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14
Q

Salmonellosis – pathogenesis of infection

A

M cells in intestinal epithelium> macrophages in lamina propria
and Peyer’s patches >transferred to mesenteric lymph nodes >via portal circulation to liver

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15
Q

Peracute Septicemic Salmonellosis

A

Multisystemic vascular lesions with fibrinoid change, thrombosis and necrosis
Disease of calves, foals and pigs – younger animals most sensitive
Usually fatal in animals 1-6 months of age

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16
Q

Signs of Peracute Septicemic Salmonellosis

A

petechiation and blue discolouration (cyanosis)
of ventral abdomen, extremities (ears commonly affected)

17
Q

Peracute Septicemic Salmonellosis cause of death

A

Disseminated intravascular coagulation (DIC)

18
Q

Acute Enteric Salmonellosis mostly affects….

A

Horses

19
Q

Pathogenic effects of Acute Enteric Salmonellosis

A

Interference with Chloride channels = Secretory diarrhoea
induction of enterocyte apoptosis + recruitment of neutrophils
endotoxins = vascular thrombosis

20
Q

Button ulcers are commonly caused by

A

Chronic Enteric Salmonellosis

21
Q

Lawsonia intracellularis mostly infects

A

Swine

22
Q

Swine clinicopathological presentations

A

Porcine Proliferative Enteropathy (PPE)
- Porcine Intestinal Adenomatosis (PIA)
- Necrotic enteritis
- Proliferative Haemorrhagic Enteropathy (PHE)

23
Q

Diagnosis of Lawsonia intracellularis

A

ELISA (serum) L. intracellularis specific IgG
(indicating exposure to infection rather than active disease)

PCR on faeces L. intracellularis DNA
(indicating active infection with faecal shedding)

Distinctive gross PM findings

Immunohistochemistry

24
Q

Bacteria that causes suppurative bronchopneumonia in foals and ulcerative colitis

A

Rhodococcus equi

25
Q

Mechanisms of Clostridial disease

A
  1. Local effects of toxins on the mucosa- haemorrhagic, fibrinous or necrotic enteritis
  2. Secretory effects of locally acting enterotoxin- diarrhoea and minor mucosal lesions
  3. Systemic absorption of (entero)toxins- affects sites distant from the gut
26
Q

Causes of massive expansion of enteric populations of clostridia

A

Changes in the enteric microenvironment
- change in feed, abnormally nutrient-rich digesta – CHO dumping
- antibiotic therapy
- altered pancreatic exocrine function or trypsin inhibitors
- reduced intestinal motility
- primary infections (CPV-2 in dogs or Coccidiosis in piglets & chickens)

27
Q

Focal symmetrical encephalomalacia (FSE) Pulpy kidney disease is caused by…?

A

Cl. perfringens type D enterotoxaemia

28
Q

Haemorrhagic canine gastroenteritis is caused by….?

A

Clostridium perfringens type A

29
Q

Necrotising-haemorrhagic enteritis in foals / enterocolitis in adult horses is caused by…?

A

Clostridium perfringens type A

30
Q

Potomac Horse Fever (Equine Monocytic Ehrlichiosis) is caused by ..?

A

Neorickettsia risticii

31
Q

Idiopathic Inflammatory Bowel Disease (IBD) pathophysiology

A

Villus blunting (and possible alteration of superficial epithelium)
Variable crypt dilation (filled with mucus and cellular debris)
Possible crypt epithelial hyperplasia
Inflammatory cell infiltration in lamina propria (and variably intraepithelial)

32
Q

Breeds predisposed to IBD

A

Basenji
German Shepherds
Boxer (see GCB)
Irish Setter- enteritis associated with familial hypersensitivity to wheat protein

33
Q

Diagnosis of Inflammatory Bowel Disease (IBD)

A

Endoscopic biopsies
Diagnostic pathology approach & work up
Histological assessment (revised WSAVA standards / other algorithms)
Differential diagnosis with intestinal lymphoma small cell (EATCL-2)
Immunohistochemistry