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Alimentary > Infection & Immunology > Flashcards

Infection & Immunology Flashcards

1
Q

SA of GI tract

A

400m2

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2
Q

4 major phyla of bacteria

A

Bacteroidetes
Firmicutes
Actinobacteria
Proteobacteria

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3
Q

What leads to increased cell numbers/ decreased cell number?

slide 7, lecture 8

A

-

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4
Q

Relationship between chemical digestive factors produced by host and bacterial content throughout GI

A

Most amount of microbiota are where there are no digestive factors of the host

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5
Q

Dysbiosis

A

Altered microbiota composition

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6
Q

Immunological equilibrium
Immunological dysequilibrium
(slide 8, lecture 8)

A

Immunological equilibrium - equilibrium between symbionts (regulation), commensals, pathobionts (inflammation)

Immunological dysequilibrium= arrival of pathogens = imbalance towards pathogens compared to symbionts

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7
Q

Cause of immunological dyequilibrium

A 
Infection
Diet
Xenobiotics
Hygiene
Genetics
These turn healthy microbiota into dysbiosis
Production of bacterial metabolites and toxins affect:
Brain
Lung
Liver
Adipose Tissue
Intestine
Systemic disease
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8
Q

Mucosal defense

A

Physical barriers:
Anatomical (peristalsis, epithelial barrier: mucus layer= goblet cells, epithelial monoloayer= tight junctions prevent entry of pathogens, Paneth cells (small intestine)= bases of crypts of Lieberkuhn+ secrete antimicrobial peptides (defensins) and lysozyme)
Chemical (enzymes, acidic pH)

Commensal bacteria: occupy ecological niche

Immunological: following invasion when bacteria has cross epithelial lining
MALT (mucosa associated lymphoid tissue)
GALT (gut associated lymphoid tissue)

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9
Q

MALT

A

Found in the submucosa below the epithelium, as lymphoid mass containing lymphoid follicles (collection of lymphocytes)
Follicles are surrounded by HEV postcapillary venules, allowing easy passage of lymphocytes
The oral cavity is rich in immunological tissue.
Diagram at slide 11, lecture 8

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10
Q

GALT
Responsible for?
Contains?
Types? Each one contains?

A

Responsible for both adaptive & innate immune responses through generation of lymphoid cells & Abs.
Contains innate and capability to produce ABs

Types:
Not organised
Intra-epithelial lymphocytes – Make up one-fifth of intestinal epithelium, e.g., T cells, NK cells
Lamina propria lymphocytes

Organised
Peyer’s patches (small intestine)- collection of lymphoid follicles
Caecal patches (large intestine)
Isolated lymphoid follicles
Mesenteric lymph nodes (encapsulated)
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11
Q 
Peyer's Patches
Found in?
Description?
Development requires?
Important cells?
A

Found in small intestine – mainly distal ileum.
Aggregatedlymphoid follicles covered with follicle associated epithelium (FAE).
FAE - no goblet cells, no secretory IgA, lack microvilli.
Organised collection of naïve T cells and B-cells.
Development requires exposure to bacterial microbiota (50 in last trimester foetus, 250 by teens).
Antigen uptake via M (microfold) cells within FAE. M cells can sample Ag in gut lumen and uptake them from lumen, presented to lymphocytes, cause activation
M cells expressIgA receptors, facilitating transfer of IgA-bacteria complexinto the peyer’s patches. B cells produce IgA, complexes with bacteria, neutralised. Usually its fine but if it causes a build up, M cells uptake it and can cause phagocytosis

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12
Q

Antigen sampling

A

Trans-epithelial dendritic cells
Dendritic cells through thin extensions can sample and bring to lymphoid tissue
Forms such a tight junction with epithelial that it doesn’t allow any pathogens through barrier

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13
Q

B cell adaptive response

A

1) Thymus dependent B cell maturation: foreign antigen with matching specificity binds+ presented to Th cell. Th cell secretes CD40L + some cytokines which activates B cell
2) Mature naïve B-cells express IgM in PPs.
3) Upon antigen presentation class switch to IgA.
4) T-cells & epithelial cells influence B cell maturation via cytokine production.
5) B cells further mature to become IgA secreting plasma cells.
6) Populate lamina propria+ start mass production of IgA- exists in dimer form in gut

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14
Q

Formation of secretory IgA

A

1) Plasma cells produce dimeric IgA
2) Dimeric IgA binds to Poly-Ig receptor on basolateral membrane of epithelial cell
3) endocytosed through epithelial cells towards luminal side
4) Enzymatic cleavage in vesicle frees up Poly-Ig receptor
5) secretory IgA has secretory component attached to it with form of protection from harsh environment of gut

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15
Q

How much gut B-cells secrete what type of Ab?

A

Up to 90% of gut B-cells secrete IgA.

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16
Q

Action of IgA

A

sIgA binds luminal antigen, thereby preventing its adhesion and consequent invasion.

17
Q

Immune adaptation of large intestine

A

Outer mucus layer- very thick so doesn’t let bacteria

18
Q

Most commonly found organised GALT in large intestine

A

Caecal patch (NOT peyer’s patch)

19
Q

Lymphocyte homing and circulation
(slide 20, lecture 8)
What facilitates gut homing?

A

Naïve lymphocytes travel from primary to secondary lymphoid organs
If antigen is met, becomes activated, go back to circulation through thoracic duct and can go other lymphoid organs or to lamina propria (which is what is prefers because that’s where it was activated so its likely that the pathogen will be there)
If the antigen wasn’t met it will probably recirculate around the body

α4β7 integrin (on lymphocyte)/MAdCAM-1 (presented by epithelial cells) adhesion, facilitates rolling, activation, arrest in HEV venule

20
Q

Cholera Mechanism
Caused by?
Mechanism?

A

1) Cholera is an acute bacterial disease caused by Vibrio cholerae serogroups O1 and O139 (cholera toxin).
2) The bacteria reaches the small intestine where on making close contactwith the epithelium releasescholera toxin.
3) Cholera toxin on entering the epithelial cell, starts a series of biochemical reactions resulting in exit of ions such as Na+, K+, Cl- and water from the epithelial cell.

21
Q

Cholera Transmission & Symptoms

A

1) Transmitted through faecal-oral route, and spreads through contaminated water & food.
2) Main symptoms – Severe dehydration and diarrhoea (watery).
3) Other symptoms - vomiting, nausea & abdominal pain.

22
Q

Cholera Diagnosis & Treatment

A

1) Diagnosis: bacterial culture from stool sample on selective agar is the gold standard, rapid dipstick tests also available.
2) Treatment: oral-rehydration is the main management; up to 80% of cases can be successfully treated.
3) Vaccine: Dukoral, oral, inactivated.
4) Globally 1.3 - 4 million cases, avg. 95,000deaths/year (last indigenous UK case 1893: 2017 - 13 cases).

23
Q

Other causes of infectious diarrhoea

A

Viral
Rotavirus (children)
Norovirus “winter vomiting bug”

Protozoal parasitic
Giardia lamblia
Entamoeba histolytica

Bacterial
Campylobacter jejuni
Escherichia coli
Salmonella
Shigella
Clostridium difficile
24
Q 
Rotavirus
Description
Epidemiology
Treatment
Vaccination
A

Description: RNA virus, replicates in enterocytes. 5 types A – E, type A most common in human infections.

Epidemiology: Most common cause of diarrhoea in infants and young children worldwide.

Treatment: oral rehydration therapy, but still cause about 200,000 deaths per year.

Before vaccine, most individuals had an infection by age 5, repeated infections develop immunity.

Vaccination: Live attenuated oral vaccine (Rotarix) against type A introduced in UK July 2013.

25
Q 
Norovirus (genus) Norwalk virus (species)
Description
Diagnosis
Epidemiology
Symptoms
Transmission
A

Description: RNA virus. Incubation period 24-48 hours.

Diagnosis: Sample PCR.

Epidemiology: Estimated 685 million cases per year because easily transferrable

Symptoms: Acute gastroenteritis, recovery 1 – 3 days.

Transmission: Faecal-oral transmission. Individuals may shed infectious virus for up to 2 weeks.

Outbreaks often occur in closed communities.

26
Q 
Campylobacter “curved bacteria”
Most common species
Transmission
Epidemiology
Treatment
A

Most common species: Campylobacter jejuni, Campylobacter coli

Transmission: Undercooked meat (especially poultry), untreated water and unpasteurised milk. Low infective dose, a few bacteria
(<500) can cause illness.

Epidemiology: Estimated 280,000 cases per year in UK, 65,000 confirmed. Most common cause of food poisoning in the UK.

Treatment: Not usually required, azithromycin (macrolide) is standard antibiotic, resistance to fluoroquinolones is problematic.

27
Q

Escherichia coli (E. coli)

A

Diverse group of Gram negative intestinal bacteria, most harmless but 6 ”pathotypes” associated with diarrhea (diarrhoeagenic)

28
Q

Clostridium difficile

Management

A

Isolate patient (very contagious)
Stop current antibiotics
Metronidazole, Vancomycin
Recurrence rate 15-35% after initial infection, increasingly difficult to treat.
Faecal Microbiota Transplantation (FMT) – 98% cure rate- releases stool of healthy donor to transplant healthy microbiota

29
Q 
Coeliac disease
Mechanism
Symptoms
Diagnosis
Treatment
A

Mechanism: Gliadin (33aa peptide component of gluten) is not broken down in the stomach, reaches small intestine, binds to sIgA and is transferred to the lamina propria.

Symptoms: Abdominal distension (bloating), Diarrhoea

Diagnosis: Ab blood tests -anti-gliadin, Biopsy test of duodenum

Treatment: Diet management – gluten-free diet (wheat, barley, rye exclusion).

30
Q

Irritable bowel syndrome (IBS)
MECHANISM/ Triggers
SYMPTOMS
TREATMENT

A

Mechanism/ Triggers: Visceral hypersensitivity, Triggered by diet / stress

Symptoms: Recurrent abdominal pain, Abnormal bowel motility, Constipation and/or Diarrhoea

Treatment: Diet modification - Avoiding certain foods such as apples, beans, cauliflowers, Treatment of constipation - soluble fiber, stool softeners and osmotic laxatives, Treatment of spasms and pain - anti-diarrheals, anti-muscarinic, Management of stress, anxiety, depression.

31
Q

Inflammatory bowel disease (IBD)

Mechanism

A
  1. Triggers before onset of disease (Genetic/ Environmental)
  2. Leads to dysbiosis= destruction of epithelial lining= pathogens enter lamina propria
  3. Pathogens induce immune cell activation+ regulation of it fails= constant activation of T cells etc
  4. Leads to chronic inflammation which is very harmful
32
Q

2 forms of Inflammatory bowel disease

A

Crohn’s Disease

Ulcerative colitis

Alimentary (12 decks)

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