infection and immunity Flashcards

1
Q

4 methods of protection against infection

A

physical barrier
chemical barrier
bacteria protection
immunological

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2
Q

physical barrier

A
tight epi wall 
glycolyx
mucous and unstirred layer 
peristalsis - keep things moving 
epi barrier - Paneth cells - secrete defensins and lysozyme
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3
Q

chemical barrier

A

bacteriacidal enzymes from Paneth cells

acid - stomach

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4
Q

bacterial protection

A

commensal bacteria maintain immune system priming
may attack foreign species
occupy niche

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5
Q

immunological

A

MALT - rich in T and B cells
GALT
BALT - bronchus

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6
Q

GALT

A

adaptive and innate
generate AB
peyer’s patches, caecal patches- lymphoid tissue - in SI
lymphocytes - mesenteria and lymph nodules (where the lymph from villi drain) and isolated lymphoid follicles
disorganised sites of lymphocytes in lamina propria and lymphocytes in interstitial space between basolateral membrane of epithelium - intra-epithelial cells eg T cells and NK cells
NOT GALT - kuppfer cells in liver - phagocytose

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7
Q

what is the GI immune system tolerant against

A

food antigens

commensal bacteria

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8
Q

what is essential for the gut immune system

A

the bacterial microbiota

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9
Q

describe the gut microbiota

A

more bacteria than the cells in our body
4 phyla
many more genes - provide us with the ability to digest

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10
Q

gut microbiota through the GI

A

stomach - pH = few bacteria
colon = exponential increase

number increased with ingested and secreted nutrients
decrease with peristalsis, contractions, defecation

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11
Q

symbiotic bacteria

A

take and provide nutrients and regulation

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12
Q

commensal bacteria

A

occupy a niche

prevent adhesion of pathogens

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13
Q

pathogens

A

cause inflammation

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14
Q

describe dysbiosis

A

regulation interrupted and inflammation occurs

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15
Q

causes of dysbiosis

A
infection 
diet 
xenobiotics 
hygiene 
genetics
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16
Q

diseases caused by dysbiosis

A

brain - stress, autism, MS
lung - asthma
liver - NAFLD, NASH
adipoise tissue - obesity, metabolic disease
intestine - IBD, coeliac
systemic disease - T1DM, atherosclerosis, rheumatoid arthritis

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17
Q

MALT

A

submucosa below epithelium
contain lymphoid follicles
follicles surrounded by HEV postcapillary venules = easy passage of lymphocytes
eg oral cavity

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18
Q

peyer’s patches

A

aggregated lymphoid follicles
covered by follicle associated epithelium
this has no goblet cells, secretory IgA or microvilli
have M cells
in SI - most in distal ileum
immune sensors - monitor local bacteria, protect against pathogenic bacteria
development needs exposure to bacterial flora
hit maximum 250 by teenage years
rich in B cells, T cells, macrophages and dendritic cells

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19
Q

M cells

A

the way that antigen uptake occurs in FAE
have IgA receptor
facilitate transfer IgA bacteria complex into Peyer’s patches
antigens presented to lymphocytes = activation

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20
Q

describe trans-epithelial dendritic trees

A

DC
perform antigen sampling
thin extension - bring back into organ
DC form TJ with epi - doesn’t allow entry of pathogens

21
Q

describe the actiation of B cells

A

mature naïve B cells express IgM
when antigen presented to B cell - class switch to IgA
T cell and B cell influence maturation by cytokines
B cell mature to become mature IgA secreting plasma cells
populate the lamina propria

22
Q

describe thymus dependant B cell maturation

A

B cell meets antigen
if correct antigen - T cell gives B CD40L
B cell is activated

23
Q

describe the formation of secretory IgA

A

in submucoisa - dimeric IgA binds to poly-Ig receptor on basolateral membrane
taken into vesical
enzymatic cleavage
makes secretory IgA

24
Q

action of sIgA

A

neutralisation

25
Q

action of secretory component

A

protects against the gut

26
Q

mucus in LI

A

there is a lot

doesn’t let bacteria in

27
Q

describe lymphocyte homing

A

lymphocyte in circulation and secondary lymphoid tissue
if find correct antigen - most likely to go back to organ it found the antigen - thinsk more likely to meet more antigens

28
Q

describe extravasation of lymphocytes

A

rolling fascilitated by weak binding of selectin
strong α4β7 integrin (on lymphocyte)/MAdCAM-1 (on epi) binding causes activation and arrest of lymphocyte - homing back to gut

29
Q

mechanism of cholera infection

A

acute bacterial disease - vibro cholerae serogroups O1 and O139 - cholera toxin
gram -ve
comma shaped
bacteria reach SI
make close contact with epi - releases toxin
cause exit of Na K Cl and water = diarrhoea

30
Q

transmission of cholera

A

faecal oral - contaminated water and food

31
Q

symptoms of cholera

A

severe dehydration and diarrhoea
vomiting
nausea
abdominal pain

32
Q

diagnosis of cholera

A

bacteria culture from stool sample on selective agar

rapid dipstick tests are also available

33
Q

treatment of cholera

A

oral rehydration

vaccine - for travellers - Dukoral, oral, inactivated

34
Q

viral infections causing diarrhoea

A

rotavirus

norovirus

35
Q

bacterial causes of diarrhoea

A
campylobacter jejuni 
E coli
salmonella 
shigella 
C difficiile
36
Q

protozoal parasitic

A

giardia lambia

entamoeba histolytica

37
Q

describe rotavirus

A

RNA
replicates in enterocytes
types A - E
A most common - human infections
most common cause diarrhoea in infants and young children ]
treatment - oral rehydration therapy
vaccination - live attenuated oral vaccine - rotarix against Type A

38
Q

describe norovirus

A
RNA 
diagnosis - PCR 
symptoms - acute gastroenteritis 
recovery - 1-3 days 
transmission - faecal-oral route - up to 2wks 
outbreaks occur in closed communities
39
Q

descrive campylobacter

A

transmission - undercooked meat, untreated water, unpasteurised milk - low infective dose
treatment - not necessary, azithromycin, fluroquinolones - resistance so means problematic

40
Q

describe enterotoxigenic E coli

A

cholera like toxin

watery diarrhoea

41
Q

describe entrovasive E coli

A

shigella like illness

bloody diarrhoea

42
Q

describe enterohaemorrhagic or shiga toxin producing E coli

A

loss of kidney function

43
Q

describe C difficile

A

normally in epi - do no harm
on AB microbiota killed
C difficile = pathogenic
destroy lining = leakage of neutroohil and RBC = bloody diarrhoea
treatment - stop current AB
treat with metronidazole, vancomycin
high recurrence - increasingly difficult to treat
can treat with faecal microbiota transplantation

44
Q

describe coeliac disease

A

gliadin not broken down in stomach - reach SI - bidn to sIgA - transferred to lamina propria
innate immune detection -T cell developmet - T and B co-stim - cytokines, chemokines and their receptors
symptoms - abdominal distension, diarrhoea
diagnosis - Ab blood tests- anti-gliadin, biopsy of duodenum
treatment - gluten free diet

45
Q

describe IBS

A

visceral hypersensitivity - triggered by diet and stress
symptoms - recurrent ab pain, abdominal bowel motility, constipation/diarrhoea
treatment - diet modiufication (avoid apples, beans cauliflowers, constipation - soluble fibre, stool softeneers, osmotic laxitives, spasms and pain - anti-diarrheals, anti-muscarinic
management of stress, anxiety and depression

46
Q

describe crohn’s disease

A

distal ileum and colon
patches of inflammatory damage - cobblestone appearance
symptoms - diarrhoea, ab cramp, fever, anaemia, weight loss and fatigue
diagnosis - Ab blood tests, endoscopy and barium x-ray
treatment - anti-inf drugs, immunosuppressants, surgery - not curative

47
Q

describe ulcerative colitis

A

colon only
continuous inflammation
bloody diarrhoea, ab cramp, anaemia, weight loss, fatigue
diagnosis - Ab blood tests, endoscopy and barium x-ray
treatment - treatment - anti-inf drugs, immunosuppressants, colorectomy - curative

48
Q

mechanism of IBD (irritable bowel disease) ie Crohn’s and ulcerative colitis

A
2/3 genes identical 
lining destroyed 
bacteria entry 
stimulate immune celk 
regulation falls 
constant action
chronic infection
colon cancer