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mcrb 265 > host-microbe interactions > Flashcards

host-microbe interactions Flashcards

1
Q

types of interactions

A

mutualism, commensalism, competition, parasitism, pathogenesis

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2
Q

commensal vs synergism vs mutualism

A

commensal = 0/+
syn: +/+ - protocooperation

mutualism (symbiosis) +/+

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3
Q

competition
amensalism
predation
parasitism

A

c: -/-
a 0+/-
p +/-
p +/-

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4
Q

rumen microbiology - mutualism in cows.

A

rumen is 1 part of cow stomach.

ton of bacteria in there - fermentation. lots of methane release

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5
Q

what is endosymbiosis

A

1 guy lives in the other. both act as 1 - benefit

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6
Q

human-microbe interactions

-application of ecological principles

A

many interactions btw human + normal microbial flora.

- human body is diverse enviro for microbes. usually benign

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7
Q

Normal human flora

A

microorganisms living on body surfaces of healthy individuals

  • 10^3 bacteria + archaea in average adult
  • most in gut, some on skin, mouth, resp tract, urogenital tract.
  • normal are opportunistic pathogens
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8
Q

bacteria associated with mucous membranes

A
  • frequent sites of infection bc favourable for bacterial growth.
    bacteria can grow - close access to epithelial resources. invade = infect
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9
Q

mouth microbes - adhere to?

A

adhere to gums + teeth

  • > not removed by brushing. acidify = plaque, cavities, gingivitis, periodontal disease
  • mouth covered in microorganisms from surrounding enviro within hours following birth
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10
Q

how bacteria bind to tooth?

A

attach to glycoprotein deposited by saliva.
- oral microbes continue to grow = thick bacterial layer AKA dental plaque. hard, strong biofilm. if thick enough = anaerobic - fermentation = degrade teeth

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11
Q

GI tract microbes

A

stomach: high acidity kills most microbes.
- some survive if pass thru quick, or in food particles.
- H.pylori is exception.
- small intestine: few organisms
- large intestine: larges microbial popln in body (10^13 -10^14)

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12
Q

large intestine - elimination, replaced, metabolism?

A

eliminated by peristalsis, desquamation + movement of mucus

  • replaced rapidly due to quick doubling times (similar to continuos culture
  • most are anaerobes
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13
Q

name few large intestine bacteria

A

streptococcus, enterococcus, escherichia, lactobacillus,

methanobrevibacter

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14
Q

what things do large intesince bacteria do?

A 
vitamin synthesis
gas production
odour production
organic acid production
glycosidase reactions
steroid metabolism
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15
Q

H.pylori

- characteristics + functions

A

flagella - motile, chemotaxic

urease- neutralize gastric acid

lipopolysaccharides - adhere to host cell

-type 4 secretion system: like pillus= changes in host , virulence factor kills host cell.

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16
Q

H.pylori - how to get ulcers? then + now

A

past: stress caused. take antacid to healh
now: H.pylori infection = ulcer. inflammation, could be painful, perofation, bleeding etc.

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17
Q

bacteroides thetaiontaomicron

A

colonizes exfoliated host cells, food particles + sloughed mucus.

  • attach or eliminated
  • adhere to particles in gut, not gut itself.
  • degrades complex carbs along with methanogens
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18
Q

microbe diversity in body

A

areas we though were sterile are not.

ex: brain, stomach, skin, repro system..
- aura of bacteria match microbial fingerprint.

bacteria make habitat in warm, dark , wet enviros

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19
Q

biodiversity + functional genomics in human microbiome - stage of life

A

young - low microbiome diversity
mddle age = greatest diversity in gut.
old - lower diversity = more infection

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20
Q

human microbiome project

A

generally found microbiome is stable over time.

  • more diverse microbiome = healthier you are.
  • diff area of body - diff microbiomes, but same area of body across popln is v simiar microbiome
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21
Q

babies birth - c-section vs vaginal

A

diff microbiome. bc diff inoculation of bacteria.

same w formula vs bottle fed

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22
Q

dysbiosis

A

imbalance in microbiome

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23
Q

theory of dysbiosis linked w disease

A

distinct pattern due to habitat, live w animals? diet, health.
- microbes evolve with us.

need to know what homeostasis is for individual to know what dysbiosis looks like

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24
Q

rebiosis

A

return of microbial community ecology to “normal”

- infant anitbiotic in 1st year = may affect health long term

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25
dysbiosis linked to disease
bowel disorders, crohns, obesity, celiac, allergies, autism, depression, parkinsons
26
pathogenicity
ability of organism to produce pathological change or disease that impars host function - disease-producing, parasite, opportunistic
27
define virulence
quantitative measure of pathogenicity
28
define infection
any situation in which organism is established + growing. | - doesnt have to be pathogenic
29
attenuation
decrease or loss of virulence
30
toxicity
ability of organism to cause disease through making toxin that inhibit host cell function/kills host cells = toxins can travel
31
invasinveness
ability of pathogen to grow in host tissue at densities that inhibit host function - damage without toxin
32
steps to pathogenic life cycle
1. exposure 2. adherence to skin/mucosa 3. invasion through epithelium 4. colonizaiton + growth => back to 1 or 5. toxicity, invasiveness 6. tissue damage, disease
33
adherence of pathogen
needed to gain access to host tissue - attach to epithelial cell. -direct attachement: to surface cell/host indirect attachment: capsule attaches to host
34
four factors involved in adherence to host cells
- capsule/slime layer - adherence proteins - lipoteichoic acid - fimbriae (pili)
35
invasion
starts at site of adherence. - spread through circulatory, lymphatic systems = availability of nutrients important in affecting pathogen growth. - pathogens grow locally at invasion or spread throughout body
36
measure virulence
LD50 - lethal dose that kills 50% of animals in test group | - lower number? more virulent
37
high virulence + # of cells for LD100
small range. hgihly virulent, kill in small quantities
38
enzyme virulence factors
- enhance virulence by breaking down/altering host tissue to provide accessto nutrient = hyaluronidase breaks down hyaluronic acid that glues animal cells together -protect pathogen by interfering w normal host defense mechanisms = coagulase breaks down collagen netwrok
39
virulence factors in bacteriophage
erythrogenic toxin, shiga-like toxin, enterotoxins, neurotoxins ,diphtheria toxin
40
plasmin virulence factors
enterotoxins, hemolysin, urease, edema factor, coagulase, fibrinolysin
41
transposon virulence factors
enterotoxin shiga toxin cholera toxin
42
salmonella virulence factors
o antigen = inhibits phagocyte killing in LPS layer of g(-) CW endotoxin in LPS layer = fever enterotoxin = diarrhea (symptom) - effect small intestine siderophores = pick up Fe to aid growth type 1 fimbriae = adherence
43
exotoxins + 3 categories
proteins released from pathogenic organism as it grows 1. cytolytic toxin 2. AB toxin 3. superantigen toxin
44
cytolitic toxins work
by degrading cytoplasmic membrane integrity - host cell lysis + death - hemolysins too.
45
cytolytic toxin ex:
staphylococcal a-toxin | form mutlimer in PM = pore.
46
what is AB toxin do?
A + B units. B binds to host cell receptor A transfers damaging agent to host
47
ex of AB toxin
diphtheria toxin | - catalyze ADP-ribosylation of elongation factor 2 + prevent aa transfer to grwoing peptide chain in ribosome
48
ex of botulinum toxin
blocks release of aCh to muscle tissue = permanent relaxed state
49
superantigen toxins
stimulate large numbers of immune cells | - result in extensive inflammation + tissue damage = cells gorw elsewhere cause not viable there
50
endotoxins
lipopolysaccharide portion of CW of certain g(-) bacteria. toxin when solubilized. - less toxic than exotoxins. - only when cells are present
51
innate resistance to infection
nonspecfic barriers prevent colonizationof host by most pathogens - lack of defenses = more susceptible to infection + colonization
52
risk factors for infection
compromised host: 1+ resistance mechanisms inactive = infection increases (AIDs, pregnant) age: young + old more susceptible stress: decrease immune function due to cortisol diet + lifestyle affect microbiome genetic condition
53
specific (adaptive) immunity
complex, mutli-path systems - innate immunity - t-cell immunity - antibody-mediated immunity - organism recognized, person is immune . immune memory is specific
54
immunization - vaccination
inoculation with attenuated/killed pathogen or chemically modified exotoxin
55
immune system response
recognize specific antigens - develops antibodies against. | - flu/antigens can mutate = need new flu vaccine yearly
56
herd immunity
when 90% or more of popln have immunization/vaccine against - infection cant pass easily. non-immune not as susceptible.
57
transmission mechanisms
``` person-to-person zoonotic + vectorborne soilborne waterborne foodborne ```
58
types of person-to-person transmission
airborne direct contact sexually transmitted
59
diff vtw zoonotic + vectorborne
zoo: animals. | vector = insect usually. animals can be vectors tho too
60
airborne pathogens
smaller particles, stay in air longer. more dangerous bc aerosolized
61
seasonal flu - kind of virus? characteristics?
RNA virus. ss, negative sense, helical RNA - surrounded by envelope - protein + lipid bilayer + glycoproteins - DNA on 8 segments = high reassortment between strains
62
antigenic shift vs drift
shift: unique reassortments drift: minor mutations in envelope genes (cell recognies this slow change)
63
endemic, epidemic, pandemic - timig?
en: annual epidemic: 2-3 years (large regions) pandemic - 10-14 years (widespread infection
64
why were so many killed in 1918 flu pandemic?
secondary bacterial pneumonia | - new virus occurred at time
65
H1N1
combo of human avian. - reassorted in swine. - majority of infections are mild or have no symptoms
66
who does H1N1 tend to afffect?
younger, healthier ppl. more from H1N1 than seasonal flu | - may be penetrate deeper into lungs?
67
infection + fatality rate or seasonal flu vs H1N1
more ppl infected with seasonal flu. but proportionally, 1% ppl died from H1N1, less than 01% died from seasonal flu
68
HIV AIDS - what is it?
HIV: virus infects immune system cells = macrophage + t-cells. = CD4 surface protein leads to AIDS (immune deficiency) - death due to secondary opportunistic infections.
69
secondary opportunistic infections assoc w HIV/AIDs
kaposi's sarcoma = co-infection of herpes + HIV = specific cancer penumocystic carnii pneumonia tuberculosis gastorintestinal and neurological infections
70
HIV/AIDs disease progression
- RNA retrovirus. copies itself + makes RNA. makes cDNA and inserted into genome. = slowly replicates. = need protease to inhibit progression of disease. symptom free: normal range or t-cells. swollen lymph nodes = increase in t-cells subclinical immune function - severe t-cell depletion. opportunistic infections and systemic immune deficiency = lots of HIV RNA copies, few t-cells
71
Malaria
parasitic infection - deadly, transmitted by insect vector. sporozite is most infectious. - grows in liver of human, infects RBC - parastie grows + lyses cell = anemia.

mcrb 265 (14 decks)

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