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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
Q

dysbiosis linked to disease

A

bowel disorders, crohns, obesity, celiac, allergies, autism, depression, parkinsons

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26
Q

pathogenicity

A

ability of organism to produce pathological change or disease that impars host function
- disease-producing, parasite, opportunistic

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27
Q

define virulence

A

quantitative measure of pathogenicity

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28
Q

define infection

A

any situation in which organism is established + growing.

- doesnt have to be pathogenic

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29
Q

attenuation

A

decrease or loss of virulence

30
Q

toxicity

A

ability of organism to cause disease through making toxin that inhibit host cell function/kills host cells
= toxins can travel

31
Q

invasinveness

A

ability of pathogen to grow in host tissue at densities that inhibit host function
- damage without toxin

32
Q

steps to pathogenic life cycle

A
  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
Q

adherence of pathogen

A

needed to gain access to host tissue - attach to epithelial cell.

-direct attachement: to surface cell/host
indirect attachment: capsule attaches to host

34
Q

four factors involved in adherence to host cells

A
  • capsule/slime layer
  • adherence proteins
  • lipoteichoic acid
  • fimbriae (pili)
35
Q

invasion

A

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
Q

measure virulence

A

LD50 - lethal dose that kills 50% of animals in test group

- lower number? more virulent

37
Q

high virulence + # of cells for LD100

A

small range. hgihly virulent, kill in small quantities

38
Q

enzyme virulence factors

A
  • 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
Q

virulence factors in bacteriophage

A

erythrogenic toxin, shiga-like toxin, enterotoxins, neurotoxins ,diphtheria toxin

40
Q

plasmin virulence factors

A

enterotoxins, hemolysin, urease, edema factor, coagulase, fibrinolysin

41
Q

transposon virulence factors

A

enterotoxin
shiga toxin
cholera toxin

42
Q

salmonella virulence factors

A

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
Q

exotoxins + 3 categories

A

proteins released from pathogenic organism as it grows

  1. cytolytic toxin
  2. AB toxin
  3. superantigen toxin
44
Q

cytolitic toxins work

A

by degrading cytoplasmic membrane integrity

  • host cell lysis + death
  • hemolysins too.
45
Q

cytolytic toxin ex:

A

staphylococcal a-toxin

form mutlimer in PM = pore.

46
Q

what is AB toxin do?

A

A + B units.
B binds to host cell receptor
A transfers damaging agent to host

47
Q

ex of AB toxin

A

diphtheria toxin

- catalyze ADP-ribosylation of elongation factor 2 + prevent aa transfer to grwoing peptide chain in ribosome

48
Q

ex of botulinum toxin

A

blocks release of aCh to muscle tissue = permanent relaxed state

49
Q

superantigen toxins

A

stimulate large numbers of immune cells

- result in extensive inflammation + tissue damage = cells gorw elsewhere cause not viable there

50
Q

endotoxins

A

lipopolysaccharide portion of CW of certain g(-) bacteria. toxin when solubilized.

  • less toxic than exotoxins.
  • only when cells are present
51
Q

innate resistance to infection

A

nonspecfic barriers prevent colonizationof host by most pathogens
- lack of defenses = more susceptible to infection + colonization

52
Q

risk factors for infection

A

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
Q

specific (adaptive) immunity

A

complex, mutli-path systems

  • innate immunity
  • t-cell immunity
  • antibody-mediated immunity
  • organism recognized, person is immune . immune memory is specific
54
Q

immunization - vaccination

A

inoculation with attenuated/killed pathogen or chemically modified exotoxin

55
Q

immune system response

A

recognize specific antigens - develops antibodies against.

- flu/antigens can mutate = need new flu vaccine yearly

56
Q

herd immunity

A

when 90% or more of popln have immunization/vaccine against - infection cant pass easily. non-immune not as susceptible.

57
Q

transmission mechanisms

A 
person-to-person
zoonotic + vectorborne
soilborne
waterborne
foodborne
58
Q

types of person-to-person transmission

A

airborne
direct contact
sexually transmitted

59
Q

diff vtw zoonotic + vectorborne

A

zoo: animals.

vector = insect usually. animals can be vectors tho too

60
Q

airborne pathogens

A

smaller particles, stay in air longer. more dangerous bc aerosolized

61
Q

seasonal flu - kind of virus? characteristics?

A

RNA virus. ss, negative sense, helical RNA

  • surrounded by envelope - protein + lipid bilayer + glycoproteins
  • DNA on 8 segments = high reassortment between strains
62
Q

antigenic shift vs drift

A

shift: unique reassortments
drift: minor mutations in envelope genes (cell recognies this slow change)

63
Q

endemic, epidemic, pandemic - timig?

A

en: annual
epidemic: 2-3 years (large regions)
pandemic - 10-14 years (widespread infection

64
Q

why were so many killed in 1918 flu pandemic?

A

secondary bacterial pneumonia

- new virus occurred at time

65
Q

H1N1

A

combo of human avian.

  • reassorted in swine.
  • majority of infections are mild or have no symptoms
66
Q

who does H1N1 tend to afffect?

A

younger, healthier ppl. more from H1N1 than seasonal flu

- may be penetrate deeper into lungs?

67
Q

infection + fatality rate or seasonal flu vs H1N1

A

more ppl infected with seasonal flu. but proportionally, 1% ppl died from H1N1, less than 01% died from seasonal flu

68
Q

HIV AIDS - what is it?

A

HIV: virus infects immune system cells
= macrophage + t-cells.
= CD4 surface protein

leads to AIDS (immune deficiency)
- death due to secondary opportunistic infections.

69
Q

secondary opportunistic infections assoc w HIV/AIDs

A

kaposi’s sarcoma = co-infection of herpes + HIV = specific cancer

penumocystic carnii pneumonia

tuberculosis
gastorintestinal and neurological infections

70
Q

HIV/AIDs disease progression

A
  • 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
Q

Malaria

A

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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