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BMSC 210 > Module 10 > Flashcards

Module 10 Flashcards

Host microbe interactions

1
Q

Commensal

A

host provides shelter/environment for bacteria (benefit bacteria)

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2
Q

Mutualistic

A

mutual benefit

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3
Q

Pathogenic

A

damages host

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4
Q

microbiome

A

functional collection of different microbes in a system

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5
Q

microbiota

A

community of microorganisms present in a habitat

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6
Q

Metagenomic

A

genetic material in a given environment

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7
Q

colonization

A

microbes present and grow on non sterile external body surface

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8
Q

basic steps to infection

A

enters body sites, overgrows, induces immune response

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9
Q

disease

A

damages caused by infection

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10
Q

normal microbiota

A

total microbial population associated with a human
mainly bacteria
10^13 human cells + 10^14 bacteria cells

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11
Q

different classes of microbes and explain

A

transient: short term, highly variable, high external influence
resident: long term, stable, limited external influence

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12
Q

functions of micrbiota

A

digest nutrients
provide nutrition
educate/prime host defenses
colonization resistance

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13
Q

how is microbiota esablished

A

at birth by feeding

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14
Q

how is microbiota unstabilized

A

hormone fluctuations during puberty

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15
Q

factors in microbiota development

A

drivers(host and microbiota)
microbe-microbe interactions
habitat filtering

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16
Q

skin microbiome (3)

A

low diversity (dry and salty)
transient populations on surfaces, resident in pores
mostly commensal, some mutualistic

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17
Q

respiratory tract microbiome (4)

A

site specific composition
oral cavity: biofilm communities
nasal and upper: similar to skin/mouth
lower: few transient

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18
Q

genito-urinary microbiome

A

urine is sterile, first 1cm of urethra has transient
vaginal has non specific defenses, acidic

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19
Q

intentional microbiota alteration

A

fecal transplant
probiotics
prophylactic antibiotics
antispetics

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20
Q

intestinal microbiome

A

highest populations and great diversity
mutualistic
composition impacted by diet

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21
Q

unintentional microbiota alteration

A

dysbiosis from antibiotic use

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22
Q

FMT cure rate and use

A

60-90% cure rate
only used to combat recurring C diff
works by creating competition not wiping out

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23
Q

probiotic

A

living microorganisms for competitive exclusion

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24
Q

prebiotics

A

nutrients to help out microbes

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25
symbiotics
mix of pre and probiotics
26
original koch postualte
suspect causative agent not in healthy suspect must be isolated, grown, and put into organism to test
27
issues with koch postulate original
not designed for virus does not account for asymptomatic carriers no longer ethical to deliberately infect
28
pathogenicity
ability to cause disease
29
virulence
degree of pathogenicity
30
ID50
infectious dose
31
LD50
lethal dose
32
periods of disease
incubation prodromal (general signs) illness (severe symptoms) decline convalesence
33
stages of pathogenicity (list)
exposure adhesion invasion disease transmission
34
exposure
mode of transmission varies with portal of entry
35
adhesion
capability of microbe to attach to cell works with adhesins that bind to certain receptors on host and form biofilm
36
bacteria adhesins
fibrae, capsules
37
protozoa adhesin
cilia
38
virus adhesins
capsid spike proteins
39
invasion
dissemination in local tissue using exoenzymes and toxins
40
disease
successful multiplication
41
local disease
small near entry port
42
focal disease
spread to secondary location
43
systemic disease
disseminated, lesions not at site of entry)
44
transmission
required for success
45
molecular koch posulates
-gene is pathogenic members of species -inactivating/deleting gene decreases virulence -reversion or allelic replacement can bring back pathogenicity
46
how do pathogens damage
inject effectors and reprogram cell enzymes distryo/affect tissue integrity produce toxins
47
exoenzymes
act as spreading (invading) factors
48
intoxication
ingest toxin, rapid (1-12hrs)
49
infection
bacteria, delayed (12-72hrs)
50
endotoxins
part of bacterial structure released by lysis
51
exotoxins
secreted proteins
52
type 1 toxin
target cell surface, superantigens
53
type 2 toxin
target euk cell membrane, pore forming
54
type 3 toxin
AB type toxin
55
how do superantigens cause damage
entering blood stream, forming cytokine storm,
56
what are membrane disrupting toxins, how do they work
kill host cells (phagocytes) and escape phagosome 1. form channel/pore, water rushes in lysing cell 2. attack phospholipids cleaving head
57
functional subunits of AB toxin
A subunit-toxic enzymatic activity B subunit- bind to receptor carries A
58
single peptide AB toxin
gram positive
59
multiple peptide AB toxin
gram negative
60
ADP ribosyltransferase
targets NAD+
61
genotoxin
targets host DNA
62
deaminases
target rRNA
63
botulism toxin
flaccid paralysis stops muscle contration
64
tetanus toxin
uncontrollable contraction spastic paralysis
65
options for pathogen invasion
camouflage disguise resistance
66
camouflage
coating surface with host proteins, host mimicry
67
disguises
change structures on cell surface antigenic variation, phase variation, epigenetic variation, LPS modification
68
resistance
vary LPS length (longer is harder for host to attack) capsule surface enzymes
69
influenzavirus (disease, adhesin, attachment site)
influenza hemagglutinin sialic acid of respiratory and intestinal cells
70
herpes simplex virus 1 or 2 (disease, adhesin, attachment site)
oral/genital herpes glycoprotein: gB, gC, gD heparan sulfate on mouth/genital mucosal cells
71
human immunodeficiency virus (disease, adhesin, attachment site)
HIV/AIDS glycoprotein: gp120 CD4, CCR5 of immune system cells
72
mycotoxicoses
poisoning due to consumption of fungal metabolic product
73
cutaneous mycoses
fungal infection on outermost layers spreads through direct contact
74
subcutaneous mycoses
fungal infection of skin and SQ tissues affects pre existing wounds
75
systemic mycoses
fungal infection of internal organs start airborne and spread very severe to fatal

BMSC 210 (10 decks)

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