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Microbio Test 3 Review (ch 8, 10, 11) > Ch 11 > Flashcards

Ch 11 Flashcards

(67 cards)

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1
Q

What is normal microbiota?

A

permanently colonize the host and either cause no harm to the host or are beneficial to their host

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2
Q

transient microbiota

A

may be present for days, weeks, or months, more easily lost but are not harmful to the host

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3
Q

types of symbiosis

commensalism

A

one organism benefits
other is unaffected

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4
Q

types of symbiosis

mutualism

A

both organisms benefit

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5
Q

types of symbiosis

parasitism

A

one organism benefits and the expense of the other

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6
Q

How can normal flora cause disease?

A

Cause disease when in a new area of the body or host is immunocompromised aka opportunistic pathogens

Ex ecoli UTIs

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7
Q

primary infections

A

Acute infection that causes the
initial illness

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8
Q

secondary infections

A

Opportunistic infection after a
primary (predisposing) infection

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9
Q

Know a few factors that make us predisposed to disease

A

age
lifestyle
fatigue

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10
Q

What is a reservoir?

A

Continual sources of infection; living or nonliving

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11
Q

examples of reservoirs

humans

A

AIDS, gonorrhea

carriers may have subclincal (unapparent) infections or latent diseases

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12
Q

example of reservoirs

animals/ insects

A

rabies, lyme disease

zoonoses may be transmitted to humans from non-human reservoirs

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13
Q

examples of reservoirs

nonliving/ abiotic

A

botulism, tetanus

spores of clostridium species are found in soil and water

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14
Q

What are the 3 main routes of transmission?

A

direct

indirect

contact

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15
Q

direct transmission

A

droplet (aerosol)

body fluid exchange

fecal-oral

contact (STDs)

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16
Q

indirect transmission

A

foodborne

water-borne

fomite (inantimate object contact)

insect vectors/ animal zoonoses

environmental

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17
Q

contact transmission

A

direct: with infected/ reservoir

indirect: with inanimate object as intermediate

congenital: mother to fetus or to newborn at birth

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18
Q

What is a fomite?

A

indirect transmission

carry infectious microbes between hosts

ex. hypodermic syringe

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19
Q

transmission of arthropods

mechanical

A

arthropod carries pathogen on feet to host

host causes further contamination to self

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20
Q

transmission of arthropods

biological

A

pathogen reproduces in vector (insect) and is injected when insect bites host

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21
Q

What is MRSA?

A

methicillin resistant Staphylococcus aureus

resistant to the broad-spectrum antibiotics commonly used to treat it; can be fatal

mostly occurs in hospital aka healthcare-associated (MRSA or HA-MRSA)

older adults and people with weakened immune systems are at most risk of HA-MRSA

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22
Q

What are some factors that contribute to emerging and reemerging diseases?

A

genetic recombination

inappropriate use of antibiotics and pesticides

evolution of new strains

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23
Q

3 basic types of epidemiology.

A

descriptive

analytical

experimental

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24
Q

types of epidemiology

descriptive

A

collection and analysis of data

john snow

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25
**types of epidemiology** analytical
comparison of a diseased group and a healthy group nightingale23e4
26
**types of epidemiology** experimental
controlled experiments to learn how to prevent the spread of disease
27
What are features and examples of nosocomial infections?
aka healthcare associated infections acquired during a hospital stay affects 5-15% of all patients reduced by following proper aseptic techniques during patient care and procedures
28
examples of nosocomial infections aka healthcare associated infections
Urinary tract infections (UTIs) surgical site infections lower respiratory infections
29
In what ways can opportunistic bacteria cause disease?
causes disease when in new area of body OR host is immunocompromised ex e coli UTIs
30
Know all terms involved in pathogenicity, virulence, and toxicity
31
**3 main characteristics of pathogens that determine virulence** infectivity
ability to establish focal point of infection
32
** 3 main characteristics of pathogens that determine virulence** invasiveness
ability to spread to adjacent tissues
33
**3 main characteristics of pathogens that determine virulence** pathogenic potential
degree to which potential can cause damage to host
34
What are the 3 main routes of entry into the body?
mucous membranes skin oral-fecal route
35
ID50
infectious dose for 50% of the test population the amount of pathogen it takes for 1/2 of the individuals tested to become infected
36
LD50
lethal dose (of a toxin) for 50% of the test population the amount of toxin required to kill 1/2 of the individuals tested
37
Do microorganisms have a preferred portal of entry? What does that mean?
most pathogens do have a preferred portal of entry the portal of entry determines how many spores the bacteria will produce which will show how many bacteria are required to establish infection
38
What are adhesins?
bind to receptors on host cells-INVASION
39
ex of adhesions
glycocalyx: Streptococcus mutans fimbriae: Escherichia coli M protein: Streptococcus pyogenes
40
What are some ways in which pathogenic bacteria have evolved ways to get around the immune system
cell wall: evasion capsules: cover surface markers in their cell walls enzymes: evasion and damage hemolysins: lyse RBCs to release iron for pathogen use
41
exotoxin
gram pos proteins with 2 subunits (A-B) heat unstability b/c these are proteins high temp denatures them high toxicity neutralized by antitoxin small lethal dose
42
endotoxin
gram neg lipid heat stability b/c high temp does not kill lipids low toxicity not easily neutralized by antitoxin larger lethal does
43
exotoxin A subunit B subunit
A subunit does the damage / is toxic to the host cell B subunit extoxin is responsible for binding it to the target cell and transporting the A subunit into the target cell
44
What are the general steps of entry of an A-B exotoxin?
1. bacterium produces and releases exotoxin 2. B (binding) component of exotoxin attaches to host cell receptor 3. A-B exotoxin enters host cell by endocytosis 4. A-B exotoxin enclosed in pinched-off portion of plasma membrane during pinocytosis 5. A-B components of exotoxin seperate The A component alters cell function by inhibiting protein synthesis The B component is released from the host cell
45
membrane-disrupting exotoxins
Lyse host cells by making protein channels in the host cell membranes
46
What are superantigens
cause an intense immune response due to a massive release of cytokines from host cells * Intense immune response occurs because they activate more immune cells than normal by binding non- specificall
47
**stages of disease** 1. incubation period
time between infection with a microbe and the onset of symptoms
48
**stages of disease** 2. prodromal period
first appearance of mild or nonspecific signs and symptoms of an illness
49
**stages of disease** 3. acute illness
most severe signs and symptoms
50
**stages of disease** 4. convalescence
the recovery period after an illness
51
infection
invasion and growth of bacteria
52
intoxication
Disease that results from a specific toxin which may or may not have been produced during the infection (some toxin are very stable!
53
**capsules: evasion** pathogens can avoid detection by host phagocytes by
covering surface markers on their cell walls
54
**capsules: evasion** is used by
Streptococcus pneumoniae, Bacillus anthracis Haemophilus influenzae
55
**capsules:evasion** Otherwise host phagocytes recognize pathogen cell markers with receptors on their surfaces
Bacterial markers and host phagocyte receptors interact to initiate **phagocytosis** * Once ingested: **Lysosomes** use a complex mixture of digestive enzymes and destructive oxygen radicals (e.g. super oxides) to destroy pathogens
56
process of phagocytosis
1. chemotaxis and adherence of microbe to phagocyte 2. ingestion of microbe by phagocyte 3. formation of a phagosome 4. fusion of the phagosome with a lysosome to form a phagolysosome 5. digestion of ingested microbe by enzymes 6. formation of residual body containing indigestible material 7. discharge of waste materials
57
**cell wall components: evasion** Many pathogenic bacteria have cell wall
factors that help them evade the host’s immune system
58
**cell wall components: evasion** M protein
in Streptococcus pyogenes (also used in adherence to host cells) helps resist phagocytosis
59
**cell wall components: evasion** Opa proteins
inhibits interactions between Neisseria gonorrhoeae and T helper cells due to very tight packing between bacterial cells mediated by Opa proteins
60
**cell wall components: evasion** mycolic acids
in (acid fast bacteria) Mycobacterium tuberculosis and Mycobacterium leprae make it difficult for phagocyte lysozomes to digest/destroy the pathogen
61
**enzymes: evasion and damage** some pathogenic bacteria produce enzymes that help them establish
an infection and/or cause damage to their host
62
**enzymes: evasion and damage** Coagulase
causes clotting of the blood; converts fibrinogen to fibrin which coats the bacteria to help it evade phagocyte detection
63
**enzymes: evasion and damage** Kinases
ex. streptokinase digests fibrin clots which allow pathogens to escape from a clot and spread
64
**enzymes: evasion and damage** Hyaluronidase
hydrolyzes hyaluronic acid which helps hold cells together, allowing easy spread in host tissues
65
**enzymes: evasion and damage** Collagenase
hydrolyzes collagen to allow pathogen to spread in connective tissues
66
**enzymes: evasion and damage** IgA protease
destroys IgA antibodies produced by the host
67
**enzymes: evasion and damage** Hemolysins
lyse red blood cells to release iron for pathogen use

Microbio Test 3 Review (ch 8, 10, 11) (5 decks)

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