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BHSC3329 MT 1 > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

Define niche

A

a compartment with unique properties (temperature, pH, nutrients) (able for microbe colonization)

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2
Q

Define commensalism

A

one organism benefits without harm to the other (aka normal resident microbiota, indigenous microflora, commensals)

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3
Q

Mutualism

A

two organisms cooperate to both benefit (aka symbiosis, cows + bacteria to digest grass, bees + flowers)

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4
Q

Parasitism

A

one organism benefits at the expense of another

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5
Q

What protects the womb from vaginal microbes?

A

fetal membrane

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6
Q

Colonization of a newborn occurs in 3 ways. Name them.

A

1) by birth 2) by feeding 3) by caregiver/environment

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7
Q

Microbes bottle fed babies are exposed to:

A

coliforms lactobacilli enteric streptococi staphylococci

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8
Q

Microbes breast fed babies are exposed to:

A

primarily Bifodobacterium

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9
Q

What are transient microbes?

A

microbes that temporarily colonize the body

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10
Q

What are resident microbes?

A

microbes that permanently colonize the body

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11
Q

Microbial antagonism:

A

when good microbes defend us against harmful ones

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12
Q

Pathogens:

A

parasitic microbes with the potential to cause disease

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13
Q

True/primary pathogen:

A

likely to cause disease persons with normal immune system

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14
Q

Opportunistic pathogens:

A

cause disease in immunocompromised persons

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15
Q

Invasion:

A

microbes enter into germ-free tissues or cells

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16
Q

Infection:

A

microbe spreads throughout the tissues and body

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17
Q

Sterile organs:

A

heart + circulatory system liver kidneys + bladder brain + spinal cord muscles bones ovaries/testes glands (pancreas, salivary) sinuses middle + inner ear internal eye

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18
Q

Sterile fluids:

A

blood urine in kidney, ureters, bladder CSF saliva priof to entering the oral cavity semen prior entering the urethra amniotic fluid surrounding the embryo + fetus

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19
Q

Virulence:

A

the degree of harm caused by a pathogen (morbidity/mortality)

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20
Q

Virulence factors:

A

intrinsic characteristics of pathogens that contribute to virulence

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21
Q

Infectious dose (ID):

A

minimum number of microbes to cause illness

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22
Q

Lethal dose (LD):

A

minimum number of microbes to cause death

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23
Q

Do we what ID and LD to be high or low?

A

We want both high ID and LD. Higher amount of microbes needed for ID and LD, means decrease or harder chance to become ill/die.

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24
Q

E. coli (O157: H7)

Name 4 characteristics

A
  • in the lower intestine of warm-blooded animals
  • mostly harmless/beneficial; some strains -> food poisoning
  • produce toxins to break down the gut lining
  • ingesting as little as 10 cells may cause illness (low ID)
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25
Q

Vibrio Cholera (3 char)

A
  • found in small intestine of people & some aquatic habitats
  • produces “cholera toxin”: draw salts + water into the intestine -> severe diarrhea
  • ingetings 10^6-10^11 are required to cause illness (high ID)
26
Q

ID50

A

min amount of microbes required to infect 50% of a given population

27
Q

LD50

A

amount required to kill 50% of a given population

28
Q

Can toxins have ID and LD?

A

Toxins do NOT have ID, but can kill without infecting (therefore LD50 can be determined)

(only infectious agents can infect and kill; ID50 + LD50)

(the lower the ID50 + LD50, the “more virulent” the pathogen)

29
Q

6 Virulence factors:

A

1) adhesion 2) immune evasion 3) invasiveness 4) toxins 5) nutrient competition 6) genetic

30
Q

Adhesion:

A

adsorption to host cells and tissues

31
Q

2 Bacteria adhesion factors:

A

1) fimbriae: hair-like structure (sticky)
2) capsule: simy outer layer (made of carbs, sticky) Both nonspecific

32
Q

2 viruses adhesion factors:

A

1) glycoproteins: adsorb to cells because of specific interactions with cellular proteins (receptors) (e.g. HIV uses C4 to get into cells; specific)
2) hemagglutinin: protein spikes of influenza that bind to surface of respiratory tract (nonspecific)

33
Q

Evasion: antiphagocytic factor Name 4 strategies to avoid phagocytosis

A

1) capsule: slimy layer masks antigens by sugar
2) toxins: defense against phagocytic cells
3) leukocidins: toxins that directly kill WBC
4) intracellular microbes: hide inside host cells (secrete molecules into a target cell to make it easier to enter - similar to phagocytosis w/o digestion)

34
Q

Evasion of host defense:

1) Physiological example:
2) Immunocompromise example:

A

1) H. pylori survives in stomach acid because of enzyme urease that produces ammonia - basic pH
2) HIV-1 (human immunodeficiency virus) binds to cells using CD4 receptor proteinon the cell surface

Then HIV-1 integrates into and becaomes part of the host genome

35
Q

>Function of CD4 T cells

>HIV-1 effect on CD4 T cells

>What must the CD4 T cells level # be, to be identified as positive for AIDS

A

>CD4-expressing T cells regulate the immune system *by producing cytokines*

>HIV-1 cripples the immune system >HIV may appear to have been cleared by the immune system but it continues to kill CD4 T cells

>CD4 T cells <200/ul blood = AIDS

36
Q

Invasiveness: exoenzymes:

A

secreted by cetrain pathogens to help them disrupt and “dig” deeper into tissues

37
Q

Invasiveness: exoenzymes > MUCINASE + example

A

disrupts protective mucous membranes (e.g. dysentry)

38
Q

Invasiveness: exoenzymes > KERATINASE + example

A

digest main protein of skin and hair (e.g. ringworm)

39
Q

Invasiveness: exoenzymes > COLLAGENASE + example

A

digests connective tissue (e.g. Clostridiun)

40
Q

Invasiveness: exoenzymes > HYALURONIDASE + example

A

digests hyaluronic acid that cements tissues together (e.g. flesh eating disease) - Hyaluronidase - spreading factor - breaks down H.a. - H.a. is a tissue phospholipid -> connective tissue “glue” that holds other tissues in place - increase pain for decrease wound; high fever; rapid spread (of tissue breakdown)

41
Q

Invasiveness: exoenzymes > COAGULASE + example

A

prevents blood clotting (e,g, Stapholococci)

42
Q

3 ways of invasion + examples:

A

1) break down tight junctions (e.g. Tersubia, black plague)
2) kills cells (e.g. E. coli) 3) endocytosis (e.g. Salmonella enterica)

43
Q

1) Invasion of tight junctions between cells via
2) Invasion via killing surface epithelial cells via

A

1) usually exoenzymes (e.g. Yersinia, black plague)
2) toxins (e.g. E. coli)

44
Q

Salmonella enterica - explain its process of invasion

A
  • uses secretion system to inject proteins in gut epithelial cells
  • these proteins change the nature of the cell membrane, causing it to endocytose the Salmonell cell
  • the pathogen can exist, even multiply inside the cell (hiding from antibodies + phagocytes)
  • gets released by exocytosis (now inside the body)
45
Q

Toxins - Do they cause virulence?

A

Yes! They cause harm!

46
Q

Exotoxins vs. endotoxins

  1. toxicity
  2. effects on the body
  3. chemical composition
  4. heat denaturation at 60 degrees
  5. toxoid formation
  6. immune response
  7. fever stimulation
  8. manner of release
  9. typical sources
  10. examples of disease
A
47
Q

Exotoxins (3 char)

A
  • generally protein
  • consists two parts: binding doman and active domain
  • are heat labile (exceot for S. aureus and B. cerus emetic toxin) (denature-able)
48
Q

Enterotoxins:

  • Examples (2-3)
  • Clinical manifestations
A
  • GI tract -> diarrhea (sometimes bloody diarrhea ex. Shigella infection)
  • S. disenteriae (shiga toxin) = E coli 0157 verotoxin (degrades the lining of blood vessels -> bloody stool)
  • Choleragen produced by Vibrio chlolera O1 (stimulates water secretion into gut -> rice-water stools)
49
Q

Neurotoxins

  • 2 examples + its clinical manifestations
A
  • effects the nervous system
  • botulism toxin: cause flaccid paralysis (numbness, no strength in the muscle)
  • tetanus - tetanospasmin: spastic paralysis (constant muscle contraction, fails to relax)
50
Q

Hemolysins (exotoxin)

  • 1 example + clinical manifestation
A
  • it destorys RBC in the circulatory system
  • ex. Streptococcus pyogenes (Group A Streptococcus)
  • characterized by growing on blood agar
51
Q

Agar:

Blood agar:

Chocolate agar:

A
  • jello-like surface where individual bacteria can be separated into single cells that grow into single colonies
  • agar mixed with nutrient growth medium as well as living RBCs
  • growth medium for fussy (opportunistic) bacteria (RBC has been lyse to relase iron content)
52
Q

a-hemolytic:

b-hemolytic:

g-hemolytic:

A
  • partial RBC hemolysis (incomplete digestion of RBC, RBCs turn green from S. viridans)
  • compete RBC hemolysis (RBC lysate forms halo around colonies from S. haemolyticus)
  • not hemolytic
53
Q

Leukocydins (exotoxin)

A
  • destroys WBC in immune system esp. phagocytes such as neutrophils
  • (neutrophils are gateway/first responders that send chemokines - killing it greatly impacts immune system)
  • ex. Streptococcus aureus: necrotizing pneumonia kills patients within 72 hours
54
Q

Virulence factor: competition for nutrients with host

Define siderophores

Name 3 hemoproteins

A

siderophores: bacteria proteins used to scavenge free iron by dissolving iron bound to host hemoproteins (e.g. transferrin, ferritin, lactoferrin)

55
Q

Examples of siderophores

Mycobacterium tuberculosis (TB)

Escherichia coli

Bacillus anthracis (Anthrax)

Vibrio cholera (Cholera)

Versinia pestis (Black Plague)

A

Myctobactin

Enterobactin

Bacillibactin

Vibriobactin

Yersiniabactin

56
Q

Virulence factor: Genetic

How pathogen can avoid recognition as non-self

A
  • antigenic variation: pathogen just has the change the 3D shape of the antigen so that it does not “feel” the same (T cells PRR can feel from PAMPs)
  • almost always variable surface glycoproteins (VSGs)
57
Q

African sleeping sickness: trypanosome

A
  • a protozoan parasite
  • changes its VSGs in repsonse to immunological challenge
  • “ping pong effect”
58
Q

Antigenic drift vs. antigenic shift

A

antigenic drift: minor changes -> localized outbreak or epidemic (expansion in a population with resistance) (ex. seasonal flu)

antigenic shift: dramatic antigenic alterations -> pandemic (expansion into a population with no resistance) (ex. swine, avian flu)

59
Q

How do influenza virus survive?

A

If mistakes in RNA is made, they are retained -> evolution

60
Q

Avian flu

Name 2 antigens

A
  • two important antigens: hemagglutenin (HA) (adhesion) and neuraminidase (NA)

BHSC3329 MT 1 (2 decks)

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