S2 I&i Normal Flora/pathogens

Front 1

Normal flora

Back 1

microorganisms routinely found on/in bodies of healthy individuals

Front 2

Resident flora

Back 2

flora that inhabit body sites for extended periods

Front 3

Transient flora

Back 3

flora that inhabits body sites for brief time

Front 4

What parts of the body are normally sterile (have no flora)?

Back 4

blood
body fluids
tissues

(may have transient flora, but removed by immune)

Front 5

staphylococci, Propionibacterium are normal flora on the ________

Back 5

skin

Front 6

Bacteroides, Clostridium, Escherichia coli are normal flora on the __________

Which are obligate anaerobics & which are facultative anaerobes?

Back 6

Intestinal tract (colon)

Obligate Anaerobes: Bacteroides, Clostridium
Facultative anaerobes: Escherichia coli

Front 7

Potential pathogens such as pneumococci, meningococci, Haemophilus may invade the ________


what is an Ex of normal flora in this location?

Back 7

Respiratory tract



Staphylococcus aureus

Front 8

Lactobacillus is a normal flora present in the ______________

What is the most common pathogen here?

Back 8

Urinary Tract


E. Coli (especially for UTI)

Front 9

Advantages of normal flora

Back 9

1. Protection
2. Prevention

(of harmful microorganism)

Front 10

How does normal flora prevent harmful microorganisms from becoming pathogenic?

Back 10

Blocks pathogen binding sites (can't adhere)
Consume available nutrients (can't grow/multiply)
Produces toxic compound (kill)
Produce essential nutrients for host (vitamins,etc)
Help develop immune system (build immunity)

Front 11

What is the difference btwn primary & opportunistic pathogens?

Back 11

primary pathogens can cause disease in healthy individuals

opportunistic cause disease in compromised individuals or in unusual locations only (UTI)

Front 12

What is virulence?

Back 12

the degree of pathogenicity of an organism
(how toxic)

Front 13

Define commensalism

Back 13

Microbe benefits from unaffected host

(staphylococcus aureus (host) & clostridium (microbe))

Front 14

In order for a microorganism to be pathogenic it must be able to _________, __________, & __________

Back 14

INVADE (host), INFECT (replicate & spread), & TRANSMIT (transmit to new hosts)

Front 15

In order for a host to prevent microorganism from causing disease it must ________ & _________ infection

(via innate & adaptive immunity)

Back 15

Control & eliminate infection

Front 16

Means for microbial invasion/entry into host cells

Back 16

Damaged mechanical barrier (skin, mucus)
Natural breech (insect bite)
Intentional breech (needle prick)

Front 17

Once a microbe has successfully invaded, it must __________ to infect host cell (become pathogenic)

Back 17

adhere/attach (to host cell)
(via adhesin)

Front 18

What are the 3 types of adhesins

Back 18

1. Pili (fimbriae)
-bind directly to residues on host surface

2. nonpilin (afrimbriael) ahesins
-outer membrane proteins allows contact btwn host ECM & microbe

3. biofilm
-Microbe EPS (exopolysaccharide matrix) produces IgA protease to break down mucus
-Microbe binds to Fc region (=adherence)

Front 19

Microbe binding to Fc region provides adherence to host cell receptors AND allows what?

Back 19

allows microorganism to hide from immune system (macrophages, etc can no longer bind to Fc)

Front 20

Give examples of Obligate & Faculative intracellular Bacterial pathogens

(intracellular pathogens are harder for immune system to reach bc they are not on cell surface, w/i)

Back 20

Obligate intracellular pathogens:
Chylamidia, Rickettsia

Facultative intracellular pathogens:
Salmonella, Shigella, Legionella, Mycobacterium

Front 21

What do invasins do?

Back 21

Trigger signals in host cell facilitating entry of microorganism into host cell (membrane-membrane interaction)

Front 22

Once microorganisms invade & adhere, how do they actually cause disease?

Back 22

-production of ingested toxins
-surface clonization, then toxin production
-invasion of host tissues
-invasion, then toxin production

Front 23

How do Clostridium botulinum, Staphylococcus aureus, Claviceps purpurea cause disease?

Back 23

produce toxins (in food, etc) that are ingested (by host)

Front 24

How do Vibrio cholerae, E. coli O157:H7, Corynebacterium diptheriae cause disease?

Back 24

colonize on surface of host, then produce toxins (damage host)

Front 25

How do Mycobacterium tuberculosis, Yersinia pestis cause disease?

Back 25

damage host through invasion of tissues

Front 26

How do Shigella dysenteriae, Streptococcus pyogenes cause disease?

Back 26

invade host tissuses, then produce toxins (that damage host)

Front 27

A-B toxins, Membrane damaging toxins, & superantigens are all (exotoxins/endotoxins)

Back 27

exotoxins

Front 28

Describe A-B extoxin mechanism of host damage

Back 28

A-B sections on toxin
B binds host receptor
toxin enodcytosed into vacuole
Vacuole becomes acidic & A-B cleaved
A causes toxic effects on cells
B is exocytosed

Front 29

What are the 3 subtypes of A-B exotoxins?

Back 29

1. neurotoxins - block inhibitory neurons or nerve signals (clostridium tetani & butulinum)
2. enterotoxins- modify regulatory proteins to induce electrolyte & water secretion (cholerae)
3. cytotoxins- inhibit protein synthesis (Shigella)

Front 30

Describe Membrane-damaging exotoxin (cytotoxins & hemolysins) mechanisms of host damage

Back 30

2 mechanisms:
1. insert into membrane & form pore (Strep O)
2. remove polar heads of membrane phospholipid (phopholipases)

*both damage membranes leaving cell open to invasion

Front 31

Describe Superantigen exotoxin mechanism of host damage

Back 31

-bind to MHC 2 on BOTH antigen presenting cell & T-cell receptor= circumvent antigen processing
- cause T cells to release large amount of cytokines
--> cytokines lead to shock, organ system failure
--->death apoptosis of overstimulated T-cells leads to compromised immune system

Front 32

LPS is an (exotoxin/endotoxin)

Back 32

endotoxin

Front 33

Describe LPS endotosin mechanism of host damage

Back 33

lipid A on LPS activates innate immune system-->
macrophages release TNF & IL-1-->
fever occurs initially-->
large scale leads to inflammation-->
hypotension, reduced PMN, hemorrhage, DIC, shock