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Microbiology > 02- Microbio of patogenic factors > Flashcards

02- Microbio of patogenic factors Flashcards

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1
Q

Pathogenic factors

A

process by which microorganisms cause infection

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2
Q

The Microbe

A

● Few are pathogenic
● Many benefit the host
○ Some can provide resources for us → vitamin K

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3
Q

t/f: Host factors greatly influence the relationship between microbe and host

A

true

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4
Q

t/f: Our normal flora is only as healthy as we are

A

true; ● As our health diminishes with age and nutrition → decline in quality of normal flora

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5
Q

Commensalism

A

One organism benefits from the relationship
ex. Saprophytic mycobacteria of the ear and external genitals
○ Live on secretions and sloughed-off cells
○ Cause no benefit or harm to the host

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6
Q

Mutualism

A

● Both organisms benefit from the relationship
● We measurably are better with microorganism present
○ We can quantify this

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7
Q

Parasitism

A

● One organism benefits from the relationship at the expense of the other
● Host is harmed
● This is an infectious process

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8
Q

Two types of flora are

A

Resident microbiota & Transient microbiota

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9
Q

Resident microbiota

A
  • permanently colonize the host
    ○ Acquire this normal flora after birth
    ○ Through every exposure on the earth
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10
Q

Transient microbiota

A

temporarily colonize the host
○ Commensal or mutualistic relationship
○ Not part of our normal flora
○ Acquired due to changes in our environment

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11
Q

Difference between flora of the gut and flora of respiratory

A 
●	Normal flora of gut is different from that of resp tract, skin, urogenital, etc
●	The environment in each are completely different
Skin
○       Dry 
○	Exposure to sun
○	Different textures/frictions
Respiratory tract
○	Wet
○	Moist
○	Dark
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12
Q

Distribution and composition of normal flora determined by the following factors:

A
  • nutrients
  • physical and chemical factors
  • mechanical factors
  • other host factors such as age, nutritional status, disability, stress, personal hygeine, lifestyle, geography, occupation
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13
Q

Normal Flora

A

Normal conditions → normal flora colonizes the host without causing disease
● In many circumstances the normal flora benefits host
○ Preventing growth of pathogenic microbes
○ Make it more difficult for us to be infected b/c they colonize the sites
● Process commonly referred to as Microbial Antagonism

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14
Q

t/f: the flora is better at getting nutrients than pathogens

A

true

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15
Q

Microbial Antagonism

A

● Normal flora is fit → more resilient against infections

● Makes us stronger than if we did not have normal flora

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16
Q

Microbial Antagonism example

A

● E. coli produce bacteriocins
○ Protect the turf
● These proteins inhibit growth of closely related species of bacteria
○ Such as Salmonella and Shigella
○ These can cause serious GI infections or gastroenteritis
○ Bacteriocins kill theses species
● E.coli present → we need to be exposed to a lot of salmonella and shigella to actually get sick

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17
Q

Balance btw normal flora and pathogenic microbe is altered:

A

● Microbial antagonism fails
● Immune system cannot eradicate the microorganism
● Disease can result

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18
Q

Disruption of this balance may be induced by a number of factors, including:

A

● Age
● Antibiotic use
● Changes in hygiene
● Nutritional status

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19
Q

Normal flora changed vs unchanged

A

Normal flora unchanged → C. diff does not cause disease

Normal flora changed → C. diff grows, reproduces, and causes disease

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20
Q

Opportunistic infections occur when:

A
  1. Microbes from the host normal flora move from their normal habitat → causing disease
  2. The host’s immune system is weakened/compromised
  3. Changes occur in the composition of the host normal flora
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21
Q

Most pathogenic microorganisms cause disease via the process outlined below:

A 
●	Contact/Exposure
●	Adherence
●	Evasion of Host Defenses and Penetration
●	Damage of Host Cells
●	Transmission
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22
Q

Contact/Exposure: Portals of entry

A
  1. Mucous membranes → represent a significant portal of entry
  2. Skin
  3. Direct deposition beneath mucous membranes or skin
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23
Q

Adherence

A

● Pathogen attaches itself to host tissues at portal of entry
● Adhesins on cell surface molecules located on the pathogen
○ Binding specifically to surface “receptors” located on the cells of host tissues
● Adhesins are host specific and tissue specific

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24
Q

Adherence

A

● Has to be a match btw host and microorganism receptor in order for adhesion to occur
● No adherence = no infection
● Mismatch = no harm = no infection

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25
Q

Bacterial Structures

A

Fimbriae/Pili, flagella

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26
Q

Adherence proteins

A

M protein, Opa protein, etc…

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27
Q

Glycocalyx

A

Capsule, slime layer

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28
Q

t/f: Has to be a match btw host and microorganism receptor in order for adhesion to occur

A

true
● No adherence = no infection
● Mismatch = no harm = no infection

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29
Q

adhesins

A

● Microorganisms must produce

● Adhesins will bind to the receptors that are aligned with host cells

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30
Q
  1. Bacterial structures
A

● Adhesins are present on the fimbriae and flagella of many pathogenic bacteria
● Fimbriae help bacteria hold onto the host cell

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31
Q
  1. Adherence Proteins
A

● M proteins produced by Streptococcus pyogenes (GAS)
○ M protein allow it to bind to cell surface
● Appear as hair-like projections from the cell surface
● Mediates attachment of bacteria to epithelial cells of the host
● Many subtypes
○ Some more strongly associated with specific diseases than others
● More wide variety of adhesins → more type of tissues and organs it affects

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32
Q
  1. Glycocalyx
A

Well organized and firmly attached to cell wall → “capsule”

Unorganized and only loosely attached to the cell wall → “slime layer”

33
Q
  1. Glycocalyx: Unorganized and only loosely attached to the cell wall → “slime layer”
A

● Facilitates formation of biofilms
● Not restricted to organism that is producing it
○ Can also protect other organisms

34
Q
  1. Glycocalyx

Well organized and firmly attached to cell wall → “capsule”

A

● K1 capsule associated with some strains of Neisseria meningitidis type b
○ Leading cause of gram negative bacterial meningitis
● This adhesin binds to epithelial cells of the ventricles and vascular endothelium of the brain
○ Without adhesin → decreased opportunity to cause meningitis
● Causing meningitis

35
Q

Biofilms

A

● Colony of bacteria that adheres to surfaces (living and nonliving)
○ Organic → host tissues
○ Fomites → hard surfaces, inorganic material (those inside the host too)

36
Q

where are biofilms embedded?

A

in an extracellular slime layer

37
Q

biofilms surfaces include

A 
○	Teeth
○	Medical catheters
○	Heart valves
○	Hip replacement components
○	Contact lenses
○	Industrial food equipment
38
Q

t/f: biofilms are Highly resistant to disinfectants and antibiotics

A

true
○ This is why we are careful with hip, heart valve, or knee replacement
○ Put on antibiotic to prophylactically → protect against infection
○ Bacteria is able to enter the bloodstream and land on replaced knee, hip, or heart
○ Often pre-treat individuals that underwent implantation surgery

39
Q

t/f; biofilms May involve multiple bacterial species and consist of many layers

A

t/f: true ○ Bacteria producing slime layer + other bacteria

40
Q

t/f: biofilms do not shelter microorgansims from host denfences

A

false; ○ This is why they can be resistant to antibiotics

41
Q

t/f: there are many treatments able to penetrate the slime layer

A

false: very few antibiotics

42
Q

Enzymatic bacteriophages

A

● Uses bacterial cells to replicate
○ Does not like human host but LOVES bacteria
● Viruses that have capacity to produce enzymes that destroy slime layer
○ Use bacteria to replicate
○ Rupture bacteria when they want to get out of organism

43
Q

Evasion of Host Defences

A

● Exposed to microorganism

● Microorganism is able to bind to host cell tissues

44
Q

Cannot evade host defenses → aborted infections

A

● Immune cells clear us from microbes before we become symptomatic
● Infection has not occurred

45
Q

Capsule

A

facilitates microorganisms ability to evade host cell defenses
● Impairs phagocytosis
● Prevent phagocytic cell from adhering to the microbe
● Increasing virulence of the pathogen
● With time → host will produce antibodies against the capsule

46
Q

Cell wall

A 
●	M proteins increase virulence 
●	Helping bacteria resist phagocytosis 
○	WBC e.g. Streptococcus pyogenes
●	Mycolic acid present in the cell wall of Mycobacterium tuberculosis increases virulence 
○	Inhibits phagocytosis
○	Resists digestion by phagocytosis
○	Cannot be gram stained
○	Has to be acid fast stain
47
Q

Coagulase →

A

facilitates coagulation
● Coagulate fibrinogen in the blood to form fibrin
● Fibrin clot protects bacteria from phagocytosis
○ It will be protected within the hosts fibrin, platelets, etc
○ The body will think its one of its own
● Isolates the microbe from other defenses of the host
● Produced by some Staphylococci spp.
○ Round shaped
○ Gram positive → all staph are
○ Coagulase positive → More viral

48
Q

Coagulase positive →

A

More viral

49
Q

all staph are

A

○ Gram positive

50
Q

Kinase

A

● Degrades fibrin
● Digest clots formed by the body
● Isolate the wound and clots created by the bacteria as protection from phagocytosis

51
Q

Streptokinase produced by Streptococcus pyogenes

A

● Produce kinase to bust open clots
○ Helpful if they are living in clot
○ Helpful if they want to penetrate deeper into tissues
● Can digest and degrade healthy clots → increases fitness of microorganism
○ Get deeper into tissues

52
Q

Staphylokinase produced by Staphylococcus aureus

A

● Produce kinase to bust open clots

● Can digest and degrade healthy clots → increases fitness of microorganism

53
Q

Facultative intracellular bacteria are able to survive inside immune cells via the following mechanisms:

A

Neisserias:
● They don’t have to live in host cell to survive but if they can they will
● They can inhibit the effects of lysosome on their membrane

  1. Escaping phagosomes before fusing with host cell lysosomes
  2. Preventing phagosomes-lysosome fusion
  3. Reducing effectiveness of toxic compounds within lysosome
  4. Producing cell walls resistant to lysosomal proteases
54
Q

Penetration of Host Tissues

A

● Our tissues are sterile
● The deeper into tissue you go → fewer immune cells
● Less oxygen → advantageous to certain bacteria
● Goal is to get deeper

55
Q

Hyaluronidase

A

● Degrades hyaluronic acid
● Hyaluronic acid → polysaccharide that holds host cells together
○ Allows neighbouring epithelial cells to stick together
● Allows bacteria to penetrate deeper into host tissues
● Bacteria is sheltered from outermost surface of the skin

56
Q

Collagenase

A

● Degrades collagen fibers at the base of superficial tissues
○ Collagen acts as basement membrane for epithelial cells to adhere to
● Allows bacteria to move deeper into the host
● More oxygen poor and fewer immune cells the deeper you go

57
Q

Some bacteria enter host cells that are NOT phagocytic

A

● Make cells welcome them
● Produce invasins
● Allow bacteria to invade NON phagocytic cells
○ The epithelial cells of the intestines

58
Q

Penetration of tissues; advantages

A

● Abundance of nutrients
● Protected from immune system
● Partially protected from antibiotics

59
Q

Damage to Host Cells

A

If a pathogen is successful in evading the host immune response → host cell damage and disease results
● They want us to have symptoms
○ Vomit, cough, sneeze
○ They want to move onto and transmit to someone else
● May damage us to gain nutrients
○ They want our iron to grow and reproduce

60
Q

Host cell damage can occur via the following mechanisms:

A
  1. Appropriating host nutrients
  2. Causing direct damage to tissues surrounding site of invasion
  3. Producing toxins
  4. Inducing hypersensitivity reactions (allergy)
61
Q
  1. Appropriating host nutrients
A

● Iron is required for the growth of most pathogenic bacteria
● Iron is tightly bound to iron-transport proteins in humans
○ Hemoglobin
○ Tightly controlled in human body
● Low availability of iron produces a microbial iron deficiency

62
Q

Bacteria employ several strategies to obtain iron from host:

A

Siderophores
Direct binding to host iron-binding proteins
Producing toxins

63
Q
  1. Appropriating host nutrients: Siderophores
A

● Bind to iron more tightly than host iron-transport proteins
○ Have higher affinity to iron
● Iron-siderophore complex taken up by siderophore receptors on bacteria
● Bacteria has iron to grow and reproduce

64
Q
  1. Appropriating host nutrients: Direct binding to host iron-binding proteins
A

● Bacteria-iron complex

● Takes iron up itself

65
Q
  1. Appropriating host nutrients: Producing toxins
A

● Toxins cause damage directly to host cells
● Bacterial toxins kill host cells
● Release iron stores from host
● Pathogen acquires iron via receptor binding

66
Q
  1. Direct damage to tissues surrounding site of invasion
A

● Obligate intracellular bacteria → have to be in host cell to live
○ Cannot get nutrients for themselves
○ E.g. chlamydia
○ Once nutrients diminished = need to get out → cell lysis
○ This manifests as signs and symptoms
● Intracellular bacteria/viruses metabolize + multiply in host cells
● Host cell typically ruptures to facilitate their release
● This destroys host cell
● Once released, pathogens spread to other tissues in great numbers

67
Q
  1. Producing toxins
A

● Some pathogenic bacteria produce toxins
○ This directly affects normal activity in host cells
● Wide in variety

This alters normal metabolism of host cells:
●	Inhibit protein synthesis
●	Destroy blood cells and blood vessels
○	Toxin: hemolysin → RBC
●	Disrupt nervous system function
○	Toxin: neurotoxins
●	Directly affect and destroy whole cell
○	Cytotoxin
68
Q

Exotoxins

A

produced by bacteria that are gram positive and gram negative
● Directly damage host cell
○ Called a cytotoxin
● Actively synthesized by bacteria and released

69
Q

Endotoxins

A

only associated with gram negative bacteria
● Gram negative → lipid A polysaccharide
○ Intrinsic component of gram negative bacteria membrane
● Physically a part of gram negative outer membrane
● Occurs when cell is dividing
● Little bit of outer membrane tears off and little bit of endotoxin is released
● Also released when phagocyte engulfs gram negative bacteria and destroys it
○ Endotoxin will be released
● Prescribe antibiotic that destroys cell wall
○ Cause bacteria to lysis
○ Release endotoxin

70
Q

Exotoxins

A

● Produced inside some living pathogenic bacteria as a normal part of growth and metabolism
○ Intentions → cause damage to host tissues
● Secreted into the surrounding environment, or released during cell lysis
● Soluble in bodily fluids
○ Rapidly transported throughout host
○ Systemic infection
■ Dissolves so WELL into bodily fluids
○ Highly toxic in nature
○ Exposure can be fatal

71
Q

Diseases associated with exotoxin producing bacteria are caused by

A

the effect of the toxin on host cells, not the pathogen itself
● Ingestion/exposure to the toxin is sufficient to produce disease
● Not infection but the toxin that is causing the issue
● Consume toxin that the food made

72
Q

A - B Toxins

A

Consist of A & B polypeptides:

73
Q

Part A →

A

Active enzymatic component

● This will change how the cell functions

74
Q

Part B →

A

→ Binding component
● This will bind to the host cell
● Toxin will enter the host cell

75
Q

Exotoxins: Membrane disrupting toxins

A 
Induce cell lysis via:
●	Formation of protein channels
○	Leukocidins → WBC
○	Hemolysins → RBC
●	OR disruption of phospholipid layer of cell membrane 
○	Phospholipase 
○	Adverse effects for cell function
76
Q

Exotoxins: Superantigens

A 
associated with shock and DIC
Provoke an intense immune response
●	Not processed inside macrophages
●	They bind directly to MHC Class II proteins on macrophage surface
○	Directly activate T-cells
○	Does not need an intermediate to speak to T-cell
●	Results in excessive production of:
○	IL-2 → drives septic shock
○	TNF → drives septic shock
○	Tissue factor → drives DIC
77
Q

Superantigen causes

A 
●	Fever
●	Nausea and vomiting
●	Diarrhea
●	Shock 
●	Sometimes death
78
Q

t/f: Portals of exit are generally the same as the portals of entry

A 
true
●	Respiratory tract 
●	Gastrointestinal tract
●	Genitourinary tract
●	Skin, conjunctiva, blood, etc…
79
Q

Endotoxins (Lipid A)

A

● Released when Gram negative bacteria are killed (or multiply through budding)
○ Cell wall lysis
○ Releasing endotoxin
● Gram positives are not associated with endotoxins
○ They do not have outer membrane
● All are pathogen associated molecular patterns
○ Stimulate macrophages to release high concentrations of IL–1
○ We have aggressive reaction to lipid A
● All endotoxins produce the same signs and symptoms regardless of the pathogen
○ Common mechanism of action due to excessive IL-1
○ Chills
○ Fever
○ Weakness
○ Generalized aches
● Increased production of TF
○ Activates extrinsic & intrinsic coagulation cascade
○ Associated with DIC
○ Obstructive clots in capillaries, inducing tissue death
● Shock and death of the host in severe cases

Microbiology (7 decks)

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