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Microbiology > Commensalism vs Pathogenicity > Flashcards

Commensalism vs Pathogenicity Flashcards

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Biology 101 flashcards
1
Q

What is mutalism?

A

Both organism 1 and 2 benefit

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2
Q

What is commensalism?

A

Organism 1 benefits, nothing happens to organism 2

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3
Q

What is parasitism?

A

Organism 1 benefits, organism 2 is harmed

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4
Q

Most of our normal flora are what type of -ism?

A

Commensalisms

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5
Q

What commensalism are found on our skin?

A

Gram + cocci and yeast such as; S.epidermidis, C.albicans, S.aeuros - Stay commensalism’s if kept in proper compartment (outside of skin)

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6
Q

Opportunistic infections?

A

Organism that were not harmful, become pathogenic if the opportunity presents itself.

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7
Q

Ex of opportunistic infection on skin?

A

S.aeuros can cause a wound INFECTION in an injured person

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8
Q

Commensalism’s found in Nose/Throat?

A

Strep, Staph, Neisseria - Stay commensalism’s as long as kept in proper compartments AND person is immunocompetant

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9
Q

Ex of opportunistic infection in Nose/Throat

A

If Neisseria gets into the blood stream (outside of its compartment) it can cause meningitis in an unvaccinated person (non-immunocompetant–>immunosupressed)

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10
Q

Commensalism’s found in Mouth?

A

Actinomyces, Kingella kingae

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11
Q

Ex of opportunistic infection in Mouth? #1

A

Actinomycosis - if actinomyces escapes oral cavity into jay/lymph-nodes–> formation of a “benign tumor”

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12
Q

Ex of opportunistic infection in Mouth? #2

A

HACEK endocarditis - caused when a group of organisms from the mouth enters the blood stream and causes heart valve problems

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13
Q

Commensalism’s found in GI track?

A

Large #! - Stay commensalism’s as long as kept in proper compartment AND the balance of microorganisms is correct (Antibiotics can thrown the #’s off)

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14
Q

Opportunistic infections in GI track?

A

Sepsis following colonic rupture.
Pseudomembranous colitis - gut obstruction, do to course of abs (overgrowth of certain bacteria causes this(
Antibiotics present - throw of flora –> diareah

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15
Q

Microorganism in Vagina?

A

Symbiote - Lactobacillus

Commensalism - Candida

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16
Q

What is colonization resistance?

A

A form of symbiosis in which even commensals can participate in

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17
Q

Steps in colonization of new bacteria

A

New bacteria introduced–>either colonizes or doesn’t
If is doesn’t colonize –> the PATHOGEN or non-pathogen is cleared
If colonizes –> and is non-pathogenic it becomes commensalism, but if it is pathogenic it will cause a disease
If the pathogen causes a disease –> it can kill the host OR the host becomes chronic carrier OR host kills pathogen

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18
Q

How would a pathogen (which did not colonize) be cleared?

A

Role of colonization resistance

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19
Q

How does colonization resistance work?

A

There is other bacteria (harmless) taking up space, that the new bacteria (harmful) needs in order to reproduce and survive. The pathogen must be very pathogenic in order to outcompete present bacteria.

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20
Q

What is a non-pathogen?

A

Very unlikely to cause disease
Most environmental bacteria and the normal flora are non-pathogenic
Very low virulence –> LD 50 - very high, ID 50 - high

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21
Q

What is a opportunistic pathogen?

A

Unlikely to cause disease in a healthy individual
Will take advantage of injury or immunosuppression (age-infant an the ealrderly)
Low virulance –> LD 50 - high, ID 50 - mid-low

22
Q

Ex of opportunistic infections?

A

Legionella, Pseudomonas, Enterobacter

23
Q

What is a pathogen?

A

Readily causes disease in previously healthy individual

Mid-High virulance –> LD 50 mid-low, ID 50 low

24
Q

Ex of pathogens?

A

N. gonorrheae, Shigella, Norwalk Virus

25
Q

What is ID?

A

Infectious dose - # of bacteria needed to cause colonization

26
Q

What is LD?

A

Lethal dose - # of bacteria needed to kill an individual

27
Q

What is virulence?

A

description of pathogenicity, how much is needed to cause disease

28
Q

What are virulence factors?

A

Genes found empirically to be determinants of pathogenicity

29
Q

What do virulence factors help with?

A 
Survive extreme environments
Adhesion
Immune evasion
Host cell takeover
Poison the host
30
Q

What are some virulence factors that help pathogens survive extreme environments

A

pH tolerance, siderophores, resistance to drying, resistance to detergents

31
Q

What are some virulence factors that help pathogens adhere?

A

Pili/Fimbrae/Curil - specific/non-specific
Slime Layer - non-specific
Adhesins - specific

32
Q

What are some virulence factors that help pathogens with immune evasion?

A 
Capsule
IgA protease
Macrophage Apoptosis Inducers
Antigenic Variation
Serum Resistance
33
Q

What are some virulence factors that help pathogens take over the host cell?

A

Endosome Escape Routes
Actin Polymerization Pathways
T3SS/T4SS

34
Q

What are some virulence factors that help pathogens poison the host?

A

Tissue-Degrading Enzymes
Endotoxins - part of bacteria
Extotoxins

35
Q

What are EXOtoxins?

A

Are polypeptides that are either secreted from the cell or injected by T3SS.
The most TOXIC substances known

36
Q

What are some common toxic strategies used by exotoxins?

A

Superantigenicity
Interference with signal transduction
Depolymerization of actin

37
Q

What is A-B subunit? What is it used for?

A

Several exotoxins have a similar A-B Subunit Structure.

B delivers A to site of A’s toxic activity – one common activity for A is ADP-ribosylation

38
Q

Are exotoxins heat liable?

A

Yes. The heat unfolds them, and have a hard time refolding (inactive toxins). Useful for vaccines

39
Q

What are superantigen exotoxins? Superantigenicity

A

Undermine specificity of immune response (25% instead of 0.0001-0.001%)
Can cause shock or multiple organ failure

40
Q

What are some common bacteria that cause Superantigenicity?

A

Staph aureus
Strep pyogenes
Both cause TOXIC SHOCK SYNDROME

41
Q

What mechanism do gut bacteria Cholera, E.coli and B. cereus toxins use?

A

Increase adenylate cyclase activity

Causing fluid and electrolyte loss

42
Q

What do C. difficile toxins A and B do?

A

Glucosylate Rho GTPase–> leads ti depolymerization of actin, apoptosis, and a major inflammatory response in the gut

43
Q

What does Diphtheria Toxin do?

A

Tox gene encoded by lysogenic bacteriophage

Look up what it does??

44
Q

What does MRSA OV leukocidin do?

A

Forms pores in cell membranes –> lysis

PVL genes are phage born

45
Q

What is Koch’s Postulate?

A

Is a way to determine that a certain pathogen causes a certain disease.

46
Q

What are the steps to Koch’s Postulate?

A 
Observe pathogen in sick animal
Grow pure culture of pathogen
Infect new animal from pure culture
Observe same disease in new animal
Obtain pure culture of same pathogen from new animal
47
Q

What are the steps from Illness to Recovery?

A 
Infection
Incubation Period
Prodrome
Specific-Illness Period
Recovery/Covalescence
48
Q

What makes up the infection step?

A

Pathogen Defeats Innate Immunity for Successful Colonization

49
Q

What makes up the incubation period?

A

Microbial numbers too low to produce symptoms, most rapid growth

50
Q

What makes up the prodrome period?

A

Nonspecific immunogenic symptoms as adaptive immunity is raised: fever, fatigue

51
Q

What makes up the specific illness period?

A

Pathogen-Mediated symptoms emerge as large numbers of pathogens express virulence factors

52
Q

What makes up the recovery/covalescence?

A

Immune system gains upper hand and dramatically reduces pathogen numbers; patient begins to regain strength

Microbiology (10 decks)

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