L21: Host Parasite Relations

Question 1

Commensalism

Answer 1

A type of relationship that bacteria benefit from and host is not harmed from (ex. eating sloughed-off cells in the ear)

Question 2

Mutualism

Answer 2

A type of mutually beneficial relationship between bacteria and host (ex. colon bacteria)

Question 3

Parasitism

Answer 3

A type of relationship between bacteria and host where host is harmed (ex. tuberculosis)

Question 4

Niche

Answer 4

Physical spaces and nutrients in/around body where bacteria live

Question 5

Normal microbiota (flora)

Answer 5

Commensal or mutuant symbionts adapted to specific niches and avoid directly injuring the host

Question 6

Normal microbiota in the mouth

Answer 6

Strep, mitis, and other streptococci, Trichomonas tenax, Candida

Question 7

Normal microbiota in the nose

Answer 7

S. aureus, S. epidermidis, diphtheriods, streptococci

Question 8

Normal microbiota in the throat

Answer 8

S. viridans, S. pyogenes, S. pneumoniae, Neisseria, S. epidermidis, Heamophilus influenzae

Question 9

Normal microbiota in the lungs

Answer 9

Mostly sterile but might have pneumocystitis jiroveci

Question 10

Where is the most densely populated area of the body with bacteria?

Answer 10

GI system (mostly large intestine)

Question 11

Normal microbiota of fetus

Answer 11

Generally sterile

Question 12

Colonized sites of the body

Answer 12

Skin, mucosa, intestine, urogenital tract

Question 13

Parts of the body that are normally sterile

Answer 13

Internal organs and tissue, cervix, middle ear, urinary bladder (kind of)

Question 14

Resident microbiota

Answer 14

Long-term members of the body’s normal microbiota

Question 15

Transient microbiota

Answer 15

Organisms that attempt to colonize the body but are unable to remain due to competition from resident microbiota, elimination by the body’s immune system, or physical or chemical changes within the body that discourage growth

Question 16

Example of resident microbiota

Answer 16

S. epidermidis

Question 17

Example of transient microbiota

Answer 17

Group A Strep (GAS) – S. pyogenes

Question 18

Pathogens (2 types)

Answer 18

Any microorganism that has the capability to cause disease – strict or opportunistic

Question 19

Strict pathogens

Answer 19

Organisms always associated with disease (ex. Mycobacterium tuberculosis, N. gonorrhoeae, rabies)

Question 20

Opportunistic pathogens

Answer 20

Tend to be members of the normal microbiota that take advantage of preexisting conditions, such as immunosuppression to grow and cause disease.
(ex. E. coli, Candida albicans) – CAUSE MOST DISEASE

Question 21

Cause of contamination of intravenous catheters

Answer 21

S. epidermidis, S. aureus (MRSA)

Question 22

Cause of wound/surgical site infections

Answer 22

S. aureus, K. pneumoniae, Pseudomonas aeruginosa

Question 23

Cause of bacterial endocarditis

Answer 23

Streptococci viridans group

Question 24

Cause of aspiration pneumonia

Answer 24

Polymicrobial disease (mixed infection)

Question 25

Cause of urinary tract infections

Answer 25

E. coli (moving of E. coli from anus to urethra)

Question 26

Cause of psuedomembrane colitis

Answer 26

C. diff (overgrowth due to disruption of microbiota of colon by antibiotics)

Question 27

Cause of otitis media

Answer 27

S. pneumoniae, H. influenzae, and M. catarrhalis

Question 28

Pathogenicity

Answer 28

The ability of a microorganism to cause disease

Question 29

Virulence

Answer 29

A measurement of pathogenicity

Question 30

Virulence factors

Answer 30

Factors (e.g. toxins) produced by organisms that enable it to infect, cause disease, and/or kill a host

Question 31

Carrier

Answer 31

An asymptomatic individual who is host to a pathogen | Has the potential to transmit the pathogen to others (ex. GAS, Salmonella Typhi)

Question 32

#1 mode of transition of GI disease

Answer 32

Fecal --> oral route

Question 33

Other ways of entry into host

Answer 33

- -Transplacental (mother --> fetus) - -Secretions - -Skin (cuts) - -Blood (STIs, drugs) - -Zoonotic (animal --> human) - -Arthropod (reservoir/vector)

Question 34

Barriers against pathogen entry

Answer 34

- -Mechanical (skin, cilia) - -Enzymatic (lysozyme) - -Chemical (pH) - -Immunity - -Commensals (niche) - -Physical (showering, peristalsis)

Question 35

Adhesion

Answer 35

Binding of the bacterial adhesin to host cell surface (receptor); often associated with pili and define tropism

Question 36

Biofilms

Answer 36

Sessile (stationary) bacteria encased in a exopolymeric substance of their own making; found on surfaces that are commonly moist/wet

Question 37

Difference between biofilm cells and planktonic cells

Answer 37

- -Altered metabolism (slowed down generally) - -Increased resistance to antibiotics (due to slow metabolism) - -Increased genetic exchange increases likelihood of antibiotic resistance transfer - -Resistant to disinfection

Question 38

How does invasion into cells occur?

Answer 38

Bacteria hijack host cell machinery to facilitate uptake and can also modulate maturation of the phagosome to promote survival

Question 39

How does dissemination occur?

Answer 39

Some cause pathology due to toxin production, some cause disease from sites metastatic to original site of infection

Question 40

How do bacteria cause tissue destruction?

Answer 40

Byproducts of bacterial growth are often toxic to host cells and bacteria can secrete degradative enzymes (ex. Clostridium perfringens)

Question 41

Exotoxins

Answer 41

Bacterial products that directly harms tissue or lead to destructive biologic activities: cytolytic enzymes (hemolysins, pore forming toxins) and receptor binding proteins that initiate toxic reactions

Question 42

A-B subunit exotoxins (AB toxins)

Answer 42

A = active, B = binding; inhibit protein synthesis then cause hyperactivation --> increased cAMP (ex. cholera toxin)

Question 43

Other exotoxins

Answer 43

- -C. tetani inhibits inhibitory transmitters (spastic paralysis) - -C. botullinum blocks release of transmitters (paralysis)

Question 44

Superantigens

Answer 44

Bind both T-cell receptor and MHCII without a requiring antigen; activation of large numbers of T-cells = “cytokine storm” = life-threating autoimmune-like responses (S. aureus, S. enterotoxin, and S. pyogenes)

Question 45

Mechanisms for escaping host defenses

Answer 45

- -Encapsulation - -Antigenic mimicry - -Antigenic variation/shift - -Inactivation antibody - -Resistance to complement-mediated killing - -Escaping phagocytic clearance

Question 46

Encapsulation

Answer 46

Capsules are poorly antigenic and can mask antigens and prevent binding of antibody

Question 47

Antigenic mimicry

Answer 47

Bacteria can produce compounds the host sees as self (mimicking host) (ex. S. pyogenes and S. aureus)

Question 48

Antigenic variation/shift

Answer 48

Quickly changing the antigenic makeup of proteins on their cell surface to make a "moving" target for immune system (ex. N. gonorrhoeae type IV pili)

Question 49

Inactivation antibody

Answer 49

Secretion of proteases that degrade specific antibody isotypes (ex. IgA protease)

Question 50

Resistance to complement mediated killing

Answer 50

Limiting access to the membrane through capsule, long O-antigen on LPS; degradation of components of complement

Question 51

Escaping phagocytic clearance

Answer 51

- -Inhibit opsonization - -Inhibit chemotaxis - -Kill phagocyte - -Inhibit lysosomal fusion - -Escape from lysosome - -Resistant antibacterial lysosomal action

Question 52

Main form of regulation of virulence factors

Answer 52

Quorum sensing (way for bacteria to sense size of population using autoinducers -- can regulate gene expression in response to population size)