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Microbiology > L21: Host Parasite Relations > Flashcards

L21: Host Parasite Relations Flashcards

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Biology 101 flashcards
1
Q

Commensalism

A

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

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2
Q

Mutualism

A

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

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3
Q

Parasitism

A

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

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4
Q

Niche

A

Physical spaces and nutrients in/around body where bacteria live

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5
Q

Normal microbiota (flora)

A

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

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6
Q

Normal microbiota in the mouth

A

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

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7
Q

Normal microbiota in the nose

A

S. aureus, S. epidermidis, diphtheriods, streptococci

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8
Q

Normal microbiota in the throat

A

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

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9
Q

Normal microbiota in the lungs

A

Mostly sterile but might have pneumocystitis jiroveci

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10
Q

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

A

GI system (mostly large intestine)

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11
Q

Normal microbiota of fetus

A

Generally sterile

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12
Q

Colonized sites of the body

A

Skin, mucosa, intestine, urogenital tract

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13
Q

Parts of the body that are normally sterile

A

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

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14
Q

Resident microbiota

A

Long-term members of the body’s normal microbiota

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15
Q

Transient microbiota

A

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

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16
Q

Example of resident microbiota

A

S. epidermidis

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17
Q

Example of transient microbiota

A

Group A Strep (GAS) – S. pyogenes

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18
Q

Pathogens (2 types)

A

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

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19
Q

Strict pathogens

A

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

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20
Q

Opportunistic pathogens

A

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

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21
Q

Cause of contamination of intravenous catheters

A

S. epidermidis, S. aureus (MRSA)

22
Q

Cause of wound/surgical site infections

A

S. aureus, K. pneumoniae, Pseudomonas aeruginosa

23
Q

Cause of bacterial endocarditis

A

Streptococci viridans group

24
Q

Cause of aspiration pneumonia

A

Polymicrobial disease (mixed infection)

25
Q

Cause of urinary tract infections

A

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

26
Q

Cause of psuedomembrane colitis

A

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

27
Q

Cause of otitis media

A

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

28
Q

Pathogenicity

A

The ability of a microorganism to cause disease

29
Q

Virulence

A

A measurement of pathogenicity

30
Q

Virulence factors

A

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

31
Q

Carrier

A

An asymptomatic individual who is host to a pathogen

Has the potential to transmit the pathogen to others (ex. GAS, Salmonella Typhi)

32
Q

1 mode of transition of GI disease

A

Fecal –> oral route

33
Q

Other ways of entry into host

A
  • -Transplacental (mother –> fetus)
  • -Secretions
  • -Skin (cuts)
  • -Blood (STIs, drugs)
  • -Zoonotic (animal –> human)
  • -Arthropod (reservoir/vector)
34
Q

Barriers against pathogen entry

A
  • -Mechanical (skin, cilia)
  • -Enzymatic (lysozyme)
  • -Chemical (pH)
  • -Immunity
  • -Commensals (niche)
  • -Physical (showering, peristalsis)
35
Q

Adhesion

A

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

36
Q

Biofilms

A

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

37
Q

Difference between biofilm cells and planktonic cells

A
  • -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
38
Q

How does invasion into cells occur?

A

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

39
Q

How does dissemination occur?

A

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

40
Q

How do bacteria cause tissue destruction?

A

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

41
Q

Exotoxins

A

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

42
Q

A-B subunit exotoxins (AB toxins)

A

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

43
Q

Other exotoxins

A
  • -C. tetani inhibits inhibitory transmitters (spastic paralysis)
  • -C. botullinum blocks release of transmitters (paralysis)
44
Q

Superantigens

A

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)

45
Q

Mechanisms for escaping host defenses

A
  • -Encapsulation
  • -Antigenic mimicry
  • -Antigenic variation/shift
  • -Inactivation antibody
  • -Resistance to complement-mediated killing
  • -Escaping phagocytic clearance
46
Q

Encapsulation

A

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

47
Q

Antigenic mimicry

A

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

48
Q

Antigenic variation/shift

A

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)

49
Q

Inactivation antibody

A

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

50
Q

Resistance to complement mediated killing

A

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

51
Q

Escaping phagocytic clearance

A
  • -Inhibit opsonization
  • -Inhibit chemotaxis
  • -Kill phagocyte
  • -Inhibit lysosomal fusion
  • -Escape from lysosome
  • -Resistant antibacterial lysosomal action
52
Q

Main form of regulation of virulence factors

A

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

Microbiology (20 decks)

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