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CELS191 > Microbes and Disease (L35-37) > Flashcards

Microbes and Disease (L35-37) Flashcards

1
Q

what is selective toxicity?

A

antimicrobials have selective toxicity which means it kills microbial cells but not host cells

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2
Q

why are organisms such as fungi, protozoa, and helminths harder to treat?

A

because they are eukaryotes, this means they have cells that are more similar to our own cells and antimicrobials are selectively toxic by exploiting the differences between our cells and microbes

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3
Q

what is an antibiotic?

A

a substance produced by a microorganism that inhibits the growth of and kills other microorganisms

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4
Q

what are the 3 effects that antimicrobials have on bacteria?

A 
- bacteriostatic
stop growth
- bacteriocidal
kill cells
- bacteriolytic
destroy cells
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5
Q

what is the clinical outcome of bacteriostasis? (ie-what happens to the number of total and living cells)

A

number of total and living cells remain the same but plateau after the effect of the antimicrobial has taken place

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6
Q

what is the effect on the number of total and living cells after bacteriocide has affected bacteria?

A

the number of total cells remains constant, the number of living cells declines to zero

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7
Q

effect on number of total and living cells after bacteriolysis has affected bacteria?

A

both the total number of cells and the number of living cells declines to 0

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8
Q

what are the targets for antibacterials? (6)

A
  • cell wall
  • cytoplasmic membrane (toxic)
  • protein synthesis
  • metabolic pathway
  • DNA synthesis
  • RNA synthesis
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9
Q

how does penicillin work?

A

it targets the synthesis of peptidoglycan in bacteria by inhibiting transpeptidation: the beta-lactam ring interacts with transpeptidase to inhibit it

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10
Q

what are the mechanisms for antibiotic resistance? (4)

A
  • degrade antibiotic enzymatically
  • change the function of the antibiotic (change target)
  • change the uptake of the antibiotic
  • change the efflux potential of the cell
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11
Q

describe how antibiotic resistance has developed against penicillin (4)

A
  • evolve penicillinase
  • mutate penicillin binding proteins
  • alter porins
  • efflux pumps
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12
Q

how does producing penicillinase stop the effect of penicillin?

A

destroys beta-lactam ring which is how penicillin interacts with transpeptidase

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13
Q

how does altering the penicillin binding proteins stop the antibiotic effect of penicillin?

A

penicillin binding proteins are the targets penicillin interacts with in the cell

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14
Q

how does altering porins affect penicillin function in cells?

A

prevent the uptake of antibiotics which prevents the penicillin from functioning

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15
Q

how do efflux pumps stop the effect of penicillin in cells?

A

they expel antibiotics as soon as they enter the cytoplasm of the cell - no retention of antibiotic = can’t function

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16
Q

what are porins?

A

polymeric structures on the cell walls of Gram (-) bacteria

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17
Q

what bacteria transfers genetic material via conjugation?

A

N. meningitis

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18
Q

what bacteria transfers genetic material via transformation?

A

Str. Pneumoniae

H. influenzae

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19
Q

what bacteria transfers genetic material via transduction?

A

S. aureus

20
Q

how to prevent antibiotic resistance from developing?

A
  • choose right antibiotic
  • use sufficiently high concentration
  • treat for reasonable period
  • complete therapeutic period
  • if chronic infection, treat with multiple antibiotics
  • avoid introducing antibiotics to environment
21
Q

what are Koch’s postulates?

A
  • must be able to identify organism in all individuals who have the disease
  • must be able to grow the organism from all diseased individuals
  • must show that organism is transmissible
  • same organism must be re-isolated from diseased experimental host
22
Q

what are the exceptions to Koch’s postulates? examples and reasons why (5)

A
  • can’t be done in humans due to ethics
  • can’t prove for diseases such as leprosy because cant culture in lab
  • cant prove for diseases such as syphilis because cant grow or isolate it
  • some diseases are complex and caused my multiple organisms such as liver cancer
  • diseases where normal bacteria become pathogens such as E. coli
23
Q

how do modern diagnostics work to prove that an organism causes a specific disease?

A

need to have primers for the two ends of the gene to identify the organism
if gene is present, will multiply the gene

24
Q

what are the two terms used to describe diseases caused by virulent organisms? what do they mean?

A
  • pathogenicity
    ability to cause disease (damage to tissues)
  • virulence
    ability to infect and cause disease (spread through a population)
25
Q

name the classes of bacterial virulence factors

A
  • adhesins
  • siderophores
  • capsules
  • endotoxins
  • exotoxins
26
Q

what is the function of adhesins? examples?

A 
allow organisms to attach to host cell (vital if wanting to cause infection) 
physical or chemical adhesins
e.g- N. meningitidis
N.. gonorrhoea
pathogenic E. coli
27
Q

function of siderophores and give examples

A

bind iron

e.g. Mycobacterium tuberculosis

28
Q

what is the function of capsules? give examples

A

allow bacterium to resist phagocytosis
e.g. Streptococcus pneumoniae
haemophilus influenza
N. menigitidis

29
Q

are endotoxins found in Gram (-) or Gram (+) bacteria?

A

they are endogenous and produced by Gram (-) bacteria

30
Q

what are endotoxins? (ie- molecule)

A

lipopolysaccharides

31
Q

why do bacteria need siderophores?

A

because they need iron to survive and our tissues have low iron content

32
Q

what are exotoxins? (ie- molecule)

A

proteins

33
Q

what type of bacteria are exotoxins produced by?

A

are exogenous and produced by Gram (+) bacteria

34
Q

what is the antigen strength of endotoxins? what does this mean for our immune system?

A
  • endotoxins are poor antigens

this means they are poor at stimulating the immune system so it is hard to generate protective response against them

35
Q

what is the heat tolerance of endotoxins? why?

A

they are heat stable

this is because they are lipopolysaccharides

36
Q

what is the effect of endotoxins in our body? (ie- their function)

A

they cause fever and inflammation

37
Q

what is the strength of endotoxins?

A

they are weak toxins meaning they wont kill you

38
Q

what is are the structures of endotoxins like?

A

they have similar structures

39
Q

what is the antigen strength of exotoxins?

A

they are immunogenic - good stimulants for immune system

40
Q

what is the heat tolerance of exotoxins? what is the term for this?

A

they are not tolerant to heat: heat labile - they are susceptible to denature in heat
this is because they are proteins

41
Q

how toxic are exotoxins?

A

they are potent toxins (fatal) and have neurotoxic/cytotoxic effect
they usually cause specific effects which affect your immune system or other systems like neurologic system

42
Q

what are the structures of exotoxins like? what does this mean in the immune system?

A

they have variable structures which allows the immune system to individually recognise them

43
Q

what is normal microflora?

A

the bacteria that are found in or on our body on a semi-permanent basis without causing disease

44
Q

what are opportunistic pathogens?

A

commensal bacteria that are part of the normal microflora that become harmful under changed conditions

45
Q

what are some causes for opportunistic infections to occur?

A
  • immune suppresed
  • depletion of normal microflora
  • displacement of normal microflora
46
Q

what is the major structural difference between Gram (+) and Gram (-) bacteria?

A

Gram (+) bacteria have a thick peptidoglycan cell wall whereas Gram (-) have low murein because they have a thin layer of peptidoglycan separating their inner and outer membranes

47
Q

what are some examples of exotoxins?

A
  • straphylococcus aureus
    localised infection of skin and pus
  • streptococci
    non-localised infection

CELS191 (3 decks)

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