Microbes and Disease (L35-37)

Question 1

what is selective toxicity?

Answer 1

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

Question 2

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

Answer 2

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

Question 3

what is an antibiotic?

Answer 3

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

Question 4

what are the 3 effects that antimicrobials have on bacteria?

Answer 4

- bacteriostatic
stop growth
- bacteriocidal
kill cells
- bacteriolytic
destroy cells

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

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

Answer 7

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

Question 8

what are the targets for antibacterials? (6)

Answer 8

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

Question 9

how does penicillin work?

Answer 9

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

Question 10

what are the mechanisms for antibiotic resistance? (4)

Answer 10

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

Question 11

describe how antibiotic resistance has developed against penicillin (4)

Answer 11

• evolve penicillinase
• mutate penicillin binding proteins
• alter porins
• efflux pumps

Question 12

how does producing penicillinase stop the effect of penicillin?

Answer 12

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

Question 13

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

Answer 13

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

Question 14

how does altering porins affect penicillin function in cells?

Answer 14

prevent the uptake of antibiotics which prevents the penicillin from functioning

Question 15

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

Answer 15

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

Question 16

what are porins?

Answer 16

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

Question 17

what bacteria transfers genetic material via conjugation?

Answer 17

N. meningitis

Question 18

what bacteria transfers genetic material via transformation?

Answer 18

Str. Pneumoniae

H. influenzae

Question 19

what bacteria transfers genetic material via transduction?

Answer 19

S. aureus

Question 20

how to prevent antibiotic resistance from developing?

Answer 20

• 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

Question 21

what are Koch’s postulates?

Answer 21

• 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

Question 22

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

Answer 22

• 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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

name the classes of bacterial virulence factors

Answer 25

- adhesins - siderophores - capsules - endotoxins - exotoxins

Question 26

what is the function of adhesins? examples?

Answer 26

``` 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 ```

Question 27

function of siderophores and give examples

Answer 27

bind iron | e.g. Mycobacterium tuberculosis

Question 28

what is the function of capsules? give examples

Answer 28

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

Question 29

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

Answer 29

they are endogenous and produced by Gram (-) bacteria

Question 30

what are endotoxins? (ie- molecule)

Answer 30

lipopolysaccharides

Question 31

why do bacteria need siderophores?

Answer 31

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

Question 32

what are exotoxins? (ie- molecule)

Answer 32

proteins

Question 33

what type of bacteria are exotoxins produced by?

Answer 33

are exogenous and produced by Gram (+) bacteria

Question 34

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

Answer 34

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

Question 35

what is the heat tolerance of endotoxins? why?

Answer 35

they are heat stable | this is because they are lipopolysaccharides

Question 36

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

Answer 36

they cause fever and inflammation

Question 37

what is the strength of endotoxins?

Answer 37

they are weak toxins meaning they wont kill you

Question 38

what is are the structures of endotoxins like?

Answer 38

they have similar structures

Question 39

what is the antigen strength of exotoxins?

Answer 39

they are immunogenic - good stimulants for immune system

Question 40

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

Answer 40

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

Question 41

how toxic are exotoxins?

Answer 41

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

Question 42

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

Answer 42

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

Question 43

what is normal microflora?

Answer 43

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

Question 44

what are opportunistic pathogens?

Answer 44

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

Question 45

what are some causes for opportunistic infections to occur?

Answer 45

- immune suppresed - depletion of normal microflora - displacement of normal microflora

Question 46

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

Answer 46

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

Question 47

what are some examples of exotoxins?

Answer 47

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