Module 9 12 Part 3

Question 1

Question

Answer 1

Answer

Question 2

Q: What are the two main types of bacterial resistance to antibiotics?

Answer 2

A: Bacterial resistance to antibiotics can be innate (natural and inborn) or acquired over time.

Question 3

Q: What is the focus of this discussion regarding bacterial resistance?

Answer 3

A: This discussion primarily concentrates on acquired resistance, which is a more significant clinical concern than innate resistance.

Question 4

Q: How can bacteria develop acquired resistance to antibiotics, and what are the consequences?

Answer 4

A: Bacteria can become less susceptible or lose sensitivity to antibiotics over time, and in some cases, they can develop resistance to multiple drugs. This acquired resistance can make currently effective antibiotics ineffective, leading to a clinical crisis and a continuous need for new antimicrobial agents.

Question 5

Q: What are the typical outcomes associated with antibiotic resistance?

Answer 5

A: Antibiotic resistance is often linked to prolonged hospitalization, increased morbidity (illness), and higher mortality rates.

Question 6

Q: Which bacterial species are currently posing significant problems in terms of drug resistance?

Answer 6

A: Bacteria for which drug resistance is a serious concern include Enterococcus faecium, Staphylococcus aureus, Enterobacter species, Pseudomonas aeruginosa, Acinetobacter baumannii, Klebsiella species, and Clostridiodies difficile (C. difficile).

Question 7

Q: Are there any specific resistant bacteria discussed in more detail in separate chapters, and if so, which chapters cover them?

Answer 7

A: Yes, two specific resistant bacteria, methicillin-resistant Staphylococcus aureus (MRSA) and Clostridiodies difficile (C. difficile), are discussed in more detail in separate chapters, specifically Chapters 71 and 72.

Question 8

Q: Which bacterial species have developed resistance to antibiotics, and what are the alternative treatment options for them?

Answer 8

A: Highly resistant bacteria include Enterococcus faecium, Staphylococcus aureus, Enterobacter species, Klebsiella species, Pseudomonas aeruginosa, Acinetobacter baumannii, and Clostridiodies difficile. Alternative treatments for these resistant bacteria vary and may include different antibiotics or combinations.

Question 9

Q: What are some resistance mechanisms of Enterococcus faecium and their alternative treatments?

Answer 9

A: Enterococcus faecium may be resistant to ampicillin (mutation and overexpression of PBP5), linezolid (production of altered 23S ribosomes), daptomycin (unknown mechanism), and quinupristin/dalfopristin (production of inactivating enzymes and alteration of drug target). Alternative treatments include quinupristin/dalfopristin, daptomycin, tigecycline, linezolid, and more, depending on the specific resistance.

Question 10

Q: What are the resistance mechanisms of Staphylococcus aureus and their alternative treatments?

Answer 10

A: Staphylococcus aureus may be resistant to vancomycin (thickening of cell wall and altered cell wall precursor molecules), daptomycin (altered cell wall and cell membrane), and linezolid (production of altered 23S ribosomes). Alternative treatments include quinupristin/dalfopristin, daptomycin, tigecycline, linezolid, telavancin, ceftobiprole, and ceftaroline.

Question 11

Q: What is the main focus of the discussion in this section regarding microbial drug resistance?

Answer 11

A: The focus is on understanding how microorganisms, particularly bacteria, develop resistance to antimicrobial drugs, as opposed to the patients themselves becoming resistant.

Question 12

Q: What are the key topics covered in this section?

Answer 12

A: The section explores the mechanisms by which microbes acquire drug resistance and strategies to delay the emergence of resistance.

Question 13

Q: What is the main focus of the discussion in this section regarding microbial drug resistance?

Answer 13

A: The focus is on understanding how microorganisms, particularly bacteria, develop resistance to antimicrobial drugs, as opposed to the patients themselves becoming resistant.

Question 14

Q: What are the key topics covered in this section?

Answer 14

A: The section explores the mechanisms by which microbes acquire drug resistance and strategies to delay the emergence of resistance.

Question 15

Q: What are the four basic mechanisms that microbes use to resist antimicrobial drugs?

Answer 15

A: Microbes can resist antimicrobial drugs by employing mechanisms such as decreasing drug concentration at the site of action, altering the structure of drug target molecules, producing drug antagonists, and causing drug inactivation.

Question 16

Q: Where is the typical site of action for most antimicrobial drugs in microbes?

Answer 16

A: The site of action for most antimicrobial drugs is intracellular, within microbial cells.

Question 17

Q: How can microbes resist antimicrobial drugs that act intracellularly, and what are the two basic mechanisms involved?

Answer 17

A: Microbes can resist these drugs by either ceasing the active uptake of certain drugs (e.g., tetracyclines and gentamicin) or by increasing the active export of specific drugs (e.g., tetracyclines, fluoroquinolones, and macrolides).

Question 18

Q: Why can resistance to antibiotics develop in bacteria?

Answer 18

A: Resistance to antibiotics can develop in bacteria when the structure of the target molecule, with which the antibiotic interacts to produce its effects, is altered.

Question 19

Q: Can you provide an example of antibiotic resistance due to structural changes in the target molecule?

Answer 19

A: Yes, some bacteria are resistant to streptomycin because they have undergone structural changes in their ribosomes, which are the sites where streptomycin acts to inhibit protein synthesis.

Question 20

Q: Can microbes produce compounds that antagonize the actions of drugs, and can you provide an example?

Answer 20

A: Yes, in rare cases, microbes can synthesize compounds that counteract the actions of drugs. For instance, some bacteria can increase the production of PABA, which results in resistance to sulfonamides, a type of antibiotic.

Question 21

Q: How can microbes develop resistance to antibiotics, and what is one example of this mechanism?

Answer 21

A: Microbes can develop resistance by producing enzymes that metabolize or inactivate antibiotics. For instance, some bacteria have developed resistance to penicillin G by producing increased levels of penicillinase, an enzyme that deactivates penicillin.

Question 22

Q: Are bacterial enzymes limited to inactivating penicillin, or can they affect other types of antibiotics as well?

Answer 22

A: Bacterial enzymes are not limited to inactivating penicillin; they can also inactivate other classes of antibiotics, including cephalosporins, carbapenems, and fluoroquinolones.

Question 23

Q: What is the significance of the NDM-1 gene in terms of drug resistance?

Answer 23

A: The NDM-1 gene confers extensive drug resistance by producing a powerful form of β-lactamase, which can inactivate a wide range of antibiotics containing a β-lactam ring.

Question 24

Q: Which antibiotics are affected by the β-lactamase produced by the NDM-1 gene?

Answer 24

A: The β-lactamase produced by NDM-1 can inactivate almost all β-lactam antibiotics, which include penicillins, cephalosporins, and carbapenems.

Question 25

Q: Why is the NDM-1 gene concerning, and how is it classified?

Answer 25

A: The NDM-1 gene is concerning because it is resistant to carbapenems, and organisms carrying this gene are classified as carbapenem-resistant Enterobacteriaceae (CRE).

Question 26

Q: What other resistance determinants are typically found along with the NDM-1 gene in the same DNA segment?

Answer 26

A: The DNA segment containing the NDM-1 gene often contains genes for resistance determinants, including drug efflux pumps and enzymes that can inactivate antibiotics like erythromycin, rifampin, chloramphenicol, and fluoroquinolones.

Question 27

Q: Where are these resistance genes typically located, and what is their significance?

Answer 27

A: These resistance genes are located on a plasmid, which is a mobile piece of DNA that can be easily transferred between bacteria. This transferability is significant because it can spread drug resistance to other bacteria.

Question 28

Q: Which antibiotics are NDM-1-carrying bacteria typically resistant to, and are there any exceptions?

Answer 28

A: Bacteria carrying the NDM-1 gene are usually resistant to nearly all antibiotics, with exceptions like tigecycline and colistin.

Question 29

Q: In which bacterium was NDM-1 first discovered, and in which other common bacteria has it been found?

Answer 29

A: NDM-1 was initially discovered in Klebsiella pneumoniae in 2008 and has since been found in other common enteric bacteria, including Escherichia coli, Enterobacter, Salmonella species, Citrobacter freundii, Providencia rettgeri, and Morganella morganii.