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Infectous Disease > Dr. Roane FQ EXAM 2 > Flashcards

Dr. Roane FQ EXAM 2 Flashcards

1
Q

What is considered the old quinolone?

A

Nalidixic acid

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2
Q

What is Nalidixic acid used for?

A

Simple UTI infections

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3
Q

What is the prototype of Fluoroquinolones?

A

Ciprofloxacain 2nd Gen (Cipro)

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4
Q

How are Fluoroquinolones diffrent from Quinolones?

A

Flourid-atom added to the core structure
-> Improvement in safety and efficacy

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5
Q

Spectrum activity of FQ

A

-Legionella, Salmonella, Shigella
-E. coli, Neisseria (gonorrhea) Proteus sp, Vibrio cholerae, Campylobacter jejuni

BUT IT CHANGES

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6
Q

Spectrum activity of FQ by generation

A

1st GEN: Gram (-) rods
2nd GEN: more Gram (-) rods, Gram (+) cocci, Mycoplasma and Chlamydia

3rd: retain gram (-) and Mycoplasma, Chlamydia; more specific gram (+) cocci

4th: retain gram (-), improves gram (+) cocci and bacilli, gains anaerobic coverage

JUST NEED TO KNOW: Coverage increases with GEN

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7
Q

How are Fluoroquinolones classified?

A

Older group: Ciprofloxacin, norfloxacin, and ofloxacin

Newer group (respiratory FQ): Gemifloxacin, levofloxacin, and moxifloxacin

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8
Q

Despite activity against resistant bacteria, what is the downside of FQ?

A

-variety of serious adverse effects causing multiple FQs to be withdrawn

-Grepafloxacin, Sparfloxacin, Trovafloxin, Gatifloxacin,…

-Delafloxacin (Baxdela): indicated for acute skin infections (ABSSSI) -> Blackbox warning: Tendinitis and tendon rupture, Peripheral neuropathy, CNS effects

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9
Q

What is the MOA for FQs?

A

-Binding and inhibiting DNA Gyrase (gram (-)) and topoisomerase IV (gram (+)) -> involved in unwinding DNA for replication

-Bacteriocidal

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10
Q

Where does FQ bind to inhibit the bacteria?

A

-it binds to the subunit GyrA

-The DNA Gyrase consists of the Gyr A and Gyr B subunit

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11
Q

How does the resistance of bacteria against FQ occur?

A

Ciprofloxacin binds to a specific acid -> after mutation it doesn’t bind anymore

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12
Q

Which serious disease is resistant to Ciprofloxacin?

A

Meningococcal disease caused by Ciprofloxacin-resistant N. gonorrhea (10-14% fatal)

-colonizes mucosal surfaces of the nasal pharynx -> transmitted through direct contact with the nasal secretion of infected patients

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13
Q

What is the MOA of Nitrofurantoin?

A

-When chemically reduced by bacteria, it forms highly reactive free radicals that cause DNA damage in microbes

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14
Q

Side effects of Nitrofurantoin

A

-Colors the urine brown
-Hemolytic anemia in pts. with glucose-6-phosphate dehydrogenase deficiency

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15
Q

Why might Nitrofurantoin cause harm to patients with G6PD deficiency?

A

-G6PD converts NADP+ to NADPH
-NADPH replenishes GSH (Glutathione)
GSSG (oxidized) to GSH (reduced)

-GSH is an Antioxidant which provides protection against free radicals, like those caused by Nitrofurantoin

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16
Q

MOA of Methenamine (hexamine)

A
  • At low pH in the urine Methenamine is converted to Formaldehyde -> antiseptic in the UTI (and analgesic) - no resistance against Formaldehyde

-Alternate use: topical for hyperhidrosis, antiperspirant, solid fuel for camping

17
Q

What is the consequence of DNA Replication ahead of the two replication folks?

A

-Supercoiling
-increased tension

18
Q

How is the tension relieved?

A

Topoisomerase I: cuts 1 strand -> passes the other strand through the cut -> reseals -> decrease in 1 twist on the supercoil

Topoisomerase 2: cuts 2 strands -> passes another double-strand to the cut -> reseal -> decrease in 2 twists on the supercoil

19
Q

Which bacterial enzymes is responsible for removing superhelical twist on the bacterial DNA?

A

DNA Gyrase (Topoisomerase II)

-also involved in the initiation of replication and transcription of many genes

20
Q

What does the bacterial DNA Gyrase consist of?

A

-2x Gyrase A subunits
-2x Gyrase B subunits

21
Q

What is the role of Topoisomerase IV?

A

Separating the new from the old semiconservative (1 old and 1 new strand) DNA helices

22
Q

MOA FQ Gyrase

A

-FQ binds to DNA Gyrase and Topoisomerase IV
-It stabilizes the Enzyme-DNA-complex -> breaks in the DNA -> cell death
-Interferes with DNA when binding to DNA Gyrase

23
Q

The Gyrase of which organisms are used as a target for FQ?

A

Gram-negative bacteria

24
Q

MOA FQ Topoisomerase IV

A

-In gram-positives (Staph, Strep) - Gyrase as the secondary target

-FQ disrupts the separation between the new and old DNA in the cell -> cell death

25
Q

What affects the potency and spectrum of activity of different FQs?

A

Affinity to DNA Gyrase and Topoisomerase IV or both

26
Q

How does bacteria require resistance?

A

-Mutations in chromosomal genes altering target enzymes DNA Gyrase and Topoisomerase IV

Frequency: 10^-6

27
Q

What are the factors that affect the activity of FQs after mutation?

A

Number of mutations, location of the mutations, and which of the enzymes is affected

28
Q

Where do mutations occur in Gyrases and Topoisomerase IV?

A

Gyrase: gyrA or gyrB genes
Topoisomerase IV: ParC or ParE gene

-> reduced affinity of FQ for the enzymes

29
Q

Why are FQ antibiotics with similar affinity and potency against both target enzymes beneficial?

A

Because mutation on both enzymes are required for resistance

30
Q

What kind of improvements were accomplished due to the addition of the Fluor atom to the quinolone structure?

A

-Potency
-Antimicrobial spectrum
-Pharmacokinetics
-Safety

31
Q

Spectrum of activity of Ciprofloxacin (oldest FQ)

A

Narrow mainly gram-negative

32
Q

The spectrum of activity of the “newer” FQ

A

-Gram-negative
-Gram-positive: Pneumo cocci
-atypical pathogens

->called respiratory FQ

33
Q

What are the respiratory FQs?

A

-Levofloxacin
-Gemifloxacin
-Moxifloxacin

34
Q

Common Clinical use of FQ

A

-Community-acquired pneumonia
-UTI -> compromised due to resistance (especially E.coli (most common for UTI)

Strep pneumonia
Haemophilus influenzae
Moraxella spp
atypical species

Infectous Disease (29 decks)

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