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Pharmacology (MPAS) > Lecture 18: Antibiotics 3 > Flashcards

Lecture 18: Antibiotics 3 Flashcards

1
Q

Antibiotics used in various conditions (ear, sinus, bronchitis, sore throat, colds)

A

See figure

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2
Q

Cause of symptoms of upper respiratory tract infections

A

Generally symptoms are caused by toxins released by pathogens and the inflammatory response to fight the infection

Nasal congestion, runny nose, sneezing, Sore throat, cough, Fever

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3
Q

Utility of antibiotics in upper respiratory tract infections

A

Majority of infections have a viral origin

Antibiotics are only used for bacterial infections

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4
Q

How can antibiotics be determined as necessary in upper respiratory tract infections?

A

Need confirmation of significant bacterial cultures in sputum

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5
Q

Infections of the respiratory tract that require antibiotics

A

Strept Throat: Penicillin or erythromycin in allergic patients

Pneumonia: Penicillin or erythromycin

Bacterial Sinusitis: Penicillin or flouroquinolones in allergic patients

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6
Q

Infections of the respiratory tract that do not require antibiotics

A

Croup: Acetaminophen for pain/fever relief and feed warm clear fluids

Acute Bronchitis: not recommended

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7
Q

How quickly are resistant strains discovered after new antibiotics are created?

A

Within a few years we’re identifying resistant strains.

Seems that due to better screening, we’re identifying resistant strains almost as soon as the antibiotics come on to market

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8
Q

Diseases that pose a serious threat due to antibiotic resistance

A

Carbopenem Resistant Enteritis (CRE)- Enterobacter

Vancomycin Resistant Enterococci

Tuberculosis- Mycobacterium tuberculosis

Skin infections(and septicemia)- Staphylococcus aureus (MRSA)

Food poisoning- C. difficile (Generally hospital acquired)

Sexually transmitted disease- Gonorrhea

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9
Q

Changing treatment of gonorrhoea due to antibiotic resistance

A

1950s: Treated with penicillin
1970s: Bacterial resistance to penicillin so treatment with tetracycline recommended
1993: Bacterial resistance to tetracycline so treatment changed to ciprofloxacin or cephalosporins
2007: Bacterial resistance to floroquinolones so only the oral cephalosporin (cefixime) is recommended
2015: Now combination therapy is recommended: injectable cephalosporin (ceftriaxone) + oral azithromycin

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10
Q

Antibiotics in food

A

Veterinary use of antibiotics leads to production of resistant bacteria

No oversight of antibiotics in animals

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11
Q

Causes of antibiotic resistance

A

Overuse/abuse of antibiotics in humans

Overuse/abuse of antibiotics in non-humans (veterinary populations)

Developing countries (don’t require prescription)

World travel (rapid spread)

Critically ill patients (patient 0’s)

Industry advertising/promoting

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12
Q

What increases the risk of antibiotic resistant infections?

A

Patient-related factors (Increasing age, Increasing severity of underlying disease)

Hospital-related factors (Increased length of stay, Admission to ICU, Proximity to infected patients)

Treatment-related factors (Prolonged use of broad spectrum antibiotics, Contaminated devices or procedures)

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13
Q

Hospital related spread of antibiotic resistance

A

See figure

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14
Q

Antibiotic use in developing countries

A

Antibiotics available OTC

Poor patient compliance (1-2 days)

Cost (take subtherapeutic course)

Antibiotic quality is low (counterfeit, adulterated, poor quality (potency))

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15
Q

Why are antibiotics used in animals?

A

Given to healthy animals to prevent development of infections

Use of antibiotics makes animals larger = more value

Kill off bacterium in gut, more food available to animal for growth

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16
Q

Genetics of antibiotic resistance

A

Spontaneous mutation

Acquisition of new DNA

17
Q

How do bacterial cells acquire new DNA?

A

Transformation: DNA comes from the environment after being released by another cell (plasmid DNA)

Transduction: Virus transfers DNA between bacteria

Conjugation: contact between cells as DNA crosses from

18
Q

What is the mechanism of acquired antibiotic resistance

A

Alteration in the target site

Decreased uptake

19
Q

What is the problem of beta lactamases?

A

Not long after the introduction of Pencillin, S. aureus developed beta- lactamases which inactivate beta-lactam drugs through cleavage of their central ring structure

20
Q

How do beta lactamases work?

A

They form an intermediate molecule with the antibiotic, and then water cleaves the bond

B lactam ring is cleaved

21
Q

How to overcome the problem with beta lactamases?

A

Develop inhibitors of beta lactamases (clavulanic acid)

Combine penicillin with the use of other antibiotics

Add bulkier side chains to the basic penicillin structure, hindering enzyme access to the B lactam ring beta lactam ring (second generation = methicillin)

22
Q

Mechanism of synergy with B lactamases

A

Combine beta lactamase inhibitor with B lactic antibiotics

23
Q

Mechanism of action of beta lactam + clavulanic acid

A

Usually, B lactamases sit on the outside of cell wall and breakdown penicillin. Allows bacteria to proliferate.

Clavulanic acid binds to the Beta lactamases, so penicillin can enter.

Antibiotic kills bacteria

24
Q

Mechanisms of resistance to tetracyclines

A

Decreased uptake or increased extrusion

Mg2+ dependent active efflux mediated by the TetA gene (most common)

Can also be bacterial enzymes that inactivate tetracyclines, or expression of bacterial proteins that inhibit binding of tetracycline to the ribosome

25
Q

Characteristics of tetracycline resistance

A

Widespread resistance limits clinical use

Bacteria usually have cross resistance

26
Q

Mechanisms of resistance to aminoglycosides

A

Decreased uptake of the drug: Absence of porin channels, absence of oxygen-dependent transport system

Enzymes that inactivate aminoglycosides: Acetyltransferases, Nucleotidyltransferases, Phosphotransferases

Cross-resistance is rare

27
Q

Mechanisms of resistance to macrolides

A

Decreased uptake of the drug

Increased efflux of the drug

Reduced affinity for the 50S ribosome subunit

Methylation of an adenine in the 23S bacterial
ribosomal RNA

Enzymes that inactivate macrolides: Erythromycin esterase

Cross-resistance is common

28
Q

Mechanisms of resistance to fluoroquinolones

A

Alterations to DNA gyrase

Decreased uptake

Increased efflux

29
Q

Problems related to resistance to fluoroquinolones

A

Resistance to flouroquinolones can evolve rapidly during
treatment

3-fold increase of flouroquinolone prescription in US emergency rooms

Half of these prescriptions for non-FDA approved uses such as: ear infections, acute respiratory illness, Widespread veterinary usage, Cross resistance among quinolones is common

30
Q

What organisms are resistant to ciprofloxacin?

A

S. aureus

S. pyogenes

Enterococci,

K. penumoniae

31
Q

What promoted resistance to ciprofloxacin?

A

Widespread use to treat minor infections and unapproved uses

Ear infections

Acute respiratory illness

Widespread veterinary usage

32
Q

What bacteria are inherently resistant to sulfonamides?

A

Bacteria that obtain floats from the environment

33
Q

What causes sulphonamide and trimethoprim resistance?

A

Sulfonamides: altered dihydropteroate synthase

Trimethoprim: altered dihydrofolate reductase

Reduced cellular permeability to drugs

Enhanced production of folates

34
Q

Prevalence of resistance to cotrimoxazole

A

Rare

bacteria must have simultaneous resistance to both the sulfonamide and trimethoprim drug

Emergence of antibiotic resistant bacteria has recently renewed interest in using cotrimoxazole

35
Q

What are some potential solutions to infections caused by resistant superbugs?

A

Knowledge about resistant infections

Infection control

Vaccination

Appropriate antibiotic use

Discover and develop new antibiotics

If treating a patient, treat as early as possible and kill the pathogen

Pharmacology (MPAS) (19 decks)

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