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(UNI) Chemotherapy & Selective Toxicity (3rd Year) > Anti-Mycobacterials > Flashcards

Anti-Mycobacterials Flashcards

1
Q

What is the causative agent of tuberculosis in humans?

A

Mycobacterium tuberculosis.

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2
Q

What is the causative agent of tuberculosis in cows and rarely humans?

A

Mycobacterium bovis.

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3
Q

What causes a TB like condition especially prevalent in AIDS patients?

A

Mycobacterium avium-intracellulare.

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4
Q

What is the causative agent of leprosy?

A

Mycobacterium leprae.

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5
Q

What are mycobacteria and how do they differ from other bacteria?

A

Mycobacteria are rod shaped, Gram-positive bacteria which are acid fast (Ziehl-Neelsen stain). They differ from other bacteria in that they have a unique lipid rich cell wall. This means that they are impervious to many treatments.

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6
Q

By what other names has TB been known?

A

White plague, consumption, the captain of death.

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7
Q

What proportion of the world is believed to have latent TB?

A

1/3.

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8
Q

How many new cases of TB present each year?

A

9 million.

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9
Q

How many deaths are caused by TB each year?

A

2 million.

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10
Q

What percentage of deaths from infectious disease is caused by TB?

A

10%.

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11
Q

How is TB transmitted?

A

Tuberculosis is transmitted primarily through inhalation of infected droplets when an infected person coughs or sneezes.

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12
Q

What happens when the TB mycobacteria enter a person’s body?

A

The bacteria settle in the lungs and grow. A delayed type hypersensitivity is then seen, with aggregates of macrophages forming tubercles around the bacteria. In individuals with low resistance, the infection can cause an acute lung infection, destruction of tissue and can possibly spread to other parts of the body leading to death.

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13
Q

TB is a slow-growing bacterium, how long does it take for it to double?

A

24 hours.

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14
Q

Which vaccine is given to children upon entry to secondary school to protect against TB?

A

The BCG vaccine.

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15
Q

Vaccination against TB makes which test obsolete for testing a patient for TB?

A

The Mantoux/Heaf test.

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16
Q

What diagnostic methods are used to diagnose TB?

A

Chest x-ray, Mantoux/Heaf test (in unvaccinated), Direct sputum stain (Ziehl-Neelsen, fluorescent antibody), PCR (detects TB DNA).

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17
Q

How can the Mantoux/Heaf test be used to test for TB in an unvaccinated patient?

A

The Mantoux and Heaf tests for hypersensitivity can be used to test for TB in a patient. This is an intradermal injection of the protein fraction of M. tuberculosis, tuberculin. A hardening and swelling of the area of injection indicates previous exposure not active disease.

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18
Q

A combination of what drugs are used to treat TB?

A

Isoniazid, rifampicin, ethambutol, pyrazinamide.

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19
Q

What is the main property of the mycobacterial cell wall which causes problems for antibiotic action?

A

The surface of the mycobacterium cell wall is very hydrophobic.

20
Q

What causes the high hydrophobicity of the surface of mycobacteria?

A

Mycolic acids.

21
Q

Describe the structural appearance of mycolic acids.

A

Two long hydrocarbon chains, one longer than the other, with a carboxyl and hydroxyl group on the joining end.

22
Q

What are the consequences of the high hydrophobicity of the mycobacterial cell wall?

A

Impermeability to stains and dyes, resistance to many antibiotics, resistance to acidic and alkaline compounds, resistance to osmotic lysis, resistance to lethal oxidations (including in macrophages).

23
Q

What are the two four drug programmes used to treat TB?

A

Streptomycin, isoniazid, rifampin, and pyrazinamide. Ethambutol, isoniazid, rifampin, and pyrazinamide.

24
Q

After the two months, four drug combination therapy for TB has been finished. What therapy follows?

A

This is then followed by four months of isoniazid and rifampin.

25
Q

What is the rationale behind the TB treatment strategy?

A

The key to this treatment strategy is to attack multiple targets at once as TB often has resistance to one single method of attack.

26
Q

TB patients become non-infectious after the first few weeks, why is the rest of the treatment regimen needed?

A

The remaining months are necessary to eradicate the slow-growing fraction of TB.

27
Q

How does streptomycin act to treat TB?

A

Streptomycin, along with kanamycin and amikacin, is an aminoglycoside. These drugs target the 30S ribosomal subunit, possibly binding at the interface between the ribosomal subunits. Compromising protein synthesis.

28
Q

How does streptomycin enter the mycobacterium when treating TB?

A

The mycobacteria cell wall does not seem to hamper the entrance of these very hydrophilic antibiotics; this is possibly due to entry via porins/channels.

29
Q

How does rifampin act to treat TB?

A

It specifically inhibits bacterial RNA polymerase (responsible for DNA transcription) by forming a stable drug-enzyme complex.

30
Q

How do the fluoroquinolones act to treat TB?

A

These drugs work by inhibition of the enzyme’s topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, strand supercoiling repair, and recombination.

31
Q

How does isoniazid act to treat TB?

A

Isoniazid is first activated by KatG into an unstable intermediate which reacts with NAD to give certain compounds. The resulting adduct then binds the NAD(H) recognition site of InhA and this leads to the antimycobacterial effect. InhA is involved in mycolic acid synthesis.

32
Q

How does ethambutol act to treat TB?

A

Ethambutol blocks arabinogalactan synthesis by inhibition of an arabinosyl transferase enzyme. Mycolic acids accumulate in the wall, cells become spherical and possibly more permeable to other agents. Its effect on cell wall improves the efficiency of other antibiotics (e.g. clarithromycin) which are usually ineffective on M. tuberculosis. Hence it is given with other agents.

33
Q

How does pyrazinamide act to treat TB?

A

The mechanism of action for pyrazinamide isn’t fully known. It is thought that it works by acidifying the inside of cells by becoming hydrolysed to form a carboxylic acid. This may be done by the action of a specific pyrazinamidase.

34
Q

Why is pyrazinamide active against dormant bacilli?

A

Pyrazinamide is effective against dormant bacilli since the death by acidification mechanism does not require much metabolic activity apart from a pyrazinamidase.

35
Q

Why is teixobactin a promising drug in the fight against TB?

A

Teixobactin is a very promising drug in the fight against TB as it has shown no signs of resistance developing in the bacterium.

36
Q

How does teixobactin act to treat TB?

A

Teixobactin inhibits cell wall synthesis by binding to a highly conserved motif of lipid II (precursor of peptidoglycan) and lipid III (precursor of cell wall teichoic acid). This contributes to efficient lysis and killing, by digestion of the cell wall by liberated autolysins.

37
Q

How many people are affected by leprosy each year?

A

12-15 million people.

38
Q

How many new cases of leprosy are there per year?

A

500,000.

39
Q

Leprosy is easily treated. What is the reason for its prevalence?

A

The reason for the continued prevalence of the disease is that there is a massive social stigma surrounding it that can be traced back centuries. Because of this, people are less likely to seek medical advice and let the condition progress.

40
Q

How is leprosy transmitted?

A

By air-borne secretions and prolonged close contact with an untreated person suffering from an infectious form of leprosy with an inherent immunological susceptibility to the disease in the exposed person.

41
Q

What percentage or leprosy patients are infectious if left untreated?

A

Only 10% of patients are infectious of left untreated.

42
Q

What are the symptoms of leprosy?

A

Folded lesions on the face and limbs as well as disfiguration, loss of peripheral nerves, and secondary infection. These obvious symptoms contribute to the social stigma of the disease.

43
Q

How does dapsone act to treat leprosy?

A

Its mechanism is probably similar to that of the sulphonamides; inhibition of folic acid synthesis. This may lead to selectivity issues.

44
Q

How does clofazimine act to treat leprosy?

A

It inhibits mycobacterial growth and binds preferentially to mycobacterial DNA. It also exerts anti-inflammatory properties in controlling erythema nodosum leprosum reactions.

45
Q

In what tissue type does clofazimine tend to be deposited?

A

Clofazimine tends to be deposited predominantly in fatty tissue and in cells of the reticuloendothelial system.

46
Q

What two drugs in the 4 drug programme for treating TB can be swapped out with each other?

A

Streptomycin and ethambutol.

(UNI) Chemotherapy & Selective Toxicity (3rd Year) (18 decks)

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