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Treatment of Tuberculosis

by Jeremy Brown, PhD
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    00:00 positive in patients with previous tuberculosis exposure and is not affected by the BCG.

    00:01 The treatment of tuberculosis is actually relatively straightforward, it requires antibiotics.

    00:05 However, it requires more than one antibiotic and the standard therapy is 4 antibiotics, and it requires antibiotics for a long period of time. The minimum treatment period is 6 months and if you have central nervous system disease or bone disease it often goes on for at least 12 months. So we ask the patients to take 4 drugs for 2 months and then 2 drugs for 4 months at least, and the actual dose that we give the patient is dictated by their weight. The split being 50kg, if they are below 50kg they get a lower dose, if they are above 50kg they get a higher dose. And the 4 drugs that we use are: Isoniazid, Rifampicin those are the most effective drugs and the ones that are kept going for the 6 months.

    00:50 And for the first 2 months we give the patients Pyrazinamide and Ethambutol as well.

    00:55 Ethambutol can affect the eyes and therefore we test the eyes before we start that drug. There are other things we may want to do. One is that actually with patients with brains involvement of tuberculosis or pericardial disease, we give them corticosteroids and the reason why we do that is that tuberculosis as it heals it's a very scarring infection, so you get a lot of fibrosis occurring where tuberculosis has been and in the brain that causes neurological deficits and we know that if patients are given corticosteroids then the chance of having long term brain damage is reduced. And the same for pericardial disease, we are worried about the development of constrictive pericarditis and the chances of that are reduced by giving the patients oral corticosteroids as well as their TB therapy. A very very important point is that all the cases of tuberculosis need to be notified. What we mean by that is that they need to be brought to the attention of the authorities so that there can be a screening process of that patient’s close contacts usually the family, the people they live with, but if it is a school child it will also be their school class as well.

    02:12 And what happens there is that if a patient with TB is identified then who they live with will be tested to see whether they have active tuberculosis or latent tuberculosis as well.

    02:23 By this method we can identify the source by which a patient has been infected and whether they've actually infected somebody else as well. And this is very important for the control of the disease. The testing that we use is this immunological response to infection, the Heaf testing or the IGRA and a chest X ray to look for the active disease. There are major problems for treating tuberculosis. The first we've already mentioned is that diagnosis can be slow, if it’s reliant on culture where in fact we take 6 weeks before we know somebody doesn’t have tuberculosis in a sample that’s been sent for culture.

    02:57 And the positive growth is only, it usually occurs within 3 or 4 weeks.

    03:03 The second is compliance, you are asking someone to take quite a lot of drugs for 6 months and they don’t like doing that, and in fact when patients feel better they often think they don’t need to take the medication and they feel better within a few weeks of starting the medication, and within two weeks they should be starting to feel considerably better than they have been feeling for weeks, and often patients will say “well, actually I'm feeling better now, I’ll stop taking the tablets”. The third is toxicity. The drugs that we use for tuberculosis, unfortunately several of them are liver toxic, and they cause an inflammation of the liver with an increase in the liver enzyme results and that can prevent those treatments being used. So we have to monitor the liver function test and if they go too high, we have to stop the therapy and then restart the therapy trying to identify which one of the drugs was responsible for causing the liver toxicity. And that's a complex process and delays treatment considerably. And the last is drug resistance, this is a problem if the patient is given single agent therapy. So when we first developed therapies for tuberculosis in the 1950s, only one agent was available and treatments with that led to patients developing resistance to disease very quickly and this is a problem. So this is why we give the patient 4 drugs to start with. It is to prevent resistance developing.

    04:31 And if resistance is present to one agent, if you give somebody 4 drugs, then that will prevent the resistance increasing to affect the other drugs as well. If somebody has resistant disease, you suddenly have a problem and that treatment has to go on for at least 12 months, you may be using second line drugs, which are less effective, and they need very close monitoring to ensure they are improving and that they are compliant with the drugs that are being used. If you have extensively resistant disease, those organisms that are resistant to Rifampicin and Isoniazid, and several other drugs, then actually you can get a situation where the tuberculosis is not treatable and there is a very high mortality in those patients.

    05:14 So what's the outcome? well if you have non-resistant tuberculosis of a 100 cases you can expect


    About the Lecture

    The lecture Treatment of Tuberculosis by Jeremy Brown, PhD is from the course Infections of the Respiratory Tract.


    Included Quiz Questions

    1. 3 days morning sputum samples
    2. 3 days evening sputum samples
    3. 5 days days morning sputum samples
    4. 5 days evening sample
    5. A weeks sample
    1. Blood
    2. Sputum microscopy
    3. Culture of tuberculosis
    4. Excision biopsy of extrapulmonary site
    5. Aspiration cytology
    1. The M. tuberculosis organisms must be identified in the sample for confirmation of the diagnosis.
    2. The antibodies against tuberculosis must be identified in the blood sample for confirmation of the diagnosis.
    3. A positive Mantoux test is required for confirmation of the diagnosis.
    4. The increase in the lymphocytic count is required for confirmation of the diagnosis.
    5. The identification of lipid cell wall antigens present in the sample is required for confirmation of the diagnosis.
    1. Ziehl Nelson stain
    2. Gram stain
    3. KOH stain
    4. Reticulin stain
    5. Silver stain
    1. The culture of M.tuberculosis takes more than 10 to 12 weeks.
    2. Culture helps confirm the microscopic diagnosis given.
    3. Culture and sensitivity of M.tuberculosis help provide the drugs that are resistant to treatment.
    4. Culture of tuberculosis is slow
    5. Culture of tuberculosis is performed on liquid media
    1. Sputum positive tuberculosis
    2. Nodal tuberculosis
    3. Lymph node tuberculosis
    4. Pleural tuberculosis
    5. Tuberculous meningitis
    1. PCR for Tuberculosis
    2. ELISA for tuberculosis
    3. Western blot for tuberculosis
    4. Southern blot of tuberculosis
    5. Protien gel electrophoresis for tuberculosis
    1. Caseous necrosis
    2. Liquefactive necrosis
    3. Fibrinoid necrosis
    4. Coagulative necrosis
    5. Gangrenous necrosis
    1. Sarcoidosis
    2. Tuberculosis
    3. Leprosy
    4. Cat scratch disease
    5. Hodgkin lymphoma
    1. Non caseating granulomas only
    2. Caseating granulomas only
    3. Both caseating and non-caseating granulomas
    4. Palisading granulomas
    5. Naked granulomas
    1. Both caseating and non-caseating granulomas
    2. Specifically non-caseating granulomas
    3. Specifically caseating granulomas
    4. Naked granulomas
    5. Palisading granulomas
    1. Interferon gamma release assay is confounded by previous BCG vaccination.
    2. There are two tests that commonly can be used to identify latent tuberculosis infection.
    3. Interferon gamma release assay and Mantoux test work on the similar principles of identifying patients with a previous infection with Tuberculosis.
    4. A mixture of attenuated tuberculous antigens is injected intradermally in a Mantoux test.
    5. Interferon gamma release assay is more specific than Mantoux test.
    1. 12 months
    2. 9 months
    3. 6 months
    4. 3 months
    5. 11 months
    1. Combination therapy is used to eradicate infection and prevent resistance.
    2. The dose is dictated by patients height.
    3. Isoniazid kills slowly the replicating bacteria.
    4. Rifampicin kills the bacteria rapidly.
    5. Ethambutol must be given for the full course of treatment.
    1. Pull out the previous record of his vision testing which was performed prior to the start of treatment.
    2. Accept his claim and apologise since it was the doctor's mistake.
    3. Deny his claim as ethambutol does affect the eyes.
    4. Deny claim as internet does not provide accurate information.
    5. Ignore his claim.
    1. Only military tuberculosis is supposed to be notified.
    2. The index case must be identified.
    3. The close contacts must be identified and treated.
    4. IGRA or Heaf testing can be done to the identified close contacts.
    5. Chest X-ray can be performed when then close contacts come positive.
    1. Isoniazid
    2. Rifampicin
    3. Ethambutol
    4. Pyrazinamide
    5. Ciprofloxacin
    1. The medications do NOT work effectively in treatment.
    2. The medications can cause toxicity to the patient.
    3. The medications can be resistant to tuberculosis.
    4. The compliance with the medications by the patients.
    5. The medications have to be taken for a long period of time.
    1. Eyes
    2. Ears
    3. Taste
    4. Loss of skin sensation
    5. Loss of smell
    1. Steroids reduce the scarring caused by fibrosis post treatment of tuberculous lesions of the brain.
    2. Steroids reduce the neutrophils in the tuberculous lesions of the brain.
    3. Steroids reduce the dose of the anti-tubercular drugs
    4. Steroids decrease the duration of the antitubercular therapy for the tuberculous lesions of the brain.
    5. Steroids prevent systemic symptoms in patients who have tuberculous lesions of the brain.

    Author of lecture Treatment of Tuberculosis

     Jeremy Brown, PhD

    Jeremy Brown, PhD


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