treatment and prevention of pulmonary tuberculosis

8/13/2019 Treatment and Prevention of Pulmonary Tuberculosis

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Puteri ShamillahWan Hidayu

Farhana AzmiraShazeenah

Nadeeja


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May be associated with night sweats


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TB is major cause of illness & death

worldwide

Highest in ASIA & AFRICA

In 2011, almost 1.4 million people died fromTB

(WHO, 2012)


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Physical examination

Unusual breath sounds

Swollen lymph nodes Clubbing of fingers/toes


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L BOR TORY ND PHYSIC L

TESTING1) PPD (Purified protein derivative)

2) Thoracentesis

3) Sputum Examination


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4) Chest Radiography

cavity


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4) Chest Radiography

Acute miliary tuberculosis


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5) Bronchoscopy

6)Tuberculosis antibody testing


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Isoniazid (INH, H)

Ethambutol (RIF, R)

Pyrazinamide(PZA,Z)

Rifampicin (EMB,E)

The First line Supplementary Drugs Streptomycin (SM, S)

Second line Essential Drugs

Category Action

Inhibit cell wall

synthesis

Inhibit Protein

synthesis

Inhibit DNA

gyrase

Aminoglycosides Amikacin

Thioamide Ethionamide

Polypeptide capreomycin

Fluoroquinolones Ofloxacin,

ciprofloxacin

PAS


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Drugs which interfere with mycolic acid synthesis Drugs which inhibit nucleic acid synthesis

Drugs inhibiting protein synthesis


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Drugs Duration Interval Minimum dosesIsoniazid 9 months Daily 270

Twice weekly* 76Isoniazid 6 months Daily 180

Twice weekly* 52Isoniazid and

Rifapentine3 months Once weekly* 12

Rifampin 4 months Daily 120*used directly observed therapy (DOT)

(http://www.cdc.gov/tb/topic/treatment/ltbi.htm)

Table 1: The drugs and duration of the doses used to treat latent tuberculosis
http://www.cdc.gov/tb/topic/treatment/ltbi.htmhttp://www.cdc.gov/tb/topic/treatment/ltbi.htm


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Highest ++++ High +++ Intermediate ++ Low +


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First Line DrugsHigh efficacy, low toxicity.

Always used in combination.

Bactericidal for rapid multipliers

Bacteriostatic for dormant bacteria

Effective against intracellular & extracellular M.

tuberculosisCombination with other drugs can combat

bacterial drug resistance


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Mycolate depleted cell walls structurally weak


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Used specifically as a TB treatment

Used during first two months of antibiotic therapy

to enhance the efficiency of the antibiotic therapy

Always used with isoniazid and rifampicin Bacteriostatic & bactericidal effect

Well absorbed from GI tract and can penetrate into

cerebrospinal fluid

Partially metabolised in liver


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Converted into pyrazinoic acid by bacterial pyrazinamidase

Acid accumulates inside the bacteria (acidic pH)

Inhibits the fatty acid synthesis in bacteria

Disturbs bacteria cell membrane &energy production

Approximately 70% of an oral dose is excreted in the urine


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Used for drug resistance

Affects for growing bacteria

Disturbs for the formation of bacteria cell

wall Well absorbed from GI tract

Excreted in urine and faeces


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Inhibit mycobacterial Arabinosyl transferases

Inhibit polymerizasion of arabinoglucans

Inhibit cell wall formation

Inhibit bacterial growth


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Resistance Results from an alteration in the polymerase enzyme (mutation in the

rpoB gene).

Semi-synthetic derivative of one of the rifamycins, a group of complex

macrocyclic antibiotics.

It is also considered the most important and potent antituberculosis

agent

Like isoniazid it is bactericidal and highly effective.


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Category Explanation

Absorption Well absorbed from the GI tract

Distribution -80% bound to plasma protein.

-half life: 2-5 hour

-Widely distributed throughout the body including

the CNS.

Metabolism In the liver

Excretion About 1/3 of the drug is excreted in urine, and

2/3 in the intestine. Adjust dose with decreased liver function.


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Antiarrhythmic ( i.e quinidine)Anticoagulants (i.e warfarin)

Oral hypoglycemic

Antiepileptics

Antifungals (i.e ketoconazole)

Antivirals

Oral contraceptive- alternative methodnecessary

Thyroxine


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Aminoglycoside antibiotic

Source: Streptomyces griseus

Bactericidal against the extracellular tuberculosis bacilli.

Overall only suppressive

Resistance:

Combination therapy will delay or prevent resistance.


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Category Explanation

Absorption Well absorbed by Intramuscular and intravenous.

Distribution -extracellular fluid

-34% bound to plasma protein.-half life: 4 -10 hour (Infant), 2-4 (adults)

-cross placenta- enter milk

Metabolism Does not well metabolise.

Excretion -90% in urine

-


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Drugs Significant side effects

Isoniazid Hepatotoxicity, peripheral neuropathy

Rifampin Gastrointestinal upset, hepatitis

Pyrazinamide hepatotoxicity

Streptomycin Ototoxity, Renal toxicity

Ethambutol Retrobulbar optic neuritis


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1. Skin tests (Tuberculin) detect whether body

had been exposed to TB

Used in high risk populations or in people who

may have been exposed to TB such as health care

workers

Vital for prevention of mycobacterium tuberculosis

2


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2. BCG (Bacillus Calmete Guerin) vaccination Live attenuated vaccine- derived from the bovine strain of tuberculosis

bacteria (mycobacterium bovis)

inducing an artificial primary infection leads to stimulation of acquiredresistance to possible successive infections with virulent bacilli

Recommended for:

a) Babies

b) Older children and adults (


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3. Ventilation of the room to reduce concentration of

aerosolized droplet nuclei

4. Prevent spread from those infected with pulmonary

tuberculosis -Isolation from crowded areas

5. Usage of protective measures-masks, gloves6. Implementation of education programs to educate

people about transmission and methods of

prevention


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5. Practice of several measure to eliminate

the conditions that can increase the risk of

infection

Wearing mask

Avoid spending long time in stuffy area with

infected patients

6. Implementation of education programs

Educate people about the transmission andmethods of prevention


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REFERENCES

Carroll, N. M., Uys, P., Hesseling, A., Lawrence, K., Pheiffer, C.,Salker, F., .Helden, P. D. (2008). Prediction of delayed treatmentresponse in pulmonary tuberculosis: Use of time to positivity valuesof Bactec cultures. Tuberculosis, 88(6), 624-630.

Parsyan, A. E., Saukkonen, J., Barry, M. A., Sharnprapai, S., &Horsburgh Jr, C. R. (2007). Predictors of failure to completetreatment for latent tuberculosis infection. Journal of Infection, 54(3),262-266.

Robertson, B. D., Altmann, D., Barry, C., Bishai, B., Cole, S.,Thomas, D., Young, D. (2012). Detection and treatment ofsubclinical tuberculosis. Tuberculosis, 92(6), 447-452.

treatment and prevention of pulmonary tuberculosis

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