Multi-drug-resistant tuberculosis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]; Ammu Susheela, M.D. [3]
Overview
Multi-drug resistant tuberculosis (MDR-TB) is defined as TB that is resistant at least to isoniazid (INH) and rifampicin (RMP). Isolates that are multiply-resistant to any other combination of anti-TB drugs but not to INH and RMP are not classed as MDR-TB.
Historical Perspective
Mycobacterium tuberculosis was first described by Robert Koch in 1882 and in 1970 drug-resistant tuberculosis was first reported. Since then, several drugs and strategies have been implemented to control the disease. Cases in US have decreased, however worldwide MDR-TB is increasing in developing countries.
Classification
Classification of drug resistant tuberculosis is based on drug susceptibility , pathophysiology, clinical classification and molecular classification. According to drug susceptibility it is classified as monoresistance, poly resistance, multidrug resistance, extensive drug resistance and rifampicin resistance. Clinically it is classified as acquired and primary resistance. The restriction fragment length polymorphism helps for molecular classification into unique and cluster type.
Pathophysiology
Tuberculosis is a granulomatous infection tansmitted mainly through droplets and can have pulmonary and extra pulmonary manifestations. Multi drug resistant strains of tuberculosis have been emerging at an alarming rate and they might be developed due to primaryy resistance or acquired resistance. These resistance are mainly through genetic mutations in genes like inhA, katG and rpob genes. These molecular pathophysiology can be detected through pyrosequencing, DNAsequencing and electrophoresis.
Causes
Mycobacterium tuberculosis is the bacterium responsible for tuberculosis. It is an aerobic, non-encapsulated, non-motile, acid-fast bacillus. M. tuberculosis belongs to the Mycobacterium tuberculosis complex, that also includes bacteria, such as M. bovis and M. africanum. The bacterium has a very slow rate of replication, and its genetic variations account for the geographical distribution of different strains, and are involved in drug resistance. M. tuberculosis has tropism for different kinds of human cells, with preference for cells of the lung. It may infect different species, yet human beings are its frequent natural reservoir.
Differential Diagnosis
Pulmonary tuberculosis must be differentiated from other diseases that cause cough, fever, night sweats, hemoptysis and weight loss, such as: brucellosis, bronchogenic carcinoma, Hodgkin lymphoma, bacterial pneumonia, sarcoidosis, mycoplasmal pneumonia.
Epidemiology and Demographics
Risk Factors
Risk factors for multi-drug resistant tuberculosis include exposure to an individual with MDR-TB, previous TB treatment, HIV infection, and a low socioeconomic status.
Screening
Screening for tuberculosis is generally done with using a mantoux tuberculin skin test, also known as a tuberculin skin test or a PPD. The test involves injecting a small amount of a purified protein derivative of the tuberculosis bacterium intradermally, and watching for a reaction in the following days.
Natural history, complications and prognosis
Tuberculosis has been classified as primary and post primary infection. It can have pulmonary and extra pulmonary manifestations as well as severe parenchymal, vascular, pleural and chest wall complications. The post primary infection can be due to a recent infection or reactivation of an old infection. Further multi drug resistant strains can develop through acquired resistance through inadequate treatment / treatment failure as well as slow gradual genetic mutation resulting in primary resistance. These are transmitted to healthy people resulting in emerging multi drug resistant strains. They can be rifampicin resistant, multi drug resistant, extensively drug resistant and totally drug resistant. The more the number of drugs the strain is resistant to , the poorer is the prognosis.