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Tuberculosis

Etiology

M. tuberculosis is a slender bacillus that has a waxy outer layer (1). It is only 1 to 4 microns in length (1). When visualized under a microscope, it is straight or curved in shape (1). It does not stain well with the Gram stain, so alternative methods like the Ziehl-Neelsen stain or the fluorochrome stain is used alternatively (1).

In the Ziehl-Neelsen stain, carbol-fuchisin is used (1). Mycobacteria retain the red color despite acid-alcohol washes and therefore these are called acid-fast bacilli (1). After the staining procedure is done, microscopic examination of a smear detects about 8,000 to 10,000 organisms per millilitre of specimen (1). The smear can be negative but still have M. tuberculosis growing in the culture (1). Furthermore, microscopic examination cannot distinguish between the 100+ mycobacterial species that is present or whether the organisms in the original samples were alive or dead (1). In the smear, the organisms are all dead. However, in the culture, M. tuberculosis grows slowly, and it doubles about every 20 hours (1).

Transmission

M. tuberculosis is transmitted from person to person via coughing or sneezing (1,2). When a person coughs or sneezes, small particles known as droplet nuclei are produced and they float in the air a prolonged period of time (1,2). Each one of these droplets contain one to three organisms (1,2). It is estimated that about 30% of the individuals who experience prolonged contact with an infectious TB patient become infected (1,2).

Diagnosis

The Mantoux test, which is TB skin testing with 5-TU strength of brand purified protein derivative is the preferred method for skin testing (,21). The product is injected into the skin, not subcutaneously (1). Using a fine needle, it will produce a small, raised and blanched wheal and this will be read by a medication profession in 48 to 72 hours (1). A measurement of <5mm indicates that the patient does not have TB (2,3). If the measurement is >5mm, then patient may have latent or active TB (2,3). This has to be confirmed with a chest radiograph and symptom questioning (2). Around 70% of patients will have a positive skin test and 20% of all suspects will produce a false positive skin test (2). Upon chest radiograph, a positive TB radiograph will have patchy areas in the apices of upper lobes or in the superior segment of the lower lobes (2).

Pathophysiology

Primary Infection

Primary Infection is due to inhaling droplet nuclei that contain M. tuberculosis (1). In order for the infection to reach the clinical disease, three factors are considered: (1) the number of M. tuberculosis organisms that are inhaled (this is known as the infecting dose), (2) the virulence of these organisms and lastly (3) the host’s cell mediated immune response (1). If the macrophages present in the lungs are able to inhibit or kill the bacilli, the infection can be stopped (1,4). If not, the M. tuberculosis will eventually spread throughout the body via the bloodstream (1,4). It will most commonly infect the posterior apical region of the lungs since this region is very favourable for its survival (1,4).

T lymphocytes are activated over a period of 3 to 4 weeks and they produce interferon –γ and other cytokines (1). These cytokines stimulate the microbicidal macrophages and these surround the tuberculosis foci and form granulomas to prevent further extension (1). During this stage, the infection is largely under control and the bacillary replication falls off (1). If there are any remaining mycobacteria, they are believed to reside primarily in the granulomas or within macrophages that have avoided detected and lysis (1). Over 1 to 3 months, the activated lymphocytes reach an adequate number and tissue hypersensitivity will result, which is reflected by a positive tuberculin skin test (1).

M. tuberculosis has multiple ways of evading or resisting the host immune response (4). It can inhibit the fusion of the lysosomes to phagosomes inside macrophages (4). This results in the prevention of the destructive enzymes present in the lysosomes from reaching to the bacilli captured in the phagosomes (4). As a result, this allows for the M. tuberculosis to escape into the cytoplasm (4). Very virulent M. tuberculosis are able to multiple in the macrophage cytoplasm, and it will continue their spread (4). Lipoarabinomannan, which is the major polysaccharide of the mycobacterial cell wall can inhibit the immune host response (4). It induces immunosuppressive cytokines; and blocks macrophage activation (4). It also scavenges O2, which prevents attacks by superoxide anions, hydrogen peroxide, singlet oxygen and hydroxyl radicals (4). These factors in combination make M. tuberculosis a very difficult organism to control (4).

Progressive primary disease occurs in about 5% of the patients, especially in the elderly, children and immunocompromised patients (1). At this stage, it is a progressive pneumonia and frequently spreads, leading to meningitis and other severe forms of TB (1).

Progression

10% of the infected patients will develop reactivation TB (1). Half of these reactivations will occur within the first 2 years after infection (1). 85% of these cases will result in lobe pulmonary disease (1). Ceseating granulomas (a nercosis that results in the tissue from having a cheese like appearance) will result from a vigorous immune response and liquefaction leads to local spreading (1). A pulmonary cavity will eventually form and this is a portal to the outside that allows transmission from person to person (1).

Aggravating Factors

When infected with M. tuberculosis, the lifetime risk of developing active TB is about 10% (1). Half of this risk is present during the first 2 years after the infection has been established (1). Young children, elderly, and immunocompromised patients have the greatest risks (1). HIV-infected patients that have M.tuberculosis infection are 100 times more likely to develop active TB than normal hosts due to inadequate cellular immunity (1).

TB can infect anyone but this risk varies across the country (4). Based on certain statistics from the US, it appears that TB is the most prevalent in large urban areas (4). This is due to the fact that it is much easier for an airborne disease to infect people in very population dense areas (4). The number of foreign born TB cases in the US increased annually since 1986 and in 2005, this number reached 54% (4). Being in close vicinity with someone that is TB infected is another aggravating factor as risk of infection is as high as 30% (4).

References

  1. Chisholm-Burns MA, Wells BG, Schwinghammer TL, Malone PM, Kolesar JM, Rotschafer JC et al. Pharmacotherapy principles & practice. New York: McGraw-Hill. 2008. p. 1105-1110.
  2. Gray J, editor. Therapeutic choices. 5th ed. Ottawa: Canadian Pharmacists Association; 2007. p. 1261-1276.
  3. Health Canada. Tuberculosis and tobacco smoking. [Online] 2010 [cited 2011 Feb 28]; Available from: URL:http://www.phac-aspc.gc.ca/tbpc-latb/fa-fi/tbtobacco-tabag-eng.php
  4. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 7th ed. Toronto: McGraw-Hill; 2007. p. 1839-1854.

Disclaimer

This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers


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