Recent Posts

Re: Risk factors of tuberculosis (TB) by auntiebiotic
[November 10, 2016, 15:46:01 PM]

Re: A to Z of tuberculosis (Letter B) by auntiebiotic
[November 08, 2016, 21:44:13 PM]

A to Z of tuberculosis (Letter A) by auntiebiotic
[November 08, 2016, 21:32:38 PM]

Foods that help immune system by auntiebiotic
[November 08, 2016, 20:06:05 PM]

Cats and TB (Tuberculosis) by auntiebiotic
[November 08, 2016, 18:37:25 PM]

User Info

Welcome, Guest. Please login or register.


Board Stats

  • stats Total Members: 2
  • stats Total Posts: 57
  • stats Total Topics: 53
  • stats Total Categories: 6
  • stats Total Boards: 17
  • stats Most Online: 23

  • averages Average Posts: 0
  • averages Average Topics: 0
  • averages Average Members: 0
  • averages Average Online: 1

* Stat

Author Topic: Pathogenesis of TB  (Read 57 times)

Description: The tubercle bacilli are spread through the lymphatic channels to regional lymph nodes and through the bloodstream


  • Administrator
  • Jr. Member
  • *****
  • Posts: 57
  • Karma: +0/-0
    • View Profile
Pathogenesis of TB
« on: November 03, 2016, 16:07:09 PM »

After inhalation of a droplet nucleus, it passes down the bronchial tree without settling on the respiratory epithelium and implants in a respiratory bronchiole or alveolus beyond the mucociliary system. Here the bacilli may multiply with no initial resistance from the host. The organisms are slowly engulfed by macrophages, but they may remain viable and even multiply within the cells.

The tubercle bacilli are spread through the lymphatic channels to regional lymph nodes and through the bloodstream to more distant sites. Certain organs and tissues are notably resistant to subsequent multiplication of these bacilli. The bone marrow, liver, and spleen are almost always seeded with mycobacteria, but uncontrolled multiplication of the bacteria in these sites is exceptional. Organisms deposited in the upper lung zones, kidneys, bones, and brain may find environments that favor their growth, and numerous bacterial divisions may occur before specific immunity develops and limits multiplication.

Specific immunity is usually adequate to limit further multiplication of the bacilli; the host remains asymptomatic, and the lesions heal. Overall, in approximately 5% of all infected persons, control of the replicating organisms is inadequate, and disease occurs within 1 yr of infection. In another 5%, containment of the organism fails at a time more remote from the acquisition of infection, and disease results. Thus, overall, approximately 10% of persons infected with M. tuberculosis will develop clinical tuberculosis sometime during their lives. The ability of the host to respond to the organism may be reduced by certain diseases such as silicosis, diabetes mellitus, and diseases associated with immunosuppression, e.g., human immunodeficiency virus infection (HIV), as well as by corticosteroids and other immunosuppressive drugs, and by gastrectomy. In these circumstances, the likelihood of tuberculosis developing is greater. Susceptibility to tuberculosis also may be greater during the first 2 yr of life, at puberty, and during adolescence.

The inflammatory response in tissues and subsequent necrosis, along with some of the systemic symptoms of tuberculosis, are the results of a cell-mediated immune response of the host to the living bacilli, rather than the results of the production of toxins or tissue-destroying enzymes by the bacteria. Hypersensitivity to components of the organism, as demonstrated by the development of a positive reaction to the tuberculin skin test, develops 2 to 10 wk after the initial infection. This period corresponds to the time needed to develop a cell-mediated immune response.

disease_tb3At any point after the first infection, tubercle bacilli that have spread through the body may begin to replicate and produce disease. In some infected persons, there is a relatively direct (within 1 yr) progression from the initial infection to clinical illness. In others, illness develops after an interval of 1 yr to many years when the organisms begin to grow within an old focus. The most common site for this acceleration of growth is the upper lung zone, but foci anywhere in the body can be the sites of late progression. The lung foci account for the majority of clinical cases of tuberculosis. Because this location provides the organisms with access to the outside environment and because liquefaction necrosis often occurs, airborne dissemination of infectious particles is likely.

Pleural effusion may occur at any time after the initial infection. Effusions most commonly are caused by the release of a small amount of tuberculoprotein from an unapparent form with the lung into the pleural space. This in turn causes an inflammatory reaction and the accumulation of clear, protein-rich fluid. During the initial infection, regional, hilar, and mediastinal lymph nodes are always seeded with bacilli, and other lymph nodes may be seeded also. The infection in these nodes may progress directly to clinical disease, may become active after many years, or may never become apparent.

Miliary tuberculosis occurs either as part of the early infection or at some later time when a necrotic focus erodes a blood vessel, permitting a large number of organisms to enter the vascular system within a brief period of time, seeding many organs. Involvement of the meninges follows the rupture of a caseous focus directly into the subarachnoid space. A bone and an adjacent joint may be involved together, and the infection may extend to the surrounding soft tissue, producing a cold abscess. Renal involvement occurs when organisms within a cortical focus multiply and produce a necrotic lesion that drains into the collecting system, frequently producing secondary sites of infection in the renal medulla, ureter, and bladder with stricture formation. Infection of the female genital tract is almost always caused by hematogenous seeding, whereas the male genital tract may be infected by the urine or the bloodstream.

In a normal host the immunologic response to infection with the tubercle bacillus provides a degree of protection against additional tubercle bacilli that may be inhaled subsequently in droplet nuclei. The likelihood of reinfection is a function of the risk of reexposure, the intensity of such exposure, and the integrity of the hosts immune system. In the United States the risk of reexposure to an infectious case is low. Furthermore, in an otherwise healthy, previously infected person, any organisms that are deposited in the alveoli are likely to be killed by the cell-mediated immune response. Exceptions may occur, but clinical and laboratory evidence indicate that disease produced by the inhalation of a second infecting strain is uncommon.

Recently, it has become apparent that infection with the HIV, because of its profound suppression of the normal immune response, predisposes to much more severe forms of tuberculosis. In HIV-infected persons with tuberculosis, dissemination of tubercle bacilli and a variety of extrapulmonary manifestations are common. Unusual clinical presentations of tuberculosis in HIV-infected persons thus present a special diagnostic challenge.
« Last Edit: November 08, 2016, 16:29:21 PM by auntiebiotic »


SMF spam blocked by CleanTalk