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Introduction to Tuberculosis

 

- “White Plague” of the middle ages

- Tuberculosis accounted for 30% of deaths in 17th century London à the organism spreads via aerosolization à many people in London live in closely confined spaces à easily contracted + no treatment = lots of deaths 

- Cases:

         1800’s USA  400/100,000

         1900’s USA  200/ 100,000

         1953 USA (Tx) 12/100,000

         1978 USA (Tx) 1/100,000

         2003 USA (Tx) 5.1/100,000

         Rates highest in minorities, foreign born 

* Tuberculosis rates feel until recently.  The increase seen can be attributed partially to an increase in resistance but mostly to an increase in the incidence of HIV/AIDS.  HIV/AIDS has become one of the leading reasons for new Tuberculosis cases.  Therefore, HIV/AIDS has changed the way Tuberculosis has been monitored and seen over the last 25 years. 

* When you get a new case of Tuberculosis in the hospital, it must be reported to the state.  So, if an acid-fast organism is seen on a stain it is reported.  (There are a whole bunch of contagious diseases that must be reported to the state – so remember that that’s part of your job.) 


Mycobacterium Tuberculosis

- Transmission via inhalation of airborne droplets containing viable organisms

- Whether or not you get tuberculosis depends on:

- Number of bacilli you have inhaled

- Degree of aerosolization

- Susceptibility of contact (do you take steroids, do you have diabetes, do you have anything that could make you more susceptible)

- Organisms inactivated by heat/drying/light, but not necessarily killed. (Sometimes even when organisms are dried out, they are still active.)

- Very common in the immunocompromised host (HIV) (especially Mycobacterium Avium-Intracellulare and M. Tuberculosis)

 

- There are now drug resistant strains 

When M. Tuberculosis is inhaled into the lung, it causes immediate death of the tissue around it and causes a necrotizing granuloma – this is the hallmark of tuberculosis infxn (Other organisms can also cause this, but tuberculosis is the hallmark organism). This type of necrosis is also called caseous necrosis because pathologist like food and it reminded them of cheese.  Necrotizing and caseous (or cheese-like) mean the same thing.   
 


Tuberculosis: Two forms of the disease

- Primary infection (Ghon Complex)

- Secondary (reactivation tuberculosis)

a little more info on each…


Primary Pulmonary Infection

- Children most commonly affected

- GHON complex: Local lymphatic dissemination of bacteria with hilar adenopathy

1) Parenchymal subpleural focus à where you inhale the organism and are left with a granuloma in your subpleural area (as we saw previously); causes initial infxn and damage

2) Enlarged caseous lymph nodes draining (hilar lymph nodes) the parenchymal focus (in other  words, live organisms will be drained through the lymphatics to the hilar lymph nodes causing the same type of pattern there à peripheral nodule with a central nodule; these nodules usually become fibrotic and calcify over a period of time)

- Few clinical manifestations

- usually asymptomatic

- Fever, fatigue

- Will rarely Progress from primary tuberculosis to disseminating tuberculosis 

tuberculosis nodule

The patient has inhaled a tuberculosis organism and it has caused permanent destruction of the lung subpleurally.  Over time this will calcify and you will be able to see it on an x-ray.  We don’t normally remove calcified nodules in the lung because they are usually benign and usually just old tuberculosis. 

ghon complex

To the right is a GHON complex.  Notice that you have the same histological appearance (granuloma, giant cells) in both the subpleural lesion and the hilar region.  Usually, if you are healthy, you can wall off the nodules and have calcification. 


Reactivation/Secondary Pulmonary Tuberculosis

- Adults are affected

- Have had tuberculosis as a child; have a GHON complex that has been walled off and is fibrotic/ calcified.

- Upper lobe disease (necrotizing granulomas) predominates

            - Upper lobes involved almost exclusively because oxygen tension is greatest in the apices.

- Cavitation of upper lobe

- Extra-thoracic sites of disease spread by hematologic dissemination

reactivation tuberculosis

 The lung of someone who has had reactivation tuberculosis.  All of the necrosis is in the apex, really close to the pleural space.  These areas will become fibrotic in an attempt to wall off the entire area. 

miliary tuberculosis

Miliary/disseminated tuberculosis– when the organism spreads hematologically through the lungs and other parts of the body.  Yellow areas (the little yellow dots inside the circle) are areas of necrosis.  This basically causes bronchopneumonia with no resolution once its miliary.

(Called miliary tuberculosis after the milate seed – a yellow bird seed.)

 Another picture of miliary tuberculosis. Once again, once the patient has milary TB, the organism can spread hematologically throughout the body (but, in most cases, the patients are able to wall off the infection completely and this doesn’t happen).  

tuberculosis x-ray

A chest X-ray of someone with miliary tuberculosis.  The diffuse white stuff is the tuberculosis particles on both sides of the lung. 


Causative Organisms

mycobacterium

- Mycobacterium species is usually the likely organism but there are other organisms that are acid-fast bacilli and may not be tuberculosis:

- Actinomyces

      - Nocardia 

- There are also many species associated with human infection

 

- M. tuberculosis

- M. bovis

- M. leprae

- M. africanum

- Atypical Mycobacterium

- M.avium (Seen in the HIV/immunocompromised host)

Summary (This is where it finally comes together and makes sense): In reactivation disease patients will get apical disease.  They will usually be able to wall it off and it will become fibrotic or caviteric.  In some patients, however, there will be the development of further problems with miliary tuberculosis.
 

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