TB and Atypical Mycobacteria Flashcards
1
Q
What are the stats on TB?
A
- has existed as human disease since 3000BCE
- most common infectious cause of mortality worldwide
- more than 1/3 of world population infected
- was on the decline due to antibiotics until AIDS epidemic
- multidrug resistant (MDR) and extrensively drug resistant (XDR) strains now becoming a problem
2
Q
What is the bacteriology of M. tuberculosis?
A
- stain very poorly, almost uniquely acid fast
- they have a petidoglycan layer, followed by an arabinogalactan layer, followed by Mycolic acid layer (where all of its unique properties come from, including the acid fast staining)
- grows in vitro very slowly with special nutrients
- humans are natural host and reservoir ( thus can eradicate)
- very slow growing even in human host
- can be intra or extracellular
- produce no toxins
- drug resistance is chromosomal, no known plasmids
- very hardy
- obligate aerobe
3
Q
How does one acid-fast stain?
A
- cover smear with carbolfuchsin
- steam over boiling water for 8 min. Add additional stain if stain boils off
- after slide has cooled decolorize with acid-alcohol for 15 to 20 seconds
- stop decolorization action of acid-rinsing briefly with water
- counterstain with methylene blue for 30 seconds
- rinse briefly with water to remove excess methylene blue
- blot dry with bibulous paper.
- examine directly under oil immersion
- Mycobacter with stain acid fast, TB with cords
4
Q
What are the important structural components to M tuberculosis?
A
- mycolic acids: acid fastness
- Wax D- adjuvant (used in Freund’s)
- Phosphatides- caseation necrosis
- cord factor (trehalose dimycolate)- virulence, microscopic serpentine appearance
- phtiocerol dimycocerosate- lung pathogenesis
-pathogenic in guinea pigs
5
Q
How does M tuberculosis get into a host?
A
- transmitted by inhalation of infected aerosols; rarely transdermal or GI infection
- aerosols are extremely infectious: <10 organisms can initiate infection
- alveolar macrophages phagocytose the inhaled bacilli
- naive macrophages are unable to kill the intracellular mycobacteria
6
Q
Where does M tuberculosis go in the body?
A
- it proliferates within mononuclear phagocytes, traveling to extrapulmonary sites, where it can establish latent (immunocompetent) or active (peds, HIV+, immunosenscence) extrapulmonary infection
- lymph nodes. kidney, bones, meninges
- swallowing infectious sputum infects GI
7
Q
What determines latent/dormant infection?
A
- immunocompetent hosts develop latent/dormant infection: only 5-10% lifetime risk of active TB
- current or later immunosuppression allows reactivation
- Non-TB infections may activate quiescent TN: Measles, Varicella, Pertussis
8
Q
What is the Cell-mediated Immune Response to M. tuberculosis?
A
- a CMI response terminates the unimpeded growth 2-3 weeks after initial infection
- CD4 helper T cells activate some infected macrophages to kill intracellular bacteria
- CD8 suppressor T cells lyse other infected macrophages -> caseating granulomas
- the Mycobacteria cannot continue to grow in the granulomas so they go into latency
- TNF plays an important role in latency
9
Q
Where is most likely location for active TB?
A
- 85% in lungs
- most common site of primary lesion is within alveolar macrophages in subpleural regions of the lungs
- bacilli proliferate locally and spread through the lymphatics to a hilar node forming a Ghon complex and from there can enter the bloodsteam
10
Q
What is a proliferative lesion in TB?
A
- develops where the bacillary load is small and host cellular immune responses dominate
- compact
11
Q
What is an exudative lesion in TB?
A
- predominate when large numbers of bacilli are present and host defenses are weak
- these loose aggregates of immature macrophages, neutrophils, fibrin, and caseation necrosis are sites of mycobacterial growths
12
Q
What is a Ghon complex?
A
-exudative lesion plus hilar node
13
Q
What are the dangerous possibilities for primary TB infection?
A
- Miliary TB
- TB meningitis
14
Q
What is the “normal” TB infection look like?
A
- TB enters via inhalation
- TB lesion in lung- infectious
- Replication
- Formation of Ghon complex- infectious
- Enter blood stream
- Formation of TB Granuloma- in neck lymph nodes, GI, long bones, kidney- still infectious
- 1-2 decades: Calcified TB granuloma
- reactivation if immunosuppressed?
15
Q
What can reactivation of TB infection lead to?
A
- Scrofula
- Genitourinary TB
- GI TB
- Skeletal TB
- Reactivating Pulmonary TB- infectious sputum and aerosol
16
Q
What are the risk factors for infection with M tuberculosis?
A
- crowded at risk environments (prisons, hospitals, homeless shelters, refugee camps)
- HIV
17
Q
What are risk factors for poor outcome in TB infection?
A
- uncontrolled HIV (inadequate HAART)
- steroids
- IFN gamma def
- TNF-alpha antagonists (REMICADE)
- less than 5 years old
18
Q
How are TB infections in the US?
A
- often reactivation cases from foreign travelers
- rates at an all time low but XDR strains really high proportion
19
Q
How does classic active pulmonary TB present on exam?
A
- 75% patients
- cough, weight loss “consumption”, fever, night sweats, hemoptysis, and chest pain
- On radiography- cavity formation= advanced infection. noncalcified round infiltrates could be confused with lung carcinoma
- HIV patient may look normal because of bad immune response
- fiberoptic bronchoscopy is effective for cultures (broncoalveolar lavage)
20
Q
How do patient with extrapulmonary involvement present on exam?
A
- 20% of patients
- 60% of these are sputum negative with normal chest radiograph
- nonpulmonary symptoms mimic a wide variety of diseases
21
Q
How does TB scrofula look on exam?
A
- painless, enlarging, or persistent mass
- cervical lymph node affected 2/3 of time
- systemic symptoms include fever/chills, weight loss
- usually TB scrofula in adults, usually not in children (they get the atypicals from putting things in their mouths) with cervical mass because it only happens with reactivaction in lymph nodes
- can do PPD and fine needle aspiration for culture
