Mycobacterial infections (TB) Flashcards
1
Q
Difference b/t acute and chronic cough?
A
- acute cough: only exists for less than 3 weeks and is most commonly due to an acute respiratory tract infection. Other considerations include and acute exacerbation of underlying chronic pulmonary disease, pneumonia, and PE
- Chronic: cough that has been present longer than 3 weeks is either subacute (3-8 weeks) or chronic (more than 8 weeks)
2
Q
Common causes of chronic cough
A
- post nasal drip from allergies or chronic sinusitis
- asthma
- postinfectious
- chronic bronchitis
- GE reflux
- heart failure
- medication induced (ACE inhibitors)
- enviro irritants -> pollution
3
Q
Mycobacteria infections
A
- Mycobacterium TB
- Mycobacterium Leprae
- Atypical & nontubercular mycobacterium
4
Q
Definition of TB
A
- an infectious disease caused by the tubercle bacillus, Mycobacterium tb, and characterized pathologically by inflammatory infiltrations, formation of tubercles, caseation, necrosis, abscesses, fibrosis and calcification
- most commonly affects the respiratory system
5
Q
What type of stain do you use to dx TB
A
- Acid fast bacilli stain
mycelia acid which makes up the wall of mycobacterium take up acid fast stain (won’t show up in gram - or + stains)
6
Q
TB epidemiology
A
- TB is one of world’s deadliest disease:
1/3 of world’s pop is infected with TB - each year over 9 mill people around the world are afflicted with TB
- each year, almost 2 mill TB related deaths worldwide
- TB is leading killer of individuals who have HIV
-Incidences of TB in the U.S> has been decreasing.
Increase in 1992 (18% increase compared to 1985) associated with HIV
7
Q
Is the rate of TB declining in the U.S.?
A
- yes, the TB rate has been going down in U.S. each year since 1992
- the average annual % decline in the TB rate slowed from 6.6% for 1993 through 2002, to an avg decline of 3.4% for 2003 - 2008
- rate from 2013: 3.2%
8
Q
Who accounts for most of the increase of TB cases?
A
- HIV patients account for 30-50% of increase
- HIV is the greatest known RF for reactivating latent TB infection
9
Q
Where has TB become prevalent?
A
- prevalent in populations co-infected with HIV and M. tuberculosis, such as inner city minority and injection drug users
- in some inner city tb clinics: 40% of all pts with TB are infected with HIV
- TB in foreign born individuals accounted for 53% of cases in 2004 (mexico, philippines, Vietnam, India and China)
10
Q
4 possible outcomes of TB infection
A
- immediate clearance of the organism
- chronic or latent infection (gets past initial immunity barriers into lungs)
- Rapidly progressive disease (primary disease -> rapidly spreads throughout lungs, may spread to other organs)
- Active disease many years after the infection (reactivation disease) may lay dormant for many years
11
Q
Chronic (latent) infection
A
- person comes in with positive PPD but is asymptomatic with clear CXR
- Person is infected but not infectious
12
Q
Primary disease
A
- small bacilli carried in droplets small enough to reach alveolar space
- If host system fails in clearing:
- Bacilli proliferate inside alveolar macrophages and kill the cells
- infected macrophages produce cytokines and chemokines that attract other phagocytic cells, including monocytes, other alveolar macrophages, and neutrophils, which eventually form a nodular granulomatous structure called the tubercle or Gohn focus
- if the bacterial replication isn’t controlled, the tubercle enlarges and the bacilli enter the local draining lymph nodes, this leads to lymphadenopathy, a characteristic manifestation of primary TB
- Caseation/fibrosis/calcification: ghon complex
(caseation: necrosis of cells (look like cheese in middle of complex)
- calcification is imp step in containing bacterium
13
Q
steps of Primary disease infection
A
- bacilli reach alveolar space
- proliferation inside macrophages
- initial inflammatory granulomatous tubercle formation (if bacterial replication is controlled here, pt will not develop primary disease and is said to have chronic or latent infection)
- Enlargement of tubercle and infiltration of lymph system (Gohn complex: describes an inflammatory nodule in the pulmonary parenchyma (Gohn focus) with an accompanying hilar adenopathy, in line with lymphatic drainage from the pulmonary segment
14
Q
Symptomatic primary disease
A
- those who develop active disease w/in 2-3 years after infection
- sever illness: lung necrosis, and extrapulmonary involvement
15
Q
Main symptoms of pulmonary TB?
A
Central: appetite loss, and fatigue
lungs: chest pain, coughing up blood, productive and prolonged cough
Skin: night sweats, pallor (anemia from chronic disease)
16
Q
steps of secondary/reactivation TB
A
- asymptomatic primary infection occurs
- cell-mediated immunity: has contained the infection (neutrophils, macrophages -> gohn complex probably present)
- dormancy
- then, recurrence may occur
17
Q
When does secondary/reactivation disease occur and what is it associated with?
A
- results when the persistent bacteria in a host suddenly proliferate (no longer contained b/c decreased immunity)
- clearly assoc. with immunosuppression and can be seen in the following circumstances:
HIV infection and AIDs
end stage renal disease
diabetes mellitus
malignant lymphoma
corticosteroid use - in contrast to primary disease: the disease process in reactivation TB tends to be localized, there is little regional lymph node involvement and the lesion typically occurs at the lung apices (where gohn lesion resided)
18
Q
Signs and symptoms of secondary/reactivation of TB
A
cough, hemoptysis persistent fever/night sweats wt loss malaise adenopathy pleuritic chest pain
19
Q
What is a Rasmussen aneurysm in TB?
A
- develops aneurysm and it ruptures
20
Q
What is Miliary TB?
A
- if the bacterial growth continues to remain unchecked, the bacilli may spread hematogenously to produce disseminated TB
- lung looks like it is covered with millet seeds
- Miliary TB is used to denote all forms of progressive, widely disseminated hematogenous TB even if the classical pathologic or radiologic findings are absent
