tb Flashcards
(28 cards)
intro:
* Infection by — tuberculosis
* 1/3 of the worlds population infected with tuberculosis –
the majority in Africa and Asia
* Growing incidence of — and —- strains associated with — co-infection
* TB is responsible for 1.6 million deaths worldwide in
2017 (20% HIV co-infected)
mycobacterium
mutlidrug resistant and drug resistant
HIV
factor affecting prevalence and risk of developing tb :
* Contact with high risk groups
* Origination from a — incidence country or frequent
travel to high incidence area
* Immune deficiency – diabetes, HIV, corticosteroids,
chemotherapy, chronic — disease, malnutrition
* Lifestyle factors – drug/alcohol, homelessness, hostels
overcrowding, prisons
* Genetic susceptibility – genetic —
high
kidney
genetic polymorphism
pathology of tb:
* Mycobacterium tuberculosis is an — , — pathogen
* — infection spread by — via respiratory —
* Only — number of bacteria needs to be — for
infection to develop
* People who have — TB in their lungs who cough,
spit or sneeze can spread the virus
* Patients with — TB do not spread the disease
* 90% of those infected with mycobacterium TB have — , — symptoms called LTBI with a—% lifetime chance that the latent infection will progress to a
overt — TB disease, this increases if there is co-
existent – or other –
arobic intracellular
airborne
coughing
respiratory droplets
small , inhaled
active
latent
asymptomatic latent
10%
active
HIV or immunosuppression
beginnings of infection:
* TB infection begins where the mycobacteria reach — air — of the lungs, they invade and replicate within —
* Macrophages attempt to ingest the bacterium by —
* The bacterium is stored in a — , the phagosome combines with the — to create a — where —- species try to kill the bacterium
* Mycobacterium TB has a — , — — acid capsule which protects it from toxic substances
* Mycobacterium TB is able to reproduce inside — and will eventually kill the cell
alveolar air sac
alveolar macrophages
phagocytosis
phagosome
lysosome
phagolysosome
reactive oxygen species
thick waxy mycolic acid
macrophages
granulomatous formation:
* TB is classed as one of the granulomatous inflammatory
diseases
* Granulomas, aggregates of —- are characteristic of TB
* Macrophages attack — macrophages and fuse
together to form — cells known as —
* The bacillus uses the — to avoid destruction by
the hosts immune system
* Mycobacteria inside the granuloma can become —
resulting in — infection
* The centre of the granuloma often contains —
epitheliod macrophages
infected
multinucleated
Langhan’s giant cell
granuloma
dormant
latent
caseous necrosis
formation of granuloma:
* After aerosol inhalation the first host cell is the — , but fails to kill the mycobacterium
* —- are produced these attract neutrophils, macrophages
* Tumour necrosis factor alpha, — accelerate
inflammatory cell recruitment
* — are recruited and are critical for activating the
macrophages
* In the presence of activated T cells the granuloma
becomes organised with —- at the centre, surrounded by a rim of —
* The TB bacilli may reside in granulomas in a dormant
state- relatively —
alveolar macrophages
chemokine
interferones
T cell
macrophages
lymphocyte
anaerobic
how does the body kill tb:
* The granuloma is a complex interplay between the — and the —
* The TB bacillus can be killed by —- which activate the — to kill the bacilli
*—- cells , — cells may also play a role releasing chemicals that break down infected cells
* There is cross talk between the — and — by — , as long well balanced ,the granulomas
contain the bacterium.
* If balance tips in favour of bacterium, such as — , — or other — , they are no
longer contained and can disseminate
tb bacillius and host defences
T cells CD4
macrophages
CD8 T cell and cytotoxic T cell
macrophages and T cells
mediators
ageing preggo or immunosuppression
primary tb:
* Usually occurs in —
* — , small focus — in mid zone of lung area of granulomatous inflammation, —
* Tuberculosis granulomas develop with further — being attracted
* Lymphatic spread of these macrophages to the —- and—- nodes where —- form
* The combination of the — plus —- is called the primary complex
* On initial contact of infection less than 5% of patients
develop active disease, this increases to 10% at first
year of exposure
childhood
inhalation
sub pleural
GHON FOCUS
Macrophages
tracheobronchial and mediastinal nodes
granuloma
ghon focus + hilar nodes
natural history of primary complex:
1. — , commonest result
2. Small ghon focus with —
3. The infection is spread from the — with — or — infection in the pleura, tuberculosis
empyaemia
4. Enlarged hilar nodes may cause —-
5. Damage to bronchial lymphatics may cause—-
of bronchial wall leading to—-
6. TB bronchial pneumonia can occur—
7. The infection may invade blood vessels resulting in
wide spread through the body, generalised miliary TB,
this may involve the lung only
healing
complete fibrosis
ghon focus
pleural effusion
active infection
bronchial obstruction
ulceration
bronchiectasis
early
secondary reactivation tb:
* The majority of people infected by mycobacterium, the immune system contains the — and the patient
develops cell mediated immune — of the bacteria, — TB
* The majority of active TB cases are due to the —- of
latent infection, the initial contact occurring may years before
* The lesions occur in characteristic sites, — subapical, — part of the — lobes where the aeration is in relative excess to the blood flow, rendering tissue more susceptible to infection
* — occurs, cell mediated immunity kills many
of the bacteria and macrophages
* The lesion may heal leaving a dense — or a mass
surrounded by — of — material
infection
memory
latent
reactivation
posterior , upper of lower
Caseous necrosis
dense scar
fibrosis of caseous material
natural history of 2ndary tb:
1. The necrotising process may involve a — , this may result in a — being formed
2. — occurs around cavities but also diffusely through the lung, — may occur
3. Scared apex, fibrotic cavities, bronchiectasis, diffuse
fibrosis small shrunken lungs may occur
4. Blood vessels in TB lesions are usually obliterated by —, however, vascular rupture may result in —-
5. The TB cavity may be super infected by — , —
6. TB bronchopneumonia
7. — TB
large bronchial bronchus
cavity
fibrosis
plural fibrosis
endarteritis
haemotpysis
aspergillus , myceotoma
millary tb
factors involved in reactivation of latent tb :
- Diabetes
- HIV co-infection
- Immunosuppressant therapy
- Chronic end stage renal disease
- Malnutrition
- Aging
- Gastrectomy
- Coal workers exposed to silica dust
- Laboratory workers in contact with infected material
acute tb bronchopneumonia :
* This can occur either as primary or secondary infection
Primary Tuberculosis Infection:
* In primary TB infection pneumonia may arise as an — of the — involve the —
and the material spreads to the —-
* Caseous bronchial pneumonias normally in — lobes and commonly —
* Condition is rapidly —
Secondary Tuberculosis Infection:
* Most always due to the — of the — material in cavities into the –
* Acute caseous bronchopneumonia occurs
extension of ghon focused
small bronchus
bronchial tree
lower , bilateral
fatal
movement
caseous material
bronchi
acute millary tb :
* This is due to — of — by — material containing larger number of —
* The — and — can be affected
* Miliary tubercles approx. 1-2mm are seen
* Acute miliary TB is usually a — condition and death is commonly due to TB —
* This may be confined to the — initially
invasion of blood stream
tb material
bacilli
lungs and organs
generalised
tb meningitis
lungs
extra pulomary tb ( EPTB) :
* This is an —- disease caused by mycobacterium TB that occurs in organ systems other than the –
* Epidemiological risk factors is — and high TB prevalent countries, exposure in institutional settings, homelessness, HIV infection,
immunosuppressive medications, end stage renal disease
* Diagnosis may be — as non-specific clinical manifestations that progress slowly, lower — of acid-fast bacilli smear on extra pulmonary specimens, and lack of consideration of EPTB in the
differential
* — is often required
* The sites on the body include - GI tract, CNS, spinal cord,
bone, joints, lymph nodes, miliary TB, urinary tract male and female, body cavities, pituitary gland, adrenal gland, skin,
ENT, eye, breast - just about anywhere!
* Whatever the organ there will be varying - there is tissue — , — and — , — with mass
effect, dense — , and cold —
infectious
lungs
birth
delayed , lower sensitivity
tissue biopsy
destruction, fibrosis , scarring., tuberculoma , dense exudate , abscess
extra pulmonary manifestation of tb classic examples:
Central Nervous System (CNS)
* Tuberculous — , seen in developing nations
(CSF: Lymphocytes, raised protein, low glucose)
* Spread from — to — space
* Dense fibrous —
* Numerous — tubercles close to vessels
* TB cerebral abscess
* Unless treated almost universally fatal
Lymph node involvement:
* Often in — lymph nodes
Bone involvement:
* — spread of TB bacilli can spread to — and growing ends of —
TB arthritis:
* Spine, destruction of vertebrae, caseous material tracks along psoas muscles, cold abscess, — disease
* TB — of long bones
tb meningitis
blood to subarachnoid spaces
exudate
white
neck
haemotgenous spread
spine and long bones
potts dieases
osteomyelitis
non tb mycobacteria bacteria infection:
* Mycobacterium avium-intracellulare complex usually in — , nodular — infiltrates
* Mycobacterium kansasii, pulmonary — disease
* Mycobacterium marinum soft tissue skin- – tanks
HIV
intesitital
pulomary lung
skin fish tank
- TB is acquired by — in —
Tuberculosis following exposure to someone who has — lung infection
– ~5% of those with sufficient exposure will clear the bacteria with no subsequent sequelae
– ~5% will go on to develop active pulmonary tuberculosis
– ~90% develop — TB - In latent TB a relatively small number of “ — ” bacteria are “—- ”. This causes no symptoms or
signs whatsoever and is not — - Latent TB accounts for the — of TB worldwide
breathing
mycobacterium
active
latent
dormant
walled off
transmissible
majority
- While latent TB itself causes no symptoms or signs, and is not transmissible, those with latent TB have a 5-10%
lifetime risk of — - Reactivation of TB is the “ — ” of dormant TB bacteria that begin to — and cause active TB
infection which will lead to symptoms, signs and
transmissibility
– This active TB infection could be — or — - — (weakened immune system) can increase the 5-10% risk of lifetime reactivation of latent TB.
This includes:
– —
– Immunosuppressing — such as — or medications used to treat autoimmune disease
reacitvation
awakening
replicate
pulmonary or extra pulmonary
immunospression
HIV
medications , steroids
symptoms - pulmonary tb:
* Most — TB is pulmonary. Extra-pulmonary is about
20%
* Pulmonary TB is — . A bacterial infection of lung
* However, in contrast to typical acute bacterial
pneumonia which has symptoms lasting a — number of days, TB has an — onset and symptoms are
usually present for several — to many —
* Typical symptoms include
– Drenching night sweats
– Weight loss
– Fever
– — cough
– — (coughing blood)
active
pneumonia
short
insidious
weeks to months
productive cough
hemptypsis
symptoms - extra pulmonary tb:
* Those with pulmonary TB may also have other sites of
TB infection in the body (extra-pulmonary TB)
* But extra-pulmonary TB can also occur in —
without pulmonary TB
* Commonest sites of extra-pulmonary TB include:
– — (TB lymphadenitis AKA Scrofula)
– — (TB osteomyelitis)
– — nervous system (TB meningitis)
– But it can occur anywhere in the body including the eyes
( —TB)
* A lot of extra-pulmonary TB is not — since the patient is not coughing up — like in pulmonary TB
symtpms of extra pulmonary :
* Constitutional symptoms of drenching nights sweats,
weight loss and fever are likely to be present, just as in
pulmonary TB
* Other symptoms depend on the site of infection
– TB lymphadenitis
* Swollen lymph nodes, typically cervical / supraclavicular
– TB osteomyelitis
* Pain at site of infection. Spinal TB – chronic back pain
– TB meningitis
* Drowsy, confused, headache, photophobia, neck stiffness
* Classical bacterial meningitis presents with very acute
headache, photophobia and neck stiffness
* TB meningitis may be more vague such as just drowsiness andconfusion
isolation
lymph node
bone
central nervous
ocular
not transmissible
bacilli
signs:
* —
* Pulmonary TB:
– May have — (image shown) as a result of — lung disease
– Coarse — on auscultation of the lung over area of
infection, just like in — pneumonia
* Extra-pulmonary TB:
– — , — lymph nodes
– — over site of bone involvement
– Signs of meningitis include drowsiness / confusion, low GCS, or specific signs such as — sign (image shown)
cachexia
digital clubbing
suppurative lung
crackles
typical
palpable enlarged
tenderness
Kernig’s signs
latent tb invesitgation:
* The presence of latent TB can be tested for by proving that a patient has had — to TB
* This is done in 1 of 2 ways
1. — test ( — test) involving — injection of tuberculin which the body will recognise as
TB and cause a visible reaction if positive within — hours
2. — test which is a — test measuring the body’s — response to TB. Those that have had prior TB exposure will have a — test
* Neither of these tests can confirm current active TB infection. If the test is positive it merely confirms the patient has seen TB at some stage. Therefore, these tests should never be used in the diagnosis
of active TB
* Both tests have their benefits and disadvantages
– Tuberculin test involves 2 patient visits, one to give the — , and a second — later to read the reaction.
Whereas quantiferon is a — visit.
– The tuberculin reaction is also somewhat — and
requires a health care professional familiar with interpreting it.
Quantiferon gives a more — result.
– Tuberculin test is —
– The electronic record of the result of a quantiferon test will
likely still exist in 10 years, whereas the tuberculin result
relies on the distant memory of a healthcare worker and or a
note in the patient chart on a loose sheet of paper. So I
prefer a quantiferon
prior exposure
tuberculin ( Mantoux)
intradermal
72 hours
quantiferon
blood test
immune response
injection , after 72 hours
single
subjective
objective
cheaper
active tb investigations:
* The diagnosis of active TB infection hinges on proving the presence of mycobacterium tuberculosis. The diagnosis is —
* The gold standard is — the organism which may
take a short number of days to up to 8 weeks
* Confirming the — of the organism is also crucial
to treatment (what treatment will work)
* Microscopy is also performed
(Ziehl-Neelsen stain - image)
– This can reveal the presence of AFB to the trained observer,
but this isn’t necessarily M.TB (slide 30),
and tells you nothing about what treatment will work
microbiological
culturing
sensitivity
