Tuberculosis Flashcards

1
Q

Describe the epidemiology of TB

A
  • 30% of the worlds population (2 billion) have latent TB (could reactivate to cause disease and spread to other people)
  • Disease does reactivate, 2 million people die from TB every year
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2
Q

Describe the incidence rates of TB around the world?

A

Parts of southern africa have very high incidence rates of TB.

In the UK we have had low rates but not as low as other countries.

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3
Q

Describe death rates from TB around the world?

A

South africa (despite having high incidence of TB / yr) has lower death rates, due to introduction of TB treatment programmes.

Certain countries e.g. somalia still have high death rates due to compromised healthcare delivery.

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4
Q

Describe TB cases and incidence rates in England

A

In the 1970’s TB incidence rates were around 24 new cases per 100,000 per year.

This steadily dropped until the the 1990’s, when a resurgence of cases occurred. Due to a number of reasons –> 1) drug resistance 2) TB requires prolonged tx with high level of compliance, tends to affect more vulnerable members of society who stuggle to complete course of Tx.

(6 months of tx).

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5
Q

Describe TB incidence rates in England (from 2014-2017)

A
  • North norfolk zero rates in 3 yr period
  • Couple areas in london with high rates, birmingham and leicester also have high rates of TB.
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6
Q

Describe epidemiology of new cases of TB in England

A
  • Number of UK born TB cases has been static (although should have been going down).
  • Most of new TB cases appears to be in people not born in the UK
  • This is improving now
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7
Q

TB cases in England: Country of origin that may have TB risk?

A
  • At risk populations:
    • Indian (highest rate shown due to highest population living in UK)
    • Pakistani
    • Romanian
    • Bangladeshi
    • Somalian (probably highest rate per population)
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8
Q

Describe the aetiology of tuberculosis

A
  • Tuberculosis is caused by Mycobacterium tuberculosis (and related species in the same complex).
  • TB = gram negative organsims, but is not classically gram negative in structure
  • More like a gram positive bacteria in structure
  • It has a unique cell wall, which is “waxy” and impermeable (to liquids, to stains, helps it to survive).
  • They can infect various different body tissues.
  • Divides very slowly and can become latent
  • Transmission is usually from aerolised droplets or fomites (dried out secretions).
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9
Q

Describe bacterial and mycobacterial cell walls

A

Bacterial:

Gram positive bacteria are surrounded by Peptidoglycan wall which stains purple/ violet, retains the crystal violet stain, therefore stain positive. (postitive, purple, peptidoglycan wall).

Gram negative –> Has in inner double cell membrane, thin peptidoglycan cell wall surrounded by an outer cell membrane. Therefore does not retain crystal violet stain and stains negative. (stain pink).

Mycobacteria:

Have peptidoglycan cell wall with a layer of mycolic acids surrounding it, creating waxy coat and preventing gram positive stain.

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10
Q

Describe the pathology of tuberculosis

A

Pathogenesis of TB is similar to other LRTI’s

Exposure to TB only leads to infection in 30% of cases

The primary infection only causes disease in around 10% and goes into containment/ latency in around 90% of cases. (Primary infection often goes undiagnosed as sx. are mild and self resolving.)

Containment tends to occur within a Ghon focus and hilar lymph nodes. (infection becomes sealed off and contained by the immune sx.)

(Ghon focus is an area within the lung that has become infected by TB, become necrosed and fibroses, self contained by the immune sx.)

Latent infection can stay in pt for life and never affect you. (No bacterial replication occurring.)

However reactivation and secondary disease only occurs in 10% of people.

Reates of reactivation vary enormously depending on risk factors.

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11
Q

Describe the histopathology of TB?

A

Histopathology –> granulomatous inflammation with “caseous” necrosis

Ghon lesion/ ghon focus = tuberculous caseating granuloma represents primary pulmonary TB infection

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12
Q

Where does latent TB tend to present within the lung?

What is a Ghon focus?

A

Latent TB tends to be contained within the middle or lower lobes of the lung (often the R lower lobe).

Ghon focus = Granuloma within the middle/ lower lobes of the lung, in combination with transient paratracheal or hilar lymphadenopathy. Ghon focus involves infection of adjacent lymphatics and hilar lymph nodes, it is known as the Ghon’s complex or primary complex.

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13
Q

What are the host risk factors for both primary infection and reactivation of latent TB?

A
  • Extremes of age –> younger children, older adults (more likely to cause activation straight away and reactivation)
  • Stress and starvation = specific risk factor
  • Immunocompromisation –>
    • E.g. in HIV infected host, 100x more likely to reactivate TB
    • Alcholism
    • Steroids and immunosuppresants
    • anti-TNF Rx for autoimmune diseases
  • Malignancy
  • renal failure
  • diabetes mellitus
  • vitamin D deficiency
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14
Q

What is miliary TB?

A

Miliary TB is widespread dissemination of mycobacterium tuberculosis via haematogenous spread (via blood) during primary infection and activation (only 10%, whereas 90% isolated in Ghon focus and suppressed).

Classic miliary TB is defined as millet like seeding of TB bacilli in the lung.

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15
Q

Sites of TB presentation for cases in england during 2017?

A

Half of TB presents in the lungs –> pulmonary = 54%

of which 3% was miliary TB

Half of TB presents as Extra pulmonary (58%):

  • Lymph nodes 33% (extrathoracic = 21%)
  • pleural = 9%
  • Bone = 6% (spine 4%)
  • GI 5%
  • CNS 4% (meningitis= 2%)
  • Genitourinary 2%
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16
Q

What are the clinical features of TB?

Onset

Systemic features?

pulmonary features?

lymph nodes affected?

other sites affected presents generally with?

A

Clinical features of TB vary according to the site of infection.

Sx normally have an insidious onset (median incubation time from a month to two years, however disease can emerge many years later.)

Sytemic features = fever, night sweats and weight loss

Pulmonary features –> Cough (normally dry for 2-3 weeks then productive), sputum, haemoptysis, dysponea

Lymph nodes –> typically cervical and axillary –> lymph nodes may become necrotic and affect the overlying skin (scrofula).

Other sites –> local sx of low grade inflammation and tissue necrosis

17
Q

What sites other than pulmonary can TB affect and how does it present?

A

GI –> most disease ileocaecal causes colicky abdominal pain and vomiting

Spinal TB –> local pain, bony tenderness for weeks- months.

CNS TB –> foci of infection in brain and spinal cord, foci rupture = meningitis, headache, confusion, seizures, focal neurological deficit

Genitourinary TB –> sx may be chronic intermittent or silent, LUTS sx.

Cardiac TB –> often involved pericardium, chest pain.

18
Q

What is shown here?

A

Necrotic cervical lymph nodes = scrofula

19
Q

What investigations will be done to diagnose TB? describe what you may see?

A
  • FBC –> possible leukocytosis (↑ WCC) but usually wont due to latent onset and low level inflammation
  • Urea and electrolytes –> usually normal
  • Liver function tests –> possibly raised
  • C reactive protein –> mild to moderate rise only
  • Lactate –> usually normal (unless sepsis).
  • CXR –> for 50% that present as pulmonary:
    • Cavities within upper lobes classical as the aerobic bacterium prefers higher oxygen level within upper airway = Upper lobe cavitating pneumonia
    • miliary shadowing
    • hilar lymphadenopathy
    • pleural effusion
    • pericardial effusion
  • CT/MR scans for thorax/ abdo/ spine/ bones/ head
  • Laproscopy/ thoracoscopy –> direct visualastion and biopsy
  • Other biopsies –> lymph nodes/ bones/ cold abscesses (in soft tissue)
20
Q

What signs of TB infection are on this CXR?

A
  • Cavitating pneumonia, multiple cavities in the L upper lobe
  • patient looks thin and emaciated too
21
Q

What type of TB presentation is shown in the CXR?

A

Miliary TB shown, nodular opacities, with diffuse spread of mycobacterium throughout the lung tissue (this will also be spread diffusely throughout other body tissues).

CT scan will show this even more distinctly.

22
Q

What pathology is shown?

A

Pericardial effusion from TB

23
Q

What pathology is shown?

A

Pott’s spine –> a form of TB where the bacterium infects the IV joints, charactersitically the infection starts in the IV disc, it spreads and can compress the spinal cord –> leads to neurological deficit.

24
Q

What pathology is shown in what region of the body?

A

Laproscopic image, showing portion of the bowel at the bottom of the image and peritoneal fluid, far more than normally should be there.

On the posterior abdominal wall there are deposits of TB infection.

25
Q

What are some of the microbiological investigations you can do for TB?

A

Assess the sputum –> obtain bacterial sample and stain it:

1) Zeihl neelsen stain –> stains acid-fast bacilli (AFBs), these bacteria will stain but on addition of acid, only the TB bacteria will show = pink stain
2) Auramine- Phenol stain –> AFBs = fluorescent stain

26
Q

Where can bacteria be obtained for culture?

how long can a culture take?

What can also be tried to identify TB infection?

A
  • From sputum, pleural fluid, pericardial fluid, blood, urine, CSF and biopsies
  • –> These are then cultured and tested for sensitivity. (Cultured on lowenstein jensen liquid medium)
  • Culture may take up to 8 weeks to become positive
  • PCR can also be tried but has a lower sensitivity than culture
  • Biopsies can be ZN stained to look for AFB’s (mycobacteria)
27
Q

How do we treat TB?

A
  • TB very rarely presents with sepsis
  • Multidrug tx required to prevent resistance –> all drugs used for the first two months
    • ​Rifampacin –> 6 months
    • Isoniazid –> 6 months
    • Pyrazinamide –> 2 months
    • Ethambutol –> 2 months
  • TB in CNS requires 12 months of TX as drugs do not cross BBB well.
28
Q

What other drugs may be used in TB tx (apart from 4 key AB’s)?

A
  • Pyridoxine to prevent neuropathy from isoniazid
  • Steroids if CNS or pericardial infection (inflammation from dying TB bacteria can be worse than the infection, the immune system suddenly re-recognises dying bacteria and increases inflammation- called paradoxical reactions. Occur around 3 weeks into tx, steroids to reduce the inflammation).
  • Vitamin D if deficient
29
Q

How can we prevent TB?

A
  • Prevention of primary infection:
    • For active TB cases:
      • Need to be in respiratory isolation
      • Prompt diagnosis and tx
      • contact tracing and testing
  • Vaccination with bacillus calmetter-guerin (BCG)
    • 25% prevention of primary infection
    • 70% prevention of active infection
  • Prevention of reactivation:
    • screening for latent TB infection and tx –> Tuberculin skin test (TST) and TB interferon gamma release assays (IGRA)
  • Treatment for latent TB:
    • Rifampacin and isoniazid for 3 months