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Year 2 clinical pathology > week 5 Mycobacterial disease > Flashcards

week 5 Mycobacterial disease Flashcards

1
Q

What shape are mycobacteria?

A

slender bacillus

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2
Q

What makes mycobacteria different to all other bacterial genera?

A

Unusual waxy cell wall:
High lipid content

Slow growing
Different media requirements

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3
Q

What is the staining character of mycobacteria?

A

They have poor take up with standard Gram’s stains.
They also retain certain stains without decolourisation by acid / alcohol because they are acid fast bacilli” (AFBs).
Stains used to identify them are:
Ziehl Neelsen (ZN)
Phenol auramine.

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4
Q

What type of pathogens are mycobacteria and waht type of infection do they cause?

A

They are Intra - cellular pathogens

They cause chronic infections with Latent phase of infection

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5
Q

What is the treatment of mycobacteria compared to other bacteria genera

A

They are treated with different antimicrobial agents compared to other bacteria.
The much longer courses of therapy.
Combination of agents to prevent resistance emergence

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6
Q

What mycobacteria causes Tuberculosis?

A

M. tuberculosis complex:

M. tuberculosis
M. bovis

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7
Q

What mcyobacteria caues leprosy?

A

M.leprae

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8
Q

Name 3 atypical mycobacteria that are assoicated with HIV and Fish tank granuloma?

A

M. avium complex
M. kansasii
M. marinum

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9
Q

In terms of M.tuberculosis what % of population is infected, deaths per year and what disase is a co infection with?

A

One third of world population infected

2 million deaths per year.

Co-infection with HIV: Sub-Saharan Africa

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10
Q

TB has become more common in the developed world because of what factors?

A

HIV infection

Breakdown of control programmes

Increased global migration from endemic areas

Increased travel

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11
Q

How does Tb spread?

A

Person to person - inhalation of infected respiratory droplets

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12
Q

What is the couse of the Tb infection?

A

1) Primary infection (usually pulmonary disease) - Some patients will be symptomatic (flu like) and some completely asymptomatic
2) Latent infection period

3) Reactivation of TB (does not occur in all people some people it will remain latent forever)
4) Dissemination (doesn’t disseminate to affect other organs in all people who get reactivation) NB. Primary infection may disseminate completely skipping the latent phase (this can happen in children)

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13
Q

What is the common site of primary Tb infection?

A

In the periphery of lung midzone

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14
Q

How does the body repond to Tb infection?

A

Tubercle formation (granuloma formation) via a cell mediated response

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15
Q

What is the structure, route and action of tubercles formed in TB?

A

There is a central area of epitheloid cells and giant cells. Have a surrounding lymphocytic cell infiltration, with central area caseous necrosis. Eventually getting fibrosis and calcification of lesions. The tubercles aim to contain the infection.
The bacilli slowly die or amy remain viable for 20 yeas.

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16
Q

What group of people are more likely to see a reactivation of tuberculosis?

A 
Lowered immunity 
Western countries : over 50 year old, men
Malnutrition
Alcoholism
Debilitating illness
HIV infection
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17
Q

How can you test for Tb when there is absent or mild clinical symptoms

A

Chest X ray.

Tuberculin skin test conversion

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18
Q

What 3 diseases make it more likely for reactivation of tuberculosis to occur?

A

Silicosis, chronic renal failure, gastrectomy

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19
Q

Taking what drug can increase the chances of reactivation of tuberculosis and why?

A

Taking Anti TNFα blockade (e.g. infliximab)

This is because Role of TNF alpha is to maintain the granuloma

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20
Q

Where does TB usually residde and be reactivated? Explain why

A

In the Lung apices due there highest oxygen tension.

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21
Q

What is the consequence of reactivation on tubercles of Tb.

A

Tubercles coalesce and get caseous necrosis Can also get cavitation - leading to a higher organism load so greater risk of transmission

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22
Q

What are the symptoms of reactivation of TB?

A 
Chronic productive cough
Haemoptysis
Weight loss
Fever
Night sweats.
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23
Q

What is the name for dissemianted TB? Who is susceptible?

A

Miliary tuberculosis.

Very young/old or those who are immunocompromised

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24
Q

What is the consequence of Miliary tuberculosis?

A

Causes erosion of necrotic tubercle into blood vessel in secondary diseases.

Get wide spread infection

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25
Q

What are common sites where miliary TB can spread too?

A 
Pleura
Lymph nodes
Kidneys  
Epididymis
Bone
Intestines
Brain / meninges
Pericardium
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26
Q

What is Disseminated tuberculosis?

A

It is a contagious bacterial infection in which TB bacteria has spread from the lungs to other parts of the body through the blood or lymph system

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27
Q

What are the main signs of TB meningitis?

A 
Often insidious onset
Unidentified fever
Personality change
Focal neurological deficit
Mild headache / meningism

May lack constitutional quartet
(fever, night sweats, anorexia, weight loss

28
Q

How is TB diagnosed?

A

Radiology:Chest X - ray.
Histology
Skin testing
(Blood test: Interferon- γ release assay: IGRA)

29
Q

When is the use of microbiology neccessary to diagnose TB? What type of sample is used?

A

Confirmation of diagnosis
Drug sensitivities.
Molecular typing profile: “MIRUs”.

The sample type need is: “Fresh” samples / tissue: i.e. NOT formalin fixed

30
Q

What is the procedure in collecting the sputum needed for testing TB?

A

Sputum: 3 “Early Morning” specimens.

3 taken > 8 hours apart, with > one early morning

31
Q

How is the sputum used to detect TB?

A

Direct microscopy for Acid fast bacilli (AFBs)> 5000 organisms per ml sputum: “smear positive”

Risk of transmission

32
Q

What are the two ways in which TB can be cultured?

A

Lowenstein - Jensen solid media: 3 - 4 weeks

Broth culture: automated, usually

33
Q

What processes are carried out if there is Positive AFB culture?

A

Referred to regional reference laboratory

Species identification

Sensitivities:
within two weeks

Strain typing

34
Q

In who would there be potentially a lack of sputa to test for TB and how do you get around this problem?

A

This is common in children –> Induced sputa
Nnebulised saline.
Bronchial aspirates
Gastric aspirates

35
Q

If you expect someone of having Renal TB what test do you do?

A

Early Morning Urines x3

36
Q

If you suspect someone having TB meniningitis what te CSF analyses do you do?

A

Cell count, protein, glucose
Microscopy / culture.
“Adequate” volume: > 6mls - increased yield.

37
Q

What is the advantage and disadvtange of uing TB nucleic acid amplification?

A 
It is done by PCR.
Adv --> rapid
Dis--> Less sensitive than culture
Expensive
Not 100 % specific - false positives
38
Q

How is Xpert MTB/RIF test used and in what settting would it be used in?

A

Direct to sputum which is clinically based and get result in two hours;

The Xpert MTB/RIF test is used in developing world where there is lack of access to cultures.

39
Q

What are the disadvantages of the treatment for TB?

A

Lengthy

Combined tablets which can cause poor adherence

40
Q

What is the standard treatment of TB?

A

2 months of Isoniazid, rifampicin, pyrazinamide ethambutol / (streptomycin)

4 months of: Isoniazid, rifampicin

41
Q

What is the treatment if the TB is in other sites (except for meningeal)

A

Standard 6 month regimen.

42
Q

Why is TB treatment involves multiple drugs?

A

To reduce the chance of drug resistance

43
Q

What is the treatment for TB meningitis?

A

12 months therapy

44
Q

What two types of TB will also increase initial treatment with corticosteroids?

A

TB meningitis and TB pericarditis

45
Q

What is the second line of treatment for TB?

A

Amikacin
Ethionamide / prothionamide
Cycloserine
Fluoroquinolones: ciprofloxacin, moxifloxacin

46
Q

What are common drugs that TB can become resistant to? MDRI

A

Isoniazid and rifampicin resistant.

47
Q

What drugs are invovled in extensive drug resistant?

A

MDR + Fluoroquinolone + injectable (amikacin or capreomycin)

48
Q

What new drugs are being developed for TB?

A

Bedaloquine
Delamanid
Pa-824

49
Q

What are the advantages of shorter regime of treatment for TB?

A

Improve completion rates

50
Q

What 5 factors are put in place to control TB?

A 
Notifiable disease - Chest Clinics.
Contact Tracing.
Tuberculin skin test:
Blood test: Interferon- γ release assay
Chest X - Ray.
51
Q

What are the 2 tuberculin skin test done to control TB?

A

Heaf test

Mantoux test.

52
Q

How does Mantoux test work?

A

Inject purified protein derivative (MTB extract) subcutaneously Read at 48-72 hours observing skin reaction

You get a cell mediated immune reponse

53
Q

What does Interferon gamma release assays measure?

A

Specific T-cells: IFN γ production.
TB specific antigens (ESAT6, CFP10)
DON’T cross-react with M bovis BCG.

54
Q

When can interferon gamma release assays be used to identify TB?

A

Latent TB: New entrants, contacts, immuno-suppressed (incl HIV), HCWs

Also identify Active disease:
extra-pulmonary; paediatric

55
Q

What does BCG vaccine contain?

A

Attenuated strain Mycobacteria bovis

Bacille Calmette Guerin

56
Q

When is BCG vaccine given?

A

Either to neonatal or if there is occupational risk of being exposed to TB

57
Q

What treatments of chemoprophylaxis is given to treat TB?

A

3 months Rifampicin / isoniazid; or 6 months isoniazid.

58
Q

Can a atypical non tuberculous mycobacteria be transmitted between people?

A

It is a Environmental organisms

Lack of person to person transmission

59
Q

What type of mycobacterium causes a HIV infected person to have a disseminated disease?

A

Mycobacterium avium Complex

60
Q

What type of disease would a non HIV infected adult or young child get if they have Mycobacterium avium Complex?

A

In adults: Pulmonary: tuberculosis – like disease

Young children: cervical lymphadenitis.

61
Q

How is mycobacterium avium diagnosed?

A

In a similar way, cultured, they are acid fast bacilli so can be stained in a similar way

62
Q

What is the treatment of mycobacterium avium?

A

Combination
Prolonged
Macrolide – clarithromycin or azithromycin

63
Q

What causes leprosy?

A

M. leprae

64
Q

What are the two immune responses caused by M.leprae in leprosy?

A

Tuberculoid –
macules/plaques, can cluster around nerves (ulnar and common peroneal) - not severe

Lepromatous
Subcutaneous tissue accumulation (disfiguring lesions)
Ear lobes, face - leonine facies.

65
Q

What is the treatment of leprosy?

A

Dapsone, rifampicin, clofazimine

66
Q

How is leprosy identified?

A

Genomic analysis as non culturable in vitro

Year 2 clinical pathology (21 decks)

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