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MICRO - Abbie > 7. Mycobacterial diseases > Flashcards

7. Mycobacterial diseases Flashcards

1
Q

What percentage of world’s population is infected with TB?

A

About 30%

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2
Q

What are examples of mycobacterium tuberculosis complex?

A

Mycobacterium tuberculosis and Mycobacterium bovis (BCG).

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3
Q

What are examples of mycobacterium avium complex?

A

Mycobacterium avium and mycobacterium intracellulare

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4
Q

What are examples of mycobacterium abscessus complex?

A

Mycobacterium abscessus, mycobacterium massiliense, mycobacterium bolletii

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5
Q

What are examples of ungrouped mycobacteria?

A

Mycobacterium leprae

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6
Q

What is the shape of mycobacteria?

A

Non-motile rod-shaped bacteria

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7
Q

How quickly do mycobacteria grow?

A

Relatively slow-growing compared to other bacteria

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8
Q

How is mycobacteria characterised?

A

Long-chain fatty (mycolic) acids, complex waxes and glycoproteins in the cell wall. Structural rigidity. Makes up complete Freund’s adjuvant. Has specific staining characteristics. Acid-alcohol fast.

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9
Q

What staining is used to detect mycobacteria?

A

Auramine is usually used as a screening test.

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10
Q

What are 5 features of non-tuberculous mycobacteria?

A

Ubiquitous, environmental, atypical, varying spectrum of pathogenicity, and may be colonising rather than infecting.

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11
Q

How is non-tuberculous mycobacteria transmitted?

A

NO person-to-person transmission

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12
Q

What is non-tuberculous mycobacteria resistant to?

A

Commonly resistant to the usual anti-TB therapy.

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13
Q

What are examples of slow-growing NTM?

A

Mycobacterium avium intracellulare, mycobacterium marinum and mycobacterium ulcerans.

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14
Q

How does mycobacterium avium intracellulare infect people?

A

Immunocompetent - may invade bronchial tree; pre-existing bronchiectasis or cavities. Immunosuppressed - disseminated infection

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15
Q

What causes swimming pool granuloma?

A

Mycobacterium marinum

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16
Q

What causes skin lesions (e.g. Bairnsdale ulcer, Buruli ulcer) and/or a chronic progressive painless ulcer?

A

Mycobacterium ulcerans

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17
Q

What are examples of rapid-growing non-tuberculous mycobacteria?

A

Mycobacterium abscessus, Mycobacterium chelonae, Mycobacterium fortuitum

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18
Q

How does non-tuberculous mycobacteria present?

A

Causes skin and soft tissue infections, may be found in hospital settings and isolated from blood cultures (especially when devices such as vascular catheters are being used).

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19
Q

What are risk factors for NTM?

A

Age and underlying lung disease

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20
Q

How is NTM diagnosed?

A

Combines clinical findings with microbiology findings (blood culture, bronchoalveolar lavage, biopsy). It is important to exclude other diagnoses.

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21
Q

What is the treatment for Mycobacterium avium intracellulare (NTM)?

A

Clarithromycin/azithromycin, rifampicin, ethambutol, with or without streptomycin/amikacin.

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22
Q

How is rapid-growing NTM treated?

A

Based on susceptibility testing and usually macrolide based.

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23
Q

What are the two types of Mycobacterium leprae?

A

Paucibacillary tuberculoid and multibacillary lepromatous

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24
Q

How is paucibacillary tuberculoid (Mycobacterium leprae) characterised?

A

Few skin lesions and robust T cell response

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25
Q

How is multibacillary lepromatous characterised?

A

Abundance of bacilli, multiple skin lesions, poor T cell response

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26
Q

What is the 2nd most common cause of death by infectious agent (after HIV)?

A

Mycobacterium tuberculosis (TB) - it is a multisystem disease

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27
Q

How many deaths per year due to TB?

A

2 million

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28
Q

What is the incidence of mycobacterium tuberculosis?

A

Increasing incidence since the 1980s. 9000 per year in the UK.

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29
Q

TB Disease States

A

After contact with a person with TB you could become infected, become latently infected or not become infected at all.

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30
Q

MTB complex involves 7 closely related species. What are the 3 main ones?

A

Mycobacterium tuberculosis, Mycobacterium bovis and Mycobacterium africanum.

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31
Q

What kind of aerobe is MTB?

A

Obligate aerobe

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32
Q

What is the generation time of MTB complex?

A

Generation time 15-20 hours

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33
Q

How is MTB transmitted?

A

Droplet/airborne, suspended in air. Reaches the lower airway macrophages. Infectious dose is 1-10 bacilli and air remains infectious for 30 mins.

34
Q

How can MTB be prevented?

A

Detecting cases; treating cases; preventing transmission (protective equipment, negative pressure isolation); optimisation of susceptible contacts, and vaccination (BCG).

35
Q

How does primary TB present?

A

Usually asymptomatic, Ghon focus on X-ray (granuloma in the lungs)

36
Q

What can be be seen in imaging in primary TB?

A

Ghon focus (granuloma in the lungs)

37
Q

What is primary TB controlled by?

A

Cell-mediated immunity

38
Q

What is an example of a rare allergic reaction caused by primary TB?

A

Erythema nodosum

39
Q

What does primary TB occasionally cause?

A

Disseminated/miliary TB

40
Q

What is post-primary TB?

A

This is reactivation or exogenous re-infection. Happens > 5 years after initial infection.

41
Q

What is the risk of post-primary TB?

A

5-10% lifetime risk

42
Q

What are risk factors for reactivation?

A

Immunosuppression, chronic alcohol excess, malnutrition and ageing

43
Q

Is the clinical presentation of post-primary TB pulmonary or extra-pulmonary?

A

Both. The host immune response determines the clinical outcome.

44
Q

What are some pulmonary effects of post-primary TB?

A

Caseating granuloma. Can be found in lung parenchyma and mediastinal lymph nodes. Commonly found in upper lobes.

45
Q

What are some extra-pulmonary effects of post-primary TB?

A

Lymphadenitis (AKA scrofula); gastrointestinal (swallowing of tubercles); peritoneal (ascitic or adhesive), genitourinary (slow progression to renal disease and subsequent spreading to lower urinary tract); bone and joint (haematogenous spread and spine - Pott’s disease), miliary TB; and tuberculous meningitis

46
Q

How does miliary TB present?

A

Millet seeds on CXR; progressive disseminated haematogenous TB; increasing due to HIV

47
Q

What are risk factors for post-primary TB?

A

Non-UK born; HIV or other immunocompromise; homeless; drug users; close contacts; and young adults

48
Q

How does post-primary TB present?

A

Fever, weight loss, night sweats, pulmonary (cough, haemoptysis), malaise and anorexia

49
Q

What investigations for TB?

A

CXR and other radiology; sputum x 3; bronchoscopy; biopsies; early morning urine; stains for acid-fast bacilli; culture; histology; tuberculin skin test; IGRA assay; and NAAT (nucleic acid amplification test)

50
Q

How is smear done for TB?

A

Sputum: sensitivity increases with additional samples, hence why 3 samples should be collected. Gastric aspirated in children.

51
Q

What bacteriological examinations are there?

A

Smear microscopy, culture solid medium, culture liquid medium, culture microcolonies, LPA, automated real-time PCR.

52
Q

What is the sensitivity for each of the bacteriological examinations?

A

Smear microscopy (highest): >5000 AFB/ml. Culture solid medium: +/- 100. Culture liquid medium, culture microcolonies, and automated real-time PCR: +/-10. LPA: only on positive smear.

53
Q

What is the median turn-around time for each of the bacteriological examinations?

A

Smear microscopy: 2 hours. Culture solid medium: 16 days (smear+), 29 days (smear-). Culture liquid medium: 8 days (smear+), 16 days (smear-). Culture microcolonies: 14 days. LPA: 1 day (direct testing). Automated real-time PCR: 2 hours.

54
Q

What is the additional turn-around time with DST?

A

Culture solid medium: 6 weeks. Culture liquid medium: 2 weeks (smear+) and 2 weeks (smear-). Culture microcolonies: 0 (H and R). LPA: 0 (H and R), and 21 days (indirect testing). Automated real-time PCR: 0 (R only).

55
Q

What is the gold-standard investigation for MTB?

A

Culture. (Can be done with liquid or solid systems).

56
Q

How long does culture take for MTB?

A

Up to 6 weeks. Further testing for culture isolates.

57
Q

What is the histological hallmark of TB?

A

Caseating granuloma

58
Q

What additional tests can be done for MTB?

A
  1. Speciation: NAAT - rapid diagnosis of smear positive samples and identified drug resistance mutations.
  2. Speciation: chromatography
  3. Drug sensitivity
59
Q

What does the Tuberculin Skin Test (TST) do?

A

Looks fore previous exposure to Mycobacteria

60
Q

How is the TST carried out?

A

2 units of tuberculin are injected intradermally. It is examined after 48-72 hours looking for a reaction. It is a delayed-type hypersensitivity reaction.

61
Q

What can TST cross react with?

A

This cross-reacts with BCG so can confuse the interpretation.

62
Q

What is the sensitivity of TST?

A

POOR sensitivity. May produce false negative if: HIV, age, immunosuppression and overwhelming TB.

63
Q

What does IGRAs do?

A

Investigation - detection of antigen-specific IFN-gamma production

64
Q

What are examples of IGRAs?

A

ELISpot and Quantiferon

65
Q

Any cross-reactions with IGRAs?

A

NO cross-reaction with BCG

66
Q

What are issues with IGRAs?

A

Cannot distinguish latent and active TB. Issues with sensitivity and specificity.

67
Q

What is the first-line treatment of TB?

A

As standard treatment for individuals with active tuberculosis, offer rifampicin, isoniazid (with pyridoxine hydrochloride), pyrazinamide and ethambutol hydrochloride in the initial phase of therapy; modified according to drug susceptibility testing; and continued for 2 months. After the initial phase, offer standard continuation treatment with rifampicin and isoniazid (with pyridoxine hydrochloride) for a further 4 months in individuals with active tuberculosis without central nervous system involvement. (10 months of treatment needed for CNS involvement)

68
Q

What are second-line medications for MTB?

A

Quinolones (Moxifloxacin), injectables (capreomycin, kanamycin, amikacin), ethionamide/prothionamide, cycloserine, PAS, linezolid, clofazamine.

69
Q

What are side effects of rifampicin?

A

Raised transaminases; induces CYP450; orange secretions

70
Q

What are side-effects of isoniazid?

A

Peripheral neurotoxicity (give with pyridoxine)

71
Q

What are side-effects of pyrazinamide?

A

Hepatotoxicity

72
Q

What are side-effects of ethambutol?

A

Visual disturbance

73
Q

What are other treatments for TB?

A

Vitamin D, nutrition, and surgery

74
Q

What is the cure rate of TB?

A

90%

75
Q

How can adherence to TB treatment be checked?

A

Direct observation therapy or video observed therapy

76
Q

What is multi-drug resistant TB resistant to?

A

Rifampicin and isoniazid

77
Q

What is extremely drug resistant TB resistant to?

A

Rifampicin, isoniazid and fluoroquinolones, and at least 1 injectable

78
Q

How may drug resistant TB arise?

A

These may arise due to spontaneous mutation or due to inadequate treatment

79
Q

How does risk of drug-resistant TB increase?

A

If previous TB treatment, HIV+, known contact with MDR TB, failure to respond to conventional TB.

80
Q

What treatment do those with drug resistant TB require?

A

They require 4/5 drug regimen with a longer duration: quinolones + aminoglycosides + para-aminosalicylic acid (PAS) + cycloserine + ethionamide. Current WHO recommendations state that 7 drugs should be used for 9-12 months.

81
Q

What are diagnostic challenges of HIV and TB coinfection?

A

Coinfection is common. Clinical presentation is less likely to be classical. Symptoms and signs might be absent if low CD4+. More likely to have extra-pulmonary manifestations (i.e. normal CXR). Smear microscopy and culture is less sensitive. Tuberculin skin test is more likely to be negative. Low sensitivity of IGRAs.

82
Q

What are treatment challenges of TB and HIV coinfection?

A

Timing of treatment initiation; drug interactions; overlapping toxicity; duration of treatment (adherence); healthcare resources.

MICRO - Abbie (19 decks)

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