Mycobacterial Diseases Flashcards

1
Q

What is the microbiology of mycobacteria?

A

Non motile, rod shaped
Long chain fatty acids, complex waxes and glycolipids in cell wall - structural rigidity, compete freunds adjuvant potent necrotising factor, staining characteristics
Acid alcohol fast, hold onto zn stain and auramine which has higher sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where can NTM be identified?

A

Remote streams, shower head, whirl pool (pseudomonas), fish tank (marina)
Soil, ubiquitous
Varied pathogenicity
No person to person transmission
Resistant to classical anti TB drugs
Can colonise
Use clarithromycin and drugs used for mdr TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the slow growing NTM?

A

MAI- aka m avium complex, in immunocompetent may invade bronchial tree, pre existing bronchiectasis or cavities. In immunocompromised- disseminated infection
M marinum- swimming pool granuloma
M ulcerans- skin lesions eg bairnsdale ulcer, buruli ulcer, chronic progressive painless ulcer. Surgical debridement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the rapidly growing NTM?

A

Abcessus, chelonae, fortuitum
Skin and soft tissue infections
In hospital settings
Respond to erythromycin and doxyclyin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the risk factors for NTM?

A

60/70’s, airways disease, previous TB eg cavities, asthma, bronchiectasis, complement deficient, cf, cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the diagnosis for NTM?

A

Lung disease- pulmonary symptoms, opacities, multifocal bronchiectasis
Exclusion of other diagnoses
Positive culture of more than one sample
Positive BAL
Positive biopsy with granulomata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is treatment for NTM?

A

Susceptibility testing may not reflect clinical usefulness
MAI- clari, azithryomycin
Rifampcin
Ethambutol
+/- amikacin, streptomycin
Rapid growing NTM- macrolide based 18-24 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is m leprae?

A

Paucibacillary tuberculoid- cell response is huge, peripheral neuropathy
load of bacteria and cell mediated immunity
Multibacillary lepromatous- lumps and bumps
Lateral eyebrow loss, thickened nerve?
Still common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is mtb?

A

Multi system disease
2nd most common cause of death by infectious agent after HIV
Most common opportunistic infection in HIV
7 closely related species, tb, bovis resistant to pyrizinamide, africanum
Obligate anaerobes, generation time 15-20 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the TB disease States?

A
Exposed individual 
Active TB quickly (2years) HIV 
Uninfected 
Cleared infection, natural immunity 
Contained- majority of 3rd of people who have TB, lifetime risk of activation.
Mantoux test- induration not erythema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is TB transmitted?

A
Droplet nuclei/airborne 
Less than 10microm particles 
Suspended in air 
Reach lower airway macrophages 
Infectious dose 1-10 bacilli 
3000 infectious nuclei- cough, talking 5 mins 
Air remains infectious for 30 mins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can TB be prevented?

A

Detection of cases
Treatment of index case
Prevention of transmission- Personal Protective Equipment, negative pressure isolation
Optimisation of susceptible contacts- vaccination 70-80% effectiveness in preventing severe childhood TB, protection wanes
Inflixumab- TB cases TNF link/immunocompromised link

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the natural history of TB?

A

Primary- asymptomatic, ghon focus complex
Limited by CMI
Rare allergic reactions include erythema nodosum
Occasionally disseminated
Latent
Reactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why would you get post primary TB?

A

Failure of cell mediated immunity, immune system wanes 30 years old
Immunosuppression, chronic alcohol excess, malnutrition, ageing
Pulmonary or extra pulmonary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How can the host response shape clinical outcome?

A
Less effective immune response >>
Healthy context- ltbi
Lymphadenitis
Localised extrapulmonary
Pulmonary localised/widespread- caseating granulomata, upper lobe
Meningeal
Miliary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the presentation of extra pulmonary TB?

A

Lymphadenitis- scrofula, cervical lymph nodes,abscess and sinus
GI- swallowing of tubercles (lavage in kids)
Peritoneal- ascitic or adhesive looks like crohns
Genitourinary- slow progression to renal disease, subsequent spreading to lower urinary tract sterile pyuria
Bone and joint- haematogenous spread, spinal TB venous plexus nearby, potts
Military- seeds on cxray, progressive disseminated haematogenous TB, increasing due to HIV
Meningitis- Africa and Vietnam

17
Q

What is the clinical approach to TB?

A
High index of suscpicion
Suggestive symptoms 
Ix culture and histology 
Tx
Preventing onward transmission
18
Q

What should be included in hx and examination?

A

Ethnicity, travel, contacts with TB, bcg vaccination, non specific examination findings

19
Q

What investigations are needed for TB?

A

Cxr mediastinal, para tracheal stripe widened
Sputum times 3
Bronchoscopy, biopsies, emu
Stains
Culture
NAAT- PCR point of care
Histology
Tuberculin skin test- mycobacteria, relies on lots of things, delayed hypersensitivity, cross reacts with bcg
Igra- detection of antigen specific ifn gamma production, enzyme linked immune asay. Cannot distinguish latent and active

20
Q

What is the smear in TB involving?

A

60% sensitivity
Gastric aspirates in kids
Other specimens centrifuged urine and csf
Rapid, operator dependant

21
Q

What is the treatment for TB?

A

Rifampcin- raised transaminases and induces cytochrome p450 , orange secretions
Isoniazid- peripheral neuropathy, hepatotoxicity
Pyrazinamide- hepatotoxicity
Ethambutol- visual disturbance
RI for 4 months Dot/vot
Vit d
Surgery

22
Q

What is mutli drug resistant TB?

A

Resist to r and I
Extremely drug resistant- fluoroquinolones and at least one injectable
Spontaneous mutation and inadequate treatment
Previous TB, HIV, known contact to mdr TB, 4 months positive smear, 5 months positive culture
4/5 drug regimen

23
Q

What are the challenges in TB and HIV diagnosis?

A

Clincal history- less likely to be classical, symptoms absent in low cd4 count
Chest X-ray- more likely extrapulmonary, x Ray changes variable
Smear microscopy and culture- less sensitive
Skin test- more likely to be negative
Timing of tx
Drug interaction
Overlapping toxicity
Adherence

24
Q

What categories can mycobacteria be divided into?

A

Slow growing6-8 weeks, TB MTB complex is bovia and tuberculosis. MAC- avium and intracellulare immunocompromised hosts
Rapidly growing 3-5 days- abscesssus complex, abcessus, massilense, bolletti, immunocompromised
Ungrouped- leprae