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microb - bacteria > Mycobacteria > Flashcards

Mycobacteria Flashcards

1
Q

Features of mycobacteria

A
  1. Acid Fast Bacilli
    - Ziehl-Neelsen stain, uses heat to drive stain into cells
    - mycobacteria stained with fuchsin withstand discolourisation w acid & alcohol
    - or fluorescent dye auramine, strong affinity for waxy cell wall
  2. Slow growing, strict aerobes
  3. Waxy cell wall
    - peptidoglycan layer has different chemical basis for crosslinking to lipoprotein layer
    - outer envelope contains a variety of complex lipids (mycolic acids)
    - resistant to drying & other environmental factors + pronounced adjuvant activity (promote immunologic responsiveness)
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2
Q

Examples of mycobacteria

A 
Obligate pathogens
1. Mycobacterium tuberculosis complex - M. tuberculosis, M. africanum, M. canetti, M. bovis, M. microti
2. Mycobacteria leprae
Environmental saprophytes 
3. Non-tuberculous mycobacteria
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3
Q

Transmission of M tb

A

Respiratory route (infective droplet nuclei), only need 1-5 bacilli in terminal alveolus

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4
Q

Virulence factors of M tb

A

Cord factor - inhibits acidificatio of phagolysosome - AFB survives & multiplies in macrophages

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5
Q

Pathogenesis of M tb

A

Cell mediated immune response

  • Stage 1: contact w macrophage, survival & multiplication of AFB within macrophage
  • Stage 2: blood monocytes attracted to site of infection, differentiate into macrophages but unable to kill AFB
  • Stage 3: influx of antigen-specific T cells, secrete IFN-
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6
Q

Types of TB

A
  1. Primary TB
  2. Post primary TB
  3. Miliary TB
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7
Q

Features of primary TB

A
  • often clinically silent
  • result of primary infection in a non-immune host
  • Ghon focus = small foci of inflammation consisting of few MTC surrounded by a dense granuloma in the lung
  • Primary complex = Ghon focus + enlarged regional lymph nodes
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8
Q

Features of post primary TB

A
  • months/years after pri TB, due to reinfection/reactivation of latent TB
  • can be in any organ
  • large exuberant granulomata w central cheesy caseous necrosis
  • in lungs, necrotic tissue coughed away - leaving cavities
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9
Q

Features of miliary TB

A
  • when MTC is disseminated via bloodstream, affecting many organs
  • multiple granulomata visible in organs macroscopically as small white nodules (like millet seeds)
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10
Q

Clinical presentations of TB (4)

A
  1. Systemic features - fever, weight loss
  2. Pulmonary - chronic cough, hemoptysis, dyspnea, pleuritic chest pain, pleural effusion
  3. CNS - TB meningitis, GIT, bone & joint TB, miliary
  4. Lymph node involvement
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11
Q

Diagnosis of TB (7)

A
  1. Haematology: FBC (non specific)
  2. Biochemical: adenosine deaminase (secreted by T cells) of pleural/peritoneal fluid, CSF cell count (less glucose more protein, lymphocytic instead of neutrophils), urine analysis (sterile pyuria, a lot of pus cells)
  3. Imaging (CXR, CT/MRI brain/spine)
  4. Culture of AFB - early morning sputum/NG aspirate, first pass urine, CSF, biopsy (lymph nodes, bone, pleura), fluid (peritoneal, pleural, pericardial)
    - in solid media - egg based LJ media or broth based, incubate at 35-37C for up to 8 weeks
  5. Microscopy - acid gast/auramine smear, caseating granulomas & AFB
  6. Molecular - NAATs, PCR, isothermal amplification, DNA hybridisation
  7. Mantoux Testing (latent TB, normal CXR) - inoculation of purified protein derivative intradermally into forearm, read diameter of induration after 48-72h
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12
Q

Treatment & management of TB (2)

A
  1. Anti-TB drugs
    - standard therapy: 2m of daily R+I+P, 4m of daily R+I
    - pyridoxine + isoniazid to prevent neuropathy
    - latent TB: 6-9m of I/4m of R
    - 2nd line is toxic & less effective, used in resistance
  2. Infection control - isolate pt, contact tracing, TB is notifiable
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13
Q

Transmission of M. leprae

A
  • found within macrophages in dense clumps, very slow growing

Close & prolonged contact (resp route most likely)

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14
Q

Pathogenesis of leprosy

A
  1. Chronic granulomatous infection targeting Schwann cells of peripheral nerves
  2. Nerve damage: paralysis, anaesthesia, trophic ulcers, neuropathic joint disease (Charcot)
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15
Q

Clinical presentations of leprosy

A
  1. Initial presentation is mild - hypopigmented & hypoaesthetic skin lesion
  2. Look for subtle nerve damage - nerve tenderness/thickening, muscle weakness
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16
Q

Types of leprosy

A
  1. Tuberculoid leprosy
  2. Lepromatous leprosy
  3. Borderline leprosy
17
Q

Features of tuberculoid leprosy

A
  • patients who mount a strong cell mediated immune response (Th1)
  • 1 or 2 hypopigmented skin lesions, thickening of peripheral nerves
  • biopsy of skin lesions rarely show bacilli
18
Q

Features of lepromatous leprosy

A
  • patients w absent cell mediated immune response (predominantly humoural Th2 response)
  • intense edema of affected tissue, facial lip swelling + collapse of bridge of nose (leonine facies), mycobacteremia/dissemination (nasal/pharyngeal mucosa, eye, muscles, testicles, bone marrow)
  • tissue biopsy shows undifferentiated macrophages packed w AFBs
  • highly infectious due to nasal discharge
19
Q

Features of borderline leprosy

A
  • intermediate form, unstable, small fluctuations in immune response can shift either way along the spectrum
  • lymphocytic infiltrate & epitheloid but no grant cells
20
Q

Diagnosis of leprosy (4)

A
  1. Clinical examination
  2. Biopsy for histology - skin, nerve, retina, examine slit skin smears for AFB
  3. Molecular - PCR
  4. cannot culture in vitro
21
Q

Treatment & management of leprosy (3)

A
  1. Paucibacillary leprosy: Rifampicin (monthly, supervised) + Dapsone (daily, unsupervised)
  2. Multibacillary leprosy: PL treatment + Clofazimine (Daily, unsupervised) for 2 years
  3. Correct deformities, prevent further damage to anaesthetic limbs (eg physio), treat reactions to anti-leprosy drugs, social/psychological welfare
22
Q

Features of non-tuberculous mycobacteria

A
  1. Saprophytes of soil & water
  2. Cause opportunistic infections (transplants, cancer, HIV)
  3. May colonise non-sterile specimens (contaminant)
23
Q

Clinical presentations of non-tuberculous mycobacteria (4)

A
  1. Pulmonary opportunists (M. kasasii, M. malmoense, M. xenopi) - patients with lower resp tract abnormalities eg bronchiectasis, COPD
  2. AIDS related opportunists (MAI complex, M. haemophilum, M. cookei, M. hiberniae)
  3. Skin pathogens (M. marinum: fish tank granuloma, M. ulcerans: Buruli ulcer)
  4. Rapid growers (M. fortuitum, M. abscessus, M. chelonei complex) - can cause skin infections due to contaminated injection fluids eg diabetics using sq insulin, bacteremia in IV drug users
24
Q

Diagnosis of non-tuberculous mycobacteria (2)

A
  1. Runyon’s classification
    - photochromogens - produce pigment in light only - M. kansasii, M. marinum
    - scotochromogens - produce pigment in dark & light - M. scrofulaceum
    - non-chromogens - unpigmented - MAI complex, M. ulcerans (slow), M. cheloneae, M. fortuitum (rapid)
    - rapid growers - grow on Lowenstein-Jensen agar within 1 week
  2. Biochemistry, DNA probes, high performance liquid chromatography (HPLC)
25
Q

Treatment of non-tuberculous mycobacteria

A

Difficult & prolonged, NTMs resistant to many antibiotics, need multiple drugs with various combinations

microb - bacteria (11 decks)

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