Mycobacteria Flashcards

1
Q

How many species are included in the mycobacterium tuberculosis complex (MTC)?

A

12

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2
Q

What is the morphology of Mycobacterium tuberculosis?

A
  • Thin, straight rods
  • Acid-fast
  • Appear red in Ziehl–Neelsen stain against the blue counterstain (methylene blue)
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3
Q

What are the constituents of the mycobacterial cell wall?

A
  • Mycolic acids, esterified to glycerol, trehalose, or arabinogalactans
  • Trehalose dimycolate (TDM, cord factor): prevents chemotaxis of leukocytes, gives in vitro broth cultures a serpentine appearance
  • Trehalose monomycolate
  • Lipoarabinomannan: a virulence factor
  • Peptidoglycan
  • Phosphatidyl mannosides: prevent phagosome–lysosome fusion
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4
Q

What secretion system is utilized by mycobacteria?

A

Type VII

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5
Q

What are the growth characteristics of mycobacteria?

A
  • Obligate aerobes
  • Derive energy from oxidation of simple carbon compounds
  • Very slow growth rate, doubling time about 18 hours
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6
Q

Why are mycobacteria more resistant to chemical agents than other bacteria?

A

The hydrophobic nature of their cell surface

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7
Q

What are the types of cultures for mycobacteria?

A
  • Semisynthetic agar media: Middlebrook 7H10, 7H11
  • Inspissated egg media: Löwenstein–Jenson
  • Broth media: Middlebrook 7H9, 7H12
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8
Q

What are the contents of semisynthetic agar media for mycobacteria?

A
  • Defined salts
  • Vitamins
  • Cofactors
  • Oleic acid
  • Albumin
  • Catalase
  • Glycerol
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9
Q

What are the contents of inspissated egg media for mycobacteria?

A
  • Defined salts
  • Glycerol
  • Complex organic substances (e.g. fresh eggs/yolks, potato flour)
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10
Q

What are the two types of tuberculosis by manifestation?

A
  • Latent TB (LTBI): asymptomatic, not infectious, present in up to a third of the world’s population
  • Tuberculosis disease: fatal without treatment
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11
Q

How is Mycobacterium tuberculosis transmitted?

A

Aerosols

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12
Q

How are some MTC species other than Mycobacterium tuberculosis transmitted?

A

Vehicleborne through unpasteurized milk

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13
Q

What is the rule for the distribution of outcomes in those exposed to Mycobacterium tuberculosis?

A

10/3/1: for every 10 exposed, 3 become latent, 1 becomes active (6 are not infected)

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14
Q

What is the pathogenesis of tuberculosis disease?

A
  • The mycobacteria enter the body via respiratory aerosols
  • The droplets evaporate, leaving cells small enough to be deposited in the alveoli
  • The host responds by release of cytokines and recruitment of monocytes and macrophages
  • Mycobacteria begin to multiply within macrophages. Some macrophages kill the bacterium, others are killed
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15
Q

How does latent tuberculosis infection form?

A

A granulomatous shell forms around the focus of infection, keeping the cells under control

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16
Q

How do tubercle bacilli spread after infecting the alveoli?

A
  • Upon first infection, the tubercle bacilli always spread from the initial site via the lymphatics to the regional lymph nodes
  • The bacilli may spread further by the lymphatics or by the blood (hematogenous/miliary spread)
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17
Q

Where, other than the lungs, can tuberculosis infection be established?

A
  • Pleura
  • Lymph nodes
  • Pericardium
  • Kidney
  • Spine
  • Brain
  • Abdomen
18
Q

What are the types of tuberculosis disease by pathology?

A
  • Exudative type: an acute inflammatory reaction with edema fluid, neutrophils, and monocytes around the tubercle bacilli, resembling bacterial pneumonia
  • Productive (proliferative type): a chronic granulomatous region with a central area of large multinucleated giant cells containing tubercle bacilli, a mid zone of pale epithelioid cells arranged radially, and a peripheral zone of fibroblasts, lymphocytes, and monocytes
19
Q

Where in the lung does primary infection with Mycobacterium tuberculosis occur?

A

Any part of the lung, but most often the mid-lung fields or the base

20
Q

Where in the lung does reactivation infection with Mycobacterium tuberculosis occur?

A

Almost always at the apex of the lung, where PO2 is highest

21
Q

What are the clinical manifestations of Mycobacterium tuberculosis infection?

A
  • Fatigue
  • Weakness
  • Weight loss
  • Fever
  • Night sweats
  • Productive cough and hemoptysis (coughing blood)
  • Dyspnea (chest pain and difficulty breathing)
22
Q

How is Mycobacterium tuberculosis diagnosed in the lab?

A
  • Smears with Ziehl–Neelson stain: low sensitivity
  • Cultures: gold standard
  • Nucleic acid amplification test
  • Tuberculin skin tests
  • IFN-γ release assay
23
Q

How are sputum samples for Mycobacterium tuberculosis diagnosis obtained?

A
  • Coughed up in older children and adults
  • Broncheoalveolar lavage (BAL) during bronchoscopy in young children or people with trouble coughing up sputum
24
Q

What types of culture are used in the diagnosis of Mycobacterium tuberculosis?

A
  • Mainly: Löwenstein–Jenson, M7H10
  • Radiometric broth culture (BACTEC system)
  • Mycobacterial growth indicator tube (MGIT)
25
How does the tuberculin skin test work?
* Tests for type IV hypersensitivity to purifed protein derivative (PPD), a TB antigen * Has low specificity, as it gives a positive result in those vaccinated, exposed to non-tuberculous mycobacteria, and those with latent infection
26
How does the IFN-γ release assay work?
Monocytes are extracted from the blood and tested to see if they release IFN-γ in response to TB antigen
27
How is *Mycobacterium tuberculosis* treated?
Treatment occurs for 6–8 months: 2 months of intensive therapy followed by 4–6 months of lower dose continuation * Isoniazid (INH) * Rifampin (rifampicin, RMP) * Pyrazinamide (PZA) * Either ethambutol (EMB) or streptomycin (SM)
28
Which drug is used for preventitive therapy in high risk patients with LTBI?
Isoniazid (INH) for 9 months
29
How is tuberculosis disease prevented?
* Prompt and effective treatment of patients with active tuberculosis and careul follow-up of their contacts * Vaccination, particularly with BCG
30
What are the photochromogens?
* *M. kansaii*: TB-like * *M. marinum*: causes aquarium granuloma in fishtank workers * *M. ulcerans*: infects soft tissues All are slow growers
31
What are the scotochromogens?
* *M. scrofulaceum*: causes lymphadenitis (slow grower)
32
# Define Photochromogen
Producing pigment in light but not in darkness
33
# Define Scotochromogen
Producing pigment in darkness
34
# Define Nonchromogen
Don't produce pigment
35
What are the nonchromogens?
* *M. abscessus* * *M. fortuitum* group * *M. chelonae* group All are rapid growers and infect soft tissue
36
What type of mycobacteria are those of the *M. avium* complex? What disease do they cause?
* Slow-growing nonchromogens * Cause disseminated or pulmonary infection in imunocompromised patients (particularly AIDS patients) upon expossure to bird dropings with the bacteria
37
What type of climate is suitable for growing *Mycobacterium leprae*?
Cooler temperatures (around 30ºC), which is why it preferentially infects the face and extremities
38
What is the pathology of leprosy?
* Lesions form on the cooler tissue of the body, including the skin, superficial nerves, nose, pharynx, larynx, eyes, and testicles * Neurologic disturbances occur due to nerve inflitration, resulting in anesthesia, neuritis, paresthesia, trophic ulcers, bone resorption, and shortening of the digits
39
What are the types of leprosy infection?
* Lepromatous leprosy: course is progressive and malignant with nodular skin lesions, deficient cell-mediated immunity, and skin infiltration with regulatory T cells. Give a negative skin test * Tuberculoid leprosy: course is benign and nonprogressive, with a small number of macular skin lesions and intact cell-mediated immunity. Give a positive skin test * All patients start with borderline-LL and proceed to either true LL or TL
40
How is leprosy diagnosed?
* Scrapings from skin or nasal mucosa or from a biopsy of earlobe skin are smeared for staining with Ziehl–Neelsen stain * Biopsy of skin or a thickened nerve for histologic analysis * There are no serologic tests of value