Mycobacteria (complete) Flashcards

1
Q

What are the structures of an acid fast cell wall

A
  1. peptidoglycolipids
  2. Arabinogalactan
  3. PIM (phosphatidyl-inositol mannosides)
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2
Q

What are the 3 main mycobacterial diseases in humans

A

Tuberculosis
Leprosy
Buruli Ulcer

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3
Q

what is the estimate for the portion of the worlds population that is infected with TB

A

1/3 of the worlds population

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4
Q

What bacteria causes TB

A

mycobacterium tuberculosis

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5
Q

What is the cell wall component in the virulent strains of M. Tuberculosis that is necessary to cause disease

A

cord factor

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6
Q

What are the three types of TB

A
  1. Primary TB
  2. Secondary TB
  3. Disseminated TB
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7
Q

What is primary TB

A

initial infection with M. Tuberculosis

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8
Q

what is secondary TB

A

reestablishment of an active infection after a period of dormancy. a tubercle from primary TB ruptures and spreads again

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9
Q

what is disseminated TB

A

This is when infection spreads throughout the body

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10
Q

What two things reduced the incidence of TB in the US

A

pasteurization of milk and the isolation of patients in sanatoriums

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11
Q

who is at high risk for TB

A

those in contact with infected patients and those with immunodeficiencies (HIV)

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12
Q

How is TB diagnosed

A

by stethoscope, X-rays, skin tests using PPD, culturing

and an ACID FAST STAIN OF SPUTUM

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13
Q

what does a TB skin test identify

A

individuals with previous exposure to M. Tuberculosis by the presence of a hard red, swelling at the test site

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14
Q

What does a chest X-ray do for TB diagnosis

A

it identifies individuals with active TB

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15
Q

What easy is TB treatment, and what is used

A

it is difficult with common antimicrobials because the bacteria grow slowely and live in macrophages, but months of combination therapy is used to treat the disease

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16
Q

what are MDR TB strains

A

Multi drug resistant TB strains, are at least resistant to INH and rifampin

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17
Q

how are MDR TB strains treated

A

with cipro and kanamycin for up to 2 years (100 x more expensive)

18
Q

What are XDR TB strains

A

Extensively drug resistant TB strains (INH, rifampin, fluoroquinone and one of the second line drugs)

19
Q

how is TB prevented

A

prophylactic use of antibacterial drugs for those who went from negative to positive on the skin test and those exposed to active TB
vaccine (BCG) more effective for kids, used in countries where TB is common

20
Q

What are MOTTs

A

mycobacterium other than tuberculosis

21
Q

What are common MOTTs

A
  1. Mycobacterium avium complex (MAC)
  2. Mycobacterium Kansasii
  3. Mycobacterium fortuitum
  4. Mycobacterium Marinum
  5. Mycobacterium Scrofulaceum
22
Q

what happens with mycobacterial infections in AIDS patients

A

mycobacterium avium-intracellulare is the most common amongst AIDS patients, they affect almost every organ and cause massive organ failure.

23
Q

how easily are mycobacterial infections in AIDS patients to treat

A

very difficult do to the disseminated nature of the infection

24
Q

What is the bacteria that causes leprosy

A

mycobacterium leprae

25
Q

how easily in mycobacterium leprae grown

A

hard, it has never been grown in cell-free culture

26
Q

how is leprosy transmitted

A

person to person contact, or a break in the skin

27
Q

What are the two forms of leprosy

A

Tuberculoid leprosy

lepromatous leprosy

28
Q

What is tuberculoid leprosy

A
  • high cell-mediated response
  • Low antibody
  • nonprogressive disease, loss of sensation in skin regions
29
Q

What is lepromatous leprosy

A
  • low cell-mediated response
  • High antibody
  • gradual tissue destruction
  • loss of facial features, digits, and other structures
30
Q

what are the only two places mycobacterium leprae can be cultivated

A

footpads of mice, bellies of 9-banded armadillos

31
Q

how is leprosy diagnosed

A

loss of sensation in skin lesions (tuberculous leprosy)

disfigurement (lepromatous leprosy)

32
Q

how is leprosy treated

A

dapsone and rifampin for 6 mo. (tuberculoid)

dapsone, rifampin, and clofazimine for 2 years dapsone for 10 years

33
Q

what is the mycobacterium that causes beruli ulcers

A

mycobacterium ulcerans

34
Q

where is mycobacterium ulcerans foudn

A

slow moving water

35
Q

how does mycobacterium ulcerans enter the body

A

through skin abraisions

36
Q

does mycobacterium ulcerans grow intracellularly or extracellularly

A

extracellularly

37
Q

what is the toxin make by mycobacterium ulcerans

A

mycolactone, a polyketide (lipid)

38
Q

what does mycolactone (beruli ulcer toxin) do

A

destroys subcutaneous tissue, and is a powerful immune suppressing agent

39
Q

what is the main visible symptom of a beruli ulcer

A

when the subcutaneous tissue has been destroyed by mycolactone, the skin on top dies and sloughs off producing a clean ulcer

40
Q

how is a beruli ulcer treated

A

there is no reliable drug therapy, the infected skin must be removed and replaced with a skin graft