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Microbiology Part 1 > Lec9 tuberculosis > Flashcards

Lec9 tuberculosis Flashcards

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Biology 101 flashcards
1
Q

What are koch’s 4 postulates?

A
  • bacteria must be present in every case of disease
  • bacteria must be isolated from host with disease and grown in pure culture
  • specific disease must be reproduced when pure culture of bacteria is inoculated into healthy host
  • bacteria must be recoverable from experimentally infected host
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2
Q

What are the microbiological properties of TB?

A
  • lipid rich cell wall so resistant to traditional stains and antibiotics
  • contains mycolic acid in cell wall
  • cell wall is hydrophobic so get clumping of bacteria
  • slow incubation time
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3
Q

What is mycolic acid?

A

major component of cell wall of TB

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4
Q

What is shape of mycobacteria? gram? acid fast or non acid fast? other notable characteristics?

A
  • non-motile non-spore forming aerobic
  • rods [bacilli]
  • gram null or weakly +
  • acid fast
  • cell wall contains lots of mycolic acids
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5
Q

What is acid fast staining?

A
  • first stain with carbolfuschin
  • then put on acid acohol solution, if does not decolorize with acid alcohol solution then it is an acid fast organism
  • all myobacteria are acid fast
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6
Q

What is rate of growth of class I myobacteria? does it produce yellow pigment? how frequently is it pathogenic? what are two representative organisms?

A
  • rate of growth: slow
  • produces yellow pigment
  • usually pathogenic
  • representative:
  • — M. kansasii
  • — M. marinum
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7
Q

What is rate of growth of class 2 myobacteria? does it produce yellow pigment? how frequently is it pathogenic? what is one representative organism?

A
  • rate of growth: slow
  • produces yellow pigment
  • sometimes pathogenic
  • representative:
  • — M. scrofulaceum
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8
Q

What is rate of growth of class 3 myobacteria? does it produce yellow pigment? how frequently is it pathogenic? what is one representative organism?

A
  • rate of growth: slow
  • does not produce yellow pigment
  • usually pathogenic
  • representative:
  • — M. avlum complex
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9
Q

What is rate of growth of class 4 myobacteria? does it produce yellow pigment? how frequently is it pathogenic? what are two representative organisms?

A
  • rate of growth: fast
  • does produce yellow pigment
  • sometimes pathogenic
  • representatives:
  • — M. abscessus
  • — M chelonae
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10
Q

What is rate of growth of non-runyon class myobacteria? does it produce yellow pigment? how frequently is it pathogenic? what is one representative organism?

A
  • rate of growth: slow
  • does not produce yellow pigment
  • always pathogenic
  • representative:
  • — M. tuberculosis
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11
Q

What are m tuberculosis virulence factors?

A
  • does not have toxins or capsules [traditional virulence factors]
  • major virulence factor = intracellular survival
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12
Q

What is mech of tuberculosis intracellular survival?

A
  • makes antibody and complement ineffective
  • inhibits phagosome-lysosome fusion after phagocytosis
  • interferes with toxic ROS produced in phagocytosis
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13
Q

After transmission how much time until positive skin conversion test?

A

6-8 weeks

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14
Q

How is TB transmitted?

A
  • airbone
  • can remain suspended in air for several hours
  • close contacts, cough, sneezing
  • droplet of TB enter alveoli and ingested by alveolar macrophages
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15
Q

What happens in primary infection of TB?

A
  • at first very minimal host immune response
  • get intracellular replication that destroys alveolar macrophages
  • spread via lymphatic channels and via blood stream
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16
Q

How is latent TB infection [LTBI] established from primary?

A
  • cell-mediate immune response
  • immunologic basis for skin testing
  • macrophages presenting TB antigen attract T lymphocytes
  • immune response kills most of bacilli leading to formation of granuloma
  • MTB persists within inactivated macrophages inside granuloma
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17
Q

How is granuloma formed?

A
  • aggregation of macrophages, lymphocytes, fibroblasts

- due to low pH and anoxic environment of caseating center TB does not replicate but is able to survive

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18
Q

What is ghon’s complex?

A
  • calcified subpleural [surface] granulomas in mid lung and in hilar lymph node
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19
Q

Are there any symptoms in latent TB?

A

No

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20
Q

Are patients with latent TB contagious?

A

No

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21
Q

How can you diagnose latent TB?

A
  • PPD

- interferon gamma release assay [IGRA]

22
Q

What are IRGAs [interferon gamma release assays]?

A
  • quantiferon-TB and TB-spot
  • they are Elisa tests to detect release of interferon gamma from patients after incubation with 2 synthetic peptides that are specific to TB
23
Q

What is PPD?

A
  • antigenic components [tuberculins] are extracted from culture filtrate by protein precipitation
  • if you have TB, will get delayed hypersensitivity rxn to intradermal tuberculin 6-8 wks after infection
24
Q

What are the downsides of PPD testing?

A
  • required proper intradermal administration
  • need to return 48-72 hrs later
  • false positive from BCG vaccination and non TB myobacteria
  • false negatives in patients who are immunocompromised
25
Q

What is the clinical approach to latent TB?

A
  • get chest radiograph
  • take 3 consecutive sputum AFB samples to look for evidence of active disease or of prior healed TB
  • give isoniazid for 9 months if no evidence of active disease
26
Q

What are the risk factors for TB exposure and infection?

A
  • prison
  • health care workers
  • homeless, medically underserved, low income
  • recent immigration
27
Q

What makes you at risk for developing TB once exposed?

A
  • HIV infection
  • diabetes
  • organ transplant
  • treatment wtih IF inhibitor
  • recent TB infection
  • illicit drug use
  • history of inadequately treated TB
28
Q

What are 4 disease that TNF [tumor necrosis factor] inhibitors usually treat?

A
  • crohns
  • ulcerative colitis
  • rheumatoid arthritis
  • psoriasis
29
Q

What are 3 examples of TNF inhibitors?

A
  • infliximab
  • etanercept
  • adalimumab
30
Q

What is possible complicated of TNF inhibitors?

A
  • they can cause reactivation of latent TB infection
31
Q

What happens in development of active TB?

A
  • TB bacilli multiplying extracellular in environment and overcome immune system
  • large TB load necroses wall of bronchi, lead to cavity formation, spread to other parts of lung
32
Q

What are symptoms of acute TB?

A
  • cough
  • hemoptysis
  • nigh sweats
  • anorexia
  • weight loss
  • weakness
  • dyspnea
33
Q

What is cavitary vs miliary pulmonary TB?

A

cavitary: TB has destroyed part of lung, get big hole in the lung = enlarged air space, usually occurs in reactivation
miliary: has spread via lymph nodes all over lung, get lots of tiny little nodules

34
Q

What are principles of TB treatment?

A
  • provide effective treatment for shortest duration possible
  • give 3-4 drugs with probable susceptibility to minimize risk for resistance
  • never add single drug to failing regiment
  • direct observed therapy
35
Q

What is standard TB treatment strategy?

A
  • 2 months of 4 drug regiment RIPE
  • – Rifampin [RIF]
  • – Isoniazid [INH]
  • – Pyrazinamide [PZA]
  • – Ethambutol [EMB]
  • maintenance with RIF [rifampin] and INH [isoniazid] for 4 months
36
Q

What is mech of rifampin action? bacteriostatic or bactericidal?

A
  • inhibits DNA-dependent RNA polymerase

- bactericidal

37
Q

What are adverse rxns of rifampin?

A
  • hepatotoxicity [most important]
  • thrombocytopenia
  • orange-red colored urine
38
Q

What are pharmacokinetic properties of rifampin – can it be absorbed orally? where is it excrete?

A
  • well absorbed orally

- excreted in feces

39
Q

Why does rifampin have a lot of other drug interactions?

A

because it induces hepatic cytochrome p450 enzymes so affects other drugs’ metabolism

40
Q

What is mech of action of isoniazid [INH]? bacteriostatic or bactericidal?

A
  • prodrug
  • inhibits mycolic acid synthesis [by inhibition mycolase synthetase]
  • bactericidal
41
Q

Is isoniazid absorbed orally?

A

yes well abosrbed orally

42
Q

What are adverse effects of INH [isoniazid]?

A
  • hepatotoxicity [most common]

- peripheral neuritis

43
Q

What is mech of action of PZA [pyrazinamide]? bacteriostatic or bactericidal?

A
  • mech largely unknown

- bacteriostatic

44
Q

Can PZA be given orally? how is it metabolized?

A
  • yes — well absorbed via oral administration
  • metabolized in liver by PZA deaminase
  • metabolites then excreted by kidneys
45
Q

What are adverse effects of PZA?

A
  • arthralgias aka joint pain [most common]
  • hepatotoxicity
  • hyperuricemia
46
Q

What is mech of action of Ethambutol? bactericidal or bacteriostatic?

A
  • inhibits cell wall polysaccaride syntehsis [inhibits arabinosyl transferase]
  • bacteriostatic
47
Q

What are adverse effects of ethambutol?

A
  • optic neuritis [most common]
  • decreased red-green color discrimination
  • peripheral neuropathy
48
Q

Is ethambutol absorbed orally? how is it eliminated?

A
  • absorbed well orally but impaired by food/antacid

- excreted unchanged in urine

49
Q

What is MDR?

A
  • multi drug resistant TB

- resistant to isoniazid and rifampin

50
Q

What is XDR?

A
  • extensively drug resistnat TB
  • resistant to isoniazid and rifampin
  • also resistant to fluorquinolones and at least one other 2nd line agent
51
Q

What is bedaquiline? action? concerns?

A
  • new approved TB drug
  • inhibits mycobacterial ATPase
  • concern becuase of liver inflammation and QT prolongation
52
Q

How do you prevent TB?

A
  • bacillus calmette guerin [BCG] vaccine
  • N95 respirator masks
  • negative pressure isolation rooms

Microbiology Part 1 (24 decks)

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