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ID Week 3 > ICL 2.5: Mycobacterium Tuberculosis > Flashcards

ICL 2.5: Mycobacterium Tuberculosis Flashcards

1
Q

what is the basic microbiology of mycobacterium tuberculosis?

A

gram +, rod

thick PG layer

no outer membrane

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2
Q

what are symptoms of tubercolosis?

A
  • persistent cough
  • weight loss
  • fever
  • night sweats
  • chest pain
  • shortness of breath
  • fatigue
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3
Q

what is the composition of the mycobacterium genus cell wall?

A

mycobacterium is gram + so it has a cell wall

the cell wall is hydrophobic barrier that is rich in lipids

specifically mycolic acids and trahalose dimycolate!

this thick cell wall makes them hard to penetrate both for stains and macrophages

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4
Q

what stain do you use for mycobacterium tuberculosis?

A

it’s mycobacterium that has a really thick lipid cell wall that doesn’t stain well

so instead you have to use acid-fast stain

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5
Q

is mycobacterium tuberculosis motile?

A

non-motile

no flagella

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6
Q

is mycobacterium tuberculosis anaerobic or aerobic?

A

obligate aerobes

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7
Q

how fast does mycobacteria grow?

A

slow growers

it takes 2-3 weeks for a colony to grow on solid media…

this is just not practical and there’s also otehr bacteria around that could outgrow it so you have to use a special mediate to grow it in

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8
Q

what solid media is mycobacteria grown on?

A
  1. Lowenstein-Jensen agar

2. Middlebrook’s liquid media

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9
Q

how stable is mycobacteria?

A

BAD NEWS
it survives weeks to months on inanimate objects if protected from sunlight….

it’s also resistant to freezing or desiccation

it’s so resistant because of its lipid envelope!

GOOD NEWS
it’s killed by UV light and heat over 150 F

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10
Q

what are the 5 different bacteria species that can cause TB?

A

M. tuberculosso complex has 5 subspecies:

  1. M. tuberculosis
  2. M. africanum
  3. M. bovis
  4. M. microti
  5. M. caprae
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11
Q

what is M. bovis?

A

a type of M. tuberculosis complex bacteria

it’s genome is 99.95% similar to M. tuberculosis

it’s caused by infected cattle that spread it through unpasteurized diary product!

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12
Q

what is the BCG vaccine made of?

A

it’s an attenuated strain of M. bovis

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13
Q

what is M. africanum?

A

a type of M. tuberculosis complex bacteria

it’s common in tropical africa and causes approximately half of all TB infections there

genetic variations make it distinct from M. tb and M. bovis

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14
Q

what is M. caprae?

A

a type of M. tuberculosis complex bacteria

found in goats and cattle

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15
Q

what is M. microti?

A

a type of M. tuberculosis complex bacteria

found in rodents, pigs, rabbits, llamas

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16
Q

what populations in the US have TB?

A
  1. medically underserved
  2. poor
  3. homeless
  4. prison inmates
  5. alcoholics, drug users
  6. elderly
  7. foreign-born persons from endemic regions
  8. contact with persons with active TB
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17
Q

how much of TB infections lead to disease?

A

only 5-15% of TB infections lead to active disease

most immune systems can make a granuloma and get rid of the TB

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18
Q

what is MDR TB?

A

MDR TB = multi-drug resistant TB

this means its resistant to at least isoniazid and rifampin

60% of MDR cases in China, India, Russia, Pakistan, S. Africa

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19
Q

what is XDR TB?

A

XDR TB= extensively drug-resistant TB

this means it’s resistant to isoniazid, rifampin, all fluoroquinolones, kanamycin, amikacin, and capreomycin

it’s found in 84 countries….

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20
Q

what lead to MDR TB and CDR TB?

A

antibiotic misuse

  1. regimen not completes
  2. monotherapy
  3. addition of new drug to failing regimen
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21
Q

how is TB transmitted?

A
  1. cough, sneeze sputum
  2. prolonged contact with infected person
  3. immunocompromised
  4. HIV infection
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22
Q

can TB become latent?

A

yeah for up to 20 years

latent TB is activated by immunosuppression of some kind

23
Q

which cells does TB infect?

A

alveolar macrophages

24
Q

what are the early stages of a TB infection?

A

bacteria is engulfed by macrophages and then it can be taken up by dendritic cells

the dendritic cells can either eliminate the bacteria or present it to T cells

T cells can then release IFN-γ which activates macrophages to kill TB inside of them

granulomas can form to try and kill TB

25
Q

why would TB induce apoptosis of infected cells?

A

it would induce the death of macrophages because it’s a non-inflammatory cell death!!

this way the bacteria can be released to infect other cells

26
Q

what is the pathogenesis of ruberculosis?

A

M. tb translocates through the lung epithelium and infects alveolar macrophages and dendritic cells

M. tb can bind to different macrophage receptors for entry

T cells then secrete IFNγ which activates infected macrophages but also recruits new macrophages to site of infection!!!

the damage to the tissue is actually from our own immune response!!

27
Q

what’s the structure of a granuloma?

A

in the middle there’s dead macrophages

then in the layer outside that it’s an active macrophage layer

then in the most outside layer there’s B and T cells and neutrophils to keep the macrophages activated to kill the TB that’s in the middle

28
Q

what are foam cells?

A

TB needs alot of lipids

foam cells are the cholesterol source for TB!

29
Q

what is the cell wall of TB made of?

A
  1. mycobactin
  2. glycolipids (TDM and PDIM)
  3. mycolic acids
  4. arabinogalactan
  5. peptidoglycan
  6. LAM
30
Q

what are the virulence factors of TB?

A
  1. LAM
  2. mycolic acids
  3. TDM
  4. PDIM
31
Q

how is LAM a TB virulence factor?

A

LAM = lipoarabinomannan

LAM has a mannose core with arabinose side chains and it’s anchored to the cell membrane of the TB bacteria

it functions like LPS O-antigen

  • the mannose cap binds to macrophage mannose receptors and inhibits macrophage activation so that there’s no bacterial killing!!
  • it specifically prevents phagosome fusion with lysosome

LAM is later released from infected macrophages and goes on to inhibit neighboring macrophages

32
Q

how are mycolic acids a TB virulence factor?

A

mycolic acids form a thick, hydrophobic barrier that block free radicals

they protect bacteria from dessication

they also bind C3 complement to enhance macrophage uptake but thick layer of fatty acids make M. tb resistant to complement-mediated killing

33
Q

what happens in a normal phagosome vs. a TB phagosome?

A

NORMAL:
1. pH decreases

  1. the proteolytic enzymes get turns on to kill bacteria = superoxide and NO
  2. transferrin receptor diverted away
  3. fusion with lysosome

TB
1. pH doesn’t decrease

  1. no fusion of endosome with lysosome because TB secretes factors that inhiit lysosome fusion
  2. still lipolysis
  3. shuttling of transferrin keeps going on so bacteria can get iron
34
Q

how does TDM act as a TB virulence factor?

A

Cord factor

Glycolipid attached to mycolic acids

*interferes with phagosome maturation

damages mitochondria of neutrophils

35
Q

how does PDIM act as a TB virulence factor?

A

peripheral lipid that is shed; exocytosed by infected macrophages (like LAM)

incorporates into neighbor macrophages

*interferes with MHC-II loading in vacuole; may prevent pH decrease

36
Q

how does 19 kDa lipoprotein act as a virculence factor for TB?

A

it suppresses TNF-alpha, IL-12, and MHC-II expression by macrophages

it also induces apoptosis in late stages of infection because this is a non-inflammatory cell death!

37
Q

what is the cell mediated immunity response that the body mounts against TB?

A

IL-12 and TNF-alpha from infected macrophages during early stages of infection recruit T cells and NK cells

then IFN-gamma from TH1 cells activates macrophages

then there’s also CD4 T cells that contain TB in granuloma and CD8 T cells causing tissue destruction

small granuloma controls M. tb

  • but a large/old granuloma has a necrotic center which has decreased CMI response and eventually the granuloma breaks down and releases bacteria = bad
  • humoral immunity (antibodies) play a limited role in TB infections
38
Q

what is military TB?

A

hematogenous spread of TB to the liver, spleen and CNS!

you get tons of nodules throughout the body and its because the body after a granuloma breaks and releases TB

CXR looks like speckles literally everywhere….

39
Q

what are the symptoms of tuberculosis?

A

Persistent cough with mucous; sometimes blood

Appetite loss/Weight loss

Low-grade fever

Night sweats

Chest pain

Dyspnea

Fatigue

40
Q

what are the different ways you can diagnose TB?

A
  1. sputum stain
  2. skin testing
  3. culture
  4. quantiferon
  5. PCR
41
Q

how does a TB sputum stain work?

A
  • Early morning
    only useful during active TB

Ziehl-Neelsen acid fast stain

sometimes you have to examine > 30 fields so it’s hard to actually find bacteria in sputum

42
Q

how does TB skin testing work?

A

type IV hypersensitivity reaction! it’s the normal TB test we all get

  • Purified Protein Derivative injected sub-q
  • cheap test
  • false positive if BCG vaccinated
  • false negative during active Tb
  • false negative if anergic or immunosuppressed
  • false negative if tested early during primary infection
43
Q

how does a TB culture work?

A

take a sputum sample and put it in a tube and see how fast bacteria replicates based on how much oxygen is being consumed

44
Q

how does a TB quantiferon test work?

A

blood drawn from patient

you’re measing the IFN-gamma response from macrophages

45
Q

how does a TB PCR work?

A

collect sputum sample

confirms TB infection and susceptibility/resistance to rifampicin

46
Q

how do you treat TB?

A

6-9 month therapy

first 2 months = isoniazid + rifampin + pyrazinamide + ethambutol

then for another 4-6 months = isoniazid + rifampin

47
Q

what is MDR-TB?

A

MDR = multidrug resistant

resistant to at least isoniazid and rifampin

treat with pyrazinamide + kanamycin + levofloxacin + ethionamide + cycloserine

48
Q

what is XDR-TB?

A

XDR = extensively drug-resistant strains

resistant to isoniazid, rifampin, all fluoroquinolones and second line drugs (kanamycin, amikacin, capreomycin)

49
Q

what other disease when co-infected with TB can cause treatment complications?

A

HIV-infection complicates TB antibiotic treatment

anti-retrovirals and TB drugs can lead to more severe symptoms: Immune Reconstitution Inflammatory Syndrome (IRIS); 10%

CD4 counts < 200/ml lead to TB activation and extrapulmonary TB; 50% of cases

50
Q

is there a TB vaccine?

A

in the US there’s no approved vaccine but in the rest of the world there’s the BCG vaccine

it’s a live attenuated M. bovis strain

it can cause severe legions on the skin and its efficacy against TB is somewhat limited so that’s why we don’t use it

the reason there’s incomplete protection is because most of us already have antibodies against different mycobacterium so the vaccine gets cleared too fast before it has the chance to replicate and induce cell mediated immunity

51
Q

what is sa complicated often seen with BCG vaccine?

A

TB vaccine

can interfere with diagnosis and cause false positive PPD skin test

52
Q

which diagnostic test is best for TB?

A

quantiferon is the gold standard test in the US

or xpert if you’re at a really good lab

53
Q

FLASHCARD: microbiology, pathology, epidemiology, clinical symptoms, diagnosis and treatment of mycobacterium tuberculosis?

A

MICROBIOLOGY: technically Gram + but acid-fast; hydrophobic cell wall with long chain lipids (LAM, mycolic acids, trehalose dimycolate); aerobe; slow growth (2-3 week colony) in lab on special media (lipids)

PATHOLOGY: Infect macrophages but alter phagosome; granuloma

EPIDEMIOLOGY: 1/3 world infected; 2 million deaths/yr; 5% active disease

CLINICAL: chronic cough, sputum w/ blood, appetite/weight loss, fever, night sweats

DIAGNOSIS: Latent: PPD skin test or QuantiFERON; Active: Sputum acid-fast stain, sputum growth BACTEC MGIT, sputum PCR Xpert MTB/RIF

TREATMENT: 2 mo Inh+Rif+Emb+Pza  4 mo Inh+Rif

ID Week 3 (25 decks)

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