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microimm > tuberculosis and leprosy > Flashcards

tuberculosis and leprosy Flashcards

1
Q

what does mycobacteria tuberculosis (m. tuberculosis) cause?

A

causative agent of Tuberculosis in humans (often called “TB” for tubercle bacilli)

develop lesions in lungs

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2
Q

what does mycobacteria bovis (m. bovis) cause?

A

causes TB in cows, rarely in humans

humans can be infected by consumption of unpasteurized milk

leads to extrapulmonary tuberculosis in humans – which can be treated with the BCG vaccine made of m. bovis

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3
Q

what does mycobacteria avium (m. avium) cause?

A

causes tuberculosis-like illness in humans, particularly in AIDS patients

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4
Q

what does mycobacteria leprae (m. leprae) cause?

A

causative agent of Leprosy in humans

systemic infection in armadillos

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5
Q

approximately how many people have have latent tuberculosis? how many of those will develop active TB in their lifetime?

A

2 billion; 1/4 of the world’s population

about 10% of ^^ will develop active TB in their lifetime

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6
Q

how many people die from tuberculosis each year?

A

about 1.6 million people die from TB each year

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7
Q

what is the number 1 infectious agent?

A

tuberculosis….

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8
Q

how is tuberculosis spread?

A

contagious and spread through the air by people with active TB

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9
Q

what is meant by latent infection

A

harbours organism in lungs; no symptoms & can’t transmit disease

but do develop some immune response

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10
Q

what is multi-drug resistant TB (MDR-TB)?

A

being resistant to the two most effective first-line therapeutic drugs, isoniazid and rifampin

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11
Q

what is extensively drug resistant TB (XDR-TB)?

A

resistant to first line therapeutic drugs (rifampin and isoniazid) AND resistant to the most effective second-line therapeutic drugs used commonly to treat MDR-TB

XDR-TB has been found in all regions of the world
— but strains are virtually untreatable

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12
Q

where can mycobacteria tuberculosis be found when in humans?

A

lives within macrophages

(an intracellular pathogen)

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13
Q

what’s the generation time of mycobacterium tuberculosis? what does this mean?

A

greater than 15 hours (slow generation time)

makes studying it & creating antibiotics very difficult

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14
Q

if grown on the lab in specialized media, how long does mycobacterium tuberculosis take to get small colonies?

A

4 - 6 weeks

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15
Q

describe mycobacterium tuberculosis’s cell envelope

A

unusual cell envelope with high concentrations of mycolic acid (it’s lipid-rich aka hydrophobic) – making it “waxy”

due to its mycolic acid, it’s impermeable to stains and dyes – like other mycobacteria, it’s gram+ acid fast

its cell envelope is associated with resistance to:
—– some antibiotics
—– osmotic lysis via complement deposition
—– lethal oxidative stress promoting survival inside of macrophages

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16
Q

how is acid fast stain conducted for mycobacterium tuberculosis?

A

stain w/ carbol-fuchsin dye with slow heating (to melt waxy cell envelope) on slide

wash with EtOH and HCl

counter-stain w/ methylene blue

result:
acid-fast organisms = red
non-acid fast organisms = blue

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17
Q

what are the 4 stages in the spread and progression of tuberculosis?

A

stage 1: transmission

stage 2: survival in macrophage (key virulence property)

stage 3: formation of granulomas and killing by T-cell activated macrophages

stage 4: route of transmission and cavitation

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18
Q

describe how tuberculosis is transmitted (stage 1 of the spread and progression of tuberculosis)

A

inhalation of droplets from an infected host, usually by coughing or sneezing

coughing/sneezing can generate 3000 droplet nuclei, each of which can contain up 10 bacteria

small droplets can stay airborne for extended periods of time and these droplets can be inhaled directly into the lungs

—– a single bacteria can cause lesions in the lungs

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19
Q

describe tuberculosis survival in phagocytes (stage 2 of the spread and progression of tuberculosis) and what do TB cells do once in the macrophage?

A

lung (alveolar) macrophages phagocytose TB cells

TB blocks acidification of the phagosome

TB inhibits the fusion of the lysosome to the phagosome

TB delays dendritic cell migration to lymph nodes

TB multiplies in macrophages. the macrophages then lyse and release TB cells to infect more macrophages

20
Q

describe the formation of granulomas and killing by T cell activated macrophages (stage 3 of the spread and progression of tuberculosis)

A

infected macrophages many form granulomas

TB granulomas are “tubercles” of immune cells that try to destroy invading pathogens (typically formed by macrophages)

the granulomas represent a “balance” between the pathogen and the host – the latent infection
—- TB can’t escape but the immune system can’t kill them all – stalemate: can have this for your whole life!

T cell activated macrophages can kill TB cells
— activated T cells can secrete cytokines (IFN-gamma) to activate the macrophages
— macrophages at the center of the granuloma remain hard to be activated by T cells which leads chronic inflammation causes “cheese-like” necrosis – aka caseous necrosis (cell death in which tissue maintains cheese-like appearance)

21
Q

what is caseous necrosis?

A

cell death in which tissue maintains cheese-like appearance

seen during stage 3 of the spread and progression of tuberculosis: the formation of granulomas and killing by T-cell activated macrophages

22
Q

describe the route of transmission and cavitation (stage 4 of the spread and progression of tuberculosis)

A

some macrophages remain
unactivated and infected

the tubercle grows

granuloma erodes into
the airway provides the route of transmission

deterioration of host immunity can result in active tuberculosis, a life threatening infection – most likely due to break down in T cell repsonses

the caseous center can liquefy leading to cavitation, essentially a granuloma post-mortem

23
Q

what’s extrapulmonary tuberculosis? who is it more likely to occur in?

A

infection outside the lungs

can infect multiple organ systems (bone, joints, liver, spleen, gastrointestinal tract and brain)

more likely to occur in immunocompromised (e.g. HIV infected patients) individuals and young children

24
Q

what is miliary tuberculosis?

A

a type of extrapulmonary tuberculosis that is more widespread

almost always fatal

25
Q

what are ESX secretion systems? how many are there? what functions do they have?

A

5 ESX systems exist in mycobacteria tuberculsos

they enable the transport of select bacterial molecules across the thick cell envelope of mycobacteria tuberculsos

they also help damage the membrane of phagosomes in macrophages and also inhibit the immune responses

26
Q

how is tuberculosis tested and diagnosed for?

A

tuberculin test = PPD or purified protein derivative from mycobacteria tuberculosis
— causes a T-cell mediated response
— if positive, will see red swollen circle at 48 hours
— a person is considered infected if they convert from negative to positive on a TB skin test
——- essentially, we look for if they have T cells that recognize TB antigens!

27
Q

what does a positive result on TB testing mean?

A

latent or active TB

BCG vaccinated

previously infected and have been treated

28
Q

what does a negative result on TB testing mean?

A

not infected

immunocompromised (e.g. AIDS)

not infected long enough

29
Q

what do we look for on TB testing to see if someone is infected?

A

if they convert from negative to positive on TB skin test

30
Q

if a TB test turns out positive, what must be done?

A

must collect careful history and chest x-ray

with an x ray, you’ll typically see upper lobe “shadowing” aka lesions – the x ray can also show calcified granulomas

can also conduct staining of sputum for acid fast bacilli and culturing AND interferon-gamma response assay

31
Q

what is the treatment for tuberculosis?

A

six months of antibiotics for short treatment
– slow growth means long treatments

generally, multiple types of antibiotics are used:
– Rifampin (inhibits RNA polymerase)
– Isoniazid (inhibits mycolic acid synthesis)
– others…

multiple antibiotics are used to minimize chance of developing resistance (multiple strains surviving) – so e.g. if a cell develops resistance to rifampin, isoniazid will kill it

— don’t use antibiotics if you have the BCG vaccine!

32
Q

if untreated, how many people could active tuberculosis kill?

A

active TB can kill approximately 2 out of 3 people if untreated

33
Q

as an antibiotic used for TB, what does rifampin inhibit?

A

RNA polymerase

34
Q

as an antibiotic used for TB, what does isoniazid inhibit?

A

mycolic acid synthesis

35
Q

describe the BCG vaccine

A

bacille calmette guerin

live, reduced vaccine prepared from cultured M. bovis – grown in the lab many times, losing its virulence properties (lacks the ESX-1 secretion system)

BCG has shared antigenicity with TB

effective against miliary TB BUT has variable efficacy (0-80%) for pulmonary TB - thus controversial

—– can also leave large scars

recommended for individuals with high risk to exposure

NOT USED IN CANADA – we use a less effective vaccine to minimize scarring

36
Q

describe the relationship between tuberculosis and HIV/aids (give stats)

A

those infected with HIV are more likely to develop active TB
—- 1/3 people with HIV are co-infected with TB

TB is leading cause of death in HIV-positive people
— Massive problem! the two are now intersecting

37
Q

what is leprosy sometimes called?

A

hansen’s disease

38
Q

how long is the incubation period of leprosy?

A

approximately 5 years

very slow progession

39
Q

describe the permanent damages caused by leprosy?

A

can cause permanent damage to skin, nerves, limbs, and eyes

approximately 2 million people are permanently disabled by leprosy, mainly in tropical developing countries (this may be a low estimate due to low ragtes of reports because it’s a stigmatized disease)
——- but note it’s very rare in developed countries

40
Q

where can mycobacterium leprae be found when in humans?

A

macrophages of skin

schwann cells in nerves
— schwann cells are normally wrapped around peripheral nerves and helps with action potential

41
Q

why has mycobacterium leprae not been studied well?

A

cannot be cultivated in vitro

— it’s less well studied than mycobacterium tuberculosis

42
Q

why, compared to tuberculosis, victims of leprosy are ostracized?

A

lesions in leprosy are visible but lesions in tb are hidden

weird, cause leprosy is much LESS infectious than TB!

43
Q

what are the 2 major forms of leprosy?

A

tuberculoid leprosy

lepromatous leprosy

44
Q

describe tuberculoid leprosy

A

cell-mediated immunity present
—- macrophage can contain
the bacteria

light coloured lesions with
“anesthetic” (no sense of feeling) areas
—- sometimes loss of hair and
pigmentation

patients become tuberculin positive (active T cell-mediated responses)
—- bacterial cells are generally not recoverable from lesions

tuberculoid Leprosy can be
self-limiting
—- immune system wins out and kills the organism

45
Q

describe lepromatous leprosy

A

cell-mediated immune responses are absent
—- macrophages are not activated

M. leprae survives and multiples in macrophages and schwann cells
—- schwann cells provide myelin to peripheral nerves

nerve damage and loss of sensation leads to inadvertent traumatic lesions on the face and extremities
—- can cause loss of eyebrows, thickening and enlarged nares (nostrils), ears
and cheeks – a “lion like” appearance

lesions can become secondarily infected, eventually resulting in bone resorption, disfigurements and mutilation

46
Q

how is leprosy transmitted?

A

most likely due to close/direct contact for extended periods of time

47
Q

describe the treatment for leprosy?

A

also multiple drug therapy but with rifampin, dapsone, clofazimine
—- used for 6 months to 1 year for a full course of treatment

patients no longer transmit the disease after 1 dose of multiple drug therapy (MDT)
— can eventually eradicate this disease if everyone with leprosy takes drugs properly

microimm (30 decks)

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