Mycobacteria Flashcards
what bacterium causes leprosy
Mycobcteroum Leprae
what are the cardinal features or leprosy
skin lesions
Thickened peripheral nerves
Acid-fast bacilli on smears or biopsy
what type of bacterium are mycobacterium
a)Gram +ve
b)Gram -ve
c) Acid fast +ve
C
Is evolutionarily gram +ve but doesn’t stain +ve. Is positive with the ziehle neelson stain
what is the shape of mycobacteria
Rod (bacilli)
How much bacteria do you need to diagnose TB via acid fast staining
10,000 per ml of sputum
Mycobacteria tend to be
A) Aerobic
B) Anaerobic
aerobic
Mycobacteria are motile
T/F
F
Briefly describe the cell wall of mycobacteria
High molecular weight lipids
-Mycolic acids + lipoarabinomannan
Mycobacterium is slow growing
T/F
T
Mycobacterium can survive inside macrophages
T/F
T
What are the challenges to treating mycobacterium (not medication)
Slow growing
Slow reproduction
Slow growth in culture
Slow response to treatment (6mnths minimum)
State four examples of disease caused by mycobacteria
Leprosy, M.leprae
Buruli Ucler, M.ulcerans
Fish tank granuloma, M. marinum
Tuberculosis, M.tuberculosis
Describe the classification of mycobacteria, e.g. intracellular or can grow on artificial media etc.
can grow on artificial media –> cell walled –> single celled –> rods
Describe the structure of mycobacteria and what is used to stain it.
Aerobic, slightly curved, beaded, non-motile bacilli with high molecular weight lipids in the cell wall
Ziehl-Neelson stain (contains carbol fuchsin, acid alcohol and methylene blue)
Describe the causes of TB, and factors that make it harder to treat, how is it transmitted?
Caused by Mycobacterium tuberculosis
Thick lipid-rich cell wall makes immune cell killing + penetration of drugs challenging
Slow growth with gradual onset of disease –> takes longer to diagnose + treat
Aerosol transmission
Describe primary tuberculosis
Initial contact by alveolar macrophages
Bacilli taken in lymphatics to hilar lymph nodes
Decsribe latent tuberculosis
Cell mediated response from T cells
Primary infection contained but cell mediated immune (CMI) response persists
There is no clinical disease, but is detectable CMI to TB on the tuberculin skin test
Describe Pulmonary tuberculosis
Granulomas form around bacilli that have settled in apex (where there is ++ air, - blood supply –> less white cells to fight infection)
TB may spread in lung, causing other lesions
Can occur immediately after primary infection, or a month later after reactivation
What are the constituents of the tuberculosis primary complex?
lymphatics
Lymph nodes
Granulomas
Describe where TB could spread to beyond the lungs
Bacilli in lung + lymph nodes could spread to:
Genito urinary system to genitourinary TB
Pleural TB
Miliary TB
Bone and joint TB
What is the consequence of TB in the spine?
Gibbus formation
Describe the immune response to mycobacteria
Mycobacteria are phagocytosed by macrophages + traffic to phagolysosomes
The bacterium has adapted to the intracellular environment and aims to withstand phagolysosomal killing, to escape to cytosol
Effective immunity requires CD4 T cells to generate interferon-gamma –> activate intracellular killing by macrophages
What are the two consequances of granuloma formation?
Granuloma is effective –> mycobacteria shut down
metabolically –> dormancy
Granuloma fails –> formation of a cavity full of live
mycobacteria –> disseminated disease (consumption)
what is a granuloma made of
Macrophages and Th1 capable of synthesysing interferon gamma, and other cytokines, e.g. TNFa
What is the standard and second line therapy in Anti-TB drugs?
Standard therapy - INH, RIF, PZA and ETH x 2 months, followed by INH and RIF for further 4 months
Second line - injectable agents, e.g. streptomycin, cycloserine, capreomycin
Which strain of TB is multi drug resistant? How is it treated?
XDR-TB, resistant to four commonly used TB drugs
With BPal Regimen:
Bedaquiline, Pretomanid, Linezolid
all for 6 months
