Lecture 28 - Mycobacteria Flashcards
(21 cards)
describe the mycobacteria genera
- mould-like pellicle on liquid = no spore/hyphae
- related to corynebacterium
- weak G+ve, rod, non motile, branching, slow growth, strict aerobes
- acid fast bacilli (AFB) = resists decolourisation
- 150 species
describe the structure of mycoplasma and what it’s resistant to
- mycolic acid + thin PG
- PM, lipoproteins, PG, arabinogalactan, mycolic acids, glycolipids, possible thin capsule of capsular proteins/polysacc
- resists drying, acids, alcohol, lytic enzymes, stains
list the 2 groupings by growth rate for mycoplasma
- rapid in 2-7 days
- slow in 7+ days
describe the 3 groupings by disease for mycoplasma
- MTB complex = slow growth, cord factor +ve (trehalose 6,6′-dimycolate (TDM)), cause TB
- non-TB (NTM/MOTT) = atypical, slow/rapid, cord -ve
- m leprae = no in vitro culture
what are the symptoms, transmission and risks of tuberculous mycobacterial disease?
- pulmonary/other TB
- weakness, fatigue, weight loss, fever, night sweats, cough
- slow/fast manifestation
- airborne, human-human, human-animal
- infectious status, contact, environ eg ventilation
what are the 3 possible outcomes of tuberculous mycoplasma?
- 30% infection from exposure
- 40% primary active TB
- 60% latent TB
list the 4 stages of tuberculous mycoplasma pathophysiology
- transmission to initial infection
- innate immune response
- adaptive immune response
- active disease
describe the transmission and initial infection stage of tuberculous mycoplasma
- inhale droplet nuclei containing 1-3 bacilli
- alveolar membrane
describe the innate immune stage of tuberculous mycoplasma
- phagocytoses by alveolar macrophages/dendritic cells
- macrophages = proinflammation
- survive by blocking phagolysosome fusion
- slow continuous intracellular rep for 2-8wks
describe the adaptive immune stage of tuberculous mycoplasma
- released into lymph/ocytes
- T cells activated = activate macrophage killing, trigger granulomas
- granuloma = fused macrophages, caseous core, epitheloid macrophages, B and T cells on outside
describe the active disease stage of tuberculous mycoplama
- immune system loses control = multiply and erupt from granulomas
- bacteria + inflammation erodes airways and blood vessels = severe lung dmg
describe the history of TB
- endemic, high mortality
- 1882 koch found it
- 1940s-50s = streptomycin effective
- 1950s control = mass x-ray and BCG vac
- 1980s increase in developed from immigration, HIV, poverty, MDR, reducing funding
- today = big cause of death, millions ill/died, 95% deaths in low/middle income, 25% latent, 2% decrease/yr
discuss TB and HIV coinfection
- TB rapid with untreated HIV = reactivate, progressive, short/absent latency
- delayed diagnosis bc atypical presentation and low +ve testing
- TB rifampicin interferes with anti-HIV drugs
- immune dysfunction = more opportunistic
what is the function of each of the 4 drugs used in a cocktail for tuberculous mycoplasma?
- Isoniazid = inhibits mycolic acid synthesis
- rifampin = inhibits RNAP
- ethambutol = interferes with arabinogalactan synthesis
- pyrazinamide = multiple effects after conversion to pyrazinoid acid
what 2 main ways does resistance occur in tuberculous mycoplasma?
- incorrect drugs, poor supply, poor quality, poor compliance, poor follow up, lack of resistance surveillance
- spontaneous chr mutations 1 drug @ a time eg INH 1 in a mil cells vs RIF 1 in 100mil
describe MDR and XDR forms of tuberculous mycoplasma
- MDR = resist RIF, INH, 20-26month treatment, 80% fatality
- XDR = resist RIF, INH, injectables, fluoroquinolone, 32 month treatment
where does tuberculous mycoplasma resistance mainly occur and why?
- low/middle income where it’s endemic
- russia and china hotspots from poor TB control
describe the Bacille Calmette-Guerin (BCG) vaccine and why newer vaccines havent been dvlped yet
- BCG = live attenuated, infants/young, not full protection
- no new = no animal model, preclinical doesnt match field, poor funding
describe the features of non-tuberculous mycobacteria (NTM)
- multiple spp = range of disease in lungs, skin, lymph
- slow/rapid, environ acquired only
- contamination vs pathogen by multiple isolations
describe leprosy/hansen’s disease by M leprae
- nervous disease of cooler body parts in immunocomp = nerve dmg
- tuberculoid form = limited and non-infectious bc good immune
- lepromatous form = widespread lesions in immunocomp
- tropics, close contact or droplets
- obligate intracellular = diagnose by biopsy or skin smears
- 2yr antibiotics
describe m ulcerans
- buruli/bairnsdale ulcer = painless nodule to ulcer on extremities
- tropical africa, americas, asia, new guinea, australia
- possible reservoir = slow/stagnant water = possibly mozzie/possum amplifier
