Bacteria- Ch23 Mycobacteria Flashcards
what is in the cell wall of mycobacteria
mycolic acids
describe the type of microbe mycobacteria is
- gram positive
- weak staining: use acid fast stain or specific fluorescent detection
- facultative intracellular growth in macrophages
-obligate aerobe
how is mycobacteria transferred
airborne- as few as 10 cells can result in infection
what are reservoirs for mycobacteria
humans
describe an acid fast stain
hot carbol fuchsin
describe the mycobacterial cell wall structure
cord factor- glycolipid
what are virulence factors for mycobacteria
-structural mycobacterial cell wall components- mycolic acid moiety
-inhibition of phagolysosome fusion
what does mycolic acid slow cord like growth result from
adherence of cell surface lipid mycolic acids and glycolipids
what does the virulence of mycobacteria result from
they provide a challenge to the immune response such as CD4+ T cells and macrophages because the disease is caused by the immune response not by the mycobacteria itself
what potentiates cord factor effects
sulfatides
how long does mycobacteria last in the body
lifelong, once infected you may be asymptomatic but never cured
what does a CMI to mycobacterium tuberculosis look like
TB granuloma surrounded by puncate nuclei of lung tissue and inflammatory leukocytes. central area of necrosis where nuclei have been destroyed
effective CMI is capable of _________ infection by M tuberculosis
localizing and stopping
what is the typical result of aerosol transmission of mycobacterium tuberculosis
chronic TB
what is the exception to aerosol transmission to mycobacterium tuberculosis
young children under 5 have a high risk for developing progressive TB due to insufficient immune system development
what are the outcomes of untreated TB
-91% no disease
-6% clinical TB (2% pulmonary + 3% extrathoracic + 1% both)
- 3% progressive systemic disease and death
what is another name for acute TB and what is it caused by
secondary tuberculosis or galloping consumption caused by endogenous reactivation of prior infection
what is endogenous reactivation of acute TB stimulated by
stress, malnutrition and HIV
what does the disease of mycobacterium tuberculosis arise from
tissue destruction by our immune defenses and not by damage caused by the bacterial infection
what causes impaired lung function in mycobacterium tuberculosis infections
the repeated attempts to remove foci of infection by lung macrophages cause the granulomatous lung tissue
what is breathing impairment in TB due to
the macrophage induced tissue destruction
what is the mantoux reaction
a positive tuberculin test to subdermal PPD (processed protein derivative of the cell wall of the opportunistic intracellular pathogen mycobacterial tuberculosis)
what is a positive test and strongly positive test in the mantoux reaction
-positive test: >10 mm redness
- strongly positive: >20 mm red
what is the vaccination for mycobacteria
exposure to living attenuated mycobacterium, known as bacille calmette guerin (BCG) a derivative of M bovis
what type of vaccine is BCG vaccine
- little virulence in humans (infectious in immune compromised people)
- some protective immunity ( when given to young children)
why is BCG vaccination discouraged in the USA
because it gives a positive tuberculin test, thus removing an important diagnostic screening tool
what type of disease is TB
opportunistic
what has caused a recent increase in TB
HIV and AIDS
what is the number for world wide latent M tuberculosis infections
~ 2 billion
-USA: 13 million
what is the number for world wide TB deaths
~ 1.6 million/ year
-USA: 500
what are the treatments for TB
isoniazid
what are the preferred targets for mycobacterium leprae
peripheral nerves
what happens in a Th1 response to mycobacterium leprae
-tuberculoid
-macrophages kill nerves
-macules and plaques without sensation
-good prognosis for recovery not infectious
what happens in a lepromatous infection
bad prognosis for recovery
-highly infectious
what happens in loss of CMI to mycobacterium leprae and what is this type of response called
-CTL lysis and loss of tissue including nerves
- AKA Th2 response
what do histology slides of m leprae look like
beaded acid fast rods
describe a tuberculoid plaque
without sensations, resulting from macrophage action after TH1 cytokine (IFNgamma activation)
what happens in Th2 leprosy
cytokine (IL4) activation of CTL tissue lysis
what is the multidrug therapy for tuberculoid and lepromatous leprosy
dapsone + rifampin +clofazimine
describe tuberculoid granuloma
- no or few bacteria
- low infectivity
- ag- specific Th1
- no Ag specific IgG
- normal Ig level
describe leprosy
- many bacteria inside macrophages
- high infectivity
- extensive tissue damage
- no T- response to Ag
- sometimes Ag- specific IgG
- hyper Ig level
what are the virulence factors, clinical features, treatment, and epidemiology for M. tuberculosis
- ability to survive and live in lung macrophages
- pulmonary and extrapulmonary tuberculosis
- mutlidrug therapy for 6-12 months
- aerosol, all ages, highest risk if immune compromised such as HIV
what are the virulence factors, clinical features, treatment, epidemiology for M. leprae
-ability to survive and live in macrophages
- tuberculoid-to- lepramatous leprosy
- multidrug therapy for 2+ years
- close physical contact
all pathogenic mycobacterial species have ________ growth rates
very slow
when is isoniazid used other than mycobacterium infections
prophylactically upon conversion to a positive mantoux reaction
what does ethambutol do
inhibitor of enzymes that synthesize non-mycolic acid cell wall components
what does pyrazinamide do (PZA)
mechanism of action is unknown
what type of microbe is nocardia
- gram positive
- partially acid fast
- poor stinaing
- mycolic acid in cell wall: partially acid fast
what is the difference between nocardial mycolic acid and mycobacterial mycolic acid
-nocardial: 50-62 x C
- mycobacterial: 70-90 x C
what are the virluence factors for nocardia
-opportunistic pathogen in immuno compromised patients
- antiphagocytic virulence factors of strictly aerobic nocardia
- intracellular survival and growth
- catalase
- superoxide dismutase
what are the clinical features, treatment and epidemiology for nocardia
- bronchopulmonary cutaneous infections and brain abscesses
- sulfonamides, amikacin, carbapenems, or cephalosporins
- opportunistic pathogen if pulmonary disease of T deficiency
