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88 Cards in this Set

  • Front
  • Back
metabolism of mycobacteria
obligate aerobes

facultative intracellular (except M. leprae which cannot be cultured on articial media)
structural features of mycobacteria
slow growing
mycobacterial cell walls have a triple layer and contain
mycolic (fatty) acids (absent in most other bacteria)

has two long hydrophobic chains
gram stain to identify mycobacteria ?
how are mycobacteria stained
with acid-fast procedure

red phenolic dye complexes with mycolic acids of mycobacteria and cannot be washed out with acid-alcohol. all non-acid fast bacteria are destained and only the acid-fast bacteria remain red.
in addition to mycobacteria what other organism might stain acid fast
how do corynebacteria (which also contain mycolic acids) differ from mycobacteria
they have shorter fatty acid chain lengths and are not acid fast
"cord factor"
two mycolic acids attached to disaccharide trehalose constitute cord facotr, whic is associated with virulence in mycobaterium tuberculosis
virulence factor in mycobacterium tuberculosis
cord factor
why is mycobacteria calle a "wax ball"
mycolic acids give mycobacteria high lipid content - up to 40% - 60% of the dry weight. so its like a wax ball enclosing DNA and other cellular contents
Wax D
an unuall lipid in mycobacteria - which is used by immunologists as Freunds complete adjuvant to increase immune response
what probably plays a role in the intense CMI seen in mycobacterial infections
involved in the characterisitic resistance of mycobacteria to drying and chemicals
what is the generation time for TB
15-20 hours - much slower than other bacteria - it is due to the lipid content

therefore visible growth on solid media takes 3-8 weeks
visible growth on solid media of TB takes how long
3-8 weeks
Hansens bacillus
m. leprae
temp preference of m.leprae
27-33 degrees

predeliction for cooler areas of the body (skin, nose, mucous membranes of upper resp tract)
can m.leprae be cultivated in artificial media
transmission of m.leprae
respiratory - sometimes through skin
age relationship to suseptability to m.leprae
children more suseptable
primary lesions of leprosy - characteristics
skin macule (hypo-pigmented)
raised and braown wheal-like (like mosquito bite)
incubation period for leprosy
months - 30 years

usually 2-5 years
long duration cases of leprosy show what of kidneys, liver, and spleen
leprosy mainly infovles what organs / system
skin and nerves
genesis of lepromatous (primary leasion in leprosy)
macrophage or histiocyte takes up bacilli
genesis of tuberculoid (primary lesion in leprosy)
like TB; chronic granulomatous lesions
epitheloid and giant cells present w/o caseation
Lepromin skin test results for lepromatous lesion vs. tuberculoid test
lepromatous: lepromin skin test neg
tuberculloid: lepromin skin test positive
the ability to mobilizatio T cells in lepromatous vs tuberculoid lesion
mobilization in lepromatous is much worse than mobiliztion of T cells in tuberculoid (DTH)

therefore the prognosis of the lepromatous lesion is worse
how does the amount of bacteria found in lesion differ when it comes to lepromatous and tuberculoid lesions
lepromatous lesions have many bacilli and tuberculoid have fewer (especially towards the center of lesion)
two things that illustrate cellular immunity and the link with tuberculoid lesion in leprosy
1. lepromin test positive
2. DTH intact
what is the abnormal serologic activity seen in lepromatous lesion versus tuberculoid lesion(leprosy)
polyclonal hypergammaglobulinemia in lepromatous and normal levels of IgG in tuberculoid lesion
a complication in the tuberculoid state which resembles immune complex disease and is example of the lack of antibody response correlation w/ tuberculoid state
erythema nodosum leprosum (ENL)
is there antibody to m.leprae
yes it is specific for phenolic glycolipid but not protective
diagnosis of m. leprae (4)
gross appearance of lesions,
histological examination
acid fast stains
material fromnodules -
margins of flat lesions or nasal scrapings
3 drug treatment of m.leprae (treat for 2-3 years) involves what three drugs
1. dapsone
2. rifampin
3. clofazimine
if there is ENL complicaiton in someone infected with m.leprae then you treat with
immune suppression
TB vaccine offers some protection
hospital disinfectants are judged by their ability to kill
m. tuberculosis
m. tuberc may remain viable for weeks at what temp
4 degrees C
macrophages ingest MTB, present to T cells which release what three lymphokines
IL-2 to expand CD 4
IFNg to activate MO
TNF to induce phagoolysomal fusion and kill intracellular MTB
gene that appears to regulate the phagolysosomal enviroment and confer increased suscetibility to MTB
variant allele in NRAMP1
polymorphisms in what receptor gene is associated with protection against TB in West AFrica
polymorphisms in Vitamin D
transmission of TB
person to person inhalation of droplet nuclei produced by coughing or talking -

inhaled - ingested by alveolar macrophages, transient bacteremia, granuloma formation in lung
this organisms from contaminated mild produces clinical picture of TB in developing countries
m. bovis
infection of TB is identified by what skin test
disease of TB is identified by
culture of MTB from lung or other sites or by compativble clinical syndrome
what percent of people will develop active disease

5% will progress to primary disease w/in 2 years of infeciton
5% will progress to reactivation disease w/in a lifetime
Ghon lesion and ranke complex result from
healed primary lesion from MTB
in adition to the ghon lesion - 3 clinical syndromes linked with TB
cavitary (pulmonary) TB
disseminated (miliary) TB
extrapulmonary TB: lymph, skeletal, genitourinary, CNS
scrofula is extrapulmonary TB affecting what system
Pott's disease
extrapulmonary TB infection affecting the skeleton
four places of extrapulmonary tb
lymphatics, skeletal, genitorurinary, CNS
MDR (Multipoel drug resistance) strain of TB is defined as
resistance to a least INH and rifampin
XDR-TB is defined as
resistant to at least 3 of 6 second line drugs
risk factors for MDR include what five things
1. HIV
2. Cavitary TB
3. los socioeconomic status
4. incarcerted persons
5. intial acquisiiton in certain areas
four diagnositic tools used to diagnose TB
1. AFB (acid fast bacillus) smear
2. nuclei acid amplificaiton
3. culture
4. interferon gamma response
advantage and disadvantage to diagnosis of TB by AFB
Ad: same day result
Dis: limited spcificity and sensitivity (NTM rather than TB and needs at least 10 to the 9 organisms)
how does the inteferon gamma response work in diagnosis of TB
mononuclear cells from patients with TB infection, OR disease and normal T cell immunity produce IFN in response to TB specific antigens (ESAT, CFP10)
INH (isoniazid) is cidal for what kind of organisms
rifampin is cidal for what kind of organisms
two drugs used to treat TB that acts on intracellular oragnisms
rifampin and pyrazinamide
TB drug that is static and helps prevent resistance
the four drugs used to treat TB (INH, rifampin, pyrazinamide, ethambutol) how are they administered
intensive phase: 2 months
continuation phase: for drug susceptible strains RX is reduced to INH/rif for 4 months
6 months total
MDR Treatment
INH, rifampin, pyrazinamie, and fluoroquinolone plus one more additional drugs x for more 9-12 monts. sometiems surgical resection
how might treatment of HIV patient differ from the treatment of a non-HIV patient for TB
treatment should be continued for 9 months or for 4 months after negative cultures
why is rifampin not used in treating HIv patients for TB
rifampin connot be used with protease inhibitors

rifampin binds to bacterial RNA polymerase and blocks transcription
if a person is infective they will have a positive PPD test how soon after infections
2-10 weeks
does the magnitude of the PPD reaction matter
likelihood of TB infection or disease depends what
in vitro TB testing works how
whole blood stimulated w/ TB-specific antigents and interferon response quanititated - will replace intradermal testing
treatment regiman for latent TB infection (LTBI)
INH x 9 months (best - preferred for HIV patients
INH x 6 month
Rifampin for 4 months
NTM (nontuberculous mycobacteria or atypical mycobacteria)
are normally present where
soil, water, various animals
the most common NTM causing human infection
m. avium (MAC)
causes cervical adenitis
m. avium
treatment of mycobacterium avium
combination therapy w/ macrolide (clarithromycin or azithromycin), ethambutol and rifamycin (rifampin)
the skin test which test for m. avium and suggests that 30-40% of healthy adults in most parts of the world are infected
mycobacterium avium sensitin (MAS)

many people have false positive PPD reactions due to prior MAC infection
Bacille Calmette Guerin (BCG) is used as
live vaccine against tuberculosis in humans

it is an attenuated strain of M. bovis (normally infects cows)
vaccine for y. pestis
inactivated protects against bubonic and used by us troops in vietnam
urban plague comes from what animals
urban black rat
rat dies - flea to human
animal plague
oxidase and lactose negative
why might relapse occur in someone with tularensis
intracellular pathogen persists
where does tularensis come from
rabbits, arthropod (deer w/ flea)
treatment for tularensis
vaccine for tularensis
live attenuated
fever of undetermined orgin - seen in brucellosis
why might you have prolonged symptoms in brucellosis
intracellular persistance
diagnosis of brucella
blood culture (21 I.p though)
serologic - Ab titer
treatment for brucella
stretomycin and tetracycine