Bacteriology - Mycobacteria

Front 1

metabolism of mycobacteria

Back 1

obligate aerobes

facultative intracellular (except M. leprae which cannot be cultured on articial media)

Front 2

structural features of mycobacteria

Back 2

nonspore
non-encapsulated
slow growing

Front 3

mycobacterial cell walls have a triple layer and contain

Back 3

mycolic (fatty) acids (absent in most other bacteria)

has two long hydrophobic chains

Front 4

gram stain to identify mycobacteria ?

Back 4

no

Front 5

how are mycobacteria stained

Back 5

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.

Front 6

in addition to mycobacteria what other organism might stain acid fast

Back 6

nocardia

Front 7

how do corynebacteria (which also contain mycolic acids) differ from mycobacteria

Back 7

they have shorter fatty acid chain lengths and are not acid fast

Front 8

"cord factor"

Back 8

two mycolic acids attached to disaccharide trehalose constitute cord facotr, whic is associated with virulence in mycobaterium tuberculosis

Front 9

virulence factor in mycobacterium tuberculosis

Back 9

cord factor

Front 10

why is mycobacteria calle a "wax ball"

Back 10

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

Front 11

Wax D

Back 11

an unuall lipid in mycobacteria - which is used by immunologists as Freunds complete adjuvant to increase immune response

Front 12

what probably plays a role in the intense CMI seen in mycobacterial infections

Back 12

lipids

Front 13

involved in the characterisitic resistance of mycobacteria to drying and chemicals

Back 13

lipids

Front 14

what is the generation time for TB

Back 14

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

Front 15

visible growth on solid media of TB takes how long

Back 15

3-8 weeks

Front 16

Hansens bacillus

Back 16

m. leprae

Front 17

temp preference of m.leprae

Back 17

27-33 degrees

predeliction for cooler areas of the body (skin, nose, mucous membranes of upper resp tract)

Front 18

can m.leprae be cultivated in artificial media

Back 18

no

Front 19

transmission of m.leprae

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respiratory - sometimes through skin

Front 20

age relationship to suseptability to m.leprae

Back 20

children more suseptable

Front 21

primary lesions of leprosy - characteristics

Back 21

skin macule (hypo-pigmented)
erythematous
raised and braown wheal-like (like mosquito bite)

Front 22

incubation period for leprosy

Back 22

months - 30 years

usually 2-5 years

Front 23

long duration cases of leprosy show what of kidneys, liver, and spleen

Back 23

amyloidosis

Front 24

leprosy mainly infovles what organs / system

Back 24

skin and nerves

Front 25

genesis of lepromatous (primary leasion in leprosy)

Back 25

macrophage or histiocyte takes up bacilli

Front 26

genesis of tuberculoid (primary lesion in leprosy)

Back 26

like TB; chronic granulomatous lesions
epitheloid and giant cells present w/o caseation

Front 27

Lepromin skin test results for lepromatous lesion vs. tuberculoid test

Back 27

lepromatous: lepromin skin test neg
tuberculloid: lepromin skin test positive

Front 28

the ability to mobilizatio T cells in lepromatous vs tuberculoid lesion

Back 28

mobilization in lepromatous is much worse than mobiliztion of T cells in tuberculoid (DTH)

therefore the prognosis of the lepromatous lesion is worse

Front 29

how does the amount of bacteria found in lesion differ when it comes to lepromatous and tuberculoid lesions

Back 29

lepromatous lesions have many bacilli and tuberculoid have fewer (especially towards the center of lesion)

Front 30

two things that illustrate cellular immunity and the link with tuberculoid lesion in leprosy

Back 30

1. lepromin test positive
2. DTH intact

Front 31

what is the abnormal serologic activity seen in lepromatous lesion versus tuberculoid lesion(leprosy)

Back 31

polyclonal hypergammaglobulinemia in lepromatous and normal levels of IgG in tuberculoid lesion

Front 32

a complication in the tuberculoid state which resembles immune complex disease and is example of the lack of antibody response correlation w/ tuberculoid state

Back 32

erythema nodosum leprosum (ENL)

Front 33

is there antibody to m.leprae

Back 33

yes it is specific for phenolic glycolipid but not protective

Front 34

diagnosis of m. leprae (4)

Back 34

gross appearance of lesions,
histological examination
acid fast stains
material fromnodules -
margins of flat lesions or nasal scrapings

Front 35

3 drug treatment of m.leprae (treat for 2-3 years) involves what three drugs

Back 35

1. dapsone
2. rifampin
3. clofazimine

Front 36

if there is ENL complicaiton in someone infected with m.leprae then you treat with

Back 36

immune suppression

Front 37

BCG

Back 37

TB vaccine offers some protection

Front 38

hospital disinfectants are judged by their ability to kill

Back 38

m. tuberculosis

Front 39

m. tuberc may remain viable for weeks at what temp

Back 39

4 degrees C

Front 40

macrophages ingest MTB, present to T cells which release what three lymphokines

Back 40

IL-2 to expand CD 4
IFNg to activate MO
TNF to induce phagoolysomal fusion and kill intracellular MTB

Front 41

gene that appears to regulate the phagolysosomal enviroment and confer increased suscetibility to MTB

Back 41

variant allele in NRAMP1

Front 42

polymorphisms in what receptor gene is associated with protection against TB in West AFrica

Back 42

polymorphisms in Vitamin D

Front 43

transmission of TB

Back 43

person to person inhalation of droplet nuclei produced by coughing or talking -

inhaled - ingested by alveolar macrophages, transient bacteremia, granuloma formation in lung

Front 44

this organisms from contaminated mild produces clinical picture of TB in developing countries

Back 44

m. bovis

Front 45

infection of TB is identified by what skin test

Back 45

PPD

Front 46

disease of TB is identified by

Back 46

culture of MTB from lung or other sites or by compativble clinical syndrome

Front 47

what percent of people will develop active disease

Back 47

10%

5% will progress to primary disease w/in 2 years of infeciton
5% will progress to reactivation disease w/in a lifetime

Front 48

Ghon lesion and ranke complex result from

Back 48

healed primary lesion from MTB

Front 49

in adition to the ghon lesion - 3 clinical syndromes linked with TB

Back 49

cavitary (pulmonary) TB
disseminated (miliary) TB
extrapulmonary TB: lymph, skeletal, genitourinary, CNS

Front 50

scrofula is extrapulmonary TB affecting what system

Back 50

lymphatics

Front 51

Pott's disease

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extrapulmonary TB infection affecting the skeleton

Front 52

four places of extrapulmonary tb

Back 52

lymphatics, skeletal, genitorurinary, CNS

Front 53

MDR (Multipoel drug resistance) strain of TB is defined as

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resistance to a least INH and rifampin

Front 54

XDR-TB is defined as

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resistant to at least 3 of 6 second line drugs

Front 55

risk factors for MDR include what five things

Back 55

1. HIV
2. Cavitary TB
3. los socioeconomic status
4. incarcerted persons
5. intial acquisiiton in certain areas

Front 56

four diagnositic tools used to diagnose TB

Back 56

1. AFB (acid fast bacillus) smear
2. nuclei acid amplificaiton
3. culture
4. interferon gamma response

Front 57

advantage and disadvantage to diagnosis of TB by AFB

Back 57

Ad: same day result
Dis: limited spcificity and sensitivity (NTM rather than TB and needs at least 10 to the 9 organisms)

Front 58

how does the inteferon gamma response work in diagnosis of TB

Back 58

mononuclear cells from patients with TB infection, OR disease and normal T cell immunity produce IFN in response to TB specific antigens (ESAT, CFP10)

Front 59

INH (isoniazid) is cidal for what kind of organisms

Back 59

extracellular

Front 60

rifampin is cidal for what kind of organisms

Back 60

intracellular

Front 61

two drugs used to treat TB that acts on intracellular oragnisms

Back 61

rifampin and pyrazinamide

Front 62

TB drug that is static and helps prevent resistance

Back 62

ethambutol

Front 63

the four drugs used to treat TB (INH, rifampin, pyrazinamide, ethambutol) how are they administered

Back 63

intensive phase: 2 months
continuation phase: for drug susceptible strains RX is reduced to INH/rif for 4 months
6 months total

Front 64

MDR Treatment

Back 64

INH, rifampin, pyrazinamie, and fluoroquinolone plus one more additional drugs x for more 9-12 monts. sometiems surgical resection

Front 65

how might treatment of HIV patient differ from the treatment of a non-HIV patient for TB

Back 65

treatment should be continued for 9 months or for 4 months after negative cultures

Front 66

why is rifampin not used in treating HIv patients for TB

Back 66

rifampin connot be used with protease inhibitors

rifampin binds to bacterial RNA polymerase and blocks transcription

Front 67

if a person is infective they will have a positive PPD test how soon after infections

Back 67

2-10 weeks

Front 68

does the magnitude of the PPD reaction matter

Back 68

likelihood of TB infection or disease depends what

Front 69

in vitro TB testing works how

Back 69

whole blood stimulated w/ TB-specific antigents and interferon response quanititated - will replace intradermal testing

Front 70

treatment regiman for latent TB infection (LTBI)

Back 70

INH x 9 months (best - preferred for HIV patients
INH x 6 month
Rifampin for 4 months

Front 71

NTM (nontuberculous mycobacteria or atypical mycobacteria)
are normally present where

Back 71

soil, water, various animals

Front 72

the most common NTM causing human infection

Back 72

m. avium (MAC)

Front 73

causes cervical adenitis

Back 73

m. avium

Front 74

treatment of mycobacterium avium

Back 74

combination therapy w/ macrolide (clarithromycin or azithromycin), ethambutol and rifamycin (rifampin)

Front 75

the skin test which test for m. avium and suggests that 30-40% of healthy adults in most parts of the world are infected

Back 75

mycobacterium avium sensitin (MAS)


many people have false positive PPD reactions due to prior MAC infection

Front 76

Bacille Calmette Guerin (BCG) is used as

Back 76

live vaccine against tuberculosis in humans

it is an attenuated strain of M. bovis (normally infects cows)

Front 77

vaccine for y. pestis

Back 77

inactivated protects against bubonic and used by us troops in vietnam

Front 78

urban plague comes from what animals

Back 78

urban black rat
rat dies - flea to human

Front 79

enzootic

Back 79

animal plague

Front 80

y.pestis
oxidase?
lactose?

Back 80

oxidase and lactose negative

Front 81

why might relapse occur in someone with tularensis

Back 81

intracellular pathogen persists

Front 82

where does tularensis come from

Back 82

rabbits, arthropod (deer w/ flea)

Front 83

treatment for tularensis

Back 83

streptomycind

Front 84

vaccine for tularensis

Back 84

live attenuated

Front 85

FUO

Back 85

fever of undetermined orgin - seen in brucellosis

Front 86

why might you have prolonged symptoms in brucellosis

Back 86

intracellular persistance

Front 87

diagnosis of brucella

Back 87

occupation
blood culture (21 I.p though)
serologic - Ab titer

Front 88

treatment for brucella

Back 88

stretomycin and tetracycine