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Micro > chronic necrotizing pneumonia: abscesses, MTB, NTM > Flashcards

chronic necrotizing pneumonia: abscesses, MTB, NTM Flashcards

1
Q

chronic pneumo hallmarks

A

slow, insidious (wks-mod), fever mild-high, night sweats, malaise/fatigue, anorexia (10-20 lb), dyspnea, chronic cough may become prod, hemoptytic, CP (pleur/nonpleur)

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2
Q

foul smelling sputum is pathognomonic for

A

anaerobes

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3
Q

chronic pneumo CXR

A

consolidation/infiltrates OR cavitary lesions
Apical or subapical consolidation/infiltrates in the upper lobes or superior- posterior segments of the lower lobes +/- caviation (MTB, syst. mycoses), occur over several mos

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4
Q

lung lesions are NOT

A

NOT visualized by Gs
NOT Cx on blood agar
NOT tx w. PCN, cephs

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5
Q

tx chronic pneumo empirically?

A

NO; tx too toxic, wait til dx

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6
Q 
lung abscess (hole):
(cavitary lesions often have air-water interface)
A

local suppurative(pussy) necrotizing collection w/in lung parenchyma

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7
Q

cavitary lesions caused by

A

90%: anaerobes, facult anaerobes (G+ cocci, G- rods)
via aspiration, wks-2mos
CAN visual by Gs, blood agar if facult., tx w. PCN, cephs

also caused by: prim. SCC of lung (>45yo, 30%)

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8
Q

in chronic nec. pneumo, facultative anaerobes are…

A

more virulent w/ shorter onset (2wks)

anaerobic bacteria are less virulent and onset is 4-6 wks

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9
Q

abscess pneumo s/s

A

classic chronic pneumo + foul sputum (50-60%), altered sensorium if progressed
poor dent. hyg., trauma/inj/disease

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10
Q

abscess pneumo CXR

A

solitary cavitary lesion about 4cm in diameter w/ air-fluid level

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11
Q

abscess pneumo comps

A

empyema formation from bronchopleural fistula
massive hemoptysis
spont. rupture into uninv. lung segments
non-resolution of abscess cavity

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12
Q

abscess pneumo tx

A

abx targeting orogingival anaerobes
B-lactamase-inhib/B-lactam OR 2nd/3rd gen. CEPH + clindamycin/metronidazole for 6-8 wks
past: (IV PCN + clindamycin)

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13
Q

if abx unsuccessful for abscess tx

A

resect lung/drain absecs via bronchial airway (if thru chest, non-healing open wound in lung

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14
Q

MTB spectrum

A

no illness: LTBI
localized: pulmonary/meningeal TB
massive systemic dissemination: miliary TB

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15
Q

MTB staining

A

poorly via Gx

acid-fast : resistant to destain with acid alcohol

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16
Q

MTB cell wall structure

A
  • PTG, G- wall w/ lypophilic substances
  • virulence factors:
    1. mycolic acids (LCFAs (branched), lipids bound to arabinogalactan-PTG polymers) INH target resp. for acid-fastness
    2. trehalose dimycolate (cord factor)
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17
Q

MTB deets

A

facult. IC in macrophages, obligate areobe, slow growth (2-3 wks), sp. media, resistant to drying, acids, alkalis, disinf.
sens. to UV light and moist heat (pasteurization)

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18
Q

TB transmission only occurs from person with..

A

ACTIVE pulmonary or laryngeal TB via inhalation of 1-10um airborne droplets of 1-3 bacilli (cough) AFB smear neg or pos pts! (need contact for hours) (humans sole host)
also: ingestion of m. bovis milk

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19
Q

TB affects what age groups..

A

young imm.COMPETENT (65 as REACTIVATION (pulmonary TB)

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20
Q

most MTB-infected pts control or cure their infection?

A

CONTROL
10% will reactivate (LTBI–>TB) (esp. 0-2 yrs post inf)
90% remain LTBI for life
(some will not control–>TB)

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21
Q

risk factors for ACQUIRING TB

A

foreign born (Africa, Asia, LA)
low-income (homeless, malnutr., crowding)
nursing home, correctional, homeless shelters
HCW or persons employed above

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22
Q

risk factors for developing TB once infected w. MTB

A

65,
T cell compromise(HIV, maln, chemo, steroids, SOT, old, blood ca)
IVDU, certain diseases

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23
Q

MTB patho

A

facult. IC of alveolar endothelial/epithelial cells and macrophages
- inh. TB must reach alveolar spaces (periphery), MTB are phago (not killed) by macros and PMNs, multi. IC, disseminate: locally (lungs and LNs) or systemically/lymphohematogenous (any organ)

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24
Q

MTB replication occurs in orgs/tissues w.

A

high O2 levels: apical-post. areas of lung, LN

also: kidney, brain, bone

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25
Q

MTB immunity

A

CMI (both CD4+ and CD8+)
exposure–>MTB-sp. CD4+ cells proc. IFN-y–>activate macros–>prod. ROIs that kill MTB cells phagocyt. by act. macros
MTB-sp. CD8+ cells kill MTB-inf. NON-ACT. macros–>rel. MTB cells, killed by act. macros
CMI resp. for most tissue damage and symptoms of disease, MTB does NOT produce toxins

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26
Q

host attempts to contain MTB infections–>inflammatory response–>adaptive response–>

A

GRANULOMA (caseation-seen in histo biopsy not CXR/CT/MRI)
made of macrophage-derived epithelioid cells, lymphocytes
viable MTB @ center (w. CMI: arrested, but viable for years)
if inadequate CMI: LTBI–>TB

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27
Q

CMI response converts granuloma–>organized granulomas: tubercles

A

dynamic, continuous process
core: dormant MTB, lymphos, epithel. histocytes, multinuc. Langerhans giant cells
periphery: fibroblasts, monocytes (blood), lymphos,
zone cells alive, must be replenished

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28
Q

over time tubercles can heal

A

> 1 yr

fibrosis–>scarring–>calcification (can now see on XR)

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29
Q

primary pulm. TB

A

happens when IR fails to form granuloma (inade. CMI)
old, T cell compromised, immunocompetent kiddos
(less common in US)

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30
Q

reactivation pulmonary TB due to

A

systemic immunosuppression:
advanced HIV/AIDS, Ca, old, chronic ill health
immunosupp–>brkdwn of granulomas w. LTBI–>reactivation
most common TB in US

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31
Q

miliary TB

A

massive disseminated inf. involving multiple organs (foci-size of millet seed)
other: extrapulmonary refers to other organ system

32
Q

if infection progresses in pulmonary TB…

A

consolidation happens–>cavitary lesions–>bronchiectasis

33
Q

in reactivation TB, the caseous center continues to enlarge as MTB multiply–>liquifies tissues–>

A
  • formation of air-liquid filled cavities: huge inc. in MTB #s–>abx resistance, spread
  • rupture into airways–>hemoptysis, release of caesium (spread)
  • inhal. of MTB to other parts of lung (tuberculous bronchopneumonia)
  • erosion of vein wall and leak of caesium into blood–>hemoptysis, miliary TB
34
Q

LTBI clinical manifestations

A

absence of s/s
CXR norm or shows evidence of past TB
neg. stain/sputum Cx

35
Q

LTBI proven only by

A

positive PPD
positive Quantiferon test
(CANNOT distinguish btw LTBI and active TB disease)
i.e. disease may or may not be present

36
Q

TB disease (active) dx by

A

s/s, AFB in sputum, Cx

37
Q

TB disease (active) s/s (only after inf. has progressed)

A

slow, insidious, fever (of “unknown origin”: FUO), night sweats, malaise, fatigue, anorexia + weight loss
chronic persistant cough, pleuritic pain, pleural effusions (MTB inf or IR), dyspnea

38
Q

TB in late stage of HIV/AIDS

A

mostly pulm. TB, but coin-like or cavitary lesions uncommon
diffuse pulmonary infiltrates happen due to poor CMI
(disseminated TB 1/3 cases, inc. mortality)

39
Q

PPD

A

not 100% sp/sn, injected intradermally (into not under skin)

1st detected 3-8 wks post-primary infection

40
Q

positive PPD

A

induration (50% monos/macros, 50% MTB-sp Th1 cells) 48 hrs post-inf
> 15 mm for all pops not specified
> 10 mm for foreign born (see above), IVDU, med-underserved, low income, HCW etc (see above), residents of (see above), certain conditions, kiddos
>5 mm for HIV+, close TB contacts, abnorm. CXR (upper lobe fibrosis), immunsuppr. w. at leat 15 mg prednisone/day last 1 mo

41
Q

QuantiFERON-TB Gold test

A

in vitro, measure amount of INF-y prod. by cells in whole blood that have been stim. by MTB peptides

  • mimics ESAT-6 and CFP-10 proteins, present in MTB but not BCG and NTM
  • dx for MTB, NOT dx for LTBI vs active TB
  • no boosting effect
42
Q

new IGRAs (IFN-y release assay)

A

dx both LTBI and active TB (MTB)

-QFT-GIT and T-SPOT TB test

43
Q

detection of DISEASE (active)

A

med hx, s/s CXR

report to HD

44
Q

active TB CXR

A

-consolidation/infiltrates in apical/subapical in upper lobes or sup-post segments of lower lobes +/- cavitation (or nodular/cavitary lesion w. no surrounding infiltrates)
-immunocompetent: solitary pulm. nodule 1 cm in diam. surrounded by lung parenchyma, no other abnorm., opaque due to calcification
(granuloma form. evident in biopsy specimen)

45
Q

ddx active MTB (based on CXR)

A

infectious: nocardia, actinomyces israelii, systemic mycosis (fungi) - infection, not disease
lung cancer
hamartoma/adenochondroma

46
Q

in HIV/AIDS pts, no cavitations but

A

diffuse infiltrate is common

47
Q

lab dx MTB

A 
AFB in sputum (consid. infectious, quantified)
positive Cx (confirms dx)-->drug susc/abx sens test, monitor tx response
48
Q

if extrapulm. TB suspected

A

blood cx to see if disseminating

49
Q

nucleic acid amplification (NAA) testing

A

detects MTB 1+ wks earlier than Cx, cannot dist. btw live/dead

50
Q

MTB-sp. CD4+ T cells expressed immune markers

A

CD38, HLA-DR, Ki-67+

51
Q

MTB tx for who?

A

LTBI and active TB -confirmed! not close contacts

tx too toxic

52
Q

MTB tx: 1st line drugs

A

Isoniazid: interferes w. mycolic acid syn
Rifampin: inhib. RNA syn
Pyrazinamide: bactericidal for repl. orgs
Ethambutol: inhib. cell wall sun and is bacteriostatic

53
Q

MDR-TB

A

resistance to Rifampin and INH

54
Q

XDR-TB

A

resistant to Rifampin and INH and any FQ and at least 1/3 inj. 2nd line drugs (amikacin, kanamycin, capreomycin)

55
Q

LTBI/MTB infection (not active) 2 tx regimens

HIV or non-HIV

A
  1. INH for 6-9* mos

2. Rifampin for 4 mos for LBTI + close contacts w. INH-res. TB/cannot tolerate INH/pyrazinamide

56
Q

TB disease (active) tx: drug-sens

A
  1. INH alone 18 mod
  2. INH and Rifampin for 9 mos
  3. 4 1st LD for 3 mos, 2 1st LD for 4 mos
57
Q

TB disease (active) tx: DR

A

combined chemo to prev. MDR-TB
3 drugs 6-9 mos (e.g.,
rifampin, pyrazinamide, INH for 2 months then rifampin and INH for 4 mos -still OK)

58
Q

TB disease (active) tx: MRD

A

4-5 drugs for 18-24 mos (2 yrs!)

59
Q

Tb disease tx monitored via

A 
sputum Cx (3 wks post tx)
considered inf. as long as orgs cx, cured when 3 successive neg cx
CANNOT monitor with PPD, Quantiferon test
60
Q

MDR-TB..

A

due to chromosomal mutations

high mortality rate

61
Q

extensive tx for XDR-TB

A

lung resection and antimicrobial tx

62
Q

DOTS

A

HCW observe swallowing, monitor progress, short-course (6-9 mos)

63
Q

BCG vaccine

A

M. bovis, cannot cause dis. in immcompetent person
life-long, latent infection, can reactivate latent inf–>active in immunocompromised pts
used to tx bladder Ca (IR delays Ca recurrence)

64
Q

NTM etiology

A

environment AND human NF (MTB just NF)

65
Q

NTM spp.

A

M. kansasii
M. fortuitum
M. avium complex (MAC): M. intracellulare and M. avium

66
Q

NTM deets

A 
rapid growers: 7 days
slow growers >7d-6weeks
some AF, cross-reac. Ags to MTB Ag
most MDR (esp. MAC)
incidence inc. due to HIV/immsuppr pop
affects oldies, immsuppr, underlying dis.
67
Q

NTM transmission

A

NOT person-person, NO reactivation of latent inf.

resevoir is environ. (all contrast MTB)

68
Q

NTM patho

A

may cause slight + PPD, less virulent *rarely causes dis. in immunocompetent person, diff to elim. due to MDR

69
Q

NTM slow growers: Group 1: photochromogens, Runyon group I (7d-6wks)

A

M. kansasii: water supplies, MW US, pulm dis., min. contagious (unlike MTB)
M. marinum: skin inf.
M. haemophilum: skin, jt, bone, pulm. inf. in immunocompromised persons and lymphaden. in kiddos

70
Q

NTM slow growers: Group 2 : scotochromogens (pigment in dark), Runyon group II

A

M. gordonae

M. scrofulaceum: cervical adenitis

71
Q

NTM slow growers: Group 3: noncrhomogenic, Runyon group III

A

MAC: M. avium complex: ubiquitous environ. org

SE US, inhal. and ingestion–>across mucosa–>infects macros of LP–>submucosa–>LN

72
Q

DMAC

A

disseminated MAC in HIV/AIDS pts. (20-40% of pts w. CD4 count

73
Q

DMAC manifests in AIDS pt

A

fever, night sweats, weight loss-wasting, swollen abd. LNs (unilat), diarrhea, hepsplnmeg, anemia, elev. PB liver enzymes, localized disease LESS common, but rarely in (LRT, pericarditis, GIT, CNS, skin, joints)

74
Q

Cx for slow growers req.

A

2-6 wks, alert lab!

nucleic acid testing quicker

75
Q

NTM rapid growers: (2-7 days) Runyon group IV

A

M. fortuitum, M. abscessus, M. chelonae, M. massiliense, M. bolletii (fortuitum complex)
contaminant in clinical specimens
sig. opportunistic pathogen of (skin, ST, bone, LRT (chronic), site of wound trauma, surgical prosthetic implants)
-resis to alk. glutaradehyde, low susc. to high lev. disinfect.

76
Q

NTM dx

A

Cx must be done, need repeated isolation of org for dx, ID to species level!

77
Q

NTM tx

A

depends on ID of species, sensitivity testing must be done on Cx+ isolates

Micro (61 decks)

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