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Flashcards in chronic necrotizing pneumonia: abscesses, MTB, NTM Deck (77):
1

chronic pneumo hallmarks

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)

2

foul smelling sputum is pathognomonic for

anaerobes

3

chronic pneumo CXR

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

4

lung lesions are NOT

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

5

tx chronic pneumo empirically?

NO; tx too toxic, wait til dx

6

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

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

7

cavitary lesions caused by

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%)

8

in chronic nec. pneumo, facultative anaerobes are...

more virulent w/ shorter onset (2wks)
anaerobic bacteria are less virulent and onset is 4-6 wks

9

abscess pneumo s/s

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

10

abscess pneumo CXR

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

11

abscess pneumo comps

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

12

abscess pneumo tx

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

13

if abx unsuccessful for abscess tx

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

14

MTB spectrum

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

15

MTB staining

poorly via Gx
*acid-fast* : resistant to destain with acid alcohol

16

MTB cell wall structure

-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)

17

MTB deets

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)

18

TB transmission only occurs from person with..

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

19

TB affects what age groups..

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

20

most MTB-infected pts control or cure their infection?

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

21

risk factors for ACQUIRING TB

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

22

risk factors for developing TB once infected w. MTB

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

23

MTB patho

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)

24

MTB replication occurs in orgs/tissues w.

high O2 levels: apical-post. areas of lung, LN
also: kidney, brain, bone

25

MTB immunity

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**

26

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

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

27

CMI response converts granuloma-->organized granulomas: tubercles

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

28

over time tubercles can heal

>1 yr
fibrosis-->scarring-->calcification (can now see on XR)

29

primary pulm. TB

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

30

*reactivation pulmonary TB* due to

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

31

miliary TB

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

32

if infection progresses in pulmonary TB...

consolidation happens-->cavitary lesions-->bronchiectasis

33

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

-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

LTBI clinical manifestations

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

35

*LTBI proven only by*

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

36

TB disease (active) dx by

s/s, AFB in sputum, Cx

37

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

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

TB in late stage of HIV/AIDS

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

PPD

not 100% sp/sn, injected intradermally (into not under skin)
1st detected 3-8 wks post-primary infection

40

positive PPD

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

QuantiFERON-TB Gold test

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

new IGRAs (IFN-y release assay)

dx both LTBI and active TB (MTB)
-QFT-GIT and T-SPOT TB test

43

detection of DISEASE (active)

med hx, s/s CXR
(report to HD)

44

active TB CXR

-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

ddx active MTB (based on CXR)

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

46

in HIV/AIDS pts, no cavitations but

diffuse infiltrate is common

47

lab dx MTB

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

48

if extrapulm. TB suspected

blood cx to see if disseminating

49

nucleic acid amplification (NAA) testing

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

50

MTB-sp. CD4+ T cells expressed immune markers

CD38, HLA-DR, Ki-67+

51

MTB tx for who?

LTBI and active TB -confirmed! not close contacts
tx too toxic

52

MTB tx: 1st line drugs

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

53

MDR-TB

resistance to Rifampin and INH

54

XDR-TB

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

55

LTBI/MTB infection (not active) 2 tx regimens
(HIV or non-HIV)

1. INH for 6-9* mos
2. Rifampin for 4 mos for LBTI + close contacts w. INH-res. TB/cannot tolerate INH/pyrazinamide

56

TB disease (active) tx: drug-sens

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

TB disease (active) tx: DR

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

TB disease (active) tx: MRD

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

59

Tb disease tx monitored via

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

MDR-TB..

due to chromosomal mutations
high mortality rate

61

extensive tx for XDR-TB

lung resection and antimicrobial tx

62

DOTS

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

63

BCG vaccine

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

NTM etiology

environment AND human NF (MTB just NF)

65

NTM spp.

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

66

NTM deets

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

NTM transmission

NOT person-person, NO reactivation of latent inf.
resevoir is environ. (all contrast MTB)

68

NTM patho

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

69

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

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

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

M. gordonae
M. scrofulaceum: cervical adenitis

71

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

MAC: M. avium complex: ubiquitous environ. org
SE US, inhal. and ingestion-->across mucosa-->infects macros of LP-->submucosa-->LN

72

DMAC

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

73

DMAC manifests in AIDS pt

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

Cx for slow growers req.

2-6 wks, alert lab!
(nucleic acid testing quicker)

75

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

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

NTM dx

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

77

NTM tx

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

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