MTB Flashcards

1
Q

MTB - EPIDEMIOLOGY

A

Most common cause ID-related mortality in the worldPeak: 2003WHO aims to eliminate by 2015Humans: Only reservoirTransmitted: Person - to - person (aerosols)

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2
Q

Morphological & structural characteristics

A

Obligate aerobeBacillus, non-motileHeat sensitiveCatalase +Nitrate reductase, niacin, pyrazinamidase test Structural:Cell wall - pep layer, MYCOLIC ACID (long chain FAs, hydrophobic acids/waxes)

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3
Q

Media

A

MiddlebrooksLowenstein-jensen

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4
Q

Cord factor

A

combines w/mycolic acidcreates serpentine appearanceelicits granuloma formation

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5
Q

Catalase peroxidase

A

resists host cell’s oxidative response

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6
Q

Sulfatides

A

GlycolipidInhibits phagolysosome formationPromotes IC growth

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7
Q

High mutation rate

A

requires multidrug therapy

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8
Q

Granuloma

A

macrophagesMGCfibroblastscollagen fibers

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9
Q

active primary

A

1) when granuloma breaks loose & disseminates2) CASEOUS NECROSIS: internal lysis of macrophages/MTB cells in the granulomas3) FEVER4) radiography: hilar adenopathy, pulm infiltrates - looks like pneumonia5) droplet nuclei infects middle/lower lobes6) MTB gets phagocytosed by alveolar macro & multiplies….macro kills MTB and granuloma forms7) MTB dies, macro presents to TH1 cell. IFN-g released, activated macro.

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10
Q

active secondary

A

UPPER LOBESsuppression of T cells - insidious onset of diseasenormal symptoms + hemoptysis, dyspnea (SOB)

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11
Q

disseminated forms

A

ORAL MUCOSA: ulceration/paintongue & posterior mouth. osteomyelitis. salivary gland (parotid) infectionEYE: intraocular most common. anterior uveitis

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12
Q

TST/Mantoux test

A

depends on 2 factors: size & risk of infection

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13
Q

IGRA

A

measures TB sensitized t-cell IFN-G productionnot affected by BCG1 ov only, results in 24h

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14
Q

TX

A

3-4 drugs (ripe)rifampinisoniazidpyrazinamideethambutol

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15
Q

rifampin

A

RNA synthesis

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16
Q

isoniazid

A

mycolic acid synthesis, hepatotoxic

17
Q

pyrazinamide/ethambutol

A

hepatotoxic

18
Q

dots

A

most effective formdirectly observed treatment > short course

19
Q

What species of Mycobacterium is the second leading cause of NTM infection in HIV-infected patients

A

Mycobacterium kansasii(MAC-> #1)

20
Q

MAC/MTB similarities

A
  1. Both consists of SLOW-GROWING ORGANISMS 2. Strong ACID-FAST 3. AEROBIC BACILLI4. Gram- POSITIVE5. Grows on MIDDLEBROOK agar
21
Q

MAC/MTB differences

A
  1. Reservoirs a. MAC → soil & water b. MTB → Humans 2. MAC colonies a. NO CORDING or CLUSTERING b. Small, flat, translucent, smooth colony c. Occasionally pale yellow pigment d. LACK of GRANULOMA FORMATION e. OVERGROWTH of microbe
22
Q

treatment of MAC in HIV (-) vs HIV (+) pts

A

antibiotics for both (clarithromycin, azithromycin, ethambutol, rifampin)(+): HAART(+) W/MAC: lifelong antiretroviral; or antiretroviral for 2 wks then HAART (don’t begin both = IRIS…immune reconstitution inflamm syndrome)(+) W/NO MAC: chemoprophylaxis until CD4TCELL>100cell/uL(-): antibiotics until sputum is neg for a year

23
Q

MAC=

A

M. aviumM. intracellulareno person-to-personopportunistic

24
Q

MAC IN HIV (-)

A

PULMONARYfibrocavity disease (men): COPDfibronodulary disease (ladiez): BRONCHIECTASIS & lady windermere syndromelymphadenitis (kidsz): unilateral cervical nodes

25
Q

MAC IN HIV (+)

A

PULMONARYnew infection, not latent reactivationlooks just like MTB, but GI componentDISSEMINATED (DMAC)lymphohematogenous dissemination of bactgranulomas NOT EFFECTIVEenlarged organs, organ dysfxncan’t develop CMI (no macrophage activation or granuloma formation)

26
Q

> 5mm

A

hiv + ptsimmunosuppresedrecnt contact w/TB ptsabnormal chest radiographs

27
Q

> 10mm

A

immigrantsdrug usershealthcare employeeskids <4 exposed

28
Q

> 15mm

A

positive