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Microbiology > Tuberculosis > Flashcards

Tuberculosis Flashcards

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Biology 101 flashcards
1
Q

What microbe is an obligate aerobe, rod shaped, slender, and slightly curved, non-motile, heat sensitive, and intracellular?

A

Mycobacterium tuberculosis

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2
Q

What media do you grow MTB from?

A

Middlebrooks or Lowenstein-Jensen

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3
Q

How do you describe MTB after 3-4 weeks of growth?

A

“Ruff, buff, and tuff”

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4
Q

What is the only reservoir for MTB? Who does it usually affect?

A

Humans; usually affects young adults, needs 10 bacilli to initiate infection

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5
Q

What kind of exposure is needed for TB infection?

A

prolonged, usually in crowded conditions

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6
Q

What are some possible complications of MTB?

A

Infants and immunocompromised individuals: hematogenous dissemination may result in meningitis and other symptoms
Older: failure of immune system, possible reactivation of latent infection

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7
Q

How do many children become infected?

A

By caregivers

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8
Q

What is the probability of infection for healthy individuals with no risk factors?

A

10% over lifetime

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9
Q

What is the probability of infection for individuals with HIV?

A

10% per year

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10
Q

How does mycolic acid act as a virulence factor?

A

Prevents dehydration and may resist H2O2

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11
Q

What factor is responsible for serpentine “cords” of cells in virulent strains of MTB?

A

Mycoside

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12
Q

How do sulfatides have their effect as a virulence factor in MTB?

A

Prevent phagolysosome production and promote intracellular growth

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13
Q

Which virulence factor inhibits cell mediated immunity (perhaps by interfering with macrophage activation by IFN-gamma) and scavenges ROI?

A

Lipoarabinomannan (LAM)

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14
Q

What is produced in the host by immunogenesis of MTB?

A

Caseous necrosis within granuloma, cavity formation in lungs, hematogenous spread of bacilli

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15
Q

What is the reason for immediate clearance of TB?

A

alveolar macrophages are able to clear bacteria

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16
Q

What are the four potential outcomes for TB?

A

1) immediate clearance
2) primary disease
3) latent infection
4) endogenous reactivation/secondary disease

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17
Q

What is the pathogenesis behind primary diease of MTB?

A

Enters alveolar macrophages and multiply, produce acute inflammatory reaction, exudative lesions form, and resembles bacterial pneumonia, all of which results in dev’t of primary or rapidly progressive disease

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18
Q

What are the two cytokines that are originally signaled in primary TB infection?

A

IL-12 and TNF alpha

19
Q

Where do live macrophages take up and transport MTB particles to?

A

Perihilar lymph nodes, leads to lymphadenopathy

20
Q

What causes sensitization?

A

When macrophages present MTB protein antigens to T-cells.

21
Q

What are sensitized T Cells responsible for?

A

Turning on cell-mediated immunity which multiply and return to site of infection.

22
Q

What releases IFN gamma? What does IFN-gamma do?

A

Sensitized T Cells; attracts and activates macrophages which will actively destroy intracellular MTB

23
Q

How do activated macrophages actively destroy intracellular MTB?

A

by producing lytic enzymes and ROI and RNI, generates granuloma and tubercle formation. Local tissue destruction results in caseous necrosis

24
Q

What is in an MTB granuloma or tubercle?

A

caseous necrosis surrounded by viable MTB cells, more macrophages, multinucleated giant cells, collagen fibers.

25
Q

What causes cavitary lesions in the lungs?

A

multiple granulomas and caseous necrosis coalesce, which limits the amount of O2 and eventually the TB die

26
Q

What is the Ghon Focus and Ghon Complex of primary MTB?

A

Focus: middle or lower zone of lung
Complex: Focus+perihilar lymph nodes form a fibrotic or calcified granuloma

27
Q

What marks the onset of latent TB infection?

A

When CMI contains “persistent” MTB cells, which form very low activity. If granuloma contain viable MTB in low pH and low O2, they enter a spore-like state

28
Q

What causes the reactivation of LTBI? When can it occur?

A

Impairment of CMI, HIV is most important cause. 2 years to decades after primary infection

29
Q

How does TB become airborne?

A

Caseous necroses liquify and discharge TB bacilli into bronchi

30
Q

What is miliary TB?

A

Hematogenous dissemination of MTB to the tissue surrounding BV, Millet-seed sized granulomas form and organ & system function lost due proliferation of MTB. May form Choroid granulomas

31
Q

What is Pott disease?

A

miliary MTB present in vertebral bodies, causes chronic back pain and untreated results in destruction of vertebrae and permanent disability

32
Q

What is the Xpert MTB/RIF system?

A

Analyzes 2 ml of sputum samples to look for rifampin resistance in two hours!

33
Q

Which mycobacterium is a weakly G+ aerobic bacilli, acid fast (strongly), and ubiquitous?

A

M avium and intracellulare, doubles in half the time as MTB

34
Q

What does the colony of MAC look like?

A

small, flat, translucent, smooth, occasionally pale yellow
NO CORDING or clustering
also grows well on Middlebrook agar

35
Q

How does MAC enter the body?

A

Either inhalation or ingestion, NO PERSON-TO-PERSON, does not require patient isolation

36
Q

What is the leading cause of NTM infection? #2?

A

HIV (opportunistic); mycobacterium kansasii found in tap water in the southeastern and southern US

37
Q

HIV negative individuals may conduct pulmonary MAC if there are what other preexisting conditions?

A

Elderly men with COPD (fibrocavitary)

Elderly women with bronchiectasis due to repressed couching, aka Lady Windermere’s syndrome (fibronodulary)

38
Q

What is the clinical manifestation of MAC in children (1-4)?

A

Lymphadenitis in unilateral cervical lymph nodes

39
Q

Are MAC infections due to reactivation?

A

No, always new infection starting in the GI tract. Looks like MTB, but you differentiate with diarrhea in addition to fever, weight loss, and night sweats.

40
Q

How is diagnosis of MAC made?

A

Sterile isolation of MAC, CRX, PCR to determine 16S rRNA sequence of pathogen

41
Q

What is the DOC for MAC in both HIV+ and HIV- infections?

A

Combo of clarithro or azithro + ethambutol + rifambin (check LFTs)

42
Q

What should be done for a year following MAC treament in HIV negative pts?

A

continuation of sputum cultures for 1 year

43
Q

How do you treat an HIV+ patient with no MAC infection but with exposure?

A

Chemoprophylaxis (in pts with CD4 100

44
Q

How do you treat an HIV+ infection with MAC infection?

A

Begin tx and then ART 2 weeks later, don’t flip around or it causes IRIS

Microbiology (14 decks)

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