Respiratory Pathogens Flashcards

1
Q

Three respiratory bugs (focused in this packet)

A

Mycobacteria

Mycoplasma

Corynebacteria

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2
Q

Mycobacteria shape and growth

A

Acid Fast Rods

SLOW growth (from one pole only)

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3
Q

Mycobacterium cell wall contains…

A

Mycolic acids

arabinogalactan

PG

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4
Q

3 characteristics of mycolic acids

A
  1. acid fastness
  2. protect from lysozyme + complement
  3. anchored to PG directly or by arabinogalactan
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5
Q

What is cord factor?

A

Trehalose Dymycolate + something else

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6
Q

Mycobacterium product that stimulates cytokine production?

What cytokines?

A

Lipoarabinomannan (LAM)

TNF and IL-6 (which stimulate replication of HIV long terminal repeats)

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7
Q

Mycobacterium Tuberculosis major symptoms

A

fatigue, unexplained weight loss, hemoptysis

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8
Q

Clinical pathway for TB infection

A
  1. primary infection = exudative lesion
  2. either Heals, Necrotizes lung, or makes granuloma.
  3. Granuloma is either encased or spreads via lymph and blood
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9
Q

What is miliary TB?

A

a widely-disseminated TB infection

Also hits lungs

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10
Q
  1. Cells in center of granuloma include…
  2. What eventually forms upon tissue death?
A
  1. MQ, BC’s + DC’s
  2. Caseum forms from necrotic tissue that is damaged by inflammatory response and lack of blood supply
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11
Q

How many new TB cases per year?

A

10 million

(results in 1.5 million deaths)

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12
Q

High TB risk populations? (5)

A
  1. Minorities, Immigrants
  2. HIV patients
  3. Homeless
  4. Young/old
  5. Travelers
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13
Q

TB is always spread….

A

person to person via respiratory droplets

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14
Q

Tb attaches to _______ to invade.

What 3 cellular consequences does this have

A

Alveolar MQ

  1. Prevents phagolysosome fusion
  2. cytotoxicity from cord factor
  3. Cytokine mediated inflammation
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15
Q

Long term TB latency establishes in…

A

granulomas and bone marrow cells

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16
Q

Detection of TB is dependent on…

A

presence of T memory cells

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17
Q

Two ways to detect TB? Explain them?

A

Mantoux test

QuantiFERON-Gold assay (IGRA): tests for release of IFN-g when peripheral lymphocytes are stimulated by TB antigen

(more IGN-gamma is made when effector Tmem cells are present)

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18
Q

TB control?

A

Culture takes too long (6-8 weeks) and acid fast sputum stain needs a massive infection to be able to detect.

PCR is best! Use Tb-specific primers

–98% detection

–takes 90 minutes

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19
Q

Qualifications for latent TB? Treat or let it resolve?

A

IGRA+ or PPD+ without symptoms, and with normal Xray

ALWAYS treat (Isoniazid, Rifampin, or combination of both)

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20
Q

Treatment regimens for TB

A

Chemotherapy = long term with 4 drugs (INH, P, R, E) = (4HREZ)

DOTS important!! (observe them taking medicine)

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21
Q

BCG vaccine is used where? What is a pertinent fact regarding its use?

A

Everywhere but here

It will cause PPD+

22
Q

Treatment for XDR-TB

A

NO = Beta lactams or carbapenems

YES =

  • Meropenem+clavulanate
  • Linezolid (but adverse reaction… neuropathy)

Other:

  • Delaminid (inhibits MA synthesis)
  • Bedaquiline (inhibits ATP synthase)
23
Q

M. leprae initial presentation

A

whitened, anaesthetized skin area

progresses to either Tuberculoid (paucibacillary) or Lepromatous (multibacillary)

24
Q

tuberculoid leprosy Sx

A

macular lesions

(usually) unilateral nerve involvement (sometimes bilateral)

25
Q

Lepromatous leprosy Sx

A

Progressive nodular lesions

bilateral nerve death >> bone resorption and loss of extremities

26
Q

M. Leprae tranmission and reservoirs?

A

transmitted by long-term contact

Humans and armidillos

27
Q

M. leprae pathogenesis

A

inflammatory reaction damages nerve endings

hyposensitivity = soft tissue damage

28
Q

M. Leprae treatment

A

Dapsone (sulfone) and Rifampin …(6-9 months)

Double treatment reduces sulfone resistance

29
Q

Other Mycobacteria?

A

M. avium

  • Most common nosocomial infctn in AIDS
  • disseminated bacteremia
  • Treat with clarithromycin and ethambutol for life

M. Kansasii

  • TB like symptoms, noncommunicable
30
Q

Mycoplasma types?

A

Mycoplasma pneumoniae

Mycoplasma genitalium

Ureaplasma urealyticum

31
Q

Mycoplasma organism

A

really, really smalll. 380 genes.

like really small.

32
Q

Mycoplasma cell wall

A

No cell wall!

Only a membrane, which has sterols that it steals from host

33
Q

Mycoplasma appearance on agar?

A

fried-egg appearance

34
Q

Mycoplasma presentation

A

(Walking) Atypical PNA (20%)

Tracheobronchitis (70%)

insidious onset, mild fever, lasts about 4 weeks

35
Q

Mycoplasma can trigger…

A

Autoimmune encephalomyelitis

(due to immune mimicry)

36
Q

Difference in breath sounds between typical and atypical PNA

A

Typical = bronchial breathing

Atypical = Wheeze (musical, high pitched, fine crackle)

37
Q

Mycoplasma is transmitted via

A

respiratory droplets

38
Q

Mycoplasma is common among…

A

school kids

highest in winter

39
Q

Mycoplasma major pathogenic factors?

A

Proline-rich adhesion protein = forms elongated tip to adhere to epithelial cells

Protein M covers Fab region of antibody to block it

Cytotoxic effects = H2O2, O2 radical, competition for nutrients

40
Q

Mycoplasma treatment

A

Can treat with Tetracycline or Erythromycin (macrolides)

(Azith is more common for treating lung infections right now, but resistance may become a problem)

**often do NOT treat if mild

41
Q

Other Mycoplasmas typically present as ____. What are the three we covered?

A

STD’s

  1. M. genitalium (normal flora, NGU)
  2. M. hominis (salpingitis and post-partum)
  3. Ureaplasma urealyticum: Produces urease because it requires 10% urea for growth. Cause of nongonococcal urethritis in males (bladder stone)
42
Q

Corynebacterium diptheriae shape / structure

(hint: what is weird about this organism’s structure?)

A
  • Club shaped, pleomorphic
  • Gram +
  • Aerobic
    • *contains outer membrane with mycolic acid
43
Q

Corynebacterium culturing medium? (related to cell metabolism)

A

It will show up as black colonies on tellurite blood agar

b/c it reduces potassium tellurite to tellurium metal

44
Q

Corynebacterium clinical presentation

A
  • Throat infection
  • Fever
  • Swollen lymph nodes –> Bull neck
  • PSEUDOMEMBRANE
45
Q

How are toxigenic strains of Corynebacterium ID’d?

A

Elek immunodiffusion test

  • filter paper with antitoxin placed at right angles to streaks of bacteria
  • toxin and antitoxin form a precipitate
46
Q

Corynebacterium spread via…

A

aerosolized droplets

47
Q

Corynebacterium pathogenicity

A

AB toxin from beta phage conversion

  • B binds to EGF-like receptor
  • Partially denatures toxin in vesicle, hydrolysis occurs
  • A binds to NAD–> ADP Ribosylates EF-2 transcription factor (STOPS protein synthesis)
48
Q

How are Corynebacterium pathogenic factors controlled by the cell?

A

“tox” genes are controlled by the DtxR repressor

  • Iron is a co-repressor
  • The ToxAB operon gets shut off at iron concentrations above 10uM
  • (Iron is normally kept low in the body by lactoferrin/transferrin
49
Q

Clinically, why is the Corynebacterium toxin bad?

A

It causes cardiac damage, often resulting in heart failure and death

50
Q

Do infants have passive immunity to Corynebacterium?

A

Yes!

Lasts for about two months

51
Q

Corynebacterium vaccine type/dosing

A

Formalin-treated toxoid vaccine (DTaP)

Booster given every 10 years

***important for travelers to areas of high prevalence

52
Q

Post infection control of Corynebacterium?

A

Quarantine

equine anti-toxin

PEN / **ERYTH ** (despite intoxication, not infection… it’s to keep the number of bacteria low)