Unit 4 - Bacterial Pneumonia: Atypicals Flashcards

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1
Q

describe the bacteriology of Legionella

A

poorly staining G- rods (need silver or IF)

  • faculative intracellular parasites
  • -free-living motile w/ flagella (infectious phase)
  • -intracellular nonmotile (replicative phase)
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2
Q

when has the accidental opportunistic lifestyle of legionaires arisen?

A

recently (1970s)

  • natural: form biofilms in stagnant freshwater, parasite protozoa (waterborne), full life cycle
  • unnatural: biofilms in HVAC systems, enter human lungs (aspirated), parasitize alveolar MP as dead end host (hard to remove once established)
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3
Q

how do simultaneously-exposed cases of legionella occur?

A

form in an outbreak, but are not contagious

-most common source is contaminated water supply

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4
Q

how do legionella replicate within phagocytic cells

A
  • begin living in biofilm on warm water or in soil
  • taken up by phagocytes
  • “contained” in altered phagosome (not merged to lysosome)
  • becomes motile and escapes the phagosome
  • lyses the cells and spreads to another
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5
Q

what are Legionella virulence factors

A
  • mip - unknown, required to invade monocytes
  • Dot/Icm locus - T4SS (involved in altering endosome)
  • pilE/pilD - pilus formation (attachment)
  • Mak/Mil/pmi - unknown
  • Pep/pro - Zn metalloprotease (escape)
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6
Q

what are the 3 outcomes of Legionella infection in humans

A
  1. asymptomatic seroconversion
  2. Pontiac fever
    - flulike in previously healthy patient
    - incubates hours to 2 days
    - symptoms immunogenic as immune system kills live and/or clears dead bacteria
    - resolves w/o complication
  3. Legionnaires disease
    - pneumonia in previously ill or immunosuppressed
    - suppression of kidney function; diarrhea
    - incubates 2-10 days
    - usually resolves w/ hospitalization and treatment
    - can be fatal
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7
Q

what do the different outcomes of Legionella depend on?

A
  • all 3 caused by same bacteria

- differences are in the hosts, possibly also dosage

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8
Q

what are risk factors for Legionnaire’s disease?

A
  • increasing age
  • immunosuppression
  • smoking
  • chronic heart/lung disease
  • chronic swallowing disorder
  • male
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9
Q

why is mortality of Legionnaire’s disease decreasing?

A
  • prompt diagnosis

- early use of appropriate antibiotics

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10
Q

how do nosocomial LD outbreaks occur?

A

hospitals are hot spots for LD outbreaks

  • large numbers of at-risk individuals
  • old complex plumbing
  • hot water tanks at reduced temperature to prevent scalding
  • -fix with thermal mixing valves
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11
Q

what does the presentation of LD look like?

A
  • altered mental status
  • headache
  • high fever/chills
  • pneumonia/cough/chest pain (not clinically distinct from other pneumonias, so need lab to differentiate LD)
  • pancreatitis
  • acute renal failure
  • diarrhea
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12
Q

what lab do you use to diagnose LD?

A

urine antigen test (commercial ELISA test)

  • fast
  • cell wall component excreted starting 3 days after symptom onset
  • test complete in hours
  • reiiably detects LP1 strain of L. pneumophila
  • -doesn’t detect other strains/species
  • causes 90% of LD in US
  • testing significantly associated w/ reduced mortality
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13
Q

how does the urine Ag test work?

A

Ag capture ELISA

  1. petri dish coated with Ab for LD
  2. patient sample is added; if Ag is present, Ab binds it
  3. patient sample is removed
  4. tagged secondary Ab binds other side of Ag
  5. unbound Ab is removed and TAg is assayed
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14
Q

how do you culture Legionella?

A

respiratory secretions

  • much slower; fastidious, requires special nutrients
  • technically demanding
  • detects many strains and species of Legionella
  • 27% fatality rate among culture+, urine-test- patients
  • needed to trace outbreaks
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15
Q

what is treatment for Legionella?

A
  • Pontiac fever: often resolves w/o treatment
  • LD: needs antibiotic that penetrates infected cells
  • -Levofloaxin (M. pneumoniae and S. pneumoniae)
  • -Azithromycin
  • -Old-school erythromycin
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16
Q

what is the best way to diagnose LD?

A

both urine Ag test and culture

  • biopsy not necessary, but may show bacteria if silver-stained
  • G stain will fail
17
Q

what is post-acute care for LD?

A

many patients who recovery from LD experience following for up to 17 mo, but most recover w/in one year

  • fatigue
  • neurological symptoms
  • neuromuscular symptoms
  • cough
18
Q

what is the bacteriology of C. burnetti?

A

proteobacteria (related to LD)

  • zoonosis of asymptomatic infection of ruminants
  • transmitted to humans by inhalation of aerosols of infected ruminant urine, feces, birthing matter (no vector)
  • extremely infectious <10 IUs can cause disease; dried samples remain infectious for months
19
Q

what are virulence factors of C. burnetti?

A
  • acid phosphatase
  • superoxide dismutase
  • both help bacteria survive in fused lysosome-endosomem
20
Q

how are humans sickened with C. burnetti?

A

bacteria multiply within alveolar monocytes and macrophages

  • travel to liver, spleen, BM
  • creates complications with pregnancy
  • common in Netherlands, France, Spain, Iraq
21
Q

what is the pathogenesis of C. burnetti?

A
  • fever, chills, sweats
  • severe headache
  • dry cough
  • pneumonia and hepatitis (most common)
  • complications of pregnancy
  • rarely fatal, but is reportable
  • rare: rash, endocarditis
22
Q

how do you diagnose C. burnetti?

A

same as Rickettsia

  • immunohistological methods
  • ELISA
  • immunofluorescence
23
Q

how do you treat C. burnetti?

A

same as Rickettsia

  • doxycycline
  • fluoroquinolones
24
Q

how do you prevent C. burnetti?

A

vaccine is available to farm and veterinary personnel and military stationed in Middle East

25
Q

explain mycoplasma bacteriology

-what is unique about it

A

smallest free-living organisms (0.3 um diameter)

  • strictly aerobic
  • no cell wall; little Gran staining, but penicillins and cephalosporins are ineffective
  • only prokaryotic cell membrane that contains cholesterol
  • difficult to grow on media, require special nutrients
  • colonies have a “fried egg” shape
  • only one serotype, but immunity is incomplete (can recur)
  • bacterial metabolism produces H2O2 (tissue damage)
26
Q

how does mycoplasma infect?

A

pathogenic only to humans

  • reside on mucosal surfaces of respiratory and genital tracts (assume rod shape, attachment proteins at tip)
  • transmitted by inhalation of respiratory aerosols
  • causes tracheobronchitis, bronchiolitis, 5-10% progress to atypical “walking pneumonia” due to epithelial necrosis
  • Ab against mycoplasma (cold-agglutinins) X-react with RBC membranes so patients may become anemic
  • -resolves spontaneously with disease
27
Q

what does mycoplasma cause during infection?

A

P1 adhesin binds respiratory epithelial cells

  • causes ciliostasis –> dry cough, exacerbates chronic bronchitis, asthma
  • local inflammation from bacterial wastes
  • tissue destruction by CARDS exotoxin
  • -related to pertussis toxin
28
Q

what does mycoplasma show on exam?

A

non-specific upper or lower airway

  • more prevalent in winter
  • fever, aches/pains, oropharyngeal inflammation
  • erythematous tympanic membranes
  • conjunctivitis
  • rash
  • moderate rhonchi and rales
  • CXR looks worse than patient
29
Q

when does mycoplasma resolve?

A

in 10-14 days, very low mortality even without treatment

30
Q

what does Mycoplasma diagnosis show on lab?

A

self-limited and antibiotic-responsive

  • culture and molecular labs available
  • patient may be anemic
31
Q

what is Mycoplasma treatment?

A
  • fluoroquinolones cover mycoplasma and all similarly-presenting bacterial infections
  • erythromycin, azithromycin, clarithromycin, tetracycline all work slightly better against mycoplasma
  • longer treatment courses (14-21 days) needed b/c of M’s slow growth, intracellular penetration
  • macrolide resistance is emerging in Japan and China