Bacterial Pneumonia 2- Atypical Pneumonias Flashcards

1
Q

What is the bacteriology of Legionella?

A
  • gram neg rods
  • stains poorly by gram or H&E; requires silver or IF in tissue sections
  • facultative intracellular parasites
  • free living form is motile (flagella); intracellular form is non-motile
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2
Q

What the reservoirs for legionella?

A
  • Natural- intracellular parasites of freshwater protozoa

- unnatural- biofilms in commercial water systems, aspirated by humans

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3
Q

How does Legionella replicate?

A
  • it begins living in a biofilm on warm water or in soil
  • it is taken up by phagocytosis
  • contained in an altered phagosome- NOT merged to a lysosome
  • it becomes motile and escapes the phagosome
  • lyses the cell and spreads to another
  • humans are an unnatural dead end host for legionella- eventually it runs out of alveolar macrophages to infect, can’t spread person to person
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4
Q

What are the virulence factors of legionella?

A
  • mip= unknown, required to invade monocytes
  • Dot/Icm locus- type IV secretion system (involved in altering the endosome)
  • pilE and pilD- pilus formation (attachment)
  • Mak- unknown
  • Mil- unknown
  • pmi- unknown
  • Pep/pro- zinc metalloprotease (escape)
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5
Q

What are the possible outcomes of a legionella infection?

A
  • asympomatic seroconversion
  • pontiac fever
  • Legionnaires Disease
  • all three outcomes are causes by the same organism- one outbreak may generate all three patient types, differences are in the hosts possibly also dosage
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6
Q

What is pontiac fever?

A
  • infection with Legionella
  • flulike
  • incubates hours- 2 days
  • resolves without complication
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7
Q

What is Legionnaires Disease?

A
  • infection with Legionella
  • pneumonia
  • suppression of kidney function
  • incubates 2-10 days
  • usually resolves with hospitalization and treatment
  • can be fatal
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8
Q

What are risk factors for Legionnaires Disease?

A
  • increasing age
  • immunosuppression
  • smoking
  • chronic heart or lung disease
  • chronic swallowing disorder
  • male
  • for outbreak LD, travel is a common factor: conventions and weddings at hotels
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9
Q

What is the occurrence and mortality of Legionnaires Disease?

A
  • 80% cases are isolated, 20% outbreak
  • reportable
  • outbreaks are a simultaneously-exposed group: NOT contagious
  • 8000-18000 hospitalizations/year in US; 2nd most common pneumonia ICU admit (after pneumococcal)
  • 34% mortality in US in 1985, 11.5% in 1998
  • mortality decreasing because of: prompt diagnosis, early use of appropriate antibiotics
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10
Q

Why are there Nosocomial Legionnaires Disease Outbreaks?

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: thermal mixing valves)
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11
Q

How does Legionnaires Disease present?

A
  • high fever/chills
  • pneumonia/cough/chest pain
  • pancreatitis
  • diarrhea*
  • acute renal failure
  • headache
  • altered mental status
  • not clinically distinct from other pneumonias. Need lab results to differentiate
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12
Q

How do you diagnose Legionella Infection?

A

-Urine antigen test: Commercial ELISA kit, fast: cell wall component is excreted starting 3 days after symptom onset and test complete in hours; reliably detects the LP1 strain of L pneumophilia (causes 90% of LD in US); testing significantly associated with reduced mortality

Culture of Respiratory Secretions- much slower (1 wk), technically demanding, detects many strains and species of Legionella, 27% fatality rate among culture positive, urine-test negative patients, grow on Buffered Charcoal Yeast Extract with alpha-keto-glutarate

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13
Q

How are Legionella infections treated?

A
  • Pontiac Fever often resolves without treatment, could put on cipro if concerned about Legionnaires
  • LD requires an antibiotics that penetrates infected cells: Levofloxacin (also covers M pneumoniae and S pneumoniae); Azithromycin, erythromycin (old school)
  • post acute care: they experience fatigue, neurological symptoms, neuromuscular symptoms, cough for up to 17 months most recover completely within one year
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14
Q

What is the bacteriology of Coxiella burnetii (Q fever)

A
  • previously grouped with Rickettsia, now a Proteobacteria (closest related pathogen: Legionella)
  • 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
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15
Q

How do humans become infected with C burnetii?

A
  • in humans it multiples within alveolar monocytes and macrophages (after being breathed in), travels in them to liver, spleen, bone marrow
  • fairly common in Netherlands, France, Spain and becoming a problem among military and medical personnel in Iraq
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16
Q

What are the virulence factors of C burnetii?

A
  • acid phosphatase

- superoxide dismutases- help bacteria survive in FUSED lysosome-endosome

17
Q

How does a C. burnetti infection present?

A
  • fever, chills, sweats
  • severe headache
  • dry cough
  • pneumonia*
  • hepatitis*
  • complications of pregnancy
  • rare: rash, endocarditis
  • rarely fatal
  • reportable
18
Q

How do you diagnose and treat a C. burnetti infection?

A
  • same as Rickettsia: immunohistochemical methods, ELISA, immunofluorescence
  • doxycycline or fluoroquinolones
  • prevention: vaccine is available to farm and veterinary personnel and military stationed in Middle East
19
Q

What is the bacteriology of Mycoplasma

A
  • smallest freeliving organisms (0.3 micrometer diameter)
  • strictly aerobic
  • no cell wall: little gram staining, penicillins and cephalosporins therefore 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
20
Q

What is the pathogenesis of Mycoplasma?

A
  • reside on mucosal surfaces of respiratory and genital tracts
  • transmitted by inhalation of respiratory aerosols
  • causes tracheobronchitis, bronchiolitis, 5-10% progress to atypical walking pneumonia
  • P1 adhesion binds respiratory epithelial cells
  • Ciliostasis- dry cough, exacerbates chronic bronchitis, asthma
  • local inflammation from bacterial wastes
  • tissue destruction by CARDS exotoxin (related to pertussis toxin)
  • intracellular penetration possible
  • causes 20% of community acquired pneumonias that require admission
  • VERY low mortality <0.1%
  • antibiotics against mycoplasma (cold agglutinins) cross react with RBC membranes so patients may become anemic
21
Q

How is Mycoplasma diagnosed?

A
  • exam: nonspecific upper and lower airway, fever, aches and pains, oropharyngeal inflammation, erythematous tympanic membranes, conjunctivitis, rash, lung sounds may include moderate rhonchi and rales
  • chest radiograph often looks worse than the patient
  • labs: self limited and antibiotic responsive, not usually culture and molecular available. May be anemic
22
Q

How do you treat Mycoplasma?

A
  • Fluoroquinolones cover mycoplasma and all similarly-presenting bacterial infections
  • erythromycin, azirthomycin, clarithromycin, tetracycline all work slightly better against mycoplasma
  • longer treatment courses (14-21d) needed because of M’s slow growth, intracellular penetration
  • macrolide resistance is emerging in Japan and China
23
Q

What are some other Mycoplasma?

A
  • ureaplasma urealyticum and U. parvus can cause male urethritis, possibly also premature birth
  • M genitalium can contribute to male urethritis, female cervicitis and PID
  • ureaplasma and mycoplasma may both cause bacteremic pneumonia in very premature infants
  • all can be passed by direct contact, vertically, or nosocomial