3.6.4. Atypical CAP Flashcards

1
Q

Name the following difference between typical and atypical community acquired penumonia (CAP):

Speed of Onset

A

TYPICAL

rapid onset (acute)

ATYPICAL

gradual onset over days-to-weeks (insidious)

(constitutional symptoms predominate over respiratory ones)

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2
Q

Name the following difference between typical and atypical community acquired penumonia (CAP):

Symptoms

A

TYPICAL

fever, chills

productive cough, with PMNs seen in sputum

ATYPICAL

low-grade fever (100-101 F, ~38 C)

nagging cough, often not productive

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3
Q

Name the following difference between typical and atypical community acquired penumonia (CAP):

Gram stain

A

TYPICAL

may have a positive blood culture with agents visible in Gram staining

ATYPICAL

patients are ambulatory (contributes to definition of “walking pneumonia”), no gram stain

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4
Q

Name the following difference between typical and atypical community acquired penumonia (CAP):

Responsible Agents (most common = more important)

A

TYPICAL

Associated agents:

Strep pneumoniae

Staph aureus (especially after the flu)

Gram negative opportunistic pathogens:

Klebsiella pneumoniae

Pseudomonas aeruginosa

Enterobacter

Viruses:

H. influenza (typically type b)

Adenovirus (in acute resp. syndrome)

ATYPICAL

Associated agents: all have ATYPICAL cell walls, and can be recognized because they don’t Gram stain

  • Chlamydia pneumoniae (an obligate intracellular pathogen)
  • Mycoplasma pneumoniae (no cell wall)
  • Mycobacterium tuberculosis (acid fast; produces sputum that may be bloody)

Endemic mycoses:

  • Histoplasmosis
  • Blastomycosis
  • Coccidioides
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5
Q

How does the xray of atypical CAP appear compared to the symptoms?

A

CXR may show greater involvement than expected from physical symptoms

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6
Q

Define Walking Pneumonia

A

A type of pneumonia caused by mycoplasmas, with symptoms similar to but milder than those of bacterial or viral pneumonia. It spreads easily and typically affects school-age children and adults under 40.

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7
Q

Describe the properties of Chlamydiae organisms

i.e. genome size, gram stain, cell wall, etc

A
  • Obligate intracellular bacteria
    • contain DNA, RNA, and 70S ribosomes
    • divide via binary fission
    • small genome (~1 Mbp)
    • carry plasmids that were once from bacteriophages
  • Cell envelope
    • similar to Gram (-) bacteria (has two phospholipid membranes and LPS)
    • no DETECTABLE peptidoglycan present
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8
Q

Name the two developmental forms of Chlamydia

Describe some of their properties

A
  • Elementary Body (EB)
    • Small and dense (0.25 um in size)
    • extracellular
    • INFECTIOUS FORM
    • Metabolically inactive
    • disulfide cross-linked outer membrane proteins
  • Reticulate Body (RB)
    • Large (0.6 - 1.0 um)
    • intracellular
    • REPLICATIVE form (R for Replicative)
    • Metabolically active
    • osmotically fragile
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9
Q

How does Chlamydia spread and cause infection (at the cellular level).

A
  • 1) Entry of EBs
    • rapid internalization at the bases of villi
    • uptake done via clathrin-coated pits, and likely other mechanisms
    • once in the cell, EBs become RBs.
  • 2) Then, endosomes containing RBs fuse and release them into the cell
  • 3) Multiplication/Replication
  • 4) Lysis/spread
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10
Q

Describe the developmental cycle of Chlamydia

(Hint) Stages at 0, 8, 24, 30, and 35-40 hrs

A
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11
Q

Name some examples of disease types Chlamydia can cause and which species is responsible for each

(Hint: 4 general types, 3 species)

A
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12
Q

Give some examples of diseases Chlamydia may cause along with their causative species

A
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13
Q

What is psittacosis and what causes it?

A
  • abrupt onset with fever, headache, myalgia, mild cough (generalized constitutional symptoms)
  • abnormal chest exam
  • UNIQUE SYMPTOM: confusion or altered conscious state
  • Diagnose with culture from respiratory secretions, or serology (include microimmunofluorescence)
  • typically caught from infected birds, it is a bacterial infection by C. psittaci
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14
Q

Why are Chlamydia and mycoplasma considered atypical organisms?

A
  • Mycoplasma does not have a cell wall
  • Chlamydia is an obligate intracellular organism
  • Both are technically bacteria, but they have small genomes, so they can’t encode for all the stuff they need (esp ATP-essential proteins/enzymes)
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15
Q

What are the two most common species of Chlamydia that cause respiratory disease?

A
  • C. pneumoniae
  • C. psittaci
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16
Q

Describe the distribution and frequency in pulmonary disease of C. pneumoniae. How is it spread, does it have an animal reservoir?

A
  • C. pneumoniae
    • There is a WORLDWIDE distribution
    • Seroprevalence of > 60% among adults (60% of us have encountered this at some point in our lives…)
    • C. pneumoniae causes 10% of community-acquired cases of pneumonia (10% of cases are specifically due to this, with the rest a mix of viral/bacterial/etc…)
    • Person-to-person transmission occurs via respiratory secretions (can’t dodge the snot-bullet)
    • NO ANIMAL RESERVOIR exists
17
Q

Describe the spread of C. psittaci, who is at risk, who harbors this bacteria?

A
  • C. psittaci
    • zoonotic infection (“parrot fever”) - many species of birds can harbor this bacteria, but they’re often asymptomatic
    • transmissible to humans via inhalation of aerosolized organisms in dried feces or respiratory tract secretions
    • OCCUPATIONAL RISKS: poultry industry workers, veterinarians, exotic bird owners
18
Q

Describe the unique properties of Mycoplasma species and describe their cellular features

A
  • 1- They are the smallest bacteria (0.1 - 0.25 micrometers)
  • 2- They can pass through 0.45 um filters that otherwise restrict other bacteria (are dubbed “filterable”)
  • 3- They lack a cell wall; no peptidoglycan present
  • 4- They are surrounded by lipid bilayer membranes that contain sterols (like humans - our cells are actually where these guys take their resources from)
19
Q

Describe the growth requirements of mycoplasma (growth as in a lab or on an agar plate). Do they take up gram stains? Why are they so sticky?

A
  • 4- They are surrounded by lipid bilayer membranes that contain sterols (like humans - our cells are actually where these guys take their resources from)
    • results in a pleomorphic shape that has a P1 adhesin at the tip, which allows it to stick to whatever surface it’s on. HOWEVER, they can only grow UNDER THE SURFACE of agar on plates. *** This results in a “fried egg appearance” - look for this buzzword for lab cultures to consider mycoplasma. These fried-egg colonies require serum for growth ***
      • The P1 adhesin attaches near the cilia on host respiratory epithelia and causes bronchial irritation that closely resembles asthma attacks
      • definitely worth seeking medical attention if a nagging cough presents
    • this cellular container doesn’t Gram stain
    • allows them to make small subsurface colonies
20
Q

What are the species of mycoplasma that typically cause human disease?

A
  • Typical niches for the Mycoplasmatales family (to include Mycoplasma and Ureaplasma)
    • human pathogens:
      • M. pneumoniae
      • M. hominis
      • M. genitalium and Ureaplasma species (both can cause urethritis and complications of pregnancy)
21
Q

How do we try and diagnose Mycoplasma infection? What tests are available?

A
  • Mycoplasma pneumoniae (no cell wall)
    • goal of your DDx: eliminate alternatives (basically process of elimination to confirm M. pneumoniae)
    • culture = difficult and restricted to specialized labs, so not often recommended…
    • serology = greater than or equal to a 4x rise in specific IgM antibodies to M. pnemoniae
    • test for cold agglutinins (not specific
    • NAAT = nucleotide sequencing, not available clinically…
22
Q

What is the cold agglutinin test? Is it specific?

A
  • test for cold agglutinins (not specific)
    • IgM antibodies bind the “I” antigen on human RBCs, and are produced 1-2 weeks after the initial infection
    • first, prep the blood sample with heparin to prevent clotting, then rerigerate.
    • then, when refrigerated, IgM will agglutinate said “I” antigen, BUT THIS RESPONSE IS ONLY SEEN IN 50% OF PATIENTS
23
Q

How do we test for chlamydia infections? What labs do we look for?

A
  • C. pneumoniae (obligately intracellular)
    • culture = difficult and restricted to specialized labs (same as mycoplasma)
    • serology
  • IgM: greater than or equal to 1:64
  • IgA: 4-fold increase in acute and convalescent serums (measure these serums 4 weeks apart)
  • NAAT
24
Q

What is Bordetella pertussis? What are its virulence factors and bacteriologic traits? (i.e. gram - or +, general shape)

A
  • Bordetella pertussis (causative agent of Whooping Cough, but can also cause atypical pneumonia)
    • Seen in adults after previous vaccination has worn off, and manifests as a “cold” and nagging cough
    • virulence factors include the pertussis toxin and special adhesion molecules, which allow this microbe to persist in the host’s respiratory epithelium
    • look for these bacteriologic traits: short, Gram negative rods that form “safety pin” shapes
25
Q

What are some treatment options for Mycoplasma pneumoniae?

A
  • Mycoplasma pneumoniae
    • tetracycline
    • macrolides (erythromycin or azithromycin)
    • there is increasing evidence of emerging macrolide resistance…!
    • beta-lactam antibiotics are NOT effective! these bad boys don’t have cell walls, so these antibiotics can’t inhibit cell wall synthesis if there aren’t any to begin with…
    • no vaccine available, either :(
26
Q

What are some treatment options for Chlamydia pneumoniae?

A
  • C. pneumoniae
    • Doxycycline
    • Macrolides (same as mycoplasma)
27
Q

What are some preventive measures for Bordetella pertussis?

A
  • Bordetella pertussis
    • children are vaccinated and boosted from 6 months to 6 years
    • this means that children younger than 6 mos (they’re ineligible for the vaccine) are susceptible… So, boost the mom and adolescents to build that herd immunity!