3.6.4. Atypical CAP Flashcards Preview

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Flashcards in 3.6.4. Atypical CAP Deck (27)
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1

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

Speed of Onset

 

TYPICAL

rapid onset (acute)

 

ATYPICAL

 

gradual onset over days-to-weeks (insidious)

(constitutional symptoms predominate over respiratory ones)

2

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

Symptoms

 

TYPICAL

fever, chills

productive cough, with PMNs seen in sputum

 

ATYPICAL

 

 

 

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

 

nagging cough, often not productive

3

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

Gram stain

 

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

4

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

Responsible Agents (most common = more important)

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

5

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

CXR may show greater involvement than expected from physical symptoms

6

Define Walking Pneumonia

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.

7

Describe the properties of Chlamydiae organisms

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

  • 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

8

Name the two developmental forms of Chlamydia

Describe some of their properties

  • 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

9

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

  • 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

10

Describe the developmental cycle of Chlamydia

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

11

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

(Hint: 4 general types, 3 species)

12

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

13

What is psittacosis and what causes it?

  • 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

14

Why are Chlamydia and mycoplasma considered atypical organisms?

  • 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)

15

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

  • C. pneumoniae

  • C. psittaci

16

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

  • 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

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

  • 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

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

  • 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

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?

  • 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

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

  • 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

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

  • 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

What is the cold agglutinin test? Is it specific?

  • 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

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

  • 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

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

  • 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

What are some treatment options for Mycoplasma pneumoniae?

  • 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

What are some treatment options for Chlamydia pneumoniae?

  • C. pneumoniae

    • Doxycycline

    • Macrolides (same as mycoplasma)

27

What are some preventive measures for Bordetella pertussis?

  • 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!