3.6.4. Atypical CAP Flashcards
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)
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
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
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
How does the xray of atypical CAP appear compared to the symptoms?
CXR may show greater involvement than expected from physical symptoms
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.
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
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
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
Describe the developmental cycle of Chlamydia
(Hint) Stages at 0, 8, 24, 30, and 35-40 hrs
Name some examples of disease types Chlamydia can cause and which species is responsible for each
(Hint: 4 general types, 3 species)
Give some examples of diseases Chlamydia may cause along with their causative species
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
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)
What are the two most common species of Chlamydia that cause respiratory disease?
- C. pneumoniae
- C. psittaci
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
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
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)
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
- 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 ***
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)
- human pathogens:
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…
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
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
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
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 :(
What are some treatment options for Chlamydia pneumoniae?
- C. pneumoniae
- Doxycycline
- Macrolides (same as mycoplasma)
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!
