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Microbiology Part 1 > Lec10 Atypical Pneumonia > Flashcards

Lec10 Atypical Pneumonia Flashcards

1
Q

What are signs of typical pneumonia?

A
  • abrupt onsent
  • productive cough
  • copious sputum
  • evidence of consolidation on exam
  • high WBC count
  • distinct infilitrate on chest xray
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2
Q

What are signs of atypical pneumonia?

A
  • insidious onset
  • extrapulmonary symptoms [headahces, muscle aches]
  • usually no consolidation on exam
  • fever rarely > 101
  • normal WBC
  • less distinct infiltrate on chest xray
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3
Q

What are 3 most frequent causes of atypical pneumonia?

A
  • mycoplasma pneumoniae
  • chlamydophila pneumoniae
  • legionella species
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4
Q

What are some other common etiologies of atypical pneumonia [besides the 3 main bacteria]?

A
  • coxiella burnetii [q fever]

- respiratory viruses

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5
Q

What is epidemiology of mycoplasma pneumoniae?

A
  • in mini outbreaks in households
  • incubation 2-3 wks
  • gives young children URI, others primary penumonia
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6
Q

How is mycoplasma pneumoniae transmitted?

A
  • by respiratory droplet
  • need close contact
  • much longer incubation than viral infections
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7
Q

What is structure of mycoplasma pneumoniae? shape? gram stain? etc?

A
  • lacks cell wall
  • contains RNA and DNA
  • short rod-shaped
  • not visible on gram stain
  • can grow on cell free medium
  • long doubling time so takes many days to grow in culture
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8
Q

What are extrapulmonary manifestations of mycoplasma pneumoniae?

A
  • hepatitis
  • hemolysis
  • rash [erythema multiforme]
  • rarely: myocarditis, encephalitis
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9
Q

What are the virulence factors of mycoplasma pneumoniae? who is particularly at risk?

A
  • virulence factors located intracellularly
  • patient age relates to likelhood of progression —> adolescent, young adult, elderly more at risk
  • high disease rate [and more severe infection] in sickle-cell disease
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10
Q

What is the host immune response to mycoplasma pneumoniae?

A
  • polyclonal T cell and B cell activation

- variety of antibodies produced including antibodies [cold agglutins]

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11
Q

What are cold agglutinins?

A
  • autoantibodies produced in immune response

- IgM antibodies directed at the I antigen on RBC surface

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12
Q

What are the clinical manifestations of mycoplasma pneumoniae?

A

respiratory: upper to lower
skin: erythema multiforme
cardiac: arrythmia, CHF
neuro: meningitis
other: renal, liver, musculoskeletal

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13
Q

How do you diagnose mycoplasma pneumoniae infection?

A
  • usually on clinical basis
  • can use complement-fixing antibodies to confirm diagnosis retrospectively
  • culture techniques and cold-agglutinin test not useful [not specific/sensitive/too cumbersome]
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14
Q

How do you treat mycoplasma pneumoniae?

A
  • no cell wall so can’t use penicillins/cephalosporins
  • use macrolides [erythromycins] or tetracyclines
  • most cases undetected or untreated
  • no vaccine
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15
Q

What is epi of chlamydophila pneumoniae

A
  • associated with epidemics

- older the host –> more likely to cause lower rather than upper respiratory infection

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16
Q

How is chlamydophila pneumoniae transmitted?

A

by respiratory droplets

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17
Q

What is structure/shape of chlamydophila pneumoniae?

A
  • intracellular bacteria
  • have cell walls
  • not seen on gram stain
18
Q

What is the elementary body vs reticulate body of chlamydophila pneumoniae?

A

elementary body = metabolically inacive infectious form, can survive outside the cell

one inside the cell it becomes the reticulate body = starts replicating

19
Q

What are the virulence factors for c. pneumoniae?

A
  • no specific virulence factors identified

- located intracellularly

20
Q

What is the pathogenesis of c. pneumoniae?

A
  • enters via respiratory tract

- can persist in respiratory epithelial cells for prolonged period before and after acute infection

21
Q

What are the clinical signs of chlamydophila pneumoniae?

A
  • commonly asymptomatic
  • patchy pneumonia without fever
  • occassionaly upper respiratory symptoms [rhinitis, sore throat]
  • persistent cough
  • otisis, and rarely pericarditis or pleuritis
  • may be implicated in atherosclerosis
22
Q

How is c. pneumoniae diagnosed?

A
  • usually presumed from clinial signs
  • can use IgM antibody to detect recent infection in serum
  • can use IgG antibody to detect remote or recent infection
23
Q

How is c. pneumoniae treated?

A
  • teatracyclines, macrolides [clarithromycin, azithromycin], newer fluroquinolones
24
Q

How is legionella pneumophila transmitted?

A
  • lived in aqueous habitats
  • transmit to humans though inhalation following aerosolization
  • no person-person transmission
  • incubation = 2-10 days
25
What is structure of l. pneumophila? gram?
- small bacilli - gram negative [but weakly] - aerobe - fastidious growth --> need special media to isolate - 16 serotypes but group 1 causes most human infections
26
What are the virulence factors of l. pneumophila?
- variety of toxins and protease - on surface: - -- pili promote adherence to target cell - -- flagellae promote entry into cell - -- macrophage infectivity promoter protein
27
What is the pathogenesis of L. pneumophila infection?
- organism reaches lung and phagocytoses by alveolar macrophages - grows in cell and eventually kill and infect other macrophages - neutrophils infiltrate alveoli and fluid leaks from capillaries into interstitium of lung - sever inflammatory cytokine response to dying macrophages
28
What type of host immune response?
both cellular and humoral
29
What are the clinical signs of L. pneumophila?
- prodromal illness [fever, malaise] - mild to life threatening pneumonia - hepatitis, rhabdomyolosis, renal failure, abscesses, altered mental status etc - may start with altered mental status and diarrhea
30
How is L. pneumophila diagnoses?
- culture respiratory secretions on selective media [buffered charcoal yeast extract, use silver stain] - detect antigen of serogroup 1 in urine - direct fluorescent antibody staining of respiratory secretions - insensitive to serum antibody test
31
How is L. pneumophila treated?
- macrolides [azithromycin], tetracyclines, fluoroquinolones [levofloxacin] - high mortality in immunocompromised and elderly
32
What are the two macrolide antibiotics?
- clarithromycin | - azithromycin
33
What is mech of action of macrolides [clarithromycin, azithromycin]? bacteriostatic or bactericidal?
- bind 50s ribosomal subunit - inhibit RNA-dependent protein synthesis - bacteriostatic
34
What are the PK properties of clarithromycin? [oral or intravenous, half life, elimination]
- given orally - metabolized by liver - 30% excreted unchanged in urine - 3-4 hr elimination half life
35
What are the PK properties of azithromycin? [oral or intravenous, half life, elimination]
- given orally or intravenously - if orally needs to be on empty stomach [food interferes with absorption] - wide distribution in tissues, 2-4 day elimination half life - eliminated unmetabolized through bile
36
What toxicities associated with macrolides?
frequent: diarrhea, nausea, abdominal pain | less frequent: dizziness, temporary hearing loss, ventricular arrhythmia
37
What are the 3 fluroquinolone antibiotics?
- moxifloxacin - levofloxacin - ciprofloxacin
38
Mech of action of fluoroquinolones?
- inhibit DNA synthesis by: - inhibiting DNA gyrase - inhibiting topoisomerase IV
39
What are the PK properites of fluoroquinolones? [oral or intravenous, half life]
- all 3 given orally or intravenously - absorbed well from GI - reach high conc in all tissues with long half lives
40
How is levofloxacin eliminated? ciprofloxacin? moxifloxacin?
levo and cipro by kidneys | moxi primarily via liver in the bile
41
What toxicities associated with fluoroquinolones?
most frequent: anorexia, nausea, vomiting, abdominal pain, diarrhea less frequent: headache, dizziness, cartilage erosions, tendonitis/tendon rupture, mania, seizures, hallucination - avoided in peds because of potential effect on growing cartilage
42
If you have GI problems, confusion and 2-3 days later get pneumonia what should you think?
legionella!

Microbiology Part 1 (24 decks)

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