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Bacterial Pneumonias Flashcards

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1
Q

CAP- 3 main causes

A

S. Pneumo, H. Influenzae, M. Catarrhalis

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2
Q

15% CAP caused by what 3 bacteria

A

Legionella, Mycobacteria Pneumoniae, Chlamydophila Pneumoniae

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3
Q

Less common cause of CAP (2 bacteria)

A

Klebsiella pneumoniae, Staph. aureus

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4
Q

Most common causes of HCAP

A

More likely multidrug resistant gram neg

Pseudomonas, E coli, Klebsiella or MRSA

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5
Q

Most common causes of HAP

A

Pseudomonas, E Coli, Klebsiella, Serratia marcescens

Less commonly: Legionella, viruses

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6
Q

Most common causes of VAP

A

Bacteria that colonize the skin (Staph Aureus, GAS, H. Influenza)
Enteric gram negative (E coli, Klebsiella)
Environmental (Pseudomonas)

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7
Q

Typical Pneumonia

A

Acute, shaking chills, productive cough, consolidation on CXR, no extra pulmonary symptoms

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8
Q

Atypical Pneumonia

A

Slow onset, non productive cough, extra pulmonary symtopms

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9
Q

Pathogens of Typical Pnemonia

A

S. Pneumo, H. Influenzae, M. Catarrhalis

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10
Q

Pathogens of Atypical Pneumonia

A

Legionella, Mycobacteria Pneumoniae, Chlamydophila Pneumoniae

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11
Q

Most common pathogen for Cystic Fibrosis

A

Pseudomonas and Berkholdaria

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12
Q

Most common pathogen for alcoholics

A

Klebsiella

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13
Q

Most common pathogen for COPD

A

Klebsiella

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14
Q

Most common pathogen for AIDS

A

Pneumocystis

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15
Q

Most common pathogen for Corticosteroid Therapy

A

Nocardia

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16
Q

Pathogens for AIDS, diabetes, transplant patients

A

Opportunistic Fungi

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17
Q

Empiric Therapy for CAP-outpatient

A

No previous antibiotics: Macrolide or Doxycyclin
Recent Antibiotic Treatment:
Respiratory Fluoroquinolone (Levofloxacin) or advances macrolide plus high dose amoxicillin +/- clavulanate

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18
Q

Empiric Therapy for CAP- In patient

A
  • Advanced Macrolide (Azithromycin, Clarithromycin) plus Beta Lactam
  • Respiratory Fluoroquinolone
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19
Q

What bacteria has lipotechoic and teichoic acid in their cell wall and what does it do?

A

Strep Pneumo

Induces Inflammation

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20
Q

Strep P. has hyaluronidase as a virulence factor. What does it do?

A

Breaks down CT

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21
Q

What will the gram stain of Strep P. look like?

A

Few epithelial cells, many neutrophils, purple diplococci

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22
Q

DOC for susceptible Strep P.

A

Penicillin group (penicllin, ampicillin, amoxicillin)

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23
Q

DOC for high level drug resistant Strep P.

A

Respiratory fluoroquinolone

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24
Q

Classify H. influenza

A

gram neg, pleomorphic rod

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25
Classify M. catarrhalis
Gram neg, diplococci | non hemolytic on blood agar
26
DOC for H. influenza with beta lactamase
Amoxicillin-clavulanate, 2nd or 3rd gen cephalosporins, macrolides, resp. fluoro.
27
Classify Staph Aureus
Gram pos cocci, beta hemolytic, catalase and coag postive
28
What kind of antibiotic is oxacillin? If S. Aureus is resistant what does that mean?
``` Penicillinase resistant (antistaphylcoccal penicillin) Tells you it's MRSA ```
29
What is responsible for pathology of necrotizing pneumonia?
Panton-Valentine Leukocidin
30
What organism grows on BYCE agar?
Legionella
31
Where does Legionella like to live?
Inside amoebaes in water | Facilitative Intracellular Pathogen
32
What other systems does Legionella affect?
GI, liver, kidney, CNS
33
What two tests are best for Legionella?
BYCE agar and Urine antigen test (DFA requires a lot of organisms to be present)
34
DOC for legionella
Azithromycin or Levofloxacin
35
Classify Mycoplasma P.
No cell wall, cell membrane contains only sterols They do not gram stain, not susceptible to b-lactam antibiotics and vancomycin most common older children and young adults
36
CXR of Mycoplasma
Diffuse unilateral and bilateral infiltrates involving lower lung, rarely shows consolidation
37
Manifestations of M. pneumoniae
Slow onset beginning with URT symptoms (lasts for fairly long time and don't go to doctor right away)
38
Pathogenesis of M. pneumoniae
P1 adhesion protein mediates attachment to cilia on epithelial cells, cilia stop moving and die
39
Diagnosis of M. pneumoniae
Hard, negative sputum grain stain and difficult to culture Many pts develop cold agglutinins (Coumbs +) Serology is the best
40
Treatment of M. Pneominae
No resistance to macrolides or resp. fluoroquinolones so empiric therapy is enough
41
Classify Chlamydophila
Obligate intracellular pathogens - elementary bodies (metabolically inactive, infectious form) - reticulate (metabolically active, non infectious form)
42
Clinical Manifestations of C. pneumoniae
inhalation of elementary bodies, incubation =3-4weeks, persistent non productive cough and malaise, no fever
43
Diagnosis of C. pneumoniae
Diagnosis is difficult, hard to culture, identified by immunoassay or immunofluorescence Serology is not that great: antibodies are slow to develop PCR not widely available
44
Treatment of C. Pneumoniae
Doxycycline is DOC except for children and women | Macrolide is alternative choice
45
Empiric Therapy for HAP
Antipseudomonal cephalosporin (3rd or 4th) OR carbapenem OR extended spectrum penicillin + beta lactamase inhibitor PLUS fluoroquinolone or aminoglycoside If MRSA is suspected: add vancomycin or linezolid
46
Classify Pseudomonas Aeruginosa
aerobic, catalase postive, Gram neg rod cause infections in risk patients ubiquitous organism found in soil and water
47
Virulence Factors for Pseudomonas
Pili for attachment, Pyocyanin impairs cilia, capsule, exotoxins A and S
48
Diagnosis of Pseudomonas
biopsied lung tissue is the best sample, most common is bronchoscopic or BAL, grows on blood agar or MacConkey agar
49
Treatment of Pseudomonas
Susceptibility testing essential | Antipseudomonal penicillins with an aminoglycoside (e.g. ticarcillin,-clavulanate)
50
Classify Klebsiella
Gram neg rods, catalse positive, oxidase negative | colonizes mucosal surfaces
51
Klebsiella Pneumoniae
inflammation, necrosis, cavitation and hemorrhage in the lung produces thick bloody mucoid sputum
52
Diagnosis of Klebsiella
growth on MacConkey Agar and blood agar- slimey appearance
53
Treatment of Klebsiella
Non- extended spectrum b-lactamase strains - 3rd gen chephalosporins with or without aminoglycosides EBSL strains and carbapenem resistant strains base on susceptibility data
54
Classify Tuberculosis
Acid fast, aerobic rods cell wall contains mycolic acid does not gram stain
55
Pathogenesis of Mycobacetrium Tuberculosis
infection by inhalation | Bacteria gain access to lungs, replicate within alveolar macrophages - replication is slow
56
Latent Mycobacterium Tuberculosis
immune competent will produce this infection, bacteria contained by granuloma formation 90% of initial infections are latent over time, granulomas may be calcified bacteria inside granulomas can not replicate
57
Active TB
Can result upon initial infection =primary (Miliary) OR following reactivation of latent= secondary (immune suppression allows break down of granulomas= pulmonary TB)
58
Manifestations of Reactivated TB
fever, night sweats, weight loss, anorexia, malaise, weakness - cough productive with blood tinged sputum - apical most often affected - may see cavitary lesions
59
Miliary TB
Seen w/ TB patients co infected with HIV | Infected macrophages can take organism hematogenously throughout the body
60
Diagnosis of TB
TB skin test and gamma IFN-release assay (more consistent) Acid fast stain of sputum Culture is gold standard and must be done to assess antibitoic sensitivity - can take 2-6 wks CXR- cavitations
61
What is the measurement of induration for positive TB test for normal person w/o risk factors
15 mm
62
Measurement for positive TB test for recent travel from high prevalence country
10 mm
63
Measurement for positive TB test for immunosuppressed patients (HIV, cancer, etc)
5 mm
64
Treatment of Active TB
``` Intensive phase (2 months): Isoniazid, Rifampin, Ethambutol, Pyrazinamide Continuation phase (4-7 months): isoniazid plus rifamycin ```
65
What are multi-drug resistant TB resistant to?
INH and Rif
66
What drugs are extensively drug resistant TB resistant to?
INH, Rif, any fluoroquinolone, at least one of three injectable second line drugs
67
Treatment of Latent TB
Isoniazid (6-9 months)

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