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Block 9 Week 3 Meg > Kozel: Lower Respiratory Tract Infection > Flashcards

Kozel: Lower Respiratory Tract Infection Flashcards

1
Q

Inflammation of the large and mid-sized airways; primarily viruses

A

bronchitis

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2
Q

inflammation of the bronchioles, the smallest air passages of the lungs; primarily viruses, e.g., RSV (50-90%)

A

bronchiolitis

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3
Q

Inflammation of lungs caused by microbial infection of the alveoli and surrounding lung; present for days

A

acute pneumonia

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4
Q

Characterized by moderate amounts of sputum, absence of physical findings of consolidation, only moderate elevation of WBC, and lack of alveolar exudates

A

atypical pneumonia

**back when first described, it wouldn’t grow on culture

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5
Q

Inflammation of lungs caused by microbial infection of the alveoli and surrounding lung or non-infecious causes; present for weeks to months

A

chronic pneumonia

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6
Q

accumulation of pus in the pleural cavity

A

pleural effusion and empyema

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7
Q

infection causing necrosis of lung parenchyma

A

bacterial lung abscess

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8
Q

List 3 factors that may lead to the development of pneumonia

A

defective host defense

exposure to particularly virulent microbe (“hot organisms”

overwhelming inoculum - high dose

combo of host + microbe + dose

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9
Q

What are some normal defenses in the following areas of the airway to protect against infection?

nasopharynx
oropharynx
trachea and bronchi
terminal airways and alveoli

A

nasopharynx: nasal hair, mucocilliary apparatus
oropharynx: saliva, cough reflex, bacterial interference (use of antibiotics when not necessary)

trachea and bronchi: cough, epiglottal reflex, mucocilliary apparatus, airway surface liquid (lysozyme - cleaves peptidoglycan in cell walls of gram positives)

terminal airways: alveolar lining fluid, alveolar macrophages, neutrophil recruitment

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10
Q

4 ways that the pulmonary defenses can become impaired

A

alterations in consciousness –> compromise epiglottal reflex, so easy to aspirate bugs
cigarette smoke –> disrupts mucociliary function
alcohol abuse
infection
medical treatment that bypasses or interferes with host defenses –> intubation
older patients –> decreased resistance to bugs
underlying disease –> asplenia (strep pneumonia)

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11
Q

What are the first line pathogens that cause community-acquired acute pneumonia?

A 
Strep pneumo**
Legionella pneumophila
Klebsiella pneumonia
H. influenzae
Staph aureus
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12
Q

What is the first line pathogen that causes community-acquired ATYPICAL pneumonia?

A

Mycoplasma pneumoniae

**won’t stain with normal gram stain

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13
Q

What is the first line pathogen that causes hospital-acquired pneumonia?

A

Gram-negative rods
Klebsiella spp
Legionella pneumophila

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14
Q

What are the first line pathogens that cause chronic pneumonia?

A

nocardia
Granulomatous: Mycobacterium tuberculosis and atypical mycobacteria, Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis

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15
Q

First line pathogen that causes necrotizing pneumonia and lung abscess?

A

Klebsiella pneumoniae

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16
Q

First line pathogens that cause pneumonia in immunocompromised host?

A

Pneumocystis jiroveci

Mycobacterium avium

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17
Q

Lung obstructed by viscous secretions

Persistent bacterial infection produces airway wall damage

A

Cystic fibrosis

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18
Q

What organisms can cause cystic fibrosis?

A

Staphylococcus aureus

Pseudomonas aeruginosa

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19
Q

How to treat cystic fibrosis?

A

remove viscous and purulent airway secretions
control bacterial infection with anti-bx
proper nutrition for host defense

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20
Q

How to test for pneumonia?

A

**radiology is the gold standard for making diagnosis
examine sputum
fiber-optic bronchoscopy
examine pleural effusions
blood culture
serology
urine studies including antigen detection

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21
Q

Primary cause of bacterial pneumonia and meningitis

A

Strep pneumo

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22
Q

What are the characteristics of pneumococcal pneumonia?

A 
abrupt onset
fever
sharp pleural pain
bloody rusty sputum
usu in an immunocompromised host (pts with sickle cell)
usu in lower lobes

**bloody rusty sputum

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23
Q

Abrupt onset, fever, sharp pleural pain, bloody rusty sputum
Largely a disease of a compromised host, e.g., age, physical condition, genetic (sickle cell disease)
Generally localized in lower lobes (lobar pneumonia)

A

Pneumococcal pneumonia

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24
Q

How to treat pneumococcal pneumonia? How does this bug become resistant to antibiotics?

A

Penicillin or ceftriaxone;

PBP with reduced affinity for antibiotic

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25
Q

Gram-negative enterobacteriaceae, encapsulated (anti-phagocytic), lactose-fermenting,
Encapsulated - antiphagocytic
Mucoid colonies in lab

A

Klebsiella pneumoniae

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26
Q

What are the characteristics of Klebsiella pneumonia?

A

thick, bloody mucoid sputum
patients usu comprised via immune system or impaired respiratory defenses
usu arises in hospital setting

**bloody mucoid sputum

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27
Q

What other infections can Klebsiella pneumoniae cause?

A

UTI
wound infections
bacteremia and meningitis

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28
Q

Who gets Klebsiella pneumonia? How is it spread? How to prevent it?

A

disease of sick people (healthy people rarely develop disease)
spread in hospital setting from person to person or via contamination of ventilators, IV catheters, or wounds
prevent via strict attention to infection control measures

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29
Q

How does Klebsiella pneumoniae become resistant to antibiotics?

A
  1. overproduction of a broad spectrum beta lactamase
  2. extended spectrum beta lactamases
  3. efflux pump
  4. carbapenem resistance (a beta lactam)
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30
Q

Encoded by a beta-lactamase gene
Can hydrolyze EVERY known beta lactam antibiotics –> extremely broad spectrum beta lactamase
Resistant to beta lactamase inhibitors
Leaves few (polymyxins) or no treatment options whatsoever

**polymyxins target membranes of gram negatives, but they’re toxic

A

Carbapenem-resistant Klebsiella pneumoniae

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31
Q

Thin, pleomorphic gram-negative rod
Stains poorly with common reagents
Nutritionally fastidious; requires cysteine and iron
Replicates inside MACROPHAGES; amoebae are hosts in nature
Prevents phagolysosome fusion

A

Legionella pneumophila

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32
Q

Severe, acute pneumonia
Fever, non-productive cough, shortness of breath, myalgias
Risk factors
Age, smoking, COPD,
weakened immune system, diabetes, kidney failure, immunosuppression
High mortality rate – 15-20%

A

Legionnaires disease

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33
Q

How is Legionnaires’ disease acquired? How is it infectious?

A

it is inhaled
infects alveolar macrophages
inhibits phagolysosomal fusion, and prevents exposure to free radicals
proliferates inside cells
causes inflammatory response
eventually, cell-mediated immune reaction

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34
Q

How do you diagnose Legionnaire’s disease?

A

urinary antigen test **most commonly used diagnostic test (detects serotype 1 LPS which is shed from the bacteria and detected in the urine)
culture on special media
pneumonia by x-ray or physical exam
look at sputum or endotracheal aspirate

**LPS 1 only in community acquired legionella; more than half the cases are hospital acquired, so they will not be detected

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35
Q

Where is legionella found?

A

in aqueous environments, likes warm water

acquired by exposure to contaminated aerosols - air conditioning and cooling towers**

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36
Q

Legionella is often (blank) due to number of high-risk patients

A

hospital acquired

  • *sick people
  • *contaminated water sources
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37
Q

How to prevent and control Legionella?

A

routine surveillance

clean and disinfect

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38
Q

What antibiotics can be used to treat Legionnaires’ disease? Why are most antibiotics ineffective in treatment?

A

macrolides: azithromycin
fluoroquinolones: levofloxacin
tetracycline: doxy

**Most antibiotics ineffective due to poor penetration of macrophages

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39
Q

Smallest free-living bacterium
Lack a cell wall – resistant to antibiotics that target cell wall
Cell membrane contains sterols obtained from host, e.g., cholesterol
Growth in culture requires medium containing sterols, e.g., animal serum

A

mycoplasma pneumoniae

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40
Q

How is mycoplasma pneumoniae acquired?

A

it is inhaled
adheres to respiratory epithelium via an attachment organelle (P1 protein)
it destroys cilia, then ciliated epithelial cells (leaves you susceptible to other infections)
irritation and secondary infection cause persistent cough

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41
Q

What are two clinical diseases that can be caused by mycoplasma pneumoniae? Usually asymptomatic…

A

tracheobronchitis **most common - low grade fever, malaise, headache, non-productive cough

primary atypical pneumonia - pt not terribly ill, will see patchy bronchopneumonia on chest radiograph

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42
Q

How is mycoplasma pneumonia diagnosed?

A

usu diagnosed entirely clinically

**microscopy not useful, bc lacks cell wall
culture is not commonly done
serology and nucleic acid fixation not terribly useful
cold agglutinin should not be used, but it is…

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43
Q

How is mycoplasma pneumonia acquired? Who does it infect?

A

spread via respiratory droplets, so it is inhaled;

primarily infects older children b/w 5-15 years old, but all populations are susceptible

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44
Q

How to treat mycoplasma pneumoniae?

A

macrolide: erythromycin, azithromycin
tetracycline: doxy *cheap, can’t use in kids
fluoroquinolone *expensive

45
Q 
Inhabits soil with high nitrogen content, esp bird and bat droppings
Inhalation of microconidia
Germination into yeasts
Intracellular growth in lungs
May remain localized or disseminate
A

Histoplasma capsulatum

46
Q

This type of histoplasma is found in the US in the Ohio and Mississippi River valleys. Also found in Mexico, Central and South America

A

H. capsulatum

**duboisii found in Africa

47
Q

What is the primary host defense against histoplasmosis?

A

cellular immunity

48
Q

This disease caused by histoplasmosis is common in endemic areas
>90% asymptomatic or mild influenzae-like illness
If ill: fever, headache, nonproductive cough, chills, chest pain

A

acute pulmonary histoplasmosis

49
Q

A subset of patients infected with histoplasmosis will get these two more serious diseases

A

chronic pulmonary histoplasmosis

progressive disseminated histoplasmosis

50
Q

This form of histoplasmosis will have skin and skeletal involvement

A

African histoplasmosis

**caused by H. capsulatum var. duboisii

51
Q

What does histoplasmosis look like histologically?

A

small budding yeasts with macrophages

52
Q

If you culture histoplasmosis, what does it look like?

A

hangs inside macrophages

tuberculate macroconidia (at room temp)

or

small, oval budding yeast at 37C

53
Q

Other ways to diagnose histoplasmosis?

A

antigen immunoassay **urine is best sample
serology **test for serum antibody, 10% of normal pts will test positive
skin tests

54
Q

How to treat histoplasmosis?

A

most cases of acute pulmonary infection require no treatment
can use antifungals, like itraconazole (inhibits ergosterol synthesis)
can use amph B, too (fungicidal)

55
Q

Inhabits soil containing decaying organic matter

Geographic distribution:
Ohio and Mississippi river valleys
Southeastern U.S.
Endemic areas overlap with histoplasmosis

Natural history:
Inhalation of conidia from environmental site
Germination into yeasts
Growth in lungs
May remain localized or disseminate

**Dogs are highly susceptible; not a reservoir

A

Blastomyces dermatitidis

56
Q

What disease can blastomyces cause?

A

acute pulmonary blastomycosis: often asymptomatic, but can progress to fulminant respiratory disease

disseminated disease: skin most often involved

infection in immunocompromised host, too

57
Q

What does blastomycosis look like on histopath?

A

mycelium at 20

broad-based, large, budding yeast at 37C

58
Q

How to diagnose blastomycosis?

A

really use history, location

and culture looking for broad-based budding yeast

59
Q

How to treat blastomycosis?

A

Itraconazole for mild or moderate disease
Lipid formulation of Amphotericin B
Severe disease

60
Q

Dimorphic fungus
Mycelium with “barrel shaped” arthroconidia in soil
Endosporulating spherules in tissue
Inhabits soil of dry, low-rainfall areas
Geographic distribution
Southwestern U.S. (regions of California, Arizona and New Mexico), Mexico, Central and South America

A

Coccidioides immitis

61
Q

How do you get infected by coccidioides immitis?

A

inhale arthroconidia
it germinates in lungs and forms spherules
may remain localized or disseminate

62
Q

What diseases can you get from coccidioides infection?

A

primary pulmonary coccidioidomycosis: most common presentation, cough, chest pain, SOB, fever, fatigue 7-21 days after exposure

pulmonary nodules and cavities: pleuritic pain, cough, hemoptysis

extrapulmonary dissemination: rare, usu in immunosuppressed, very serious infection, can cause coccidioidal meningitis

63
Q

What does coccidioidomycosis look like in the tissue?

A

endosporulating spherules in sputum or tissue in lung or skin

  • *this established diagnosis
  • *arthroconidia is other form
64
Q

What other tests can be used to detect coccidioidomycosis?

A

serology **can be useful, 10% of normal are positive in endemic areas

culture **less useful
skin tests **little value for diagnosis

65
Q

How to treat coccidioidomycosis?

A

oral azole: fluconazole

Amp B if advanced

66
Q

Classified as fungus on basis of rRNA sequences
Lacks ergosterol
Species varies with each host
Can’t be grown in culture
Life cycle has sexual and asexual components
All microbial forms found during human infection: free trophic form, precystic form, and cystic form

A

Pneumocystis jirovecii in humans

carinii in rats

67
Q

How does pneumocystis jirovecii infect hosts and cause disease?

A

natural resistance is high (most people are infected), but host compromise allows organisms to proliferate and fill alveolar lumens;
foamy exudate forms in alveolar space and progresses to interstitial fibrosis and edema

68
Q

What clinical diseases does pneumocystis jirovecci cause? Who gets disease from this infection? What do these patients die from?

A

interstitial plasma cell pneumonitis;
immunosuppressed pts and HIV pts

**high mortality if untreated, death due to respiratory failure

69
Q

What is the most useful way to diagnose pneumocystis jirovecci?

A

microscopy!

BAL fluid staining (high sensitivity)
Wright-Giemsa stains
Silver stain for cyst - crushed ping pong ball appearance

70
Q

How is pneumocystis jirovecci spread? What patients are at risk?

A

via airborne route; malnourished or premie infants, SCID, hyper IgM syndrome, immunocompromising meds, AIDS - all risks

  • *used to be the most common infection in AIDS pts, but is less frequent with HAART
  • *can be spread pretty easily from pt to pt
71
Q

How to treat pneumocystis jirovecci?

A

trimethoprim-sulfamethoxazone for prophylaxis and treatment;
chemoprophylaxis for AIDS pts with CD4 less than 200

(synergistic antibiotic that interferes with folic acid synthesis)

72
Q

Non-spore-forming, weakly gram-positive, acid-fast rods
Highly aerobic
Mycolic acid in cell wall with long fatty acid stains

A

Mycobacteria

73
Q

What is in the cell wall of mycobacteria? What is unique about it?

A

mycolic acid;
confers acid-fastness, resistance to gram staining, resistance to detergents, hydrophobic antibx, and survival in macrophages, causes cording of cells

74
Q

Describe the cell wall of Mycobacterium

A

inner membrane, thick peptidoglycan layer, no outer membrane
more complex than gram-positives **lipoarabinomannan is a unique component which is functionally similar to O-antigens
**lots of lipids

**like gram-positives, but these are the differences

75
Q

Different types of mycobacterium species

A

M. tuberculosis
M. bovis in cattle - spread via dairy products
Non-TB mycobacteria - atypical mycobacteria
M. leprae

76
Q

Trehalose dimycolate
Subset of cell wall mycolic acids
Plays a role in pathogenesis by binding to a macrophage surface receptor called mincle
Blocks macrophage activation by IFN-g
Induces secretion of TNF-a
Causes formation of cords - bacteria align themselves in rope-like structures

A

Cord factor

77
Q

How does mycobacterium TB cause TB?

A

bacteria are phagocytized by alveolar macs
they survive in macs by preventing fusion of phagosome w lysosome
infected macs secrete cytokines
cytokines drive T cells to become TH1 cells that secrete IFN-gamma activates infected macrophages, and kills bacteria by ROS and nitrogen species
DTH response may lead to granuloma
infection is resolved if bacteria are killed or go dormant

78
Q

Waning or loss of cellular immunity allows for outgrowth of TB bacteria
Destructive DTH response

A

reactive TB

79
Q

This type of TB is most often asymptomatic or mild fever and malaise
Radiographs show mid-lung infiltrates and hilar lymphadenopathy
May progress to reactivation or dissemination

A

Primary TB

80
Q

10% of individuals with primary tuberculosis reactivate
Usually men > 50 years
Most often associated with immunosuppression – AIDS most common
Symptoms
Dry cough that becomes productive and mixed with blood (hemoptysis)
Fever, malaise, sweating, weight loss
Cavities in lung apices; contain huge numbers of bacteria
Untreated, death in 2-5 years
More rapid course in AIDS or other T cell compromise

A

Reactivation TB

81
Q

How to diagnose TB?

A

H&P

radiology: assessing the extent and character of disease - look for patchy or nodular infiltrate in the lung apices - esp look for cavitary infiltrate
immunodiagnosis: skin test or IFNgamma release

nucleic acid based test

acid-fast staining

82
Q

What do you use for a TB skin test? How do you read a TB skin test?

A

Intradermal injection of purified protein derivative (PPD)
DTH reaction, so takes 48-72hrs

After 48-72 hours, look for INDURATION, not erythema

Should be less than 5mm for immunocompromised
Less than 10mm for high-risk groups
Less than 15 mm for low-risk groups

Positive result implies infection, but not disease

83
Q

What can cause a false positive TB skin test?

A

infection with non-Mtb mycobacteria

84
Q

What is an IFN release assay? What are the advantages of this test?

A

used in place of a TB skin test
draw whole blood from the pt, incubate it with a cocktail of 3 purified proteins
measure release of IFN gamma
The 3 proteins in the cocktail are only found in mycoTB, so this test is much more specific

advantages: no reaction in people who received BCG, no need to return to have skin evaluated, no booster effect w repeat testing

85
Q

One of the mainstays for the diagnosis of TB
Use a tissue specimen or sputum - cover the sputum with a stain - then heat the slide which allows the stain to get into the cell wall
Use a rigorous decolorization using acid

A

acid-fast staining

  • *the tough cell wall of mycobacterium will retain the stain after treatment with acid
  • *nowadays you can scan with fluorescent dyes to make it easier
86
Q

Another test that can be used to diagnose TB
Uses PCR amplification
More sensitive than acid-fast, but less sensitive than culture

A

nucleic acid-based testing

**can assess resistance gene to rifampin in the meantime

87
Q

What is the gold standard for diagnosis of TB?

A

culture!

**most sensitive of the procedures

2 types of medium:

solid: Lowenstein Jensen or Middlebrook, takes 3-8 weeks
liquid: organism will grow faster

88
Q

What are some options for antibiotic sensitivity testing for TB?

A
  1. agar proportion
  2. liquid broth systems
  3. molecular tests - look for resistance to rifampin
89
Q

How many people on the globe are infected by TB?

A

1/3 of the globe!

90
Q

How is TB spread?

A

humans are the only natural reservoir

person to person spread via airborne droplets

91
Q

How to treat TB?

A

BIG 4 antibiotics
isoniazid - inhibits synthesis of mycolic acid
rifampin - inhibits DNA dependent RNA polymerase
ehtambutol
pyrazinamide

  • *use multiple drugs to combat the emergence of resistance
  • *directly observed treatment
92
Q

First line drug for TB and what is its mechanism of action? What can be used if the primary treatment doesn’t work?

A

isoniazid - inhibits synthesis of mycolic acid;

add rifampin

93
Q

How should you administer antibiotics to TB patients?

A

DOT: directly observed treatment - must observe pt taking meds

94
Q

What are the two forms of drug-resistant m-TB?

A

multidrug resistant TB: resistant to isoniazid and rifampin

extensively drug resistant TB: resistant to isoniazid, rifampin, quinolones and at least one second-line drug
**seen in most regions of the world, potentially untreatable

95
Q

What causes TB to become multidrug resistant?

A

interrupted course of antibiotics

levels of drug can’t kill 100% of bacteria

96
Q

What is the live vaccine used for TB? Who should it be given to?

A

BCG vaccine;
should be given to young patients

  • *not widely used in the US, because low incidence of TB, also produces false-positive skin test
  • *furthermore, can produce BCG in pts that are immunocompromised (live vaccine)
97
Q

How is non-TB mycobacteria acquired? What does non-TB mycobacteria cause?

A

from environmental sources, like tap water;

Chronic bronchopulmonary disease
Skin and soft tissue disease
Lymphadenitis
Disseminated disease in immunosuppressed patient, e.g., AIDS

98
Q

Two species of mycobacterium avium? What does mycobacterium avium complex cause?

A 
M. avium and M. intracellulare
Primary infection; no reactivation disease
Chronic localized pulmonary disease
**Disseminated disease in advanced AIDS
CD4<100/mm3
Very common prior to HAART
Cervical lymphadenitis
99
Q

Mycobacterium avium complex very common in this population

A

AIDS pts

100
Q

How to diagnose mycobacterium avium?

A

blood culture for disseminated disease

**microscopy lacks sensitivity and specificity

101
Q

How do you get infected w mycobacterium avium?

A

inhaled or ingested from environmental sources,
in natural water sources, indoor water systems, pools, hot tubs

**no human-human spread

102
Q

How to treat mycobacterium avium?

A

Clarithromycin or azithromycin + ethambutol and rifabutin

Azithromycin prophylaxis if CD4 < 50 cells/mm2

103
Q

Aerobic, gram-positive, weakly acid-fast, filamentous rods
Mycolic acids in cell wall; shorter than Mycobacteria
Makes a cord factor with similar activity to TB

A

Nocardia

104
Q

What is one nocardia species to be aware of?

A

Nocardia asteroides

105
Q

What diseases are caused by nocardia?

A

bronchopulmonary disease
cutaneous infections
**mycetoma (destruction of extremities)

106
Q

How to diagnose nocardiosis?

A

multiple sputum samples
do an acid fast stain to distinguish it from Actinomyces
culture it and look for filamentous, weakly acid fast bacilli
When you put it on agar, you can see aerial hyphae like structures

107
Q

Where is nocardia found? How do you get infected?

A

ubiquitous in soil rich in organic matter
it inoculates the skin or is inhaled

**immunocompromised pts

108
Q

How to treat nocardia infection?

A

Antibiotics
Trimethoprim-sulfamethoxazole is primary antibiotic
Amikacin, imipenem or broad-spectrum cephalosporins used in combination with TMP-SMX in immunocompromised patient
Requires prolonged treatment – up to 12 months

Block 9 Week 3 Meg (10 decks)

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