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Micro Exam 3 > Jackson: Lower Respiratory Tract Infections > Flashcards

Jackson: Lower Respiratory Tract Infections Flashcards

1
Q

Lower Respiratory Tract Infections

Children vs adults:

A

• Age is a key determinant for pneumonia:
o Children: viruses are primary causes; bacteria cause secondary infections
o Adult: depends on a variety of risk factors

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2
Q

Adult pneumonia may be CA or HA/Nosocomial
CA Risks:
HA Risks:

A

o CA Risks: alcohol abuse, occupational exposure, underlying condition
o HA Risks: immunocompromise and mechanical ventilation

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3
Q

Atypical pneumonias are caused by:

also defined as:

A

• Atypical pneumonias are caused by a pathogen other than S.pneumo: also defined as primary pneumonia that did NOT involve an initiating viral infection

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4
Q 
Streptococcus pneumoniae (Pneumococcus)
Virulence Factors (Relevant to Lower Respiratory Tract Infections): (3)
A

o Polysccharide capsule (90 serotypes)
o Pneumolysin
o Cell Wall TA and Peptidoglycan

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5
Q 
Streptococcus pneumoniae (Pneumococcus)
Polysccharide capsule (90 serotypes):
Prevents: (2)
Facilitates: 
What confers host immunity?
A

o Polysccharide capsule (90 serotypes): primary virulence factor
• Prevents complement deposition (C3b)
• Prevents phagocytosis by alveolar macrophages
• Facilitates evasion of lung surfactant
• Abs to capsule confer host immunity

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6
Q 
Streptococcus pneumoniae (Pneumococcus)
Pneumolysin:
Damages membranes (related to?)
\_\_\_\_\_\_\_is cell membrane receptor 
Acts on several cell types:
A

o Pneumolysin: sulfhydryl activated cytolysin (hemolysin)
• Damages membranes (related to SLO); subunits oligomerize in cell membrane to form a pore
• Cholesterol is cell membrane receptor
• Acts on several cell types (pulmonary epithelium, PMNs and monocytes)

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7
Q

Streptococcus pneumoniae (Pneumococcus)
Pneumolysin
Role in Pathognesis

Evasion of:
Clearance from:
May permit:
Cell-bound form activates:

A
  • Evasion of the immune response and clearance from nasopharynx
  • May permit spread to bloodstream from alveoli (bacteremia)
  • Cell-bound form activates complement, contributes to inflammation
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8
Q 
Streptococcus pneumoniae (Pneumococcus)
Cell Wall TA and Peptidoglycan

Gram (+) Shock:
Activates:
Production of:

A

Gram (+) Shock: strong inflammatory response (similar to LPS in G negative); inflammation elicits fever and lung damage (bloody sputum)

  • Activate alternate complement pathway
  • Production of IL-1 and TNF alpha
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9
Q

Streptococcus pneumoniae (Pneumococcus)
Exclusively a human pathogen:
Transmission:

A

Exclusively a human pathogen: many asymptomatic carriers (transient carriage also possible)

Transmission: person to person (droplet spread)

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10
Q

Streptococcus pneumoniae (Pneumococcus)

Recurrent pneumococcal pneumonia:
Note:

A

Recurrent pneumococcal pneumonia: is a presenting manifestation of AIDS

Note: Most common cause of acute bacterial pneumonia in any age group

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11
Q

Streptococcus pneumoniae (Pneumococcus)

Establishment of Organism in Lower Respiratory Tract:
Common causes of compromised cough:

A

Aspiration of pneumococci from middle respiratory tract

Compromised cough reflex permits entry into lower respiratory tract
- Common Causes: stroke, alcoholism, drugs, anesthesia, viral infection
• Alveolar Abs usually clear pneumococci from lower respiratory tract

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12
Q 
Streptococcus pneumoniae (Pneumococcus)
Acute Pneumonia

Cough:
Inflammatory Response:

A

o Acute Pneumonia: infection of lung parenchyma
• Cough: with productive sputum (purulent material from alveoli)
• Inflammatory Response:
➢ Complement components increase vascular permeability (fluid accumulates)
➢ Disrupted gas exchange (suffocation)

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13
Q 
Streptococcus pneumoniae (Pneumococcus)
Secondary Complications

Bacteremia:

Acute Purulent Meningitis:
Pneumococci adhere to:
Pneumococci breach:

A

Bacteremia: due to inflammatory response and damage to endothelial cells

Acute Purulent Meningitis: bacteremia may lead to meningitis
- Pneumococci adhere to vascular endothelium in CNS and cause cell death
- Pneumococci breach BBB/BCB to enter CSF
.

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14
Q

Streptococcus pneumoniae (Pneumococcus)
Sputum Gram Stain:
Major Problem:

A

Sputum Gram Stain: important diagnostic tool, but issues
Major Problem: contamination with flora from oropharynx
➢ Sputum is MONOMICROBIC and contains PMNs
➢ Contaminating saliva is POLYMICROBIC and has squamous epithelial cells

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15
Q

Streptococcus pneumoniae (Pneumococcus)

G+/-?
Hemolysis:
Lancefield Grouping:

A
  • G(+) lancet shaped diplococcic
  • Alpha-hemolytic
  • No Lancefield grouping
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16
Q

Streptococcus pneumoniae (Pneumococcus)

Biochemical Tests: (4)

A
  • Capsular serotyping
  • Quelling reaction (anti-capsule Abs)
  • Optochin (P disk) sensitive
  • Bile soluble (distinguish from viridians strep
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17
Q

Streptococcus pneumoniae (Pneumococcus)

Blood Culture:

A
  • Detects bacteremia and confirms sputum sample

* Latex agglutination used to detect circulating pneumococcal Abs

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18
Q

Streptococcus pneumoniae (Pneumococcus)

Radiology:

A

o Radiology: shows bronchopneumonia that can consolidate to lobar pneumonia

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19
Q 
Haemophilus influenzae
Virulence Factors (Relevant to Lower Respiratory Tract Infections):
A

Polysaccharide capsule
• Anti-phagocytic
• Subject to Ag variation
• Hib most virulent (capsular serotype B)

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20
Q

Haemophilus influenzae

Normal Flora:
Transmission:
Peak Age Group:

A

o Normal Flora: commonly in upper respiratory tract
• Humans can be carriers of both encapsulated and non-encapsulated (non-typable) strains

o Transmission: person to person (droplet)

o Peak Age Group: 2-5 years old

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21
Q

Haemophilus influenzae
Pneumonia: can be caused by both encapsulated and non-encapsulated strains

Encapsulated:
Hib pneumonia:

A

Encapsulated: similar disease to pneumococcal pneumonia
- Hib pneumonia: increased virulence with a higher incidence of positive blood cultures (less common than non-typable because lower colonization rates)

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22
Q

Haemophilus influenzae
Pneumonia: can be caused by both encapsulated and non-encapsulated strains

Non-Encapsulated:

A

• Non-Encapsulated: less virulent

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23
Q

Haemophilus influenzae

Predisposing Factors of Nontypable Pneumonia: (3)

A

o Chronic bronchitis
o Emphysema
o Obstructive pulmonary disease

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24
Q

Haemophilus influenzae

Acute Epiglotittitis:

A

Acute Epiglotittitis: can also be caused by H.influenzae

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25
Q

Haemophilus influenzae
Sample Collection:
Cultures:

A

Sputum and blood cultures (positive in 10-15% of patients; higher with Hib pneumonia)

Cultures:
• G(-) coccobacilli
• Fastidious (requires X and V blood factors for growth)

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26
Q

Legionella pneumophilia

Etiology:

A

Parasite of freshwater and soil protozoa: Acanthomoeba, Naeglaria

Found in reservoirs for ameba/bacteria (cooling towers, AC systems, plumbing, hospital respiratory equipment); routine disinfection of cooling systems used as prevention

Existence inside ameba provides survival advantage
➢ More resistant to disinfectants
➢ Can survive over winter inside cyst of ameba
➢ May be capable of living outside of ameba in biofilms

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27
Q

Legionella pneumophilia

Transmission:

A

Transmission: inhalation (but NO person-to-person spread)

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28
Q

Legionella pneumophilia
Acute Pneumonia

virulence in humans:
Contributors to pathogenesis:

A
  • Generally low virulence in humans: most people have Abs because of it ubiquity in nature
  • Contributors to pathogenesis: nosocomial infections, immunocompromise, smoking, excessive alcohol use, old age
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29
Q

Legionella pneumophilia

Legionnaire’s Disease:

A

Legionnaire’s Disease: severe pneumonia with a 2-10 day incubation period (high mortality rate, especially in immunocompromise)

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30
Q

Legionella pneumophilia

Pontiac Fever:

A

Pontiac Fever: nonpneumonic (no pneumonia) febrile illness with a 1-2 day incubation period (self-limiting); may be immune response to inhalation of dead/low virulence strains

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31
Q

Legionella pneumophilia

Disseminated Disease:

A

Disseminated Disease: very rare; usually presents with pneumonia after a long incubation period (days-weeks)

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32
Q

Legionella pneumophilia
Disease Process

Inhaled organism has tropism for:
Has a surface protein that binds:

A

Inhaled organism has tropism for lung alveoli and bronchioles (forms microabsecesses)

Has a surface protein that binds C3 (enhances its own phagocytosis)
➢ “Coiling” phagocytosis
➢ Uptake may also occur without opsonization (bacteria-induced phagocytosis)

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33
Q

Legionella pneumophilia
Disease Process

Survives in monocytes/macrophages as:
Once in the cell, expresses 30 new proteins that:
Multiplication of Legionella is normally inhibited in:

A

• Survives in monocytes/macrophages as intracellular parasite

• Once in the cell, expresses 30 new proteins that:
➢ Prevent phagolysosome fusion and acidification of the endocytotic vesicle
➢ Induce accumulation of ribosomes and mitochondria around phagosome
➢ Facilitate scavenging of iron from transferrin

• Multiplication of Legionella is normally inhibited in an activated macrophage

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34
Q

Legionella pneumophilia
Clinical ID

Urine EIA test for:
Normal staining and culture techniques:
Gram Stain:
Growth media:

A

Urine EIA test for soluble Ag

Normal staining and culture techniques not useful:

Does not Gram stain well:
➢ May be visualized with simple stains devoid of decolorization or silver impregnation
➢ Appears thin, pleomorphic G(-) rod with filamentous forms also seen

Growth media:
➢ Requires amino acids L-cysteine, and ferric ions
➢ Also needs to be on buffered medium (pH restrictions)
➢ Slow growth (2-5 days)

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35
Q

Legionella pneumophilia
Clinical ID

Microscopic exam of tissue required:
Legionella should be suspected in cases of:
Organism is rarely found in:
Identification based on:

A

Microscopic exam of tissue required: since Gram stain not useful

Legionella should be suspected in cases of severe progressive pneumonia with no known etiologic agent

Organism is rarely found in sputum
➢ Need to collect lung aspirate, transtracheal aspirate, or lung biopsy

Identification based on antigenic structure and DNA homology tests
➢ Indirect immunofluorescence of serum (rise in Ab titer to Legionella)
➢ Difficult to assess due to high exposure rates in population

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36
Q

Legionella pneumophilia
Clinical ID

PCR: 
Serological Diagnosis (Summary Chart):
A

o PCR: used by reference lab for identification (most human infections caused by Philadelphia strain)
o Serological Diagnosis (Summary Chart): immunofluorescence

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37
Q

Acinetobacter spp.
Etiology

Environment:
Antibiotic resistant:
Frequent cause of:

A

Etiology
o Environment: lives in soil, water and on the skin of healthy people (especially healthcare workers); can survive on dry surfaces for up to 20 days
o Antibiotic resistant: innately resistant to man classes of antibiotics
o Frequent cause of nosocomial infections

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38
Q

Acinetobacter spp.

Pathogenesis:
Clinical ID:

A
  • Pathogenesis: causes pneumonia and serious blood/wound infections in immunocompromised patients
  • Clinical ID: G(-) coccobacillus (resembles Haemophilus)
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39
Q 
Mycoplasma pneumoniae
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Adhesin:
Hydrogen peroxide:

A

Adhesin: binds sialic acid containing glycolupids or glycoproteins on bronchial epithelial cells

Hydrogen peroxide: damages tissue

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40
Q 
Mycoplasma pneumoniae
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Superoxide:
Autoantibodies may be generated during infection:

A

Superoxide: damages tissue

Autoantibodies may be generated during infection: homology between host cell and mycoplasma membrane glycolipids; reactive to lymphocytes, smooth muscle, brain, lung tissue

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41
Q

Mycoplasma pneumoniae

Common age group:
Transmission:

A

o Common age group: teenagers

o Transmission: droplet spread (very low infectious dose); common in closed communities
• Organism shed both before and long after onset of symptoms

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42
Q

Mycoplasma pneumoniae
Pathogenesis

Walking Pneumonia:
Disease Process:

A

o Walking Pneumonia: less severe than other bacterial pneumonias

o Disease Process:
• Colonization of bronchial epithelium interferes with ciliary action
• Inflammation and exudate are the primary contributors to pathogenesis

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43
Q

Mycoplasma pneumoniae
Pathogenesis
Second Infection Site:

A

Second Infection Site: non-purulent otitis media

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44
Q

Mycoplasma pneumoniae
Sequelae

Immunopathology due to:
Possible complications: (3)

A

Immunopathology due to cross-reactive Abs

Possible complications:
➢ Hemolytic anemia
➢ Aseptic meningitis
➢ Pancreatitis

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45
Q

Mycoplasma pneumoniae
Culture

sputum:
culture:
Gram stain:
microscopically:

A
  • No organism in sputum
  • Organism grows too slow to culture (require cholesterol for growth)
  • No Gram stain (no cell wall)
  • Difficult to detect microscopically
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46
Q

Mycoplasma pneumoniae

Structure:
Serodiagnosis:

A

Structure:
• Lack cell wall (no Gram stain or treatment with B-lactams); bound by triple membrane containing sterols

Serodiagnosis: can be used to detect circulating Ags or complement-fixing Ab
• Ab to M.pneumoniae is diagnostic (disease has a long IP so patient presents with high titers)

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47
Q

Mycoplasma pneumoniae

DNA hybdrization or PCR:
Serological Diagnosis:

A

o DNA hybdrization or PCR: also being developed for detection
o Serological Diagnosis (Summary Chart): complement fixation or IgM titers (ELISA)

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48
Q

Chlamydia pneumoniae
Virulence Factors (Relevant to Lower Respiratory Tract Infections)
Life Cycle: (2)

A

Life Cycle:
• Elementary Body: infectious stage that carries adhesin for receptor binding (attaches and induces endocytosis into columnar epithelial cells)
• Reticulate Body: replicates once in cell; metabolically active (uses host ATP)
➢ Eventually reorganize and release infectious EB from the cell

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49
Q

Chlamydia pneumoniae

Hosts:
It causes:

A

Humans are only host: ~50% of adults seropositive, but reinfection still occurs

Causes:
• Pharyngitis
• Bronchitis
• Atypical Pneumonia (Walking Pneumonia): in school children and young adults

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50
Q

Chlamydia pneumoniae

Pathogenesis:

A

Clinical picture resembles M.pneumoniae

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51
Q

Chlamydia pneumoniae
Clinical ID

Morphology/Growth:
Detection:
Serological Diagnosis (Summary Chart):

A

Morphology/Growth:
• G(-) outer membrane, but no cell wall (cannot Gram stain or treat with B-lactams)
• Coccobacillus
• Inclusions are glycogen (-)

Detection:
• Direct immunofluorescent staining of outer membrane proteins
• DNA or RNA detection using probes and PCR
• Inclusions do not contain glycogen

Serological Diagnosis (Summary Chart): immunofluorescence or ELISA

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52
Q

Staphylococcus aureus

Acute pneumonia:

A

Acute pneumonia: secondary to some other insult to the lung (ie. influenza)

53
Q

Staphylococcus aureus

Empyema:

A

Empyema: purulent infection of pleural space (gains access by contiguous spread from infected lung)

54
Q

Staphylococcus aureus

Lung Abscess:

A

Lung Abscess: complication of acute or chronic pneumonia (may be caused by aspiration of oral or gastric contents)

55
Q

Staphylococcus aureus
Clinical ID

Samples:
Antibiotic susceptibilities:
Radiology:

A

Samples: sputum, lung abscess aspirate, blood culture (disseminated infection)
• G(+) cocci in clusters
• Catalase (+)
• Coagulase (+)

Antibiotic susceptibilities required

Radiology: used to diagnose lung absecesses

56
Q 
Mycobacterium tuberculosis
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Mycolic Acid (Cord Factor):
Resistance to:
Promotes (2):

A

Mycolic Acid (Cord Factor): long chain fatty acid
• Resistance to drying and disinfectants
• Promotes hypersensitivity granuloma
• Promotes inflammatory response (TNF) and damage to lung tissue

57
Q 
Mycobacterium tuberculosis
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Lipoarabinomamman:

A

Lipoarabinomamman: cell wall glycolipid
• Suppresses T cell proliferation
• Prevents macrophage activation

58
Q 
Mycobacterium tuberculosis
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Sulfolipids (Polyanionic Lipids):
Catalase:
Ammonia Production:

A

o Sulfolipids (Polyanionic Lipids): inhibits macrophage phagosome-lysosome fusion
o Catalase: degrades hydrogen peroxide
o Ammonia Production: prevents acidification in phagolysosome

59
Q

Mycobacterium tuberculosis

M.tuberculosis:
M.bovis:
M.africanum:

A
  • M.tuberculosis: primary cause of TB
  • M.bovis: from infected milk; has been eradicated through pasteurization (rare cause of TB)
  • M.africanum: causes TB in Africa
60
Q

Mycobacterium tuberculosis

M.avium complex (avium and intracellulare):
M.leprae:

A
  • M.avium complex (avium and intracellulare): opportunistic pathogens causing TB-like disease; cause disseminated disease in AIDS patients
  • M.leprae: causes leprosy (degenerative disease of skin and nerves; rare in US)
61
Q

Mycobacterium tuberculosis
US Infection Points

Incidence is significant amongst:
Outbreaks often occur in:
multi-drug resistant:

A

Incidence is significant amongst AIDS patients and immigrants

Outbreaks often occur in closed communities (nursing homes, shelters, prisons)

~1% are multi-drug resistant

62
Q

Mycobacterium tuberculosis

Primary Infection:
Gohn (Primary) Complex:

A

• Primary Infection: unapparent in 95% of cases

➢ Gohn (Primary) Complex: lung granuloma (due to DTH reaction) and enlarged LNs

63
Q

Mycobacterium tuberculosis

Progressive Primary TB:
Disseminates:

A

• Progressive Primary TB: occurs in ~5% of cases of primary TB (infection does not resolve)
➢ Disseminates: bloodborne or miliary TB

64
Q

Mycobacterium tuberculosis

Reactivation TB:
Common Site:

A

• Reactivation TB: low percentage of cases (risk increases with age, alcoholism, diabetes, decreased immune function)
➢ Common Site: apex of lung (highest oxygen tension- aerobic organism)

65
Q

Mycobacterium tuberculosis

Disseminated TB:

A

• Disseminated TB: either due to progressive primary TB or reactivation TB
➢ Occurs through lymph or erosion of necrotic tubercle in lung
➢ Results in infection of liver, spleen, kidney, bone or meninges

66
Q

Tuberculin Skin Test

Inject a purified protein derivative (PPD):
DTH Reaction to PPD:

A

Inject a purified protein derivative (PPD): autolyzed bacteria containing protein, lipid, polysaccharide and nucleic acid injected under the skin and reaction read in 48-72 hours

DTH Reaction to PPD: local induration and erythema is positive reaction (seen 6 weeks after primary infection)

67
Q

Tuberculin Skin Test

Positive DTH Reaction Significance:

A

Positive DTH Reaction Significance:
➢ Coincides with tubercle (hypersensitivity granuloma) formation
➢ Indicates exposure (to M.tuberculosis or cross-reactive species), but not necessarily active disease (only 5% of skin test positive cases progress to active disease)
➢ BCG vaccination renders test invalid (will always be positive)

68
Q

Tuberculin Skin Test

Negative DTH Reaction Significance:

A

Negative DTH Reaction Significance:
➢ No exposure to organisms
➢ In prehypersensitivity stage (within 6 weeks of exposure)
➢ Loss of sensitivity (disappearance of Ag from primary complex)
➢ Anergy due to immunocompromise (poor prognosis if test was previously positive)

69
Q

Mycobacterium tuberculosis

Transmission:
Engulfed by alveolar macrophages:
Resists innate defenses:
Humoral response is weak (IgM):

A

o Transmission: aerosol inhalation, enters the lungs (primary focus)
o Engulfed by alveolar macrophages: carried to LN
o Resists innate defenses: PMNs, inactivated macrophages, lysozyme
o Humoral response is weak (IgM): no effective complement-mediated killing

70
Q

Mycobacterium tuberculosis

Cell-Mediated response:

A
  • Helper and cytotoxic T cells activate alveolar macrophages to ingest organisms
  • Activated macrophages prevent replication of organism; if there is an inadequate response, the organism can replicate in the macrophage phagosome
  • Slow replication (part of pathogenesis)
  • Cytokine response to organism causes systemic TB symptoms (weight loss, fever)
71
Q

Mycobacterium tuberculosis

Containment of pathogen in tubercle (microscopic granuloma):

A
  • Made of multinucleated giant cells, activated macrophages and lymphocytes
  • Can become necrotic and caseous (cheesy)
  • Fibroblasts and collagen accumulate at lesion
  • Tissue destruction causes chronic productive cough and blood-stained sputum
72
Q

Mycobacterium tuberculosis

Potential fates of tubercle:

A
  • Become fibrotic/calcified with dead bacteria (shows up on chest X-ray)
  • Can remain dormant for years (source of reactivation)
  • Necrotic tubercles may erode into blood vessels (causing disseminated/miliary TB)
73
Q

Mycobacterium tuberculosis

DTH reaction confers long-lived memory and protection from re-infection:

A
  • Loss of prior DTH is a bad prognostic indication of rapidly progressing disease (see above)
  • Basis of tuberculin skin test
74
Q

Mycobacterium tuberculosis

Specimen collection:

A

o Specimen collection: sputum, biopsy (sometimes), blood (if miliary TB)

75
Q

Mycobacterium tuberculosis

Staining:

A

o Staining: provides diagnosis BEFORE bacteria grows (slow growing)
• Acid Fast Stain (Ziehl-Neelsen)
• Chemotherapy monitored by periodic examination for AFB counts

76
Q

Mycobacterium tuberculosis
Cultivation

Very slow growth:
Special media:

A

Very slow growth: decontamination of sputum (4% NaOH) to inhibit faster growing bacteria; appearance of visible colonies may take 2 weeks (24 hour doubling time)

Special media: Lownstein Jensen (LJ) agar or Middlebrook agar

77
Q

Mycobacterium tuberculosis

Rapid ID: (3)

A
  • rRNA and DNA probes
  • PCR to detect common insertion sequence
  • Growth in 14C-palmitic acid (catabolized to CO2 which is therefore labeled and measured)
78
Q

Mycobacterium tuberculosis

Drug susceptibilities:
Extensively drug-resistance TB (XDR TB):

A

Drug susceptibilities: done in reference labs

Extensively drug-resistance TB (XDR TB): rare type of multidrug-resistant TB (MDR TB)
• Resistant to first line and second line drugs

79
Q 
Pseudomonas aeruginosa
Virulence Factors (Relevant to Lower Respiratory Tract Infections): (5)
A 
o	Adhesins
o	Alginate
o	Elastase
o	Exotoxin A
o	Multiple resistance to antimicrobials and disinfectants
80
Q

Pseudomonas aeruginosa

Adhesins:

A
  • Protein pilus adhesin (binding to asialoGM1)

* Non-pilus adhesin (binding to mucus)

81
Q

Pseudomonas aeruginosa

Alginate:

A

Alginate: polysaccharide capsule for biofilm formation
• Permits colonization of lung and evasion of the host immune response
• Regulated in response to environmental signals

82
Q

Pseudomonas aeruginosa

Elastase:

A

Elastase: protease that degrades lung elastin (tissue damage)

83
Q

Pseudomonas aeruginosa

Exotoxin:

A

Exotoxin A: similar structure/activity to diphtheria toxin (ADP ribosylation of elongation factor 2)

84
Q

Pseudomonas aeruginosa
Multiple resistance to antimicrobials and disinfectants

Mutation leads to:
Alteration of LPS to form that does not bind:

A
  • Mutation leads to loss of porin and decreased entry of antimicrobials
  • Alteration of LPS to form that does not bind antibiotics
85
Q

Pseudomonas aeruginosa

Etiology:

A

Etiology: common environmental isolate that can cause nosocomial infections (waterborne)

86
Q

Pseudomonas aeruginosa

Conditions causes: (3)

A
  • Acute pneumonia
  • Empyema
  • Abscesses
87
Q

Pseudomonas aeruginosa
Infections in Cystic Fibrosis

CF Lung:
Increased susceptibility to infection by Pseudomonas:

A

CF Lung: increased mucus secretion due to defect in CFTR (causes decreased sialylation of surface glycolipids)

Increased susceptibility to infection by Pseudomonas: because of increase in asialoGM1

88
Q

Pseudomonas aeruginosa
Infections in Cystic Fibrosis

Resistance to phagocytosis:
physical barrier to phagocytosis =
anti-pseudomonas Abs:

A

Resistance to phagocytosis: Pseudomonas infecting CF lung phenotypically switch to mucoid form

  • Alignate gel + excess mucus in CF = physical barrier to phagocytosis
  • In addition, anti-pseudomonas Abs may be defective in CF patients
89
Q

Pseudomonas aeruginosa
Infections in Cystic Fibrosis

Resistance to antimicrobials:
Primary infection in younger age group by:

A

Resistance to antimicrobials: alginate gel + excess mucus in CF = physical barrier to drugs
- Primary infection in younger age group by S.aureus; colonizing Pseudomonas strains develop resistance to anti-staphylococcal drugs used to treat it

90
Q

Pseudomonas aeruginosa
Infections in Cystic Fibrosis

Lung tissue damage:
Infection rarely spreads beyond:

A
  • Lung tissue damage: persistent colonization and elastase release by pathogen results in tissue damage and inflammation (recruited PMNs also release protease that contributes)
  • Infection rarely spreads beyond lungs in patients with CF
91
Q

Pseudomonas aeruginosa

G+/-:
Aerobic?
Ox =/-?

A 
o	G(-) rods in sputum
o	Aerobic (OF Dextrose tubes demonstrate aerobic growth)
o	Oxidase (+)
92
Q

FUNGI CAUSING LOWER RESPIRATORY TRACT INFECTIONS: (5)

A
  • Aspergillus spp.
  • Histoplasma capsulatum
  • Blastomyces dermatitidis
  • Coccidioides immitis
  • Pneumocystis (carinii) jirovecii
93
Q 
Aspergillus spp.
Virulence Factors (Relevant to Lower Respiratory Tract Infections):

Dimorphic growth:
Infectious conidia:
Hyphae:
Alflatoxin:

A

NO DIMORPHIC GROWTH PHASE

Infectious conidia: germinate to mold form

Hyphae: bind fibrinogen and complement components

(Alflatoxin: produced by A.flavus growing on peanuts- potent carcinogen)

94
Q

Aspergillus spp.
Basics:
Predisposing Factors: (4)

A

Basics: common environmental mold that is an emerging etiologic agent of nosocomial pneumonia

Predisposing Factors:
•	Asthma
•	Chronic bronchitis
•	TB
•	Immunosuppression (opportunistic infection)
95
Q

Aspergillus spp.

Requirements for infection:

A
  • Frequent inhalation of infectious conidia

* Inhalation of fungal elements (spores) or colonization (allergic aspergillosis/Farmer’s lung)

96
Q

Aspergillus spp.

May colonize respiratory tract:

A
  • May lead to tissue invasion by hypae

- Principal host defense is pulmonary PMN killing of invasive hyphae

97
Q

Aspergillus spp.

Infections Cause: (2)

A
  • Acute Pneumonia

* Lung Abscesses

98
Q

Aspergillus spp.
Lung aspiration, bronchial lavage, or biopsy

Mold form:
Structure:

A
  • Mold form: grows rapidly and is easily identified

* Structure: typical septate hyphae with conidia (spore)

99
Q

Aspergillus spp.

Radiology:

A

Radiology: visible fungus ball can form in pulmonary cavity

100
Q 
Histoplasma capsulatum
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Dimporphic Growth Phase:

A

Dimporphic Growth Phase: mold in environment that produces infectious conidia; pathogenic yeast in tissue

101
Q

Histoplasma capsulatum

Environmental source:
Transmission:

A

Environmental source: associated with bird and bat droppings

Transmission: inhalation of conidia (exposure is common, but disease is rare); no person to person transmission

102
Q

Histoplasma capsulatum

Primary infection site:
Causes a chronic pneumonia:
Immune response:

A

o Primary infection site: pulmonary
o Causes a chronic pneumonia: grows inside macrophages and produces a granuloma similar to TB; may disseminate to infect organs of the reticuloendothelial system
o Immune response: T cell activation of macrophages to prevent intracellular growth (long term immunity to re-infection)

103
Q

Histoplasma capsulatum
Clinical ID

Radiograph:
Blood or biopsy required:
If disseminated infection:
Isolation of yeast cells:

A
  • Radiograph: granulomas resembling TB
  • Blood or biopsy required: sputum not useful
  • If disseminated infection: biopsy of liver, spleen, and LN
  • Isolation of yeast cells: in bone marrow
104
Q

Histoplasma capsulatum
Clinical ID
Cultural isolation/histological identification (firm diagnosis):

A
  • Grows slowly on BAP and Sabouraud agar
  • Fungus appears dimorphic (yeast and mold forms)
  • Mold form produces tuberculate macroconidia (finger-like projections carrying spores)
105
Q

Histoplasma capsulatum
Clinical ID
Serological Tests:

A
  • There is widespread exposure and cross-reactivity to other pathogens
  • DTH skin reaction to mycelial Ag used for epidemiological analyses
  • Complement fixing Ab test for yeast and mycelial Ags predicts prognosis
106
Q

Histoplasma capsulatum
Clinical ID
2 other tests:

A

o Immunodiffusion test

o DNA probe

107
Q 
Blastomyces dermatitidis
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Similar to Histoplasma:
Difference:

A

Similar to Histoplasma: dimorphic growth phase

Difference: yeast cells exist extracellularly, not in macrophages

108
Q

Blastomyces dermatitidis

Geographic distribution:
More common in:

A

Geographic distribution: similar to Histoplasma (middle and SE US)

More common in males: probably due to occupational exposure

109
Q

Blastomyces dermatitidis

Conidia inhaled from:
PMN infiltration:
May mimic:

A

Conidia inhaled from soil: results in pulmonary infection with yeast cells

PMN infiltration: and formation of granuloma, leading to chronic pneumonia
- May mimic pulmonary tumor or TB

110
Q

Blastomyces dermatitidis
May disseminate

Chronic infection of _____ most common

A

Chronic infection of skin and bone most common

  • May even disseminate in subclinical infections
  • Necrosis and fibrosis at infected area can lead to disfigurement

Dissemination to UG tract also possible

111
Q

Blastomyces dermatitidis

Immune response

A

T cell mediated response and cytokine-activated macrophages

Large yeast cells can resist oxidative and non-oxidative killing mechanisms

112
Q

Blastomyces dermatitidis

Clinical ID: (3)

A

Biopsy:
• Large yeast cells with broad buds
• Grows slowly on mycological media (~4 weeks)

Serodiagnosis: hampered by cross-reactivity with other fungi

No skin test

113
Q 
Coccidioides immitis
Virulence Factors (Relevant to Lower Respiratory Tract Infections)

Dimorphic growth phase:
Mold:
Spherule:

A

Dimorphic growth phase
• Mold: produces infectious arthroconidia
• Spherule: invasive tissue form that produces reproductive endospores

114
Q

Coccidioides immitis

Geographical:

A

Geographical: Southwestern US (Valley Fever)

115
Q

Coccidioides immitis

Usually mild disease:
May become chronic pneumonia:
May disseminate to:

A

Usually mild disease: Valley fever is acute pulmonary infection with cough, chest pain, and myalgia

May become chronic pneumonia: occurs with decreased T cell response (AIDS, chemo)

May disseminate: to skin, bone, joints and meninges (very rare)

116
Q

Coccidioides immitis
Disease Process

Arthroconidia ____ and converts to _____
PMNs and macrophages respond:
Release of endospores from spherules induces a strong inflammatory response:
Inflammatory response results in:

A

Arthroconidia inhaled and converts to spherule

PMNs and macrophages respond

  • Arthroconidia phagocytosed
  • Spherule grows too large for phagocytosis

Release of endospores from spherules induces a strong inflammatory response

  • Endospores phagocytosed
  • Intracellular forms can prevent phagolysosome fusion and survive

Inflammatory response results in granuloma formation (15% cavitate)

117
Q

Coccidioides immitis

Immune Response:

A

Cell mediated (PMN, T Cell) immunity to arhtoconidia or endospores

Chronic or progressive infection can result in T cell anergy
- Spherules burst and pathogen load is so heavy it induces anergy)

118
Q

Coccidioides immitis
Clinical ID

Best:

A

Best: detection of characteristic spherules in histologic sections

119
Q

Coccidioides immitis
Clinical ID
Detection of complement fixing Abs indicates prognosis

Low titers:
High titers:

A

Low titers: primary pulmonary disease with good CMI response

High titers: disseminated disease and T cell anergy

120
Q

Coccidioides immitis
Clinical ID

Skin test detects DTH, but is of limited value:
Positive:
Negative:
2 others:

A

Skin test detects DTH, but is of limited value: due to common exposure
• Positive: 1-4 weeks after onset and positive for life (indicates immunity to reinfection)
• Negative: may be performing too soon after exposure or disease has progressed to anergy

Immunodiffusion

DNA probe

121
Q

Pneumocystis (carinii) jirovecii

Etiology:

A

Very common infection of generally low virulence

122
Q

Pneumocystis (carinii) jirovecii

Causes PCP in immunocompromised hosts: (4)

A
  • Premature infants
  • Patients undergoing chemotherapy
  • Organ transplant patients on immunosuppressants
  • AIDS (primary predisposing factor)
123
Q

Pneumocystis (carinii) jirovecii

Presenting Manifestation of AIDS: (3)

A
  • Most common opportunistic infection in AIDS
  • Prophylaxis and HAART has reduced incidence
  • Occurs due to loss of T cell function (risk increases when T cell count below 200)
124
Q

Pneumocystis (carinii) jirovecii
Acute Pneumonia/Lethal Pneumonitis

Progressive, diffuse pneumonia after:
Concurrent infections:
Alveoli become filled with:

A

Progressive, diffuse pneumonia after:
➢ Corticosteroid use and leukemia
➢ AIDS onset (insidious onset; lesions outside of lung may also be seen)

Concurrent infections common (bacterial, fungal, parasitic, viral)

Alveoli become filled with desquamated cells, organisms, monocytes and fluid (foamy appearance)

125
Q

Pneumocystis (carinii) jirovecii
Clinical ID
Classification

Classified as a _____ based on morphology and drug susceptibility

Classified as a _____ based on rRNA sequence homology with other fungi

A

Classified as a protozoan based on morphology and drug susceptibility

Classified as a fungus based on rRNA sequence homology with other fungi

126
Q

Pneumocystis (carinii) jirovecii
Clinical ID

Sputum induced with:
What are more helpful?

A

Sputum induced with hypertonic saline (only usefully in AIDS patients because of larger number of organisms)

Brochoalveolar lavage and transbronchial biopsies more helpful

127
Q

Pneumocystis (carinii) jirovecii
Clinical ID

Histological:
1 other method of clinical ID:

A

Histological (Definitive):
• Extracellular cysts and trophs seen
• Latent infections characterized by scattered cysts in contact with alveolar cells

PCR

128
Q

Pneumocystis (carinii) jirovecii

Based on Symptoms: (5)

A
  • Mild or low grade fever
  • Typical signs of pneumonia absent (cough is non-productive)
  • Progressive dyspnea and tachypnea
  • Cyanosis and hypoxia
  • Death by asphyxiation

Micro Exam 3 (11 decks)

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