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Pulmonary > Bacteria > Flashcards

Bacteria Flashcards

1
Q

Two ways bacteria can survive in the phagosome?

A
  • preventing fusion of lysosome

- inhibiting acidification of the phagolysosome (lysosomal enzymes are active at low pH)

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2
Q

How do polysaccharide capsules prevent phagocytosis?

A

binds serum factor H and accelerates the breakdown of C3b (opsonin)

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3
Q

Organism with unprogrammed antigenic variation?

A

Influenza A drifts and shifts

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4
Q

Organism with programmed antigenic variation?

A

Haemophilus influenza

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5
Q

How do A-B exotoxins work?

A
  • binding subunit binds to cell membrane
  • whole toxin is endocytosed
  • active subunit dissociates and leaves endosome to ADP-ribosylate cellular enzymes, disrupting cell function
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6
Q

How do membrane active exotoxins damage cells? Three organisms that use these exotoxins?

A
  • binds, inserts, and forms a pore
  • cytoplasmic content spills out and water comes in
  • death by osmotic lysis
  • S. aureus, GAS, B. pertussis
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7
Q

What are the effects of super antigen exotoxins? Two organisms?

A
  • toxins elaborated at site of infection go into blood stream
  • bind MHC II on APC’s without processing
  • results in polyclonal stimulation of T cells with massive cytokine release (IL-1, TNF, monocyte stimulation)
  • S. aureus, GAS
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8
Q

How does hydrolytic enzyme hyaluronidase facilitate bacterial invasion of tissues?

A
  • lyses hyaluronan to lower viscosity of ECM
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9
Q

How do endotoxins differ from exotoxins?

A
  • ex’s are secreted by bacteria

- endotoxins are part of the bacterium itself

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10
Q

What is the common gram negative endotoxin and what does it do during sepsis?

A
  • LPS

- Lipid A component stimulates the excessive release of IL-1 and TNF producing fever and shock

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11
Q

Three organisms that cause atypical acute CAP?

A
  • mycoplasma pneumoniae
  • Chlamydophila pneumonia
  • Coxiella burnetii (Q fever)
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12
Q

Organism of Q fever?

A

Coxiella burnetii

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13
Q

Three organisms of pneumonia in neonates 0-3 months?

A

BIRTH CANAL ORGS

  • GBS
  • enteric gram negative rods
  • HSV
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14
Q

When does Moraxella catarrhalis become a cause of pneumonia in children?

A
  • 1-5 years

- acquires with age as a normal upper airway organism

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15
Q

What adults most often acquire acute CAP? 7 underlying diseases/co-morbidities that are RF”s?

A
  • mid 50’s to late 60’s
  • year round (peak in midwinter to early spring)
  • COPD, CVD, neurologic disorders, DM, EtOH, IC, tobacco
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16
Q

5 patient types who get aspiration pneumonia? What causes damage in this type of pneumonia?

A
  • suppressed gag and swallow reflexes: neuro impaired, tube fed, dementia, EtOH, anesthesia
  • acid from stomach induces release of pro-inflamm cytokines
  • neutrophils recruited to the lung mediate much of the damage seen
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17
Q

What organisms are seen in aspiration CAP and HAP?

A
  • mixed cultures
  • endogenous mouth flora (S. pneumonia, H. inf) in CAP
  • GNR (60%, enterobacter), S. aureus (13-40%) in HAP
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18
Q

Why do anaerobes appear in half of aspiration pneumonia cases?

A

facultative aerobes in mixed culture take up all of the oxygen which allows anaerobes to come in

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19
Q

What is the second leading hospital acquired infection and leading cause of infection-related death in hospitalized patients?

A

nosocomial pneumonia - quality and safety indicator for hospitals

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20
Q

How does acute pneumonia present clinically?

A
  • sudden onset of chill, fever/sweats, pleuritic chest pain, productive cough (mucopurulent)
  • tachypnea, tachycardia, rales, B-like symptoms
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21
Q

What cultures are collected in pneumonia cases?

A
  • 2 sets of blood cultures drawn from two sites (nearly 90% sensitive in 24 hours)
  • 1 aerobic bottle and 1 anaerobic bottle for each site
  • sputum culture
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22
Q

What two organisms can be detected with a rapid urinary antigen test? TAT?

A
  • Strep pneumo
  • Legionella
  • 15 min TAT
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23
Q

How is an inadequate sputum specimen defined?

A

reject sputum sample if greater than or equal to 10 squamous epithelial cells per LPF (implies spit - not from LRT)

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24
Q

Uses of blood agar plate?

A
  • non-selective

- detection of hemolysis (alpha, beta, gamma)

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25
Q

Selection and differential of MacConkey Agar Plate?

A
  • selective for non-fastidious GNR

- pink colonies ferment lactose

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26
Q

Uses of the chocolate agar plate?

A
  • non-selective, non-differential

- enriched medium for fastidious organisms like Haemophilus

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27
Q

MALDI-tof TAT?

A

10 min = Matrix Assisted Laser Desorption Ionization time of flight mass spec (Bruker score >2 is a good ID)

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28
Q

How does E-test Strip susceptibility testing work?

A
  • plastic strip embedded with a linear gradient of a single drug and planted onto a lawn of organism
  • 24 hours
  • used to find Mean Inhibitory Concentration of drug
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29
Q

What population of pathogens is tested for by routine cultures?

A

routine aerobic bacteria (not viruses, fungi, myco, anaerobes, fastidious orgs)

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30
Q

What are the best testing options for viral respiratory infectious disease?

A
  • Influenza A/B/RSV PCR (batch tested daily during flu season)
  • PCR battery with lots of viruses
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31
Q

Why are respiratory viral cultures not often used?

A
  • expensive
  • 21 day TAT
  • not as sensitive as PCR
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32
Q

What is the leading cause of bacterial CAP? Where does it come from and who gets infected?

A
  • Strep pneumoniae = pneumococcal pneumonia
  • organism aspirated from flora = 5-20% carrier state
  • extremes of age; >50 at greatest death risk
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33
Q

How does Strep pneumo pneumonia manifest?

A
  • lobar pneumonia

- rusty/bloody sputa

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34
Q

What common cause of bacterial CAP is not reliably ID’d by MALDI-tof?

A

Strep pneumo

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35
Q

Hemolysis, catalase, and optochin of Strep pneumo culture? Gram stain?

A
  • alpha, cat negative, inhibited by optochin
  • dimpled colonies due to autolysin presence
  • gram + diplococci (lancet shaped)
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36
Q

Diagnosis of Strep pneumo?

A
  • urinary antigen

- blood cultures only + in 50%

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37
Q

Source and presentations of H. influenza?

A
  • nasopharynx (20-80%)
  • post-viral respiratory infections are common
  • descending laryngotracheobronchitis –> lobar pneumonia
  • similar to Strep pneumo
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38
Q

Differences in H. influenzae invasive disease worldwide vs. developed countries?

A
  • Type b strains cause 90% of invasive disease peaking in age 2-5
  • non-Hib causes most invasive disease; all ages (Hib vaccine)
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39
Q

Four virulence factors of Strep pneumo?

A
  • choline binding protein (attachment, factor H)
  • capsule blocks C3b
  • autolysin
  • pneumolysin released on bacterial death (pores in respiratory epithelium directly breaks down mucosal barrier = sepsis, directly affects phagocytes)
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40
Q

In addition to pili, OMP, and capsule, what determines serotypes of H. influenzae? How does it invade?

A
  • capsular polysaccharide antigens (associated with virulence, Hib is most virulent)
  • between respiratory epithelial cells
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41
Q

Gram stain of H. influenzae? What makes it unique?

A
  • GNR

- PLEOMORPHIC – coccibacillary

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42
Q

What does H. influenza grow on?

A
  • fastidious
  • grows on chocolate in CO2 – requires both hemin and NAD (factors X and V) in RBC’s
  • may be seen satelliting around beta hemolytic colonies
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43
Q

H. influenza catalase, oxidase, MALDI-tof?

A
  • cat negative
  • ox +
  • reliable (also E test)
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44
Q

Common presentation of S. aureus pneumonia? What percent of pneumonias? Where is it found?

A
  • acute lobar pneumonia with abscess formation
  • 2-5%
  • 10-30% skin/nares colonization
  • IVDU w/ endocarditis, post-Inf A, iatrogenic infections
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45
Q

S. aureus gram stain? Hemolysis, catalase, and coagulase?

A
  • gram + cocci in clusters

- beta, cat +, coag + opaque cream rapidly growing colonies

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46
Q

Four S. aureus surface proteins?

A
  • clumping factor = mediates cell binding to fibrinogen
  • coagulase = conversion of fibrinogen to fibrin and binding of org to fibrin
  • fibronectin binding proteins
  • protein A = binds Fc of IgG
47
Q

Two S. aureus extracellular enzymes?

A
  • alpha toxin = cytolytic, pore-forming toxin

- superantigen toxins = TSS

48
Q

Where is Moraxella catarrhalis found? Who is colonized?

A
  • normal flora of oropharynx

- most children > COPD (2-10%) > normal adults (1-5%)

49
Q

Four presentations of Moraxella catarrhalis in children?

A
  • otitis media
  • acute sinusitis
  • bronchitis
  • pneumonia
50
Q

Second most common cause of COPD exacerbation in older adults?

A
  • Moraxella catarrhalis
  • 2-10% colonized
  • bronchitis and pneumonia
51
Q

Two common co-infections of Moraxella catarrhalis?

A

Strep pneumo and H. inf

52
Q

Two gram stain morphologies of Moraxella catarrhalis? What does it look similar to?

A
  • GN diplococci
  • GN coccobacilli
  • Neisseria
53
Q

Hemolysis of Moraxella? How is it distinguished from Neisseria?

A
  • gamma

- + butyrate esterase activity (spot test)

54
Q

Presentation of Legionnaire’s?

A
  • multilobar pneumonia with headache, fever, chills, dry cough, chest pain
  • males
  • very high fever
  • rapid progression (necrosis) with respiratory failure and shock within 3-6 days
55
Q

Prognosis of Legionnaire’s? How is it acquired?

A
  • 15-50% death rate

- environmental water resources (water features, shower heads, cooling towers)

56
Q

Causative organism in Legionnaire’s?

A

Legionella pneumophila

57
Q

What type of pathogen is Legionella pneumophila? Pathogenesis?

A
  • facultative intracellular pathogen
  • endocytic invasion and prevention of phagolysosome fusion
  • extracts iron from transferrin
  • inhibits oxidative killing activities of macro’s
58
Q

How does Legionella cause damage to host tissues?

A
  • facultative intracellular
  • produces pore-forming toxin that lyses the monocyte releasing the bacteria and monocyte-derived enzymes that damage tissues
59
Q

What makes gram stain diagnosis of Legionella difficult?

A

faintly staining thin GNR so it is often missed on gram stain

60
Q

Why is culture of Legionella no longer standard of care? What is SOC?

A
  • fastidious, BYCE agar only (no blood), 2-5 days to produce colonies, low sensitivity, weakly cat and ox +
  • PCR of respiratory specimen is GOLD standard (serogroup 1)
  • urinary antigen (serogroup 1 reliably, others inconsistently)
61
Q

How does GAS Strep pyogenes pulmonary disease present in normally healthy people?

A

lobar pneumonia and TSS

62
Q

How does strep toxic shock present?

A
  • begins at site of any GAS infection
  • starts with myalgia, fever/chills, severe pain
  • progression with NVD
  • ends with hypotension, shock and organ failure including renal impairment
  • sepsis seen in over half
63
Q

What percent of GAS produces super antigen toxin?

A

10%

64
Q

GAS-specific binding protein? Toxin?

A
  • M protein = binds fibrinogen, factor H, Ig

- Streptolysin O = pore-forming toxin that lyses WBC’s

65
Q

Three enzymes produced by GAS?

A
  • streptokinase = lyses fibrin
  • C5a peptidase (C5a attracts phagocytes)
  • Hyaluronidase - degrades ECM (dec viscosity)
66
Q

How does streptolysin O cause damage?

A

pore-forming toxin that lyses WBC

67
Q

Hemolysis, catalase, and colony morphology of GAS pyogenes?

A
  • beta (hemolysin O and S)
  • catalase neg
  • small, grey colonies
68
Q

Two ways to definitively ID Strep pyogenes?

A
  • Lancefield grouping latex reagent

- MALDI-tof

69
Q

Gram stain morphology of S. pyogenes?

A
  • GPC in CHAINS
70
Q

What underlying diseases are often associated with GNR pneumonias? What organism causes half of GNR pneumonias? How are the infections acquired?

A
  • COPD, CF, neutropenia
  • P. aeruginosa
  • aspiration
71
Q

What environments are P. aeruginosa found it?

A
  • water/soil associated

- usual respiratory flora in 2-10% of healthy peopl

72
Q

What 4 P. aeruginosa virulence factors mediate adherence to host cells?

A
  • LPS
  • pili
  • alginate
  • flagellum
73
Q

Two exotoxins produced by P. aeruginosa? Functions?

A
  • breakdown of respiratory epithelium
  • A = inhibits eukaryotic elongation factor preventing protein synthesis and resulting in cell death
  • S = acts on G proteins to disrupt the cell’s cytoskeleton, signaling pathways and induces apoptotic death?
74
Q

What does P. aeruginosa exotoxin A do?

A
  • inhibits eukaryotic EF preventing protein synthesis and resulting in cell death
75
Q

What does P. aeruginosa exotoxin S do?

A
  • acts on G proteins to disrupt cytoskeleton, signaling pathways
  • induces apoptotic death
76
Q

Two enzymes produced by P. aeruginosa that aid in tissue damage and dissemination?

A

elastase and phospholipase

77
Q

How does PA in CF cause serious problems?

A

mucoid slime alginate production is switched on by quorum sensing mechanisms in biofilms that form in CF patients (makes culture plates slimy)

78
Q

P. aeruginosa gram stain morphology?

A

slender GNR

79
Q

Hemolysis and oxidase of P. aeruginosa?

A
  • metallic sheen with beta

- oxidase positive

80
Q

What type of pulmonary disease is associated with enterobacteriaceae?

A

lobar pnemonia in at-risk populations (EtOH, aspiration, hospitalized patients - aspiration and ventilation)

81
Q

Where is enterobacteriaceae found in the human body?

A
  • usual gut flora

- upper airway of hospitalized patients

82
Q

Four common enterobacteriaceae?

A
  • E. coli, Klebsiella pneumoniae, serratia marcescens, enterobacter
83
Q

Three ways enterobacteriaceae cause damage?

A
  • LPS endotoxin
  • alpha hemolysin - pore-forming toxin = cell death
  • cytotoxic necrotizing factors that disrupt cellular signaling
84
Q

Four culture characteristics of enterobacteriaceae?

A
  • rapid growing facultative anaerobes
  • ferment Glc
  • reduce nitrate to nitrite
  • oxidase negative
85
Q

Gram stain morphology of enterobacteriaceae?

A
  • GNR

- some are encapsulated and some may chain

86
Q

Why is it important to do aerobic and anaerobic blood cultures for enterobacteriaceae?

A

anaerobic bottles will be positive 12 or more hours earlier than aerobic bottles in facultative anaerobes

87
Q

Which Burkholderia species is associated with worse outcomes in CF?

A

cenocepacia

88
Q

What is cepacia syndrome? Who is it seen in?

A
  • severe progressive respiratory failure and sepsis in CF patients
  • associated with higher mortality and decrease in pulmonary function following infection
89
Q

What are two virulence factors of B. cepacia?

A
  • cable pilus - mediates binding to respiratory mucus and epithelial cells
  • BCESM = epidemic strain marker associated with increased virulence in patients with CF
90
Q

What virulence factor of B. cepacia is associated with increased virulence in CF patients?

A

B. cepacia epidemic strain marker

91
Q

Gram stain morphology of B. cepacia?

A

GNR

92
Q

Media, oxidase, and catalase of B. cepacia?

A
  • selective OFPBL media that starts off producing yellow colonies that turn media green
  • ox +
  • cat +
93
Q

How does atypical pneumonia caused by Mycoplasma pneumonia present?

A
  • mild tracheobronchitis
  • sore throat, fever, malaise, headache, cough w/ scanty sputum, few/scattered rales
  • CXR unilateral scattered areas of pneumonia
94
Q

What is the disease course of mycoplasma pneumonia? How many patients are asymptomatic?

A
  • protracted with conversion from upper to lower respiratory symptoms over a 10 day period, may persist for several weeks
  • 1/3 are asymptomatic
95
Q

Who gets mycoplasma pneumonia? When?

A
  • children and adolescents 5-15 years, but may be sen in older patients
  • severity increases with age
  • 10% of CAP
  • epidemics in enclosed populations
  • year round occurrence with increased cases in late summer/fall
96
Q

What makes M. pneumonia detection difficult?

A

no cell wall so it’s hard to detect immunologically (no targets) - also NO gram stain

97
Q

How does M. pneumonia affect mucosa?

A

desquamation

98
Q

What is the virulence strategy of M. pneumonia?

A
  • bind and hid
  • adhesion via cytadhesin P1 interacting with sialic acids on the bronchial cell surface
  • interferes with ciliary action
99
Q

What is the gold standard for diagnosis of M. pneumonia?

A

PCR - difficult to grow, requires cholesterol, ferments Glc, liquid culture make take 4 weeks, binds guinea pig RBC

100
Q

Pulmonary presentations of Chlamydophila pneumonia?

A
  • sore throat, cough that may persist for weeks/months, sinusitis
  • majority of cases are asymptomatic or mildly symptomatic
101
Q

Why is serology useless in Chlamydophila pneumonia?

A
  • > 50% of adults have positive serologies

- conversion takes weeks and there is cross reactivity with other chlamydia

102
Q

Which atypical pneumonia organism is associated with 10% of CAP and 5% of bronchitis?

A

Chlamydophila pneumoniae

103
Q

What kind of organism is Chlamydophila pneumonia?

A
  • obligate intracellular PARASITE
  • infectious phase is elementary body (spore) and replication occurs via conversion to reticulate body followed by host cell lysis
104
Q

Gold standard of Chlamydophila pneumonia Dx?

A

PCR

105
Q

Three stages of Bordetella pertussis infection?

A
  • catarrhal
  • paroxysmal
  • convalescent
106
Q

What is the most infectious B. pertussis stage and how does it present?

A

Catarrhal - profuse, mucoid rhinorrhea, fever, anorexia, and sneezing for 1-2 weeks = BAD COLD

107
Q

What is the lab finding associated with the paroxysmal stage of B. pertussis?

A

HUGE LYMPHOCYTOSIS

108
Q

How does the paroxysmal stage of B. pertussis present?

A
  • persistent paroxysmal cough up to 50 times daily for 2-4 weeks
  • cough caused by inspiratory whoop and vomiting
109
Q

Who is the most vulnerable population in B. pertussis infection?

A

70% death rate in children <1 year of age

110
Q

How does disease present in vaccinated patients?

A

incomplete vaccination and waning immunity produces variable disease

111
Q

How does B. pertussis cause most of its damage?

A

TOXINS

112
Q

Three toxins from B. pertussis?

A
  • A-B toxin that ADP-ribosylates a G protein that prevents inactivation of adenylate cyclase –> lymphocytosis, insulinemia, histamine sensitization
  • pore-forming adenylate cyclase
  • tracheal cytotoxin that causes direct toxicity to ciliated cellls
113
Q

Gram stain morphology of B. pertussis?

A

tiny, GN coccobacillus (like Haemophilus) - fastidious, slow growth

114
Q

Gold standard for B. pertussis diagnosis?

A

PCR

Pulmonary (7 decks)

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