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

Jackson: Upper Respiratory Tract Infections Flashcards

1
Q

Variety of organisms colonize oropharynx and upper respiratory tract:

A

Many commensals colonize upper respiratory tract

Respiratory tract is a continuum from sinuses to alveoli

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2
Q

Professional Invaders:

A

Professional Invaders: uniquely adapted to the upper respiratory tract; infect HEALTHY respiratory tract

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3
Q

Professional Invaders

Mechanisms:

A
  • Adhesion to mucosal surfaces
  • Interfere with cilia
  • Resist alveolar macrophages
  • Damage local tissues

.

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4
Q

Secondary Pathogens:

A

Secondary Pathogens: cause infection following initial insult; infect when host defenses impaired

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5
Q

Secondary Pathogens

Mechanisms: (5)

A
  • Primary viral infection
  • Impaired local defenses (ie. cystic fibrosis)
  • Chronic bronchitis due to tumor
  • Depressed immunity (AIDS)
  • Decreased resistance (age, alcoholism)
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6
Q

Oral Anaerobes

- Virulence Factors (Relevant to Oral Infection): (2)

A
  • Lymphocyte Activators: produces by oral bacteria; induce inflammatory response
  • Activate Complement/Release of PMN Contents: exacerbate tissue damage
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7
Q

Oral Anaerobes

Etiology:

A

o Autoinfections caused by normal flora
o Usually polymicrobic
o Anaerobes typically form localized absecesses

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8
Q

Oral Anaerobes
Chronic Marginal Gingivitis

Location:
Inflammatory Infiltrate:
Bacteria do NOT invade:
Timeline:

A

Chronic Marginal Gingivitis: between teeth and gums

Inflammatory Infiltrate: PMNs and lymphocytes enter CT attached to tooth

Bacteria do NOT invade: remain part of the plaque outside host defenses

Timeline: can occur in 2 weeks without proper tooth care

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9
Q

Oral Anaerobes
Periodontitis

Results from:
Bacterial invasion may occur:

A

Periodontitis: teeth and supporting tissue

  • Results from progressive gingivitis: resorption of bone around the neck of the tooth, loss of periodontal ligament and the entire tooth itself
  • Bacterial invasion may occur: although anaerobes still also found in dental plaque next to gingival tissues
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10
Q

Oral Anaerobes

Acute Necrotizing Ulcerative Gingivitis (Trench Mouth):

A
  • Ulceration of the gingiva: can lead to bone resorption and tooth loss
    • Bacterial invasion of oral epithelium occurs
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11
Q

Oral Anaerobes
Clinical ID

Diagnosis:
Mixed anaerobic infection not differentiated:
Abscesses may be sampled:

A

o Diagnosis: via symptoms
o Mixed anaerobic infection not differentiated: no specific designation of Gram reaction or morphology
o Abscesses may be sampled: must be cultured in anaerobic conditions; mostly G(-) rods and PMNs

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12
Q

Actinomyces israelii

Etiology:
Colonizes:
Endogenous infection only occurs upon :

A

Normal flora anaerobe:
• Colonizes mucosal surfaces (oropharynx to lower intestine)
• Endogenous infection only occurs upon penetration of epithelial barrier (low O2 tension)

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13
Q

Actinomyces israelii
Pathogenesis (Cervicofacial Area)

Follows:
Progression rate:
Inflammatory sinuses fill with:
Sinus extension or aspiration can lead to:

A

Follows mouth trauma (ie. tooth extraction):
• Slowly progressing disease
• Inflammatory sinuses fill with pus and bacteria from initial site of infection
• Sinus extension or aspiration can lead to thoracic actinomycosis

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14
Q

Actinomyces israelii
Staining/Culture of Pus

G+/-?
_________ diagnostic:
Poly vs monomicrobic:

A
  • G(+) filamentaous rod (looks like fungi)
  • Sulfur granules diagnostic (yellow granules composed of Actinomyces elements and tissue exudates)
  • Polymicrobic infection (also G(-) rods in the sinuses)
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15
Q

Actinomyces israelii
Culture Conditions

Aerobic?
Growth Rate:

A

o Culture Conditions:
• Anaerobic or microaerophilic conditions
• Slow growth (contaminating bacteria may overwhelm it)

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16
Q 
Viridans Streptococci
Virulence Factors (Relevant to Oral Infection):
A

Glucans: complex polysaccharides that permit attachment to teeth

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17
Q

Viridans Streptococci

Normal flora:

A

Normal flora: of oral and nasopharyngeal cavity (S. mutans associated with dental cavities)

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18
Q

Viridans Streptococci
May Cause:
Tooth extraction lead to:

A

o May Cause Subacute Bacterial Endocarditis:

• Tooth extraction lead to transient bacteremia and colonization of damaged heart valves

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19
Q

Viridans Streptococci

Shape/Stain:
Cat +/-?
Lancefield Group:

A

o Shape/Stain: G(+) cocci
o Biochemical:
• Catalase (-)
• No Lancefield group

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20
Q 
Candida albicans
Virulence Factors (Relevant to Oral Infection)

Adhesion:
Invasion:

A

Adhesion: mannoprotein binds fibronectin receptors

Invasion:
• Invasive hyphae (bind fibronectin, collagen and laminin)
• Proteases and elastases may also play a role

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21
Q

Candida albicans

Predisposing Factors to Candidiasis: (4)

A
  • Antimicrobial therapy (depresses competing bacterial flora)
  • Compromised immune system (leucopenia, corticosteroids, AIDS)
  • Disruption of mucosa (indwelling devices or cancer chemotherapy)
  • Diabetes (increased glucose and increased surface receptors)
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22
Q

If recurrent candidiasis consider:

A

If recurrent candidiasis: consider a T cell deficiency

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23
Q

Candida albicans

Stomatitis:
Oral Thrush:

A

Stomatitis: inflammation of the oral cavity
• Oral Thrush: multiple white cheesy plaques that are loosely adherent to the tongue or palate
• Inflammatory patches on esophagus

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24
Q

Candida albicans

Specimen Collection:

A

o Specimen Collection: scrapings of infected mucosa
• KOH or Gram stains (budding round yeast with hyphae)
• Germ tube formation speciates C.albicans

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25
Q

BACTERIA CAUSING EAR AND SINUS INFECTIONS: (2)

A
  • Streptococcus pneumoniae

* Haemophilus Influenzae

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26
Q 
Streptococcus pneumoniae
Virulence Factors (Relevant to Ear and Sinus Infection): (2)
A

Polysaccharide capsule

Cell Wall Techoic Acid and Peptidoglycan

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27
Q

Streptococcus pneumoniae
Polysaccharide capsule:
Anti-________ and prevents:
Anti-_____ Abs confer immunity

A

Polysaccharide capsule: primary virulence factor
• Anti-phagocytic and prevents complement deposition
• Anti-capsule Abs confer immunity

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28
Q

Streptococcus pneumoniae

Cell Wall Techoic Acid and Peptidoglycan:

A

Cell Wall Techoic Acid and Peptidoglycan: contribute to inflammation

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29
Q

Streptococcus pneumoniae

Predisposition for URTIs. Why?

A

Predisposition for URTIs: high nasopharynx carriage rate

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30
Q

Streptococcus pneumoniae

Predisposition for Acute Otitis Media with S.pneumo:

A

Viral infection or allergies; common in infants due to short/pliant Eustachian tubes (most common cause after 3 months old)

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31
Q

Streptococcus pneumoniae

Predisposition for Sinus Infection with S.pneumo:

A

Viral infection, allergies, or anatomical blockage

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32
Q

Streptococcus pneumoniae

Acute Otitis Media:

A

Acute Otitis Media: middle ear infection

• Eustachian tube inflammation due to bacteria entering middle ear from nasopharynx

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33
Q

Streptococcus pneumoniae

Sinus infection:

A

Sinus infection: a cause of both acute and chronic sinusitis in all ages

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34
Q

Streptococcus pneumoniae

Diagnosis:

A

Diagnosis: generally based on clinical exam
• Otitis media: swollen tympanic membrane (due to pus formation)
• Sinusitis: symptoms and radiography

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35
Q

Streptococcus pneumoniae

Needle Aspiration:

A

Needle Aspiration:
• Otitis media: pus behind tympanic membrane may be collected in difficult cases
• Sinusitis: sinus wall puncture or catheterization

36
Q

Streptococcus pneumoniae
Staining:
Biochemical:

A

Staining:
• G(+) lancet shaped diplococcic

Biochemical:
• No Lancefield grouping
• Optochin (P disk) sensitive

37
Q 
Haemophilus Influenzae
Virulence Factors (Relevant to Ear and Sinus Infection):
A

Polysaccharide capsule

IgA protease

Non-pilus adhesins: direct tissue tropism (to mucosal surfaces)

38
Q

Haemophilus Influenzae
Polysaccharide capsule: (3)
What serotype is most virulent?

A

Polysaccharide capsule: most important VF
• Antiphagocytic
• Undergoes antigenic variation
• Polyribitol phosphate (PRP) capsule with 6 (a-f); serotype b (Hib) is most virulent

39
Q

Haemophilus Influenzae

IgA protease:

A

IgA protease: facilitates colonization

40
Q

Haemophilus Influenzae

Non-pilus adhesins:

A

Non-pilus adhesins: direct tissue tropism (to mucosal surfaces)

41
Q

Haemophilus Influenzae

Normal flora where?
Most normal flora have:
Most causes of:

A

o Normal flora: high carriage rate in upper respiratory tract
• Most normal flora have no capsule (non-typable)
• Most causes of otitis media non-typable (not influenced by Hib vaccine)

42
Q

Haemophilus Influenzae

Predisposing Factors:

A

Predisposing Factors: viral infection, displacement of flora into sterile sits

43
Q

Haemophilus Influenzae
Otitis media/Sinusitis

Age:
If caused by Hib, can lead to:

A
  • Common cause in kids under 5

* If caused by Hib, can lead to meningitis

44
Q

Haemophilus Influenzae

Diagnosis:
Needle aspirate:
Staining/Shape:
Culture:

A

o Diagnosis: based on clinical exam
o Needle aspirate: in difficult/refractory cases
o Staining/Shape: G(-) coccobacillus
o Culture: fastidious; requires Hematin (X factor) and NAD (V factor) for growth
o Capsule serotyping

45
Q 
Streptococcus pyogenes
Virulence Factors (Relevant to Infections of the Pharynx):
A

o Extracellular factors facilitating immune invasion
o Factors facilitating colonization
o Exotoxins

46
Q

Streptococcus pyogenes
Extracellular factors facilitating immune invasion

M protein:
Protein G/IgG Binding Protein:
Hyaluronic Acid Capsule:

A

M protein: anti-phagocytic and anti-opsonic

  • 80 different serotypes of exposed amino terminus
  • Re-infection possible due to antigenic variation
  • Cross reactive M protein Abs can cause rheumatic heart disease

Protein G/IgG Binding Protein: binds Fc portion of Abs

Hyaluronic Acid Capsule: antiphagocytic

47
Q

Streptococcus pyogenes
Factors facilitating colonization

Protein F:
M Protein:

A

Protein F: binds nasopharyngeal epithelium (regulated by O2 levels)

M Protein: binding epidermis (impetigo)

48
Q

Streptococcus pyogenes

Exotoxins: (2)

A

SLO/SLS

Spe A-C

49
Q

Streptococcus pyogenes

Spe A-C:
SpeA:
Superantigens:

A

Spe A-C: Erythrogenic/Scarlet Fever Toxins

  • SpeA: only produced by a few lysogenized GAS
  • Superantigens: with sequence homology to Staph exotoxins
50
Q

Streptococcus pyogenes
Spe A-C

Induce cytokine release:
Toxic Shock Like Syndrome:

A
  • Induce cytokine release: fever and rash (Scarlet Fever), T cell stimulation and B cell depression, enhanced sensitivity to endotoxic shock
  • Toxic Shock Like Syndrome: in GAS bacteremia
51
Q

Streptococcus pyogenes
SLO/SLS:
_____-hemolysis on BAP:

A

SLO/SLS: oxygen labile and oxygen stable, respectively

- B-hemolysis on BAP; form large pores in cell membranes (lysis of leukocytes)

52
Q

Streptococcus pyogenes
Pharyngitis

Basics:
Transmission:

A

Basics: GAS most common bacterial cause (but usually caused by viruses)

Transmission: droplet spread person to person

53
Q

Streptococcus pyogenes
Pharyngitis
Treatment:

A

Treatment: prompt antimicrobial therapy required to prevent postreptococcal sequelae caused by natural development of type-specific immunity (cross reactive Abs)

54
Q

Streptococcus pyogenes
Scarlet Fever:
Cause:
Presentation:

A

Scarlet Fever: can occur simultaneously with pharyngitis
• Cause: pyrogenic exotoxins (Spe)
• Presentation: rash spreads from mouth and face to trunk and extremities; strawberry tongue

55
Q

Rheumatic Heart Disease (Poststreptococcal Sequelae)

Course:

A

Course: begins ~3 weeks after pharyngitis (does not follow skin infection)

56
Q

Rheumatic Heart Disease (Poststreptococcal Sequelae)
Symptoms

Systemic Sx:
Cardiac Sx:

A

Systemic Sx: fever, subcutaneous nodules, chorea (neurologic), migratory polyarthritis

Cardiac Sx: carditis, cardiac enlargement, murmurs, heart failure)

57
Q

Rheumatic Heart Disease (Poststreptococcal Sequelae)
Symptoms

Rheumatic Carditis:
Subacute bacterial endocarditis:

A

Rheumatic Carditis: Aschoff body present due to cell mediated response (lesion of lymphocytes and macrophages aggregated around fibrinoid deposits)

Subacute bacterial endocarditis: damage to heart valves due to formation of vegetations, which provide site for colonization during transient bacteremia

58
Q

Rheumatic Heart Disease (Poststreptococcal Sequelae)

Cause of Heart Damage:
Abs to:
Epitopes shared with:
Progressive heart damage can result from:

A

Cause of Heart Damage: anti-streptococcal Abs that cross react with cardiac tissue; SLO, Spe and streptokinase (toxins) may also contribute directly to cardiac damage

  • Abs to cell wall, cell membrane and M protein
  • Epitopes shared with cardiac sarcolemma membranes, smooth muscle cells, and valves
  • Progressive heart damage can result from recurrent attacks with new M types
59
Q

Acute Glomerulonephritis (Poststreptococcal Sequelae)

Course:
Symptoms:

A

Course: follows respiratory or skin infection (more commonly) with GAS (10 day latent period following infection

Symptoms: edema, HTN, proliferative lesion of glomeruli

60
Q

Acute Glomerulonephritis (Poststreptococcal Sequelae)

Cause:
Anti-M protein Abs react with:
What also contribute?

A

• Cause: Ab cross-reactivity and inflammatory response
➢ Anti-M protein Abs react with glomerular proteins (associated with a few M types found in nephrogenic strains)
➢ Deposition of Ag-Ab and complement complexes in glomeruli also contribute

61
Q

Streptococcus pyogenes
Throat swab of tonsils and pharynx

Culture:
Agglutination test:

A
  • Culture: on BAP for B-hemolysis (CO2 incubation)

* Agglutination test: identify Lancefield Group A (rapid)

62
Q

Streptococcus pyogenes

Other Contaminants:
Biochemical Tests:

A

• Other Contaminants: S.pneumo, S.aureus, N.meningitidis, H.influenzae
• Biochemical Tests:
- Catalase (-)
- Bacitracin sensitive

63
Q

Streptococcus pyogenes

What is seen in patients with rheumatic fever?

A

High titers of anti-SLO Abs: seen in patients with rheumatic fever

64
Q 
Corynebacterium diphtheriae
Virulence Factors (Relevant to Infections of the Pharynx):
A

o Diphtheria Toxin: only VF

65
Q

Corynebacterium diphtheriae
Diphtheria Toxin

Structure:
B subunit binds:
Holotoxin uptake by:
Reduction in vesicle releases:

A

Structure: AB toxin (single polypeptide with nicked chain between A and B subunits)

  • B subunit binds epidermal growth factor precursor on cell membrane
  • Holotoxin uptake by receptor mediated endocytosis
  • Reduction in vesicle releases A subunit (enzymatic)
66
Q

Corynebacterium diphtheriae
Diphtheria Toxin

Mechanism:
What is needed for translocation of ribosome along mRNA?

A

Mechanism: A subunit ADP-ribosylates elongation factor 2 of any eukaryotic cell
➢ EF2 is needed for translocation of ribosome along mRNA (halts translation)

67
Q

Corynebacterium diphtheriae
Diphtheria Toxin
Genetics of Toxin Synthesis

Tox gene is carried by:
Synthesis of the gene is negatively regulated by:

A

Tox gene is carried by bacterophages (β and ω)

Synthesis of the gene is negatively regulated by iron (free iron levels are low in human host → signals bacteria to turn on toxin production)

68
Q

Corynebacterium diphtheriae

Prevalence in US:
Only _______ strains produce DT
What can occur in vivo?

A

Very rare in the US: transients, migrant workers, those who refuse immunization

Only lysogenized strains produce DT: DT required for pathogenesis
• In vivo lysogenization can also occur to convert strain to toxin-producing form

69
Q

Corynebacterium diphtheriae
Transmission:
What can also transmit?

A

o Transmission: droplet spread or contact with cutaneous infection or fomite
• Asymptomatic carriers of toxinogenic strains can also transmit disease

70
Q

Corynebacterium diphtheriae

Bacterial Toxinosis with NO Invasion:
Manifestations due to DT-Mediated Cytotoxicity: (2)

A

o Bacterial Toxinosis with NO Invasion: DT is solely responsible for ALL pathogenesis

Manifestations due to DT-Mediated Cytotoxicity:
• Pseudomembrane formation: from oropharynx down to trachea (can cause suffocation)
• Systemic manifestations: can cause organ damage (DT attack of heart and CNS)

71
Q

Corynebacterium diphtheriae

Diagnosis:
Throat swab is difficult:
G+/-?
After division:

A

Diagnosis: based mostly on clinical symptoms

Throat swab is difficult: normal resident flora of many individuals
• G(+) club shaped rods
• Cells remain attached after division (“Chinese letters”)
• Culture of organism producing toxin

72
Q 
Bordetella pertussis (Whooping Cough)
Virulence Factors (Relevant to Respiratory Tract Infections): (4)
A

o Filamentous Hemagglutinin (FHA) and Pili
o Pertussis Toxin (Ptx)
o Invasive Adenylate Cyclase
o Regulation of Virulence Factors

73
Q

Bordetella pertussis (Whooping Cough)

Filamentous Hemagglutinin (FHA) and Pili:
Directs organism to:
Can agglutinate:

A

o Filamentous Hemagglutinin (FHA) and Pili: adhesin for binding to ciliated mucosal epithelial cells
• Directs organism to macrophages
• Can agglutinate RBCs

74
Q 
Bordetella pertussis (Whooping Cough)
Pertussis Toxin (Ptx)

Structure:

A

o Pertussis Toxin (Ptx) major virulence factors

• Structure: AB with 5 non-identical B subunits (binding) and 1 A subunit (enzymatic)

75
Q 
Bordetella pertussis (Whooping Cough)
Pertussis Toxin (Ptx)

Mechanism:
Cells unable to:
Increase in __________ leads to increase in ______

A

• Mechanism: ADP-ribosylates Gi protein (therefore Gs is never turned off)
➢ Cells unable to stop production of adenylate cyclase
➢ Increase in adenylate cyclase leads to increase in cAMP

76
Q 
Bordetella pertussis (Whooping Cough)
Pertussis Toxin (Ptx)

Increase in cAMP causes: (4)

A

o Histamine sensitization
o Promotion of lymphocytosis
o Insulin secretion
o Diminished oxidative killing by macrophages

77
Q

Bordetella pertussis (Whooping Cough)

Invasive Adenylate Cyclase:
Requires:
Net effect:

A

o Invasive Adenylate Cyclase: enters cells directly to stimulate cAMP production (also increases cAMP)
• Requires calmodulin (Ca binding protein) for activation
• Net effect: interference with chemotaxis and superoxide production by PMNs

78
Q 
Bordetella pertussis (Whooping Cough)
Regulation of Virulence Factors:
A

Regulation of Virulence Factors: occurs through a 2 component signal transduction system
• BvgS
• BvgA

79
Q

Bordetella pertussis (Whooping Cough)
Regulation of Virulence Factors
BvgS:

A

BvgS: transmembrane histidine kinase; body temperature or ion changes cause BvgS to phosphorylate BvgA

80
Q

Bordetella pertussis (Whooping Cough)
Regulation of Virulence Factors
BvgA:

A

• BvgA: cytoplasmic response regulator; transcriptional activator of over 20 unlinked genes

81
Q 
Bordetella pertussis (Whooping Cough)
Temporal (Timed) Control of VF Expression:
A

Pili and FHA turned on first (adherence to ciliated epithelium)

Ptx and Invasive AC turned on later (cytotoxicity)

82
Q

Bordetella pertussis (Whooping Cough)
Disease often seen in:
Only infects:

A
  • Disease often seen in infants and preschoolers

* Only infects human respiratory tract

83
Q 
Bordetella pertussis (Whooping Cough)
Transmission:
A

Transmission: HIGHLY contagious (droplet spread)
• Even immunized patients may have mild symptoms
• Adult pertussis epidemics occur often (adults develop long-term dry cough for up to 3 mo)
• Adult carriers can be a source of infection for unvaccinated newborns

84
Q

Bordetella pertussis (Whooping Cough)
Whooping Cough:
May also cause:

A

o Whooping Cough: an acute bronchitis (prolonged disease with paroxysmal/violent cough)
• May also cause edema and hemorrhages in the brain

85
Q 
Bordetella pertussis (Whooping Cough)
Mechanism of Disease

PHA directs organism to:
Toxins kill:
Systemic effects are due to:
What leads to cough?

A
  • PHA directs organism to adhere to bronchial epithelium
  • Toxins kill ciliated cells and interfere with phagocytosis
  • Systemic effects are due to toxin, NOT bacteria
  • Local inflammatory response to bacteria in bronchi leads to cough
86
Q 
Bordetella pertussis (Whooping Cough)
Deep nasopharyngeal cultures:
A
  • Needs to be cultured immediately (does not survived well)
  • Grown on charcoal blood agar + cephalosporins (to inhibit G positives)
  • Slow growth (3-7 days)
87
Q

Bordetella pertussis (Whooping Cough)

Stain/Shape:
Direct fluorescent Ab detection:

A

G(-) coccobacillus (resembles Haemophilus)

Direct fluorescent Ab detection: should still also be confirmed by culture

Micro Exam 3 (11 decks)

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