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2. HDS Pulmonary > Upper Respiratory Treact Infections > Flashcards

Upper Respiratory Treact Infections Flashcards

1
Q

Upper Respiratory Tract

A
  • Nose
  • Pharynx
  • Paranasal sinuses
  • Middle ear
  • Larynx
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2
Q

URT

Normal Flora

A

Primarily coagulase-⊖ Staph and diphtheroids.

Colonization with Pneumococci, S. aureus, Moraxella, Haemophilus frequently present.

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3
Q

URT

Sterile Sites

A

Sinuses

Middle ear

Larynx

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4
Q

URT

Infections

A
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5
Q

Pharyngitis

A

Acute inflammation of the throat ⇒ pain on swallowing and a red, swollen phryngeal mucosa.

  • 50-75% caused by viruses and Group A Strep
    • Adenovirus 25%
    • Rhinoviruses 20%
    • Group A Strep 15-30%
  • Peak incidence is 3-18 y/o
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6
Q

Otitis Media

A

Acute inflammation of the middle ear with fever and local pain.

  • Purulent fluid accumulates behind a tense, red TM
  • May discharge externally after TM rupture
  • Common in children < 3 y/o
    • Most get 2-3/yr
  • Frequently follows URT infection
  • Most commonly caused by:
    • Strep. pneumoniae
    • Non-typable strains of Haemophilus influenzae
    • Moraxella catarrhalis
  • Treatment problematic d/t inc. abx resistance
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7
Q

Otitis Media

Risk Factors

A
  • Eustacian tube flatter and more narrow in children
  • URT can trap fluids ⇒ colonization by normal flora
  • Feeding tilts child into position where tube is flatter & more connected to OP ⇒ fluid can back up
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8
Q

Otitis Media

Treatment

A
  • ⅔ improve within 24 hours without abx
    • 80% within 2-5 days
  • Advise use of OTC pain relievers, anesthetic drops
  • Wait 24 hours before giving abx
    • 24 months or older
    • Otherwise healthy
    • Mild sx or unclear dx
  • Offer observation in 6-24 month olds
  • Pathogens can cause meningitis ⇒ must monitor
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9
Q

Otitis Media

Bacterial Pathogens

A
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10
Q

Moraxella

Overview

A
  • Moraxella catarrhalis ⇒ most important
  • Related to Neisseriae
  • Gram ⊖ diplococcus
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11
Q

Moraxella

Transmission

A
  • Transmitted by respiratory secretions
  • Transient carriage/colonization normally
  • Colonization of URT in 40-50% of school children
  • Endogenous infection
    • Usually precipitated by URT infection
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12
Q

Moraxella

Clinical Syndromes

A
  • 3rd highest cause of otitis media and sinusitis
  • Also causes bronchitis, PNA, and conjunctivitis
    • Esp. the elderly, immunocompromised, or those with chronic pulmonary disease
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13
Q

Moraxella

Diagnosis

A
  • Small, coffee-bean shaped gram ⊖ diplococci
    • Likes to lie side by side
  • Strict aerobe
  • Oxidase ⊕
  • Does not ferment carbs
    • Unlike Neisseriae
  • Grows well on blood agar
  • Prefers chocolate agar
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14
Q

Moraxella

Treatment

A

~100% of strains are beta-lactamase producers

PCN resistant

Usually treat with cephalosporins

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15
Q

Haemophilus influenzae

Characteristics

A
  • Small, gram ⊖ rods (cocco-bacillus)
  • Complex nutritional requirements
    • X factor ⇒ hematin
    • V factor ⇒ NAD or NADP
  • Grows well on chocolate agar
  • Grows poorly on blood agar
    • Small satellite colonies grow around colonies of S. aureus or other factor V excreting organisms ⇒ satellite phenomenon
  • ± polysaccharide capsules
  • Classified based on capsule type ⇒ typable vs non-typable
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16
Q

H. influenzae

Typable Strains

A
  • Encapsulated ⇒ Types a-f
    • Typed based on antisera rxn to capsular polysaccharide
    • HiB most invasive
    • HiF incidence increasing
  • Exogenous transmission
  • Colonization uncommon
    • ~5% of children
    • < 0.5% of adults
  • 1° pathogens ⇒ meningitis, bacteremia, epiglottitis
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17
Q

H. influenzae

Non-Typable Strains

A
  • Non-encapsulated
  • Colonize 60-90% of children, 30-50% of adults
  • Endogenous transmission
  • Opportunistic ⇒ otitis media, sinusitis, pharyngitis, PNA
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18
Q

H. influenzae

Transmission & Epidemiology

A
  • Transmitted by respiratory secretions
  • Severe disease 1° in children 6-18 m/o and the elderly
    • Ab levels lowest
    • PRP polysaccharide is a T-cell independent Ag
    • B-cell response to PRP poor under 18 m/o
  • Systemic spread only typical for encapsulated strains
    • Esp. HiB
  • Bacteremia can lead to infection of CNS, bones, and joints
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19
Q

H. influenzae

Virulence Factors

A
  • Polysaccharide capsule
    • Antiphagocytic
    • Blocks complement activation
  • IgA protease
    • Avoids immune response at mucosal surface
  • Outer membrane proteins
    • Attachment and adherence
  • Endotoxin
    • Gram ⊖
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20
Q

H. influenzae

Type B

A
  • Most invasive strain
  • Causes 90% of all H. influenzae infections
  • Virulence due to unique polyribose-ribitol phosphate (PRP) capsule
    • Contains pentose sugar
    • ⊗ Phagocytosis
    • ⊗ Alternative complement activation
    • ⊗ Ciliary function
    • Damages respiratory epithelium
    • Penetrates epithelial and endothelial walls ⇒ dissemination
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21
Q

H. influenzae

Clinical Syndromes

A
  • # 2 cause of otitis media and sinusitis
  • Epiglottitis
    • HiB only
  • PNA
    • Prominent in pts w/ underlying lung disease or debilitating conditions like malnutrition, lung CA, alcoholism
  • Bacteremia
    • Mostly encapsulated strains only
  • Meningitis
    • HiB only
    • Usually follows URT infection
    • Most common in unimmunized children 5 m/o-5 y/o
    • More cases before vaccine available
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22
Q

Acute Epiglottitis

A
  • Caused by HiB only
  • Inflammed, swollen, cherry-red epiglottis
    • Protrudes and obstructs airway
  • Fever, sore throat, hoarseness, barking cough
  • Can result in death due to suffocation if untreated
  • Children < 6 y/o most at risk d/t smaller airways
  • Local invasion ⇒ bacteremia ⇒ epiglottis
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23
Q

H. influenzae

Lab Diagnosis

A
  • Fastidious
  • Specimen from NP swab, pus, blood, or CSF for smears and culture
  • Grows on chocolate agar or BAP with X factor (hematin/hemin) and V factor (NAD)
    • Does not grow on normal blood agar
  • PRP capsular Ag of HiB released into body fluids
    • Antigen detection methods ⇒ latex agglutination
24
Q

H. influenzae

Immunity

A
  • Passive protection by maternal Ab
    • No episodes until after 6 m/o
  • Opsonizing anti-capsular Ab
    • Capsule-type specific
    • Enhance phagocytosis by PMNs
    • Bacteriolytic in presence of complement
  • Active acquired Ab gradually increases up to ~ 10 y/o
25
Q

H. influenzae

Treatment

A
  • Ampicillin for 5-10 days
  • Some are beta-lactamase producers
    • ~ 25% of HiB
    • Higher % of unencapsulated strains
    • Varies with region
    • Via transmissible plasmid
  • Newer cephalosporins are drugs of choice
    • Ceftriaxone, cefotaxime
26
Q

H. influenzae

Prevention

A
  • Vaccine composed of PRP + diphteria CRM197 protein
  • Immunization of infants at 2, 4, and 6 m/o
  • Greatly ↓ invasive disease esp. meningitis in young children
27
Q

Bordetella

A
  • Cause infection of human tracheobronchial epithelium
  • Bordetella pertussis most important
    • Causes Pertussis aka “Whooping cough”
28
Q

Pertussis

Epidemiology

A

“Whooping Cough”

  • 30 mil cases and 300k deaths per year worldwide
  • 21k cases and 7 deaths in US in 2016
29
Q

Bordetella pertussis

Characteristics

A
  • Gram ⊖ coccobacilli
  • Strict aerobe
  • Extracellular organism
  • Fastidious and slow growing ⇒ takes 3-7 days
  • Requires specialized media
    • Charcoal blood agar
    • Bordet-Gengou agar (blood-potato-glycerol)
  • Solely a human pathogen
30
Q

B. pertussis

Transmission & Epidemiology

A
  • Exogenous transmission via respiratory secretions
  • Highly communicable
    • Attack rate 90% in susceptible individuals
  • Survives briefly outside of human respiratory tract
  • Infection most common in children < 1 y/o & preterm infants
  • Esp. dangerous during first 6 months of life
31
Q

B. pertussis

Virulence Factors

A
  • Adhesins ⇒ pili proteins that mediate attachment to ciliated epithelium
    1. Filamentous hemagglutinin (Fha)
    2. Agglutinogens
  • Toxins ⇒ cause cell and tissue damage
    1. Pertussis Toxin (PT)
      • Major virulence factor
    2. Invasive adenylate cyclase
      • Enters host cell and ↑ cAMP levels
      • Hemolytic
      • Interferes with chemotaxis and superoxide production of PMNs
    3. Tracheal cytotoxin
    4. Hemolysin
    5. Dermonecrotic heat-labile toxin
32
Q

Pertussis Toxin

(PT)

A

Major virulence factor

  • ADPR-transferase
  • Classic A-B type exotoxin
    • A subunit (active) ⇒ transfers ADP-ribose from NAD to G protein that regulates adenylate cyclase activity
      • Host cell cannot turn off cAMP production
      • Cell loses control of ion flow and cellular processes
    • B subunit (binding) ⇒ mediate attachment to carb moieties on host cell surface
      • Translocates A subunit across the membrane
  • Biological effects depend on cell type
    • Histamine sensitization
    • Lymphocytosis
    • ↑ Mucus production
    • Insulin secretion ⇒ hypoglycemia
    • Alteration of immune effector cell functions
      • ↓ Oxidative killing capacity
33
Q

B. pertussis

Pathogenesis

A

Organism remains in the URT.

Exotoxins move to LRT and throughout body.

34
Q

Pertussis

Clinical Stages

A

Colonization of ciliated bronchial epithelium ⇒ incubation for 7-10 days.

Immobilization and destruction of epithelial cells.

No tissue invasion or dissemination.

3 stages of disease:

  1. Catarrhal stage (1-2 weeks)
    • Malaise, fever, sneezing, anorexia
    • Profuse and mucoid rhinorrhea
    • Highly communicable with large # of organisms in NP and mucoid secretions
  2. Paroxysmal coughing stage (2-4 weeks)
    • 40-50 coughing episodes per day
    • Characteristic inspiratory whoop
      • Air drawn through narrowed glottis
    • Coughing and breathing disruption ⇒ child turns red or blue
    • May result in vomiting or choking on respiratory secretions
    • Lymphocytosis w/ 70-80% lymphocytes
  3. Convalescent stage (3-4 weeks)
    • Gradual fade of sx
    • At risk for secondary complications
35
Q

Pertussis

Complications

A

Usually limited to the URT.

Infrequent complications may include:

  • Bronchopneumonia
    • Either due to B. pertussis or superinfection
      • Staph, S. pneumoniae, H. influenzae
  • Acute encephalopathy
    • See convulsions resulting in death or permanent brain damage
36
Q

Pertussis

Adolescent/Adult Disease

A
  • Mild URT infection
  • Cough with vomiting
  • Cough persisting > 2 weeks
  • Whooping variable
  • Source of transmission to non or partially immune infants
37
Q

Pertussis

Lab Diagnosis

A
  • NP swab ⇒ must be dacron or calcium alginate
  • Culture during first 4 weeks of infection
  • Grown on charcoal blood agar (Bordet-Gengou medium)
  • Takes 3-7 days for final ID
  • PCR in conjunction with culture ⇒ becoming the standard
  • Direct Immunofluorescent Assay ⇒ can be performed on swab specimens
    • Sensitivity ~ 50%
    • Most useful in ID’ing B. pertussis after culture
  • Mainly a clinical dx
38
Q

Pertussis

Treatment

A
  • Macrolides
    • Effective during catarrhal phase
    • Preventative therapy
    • Erythromycin ⇒ drug of choice
  • Supportive therapy
    • Only option once paroxysmal phase reached
    • Manage paroxysms, apnea, cyanosis, feeding difficulties
39
Q

Pertussis

Immunity

A
  • Infection or immunization ⇒ protective immunity
    • Not life-long
    • sIgA prevent attachment
    • Ab’s that neutralize PT
  • Repeat infections are mild
40
Q

Pertussis

Prevention

A
  • 1st gen ⇒ heat-killed prep of whole organism
    • Post-vaccinal encephalopathies
  • 2nd gen ⇒ acellular vaccine
    • Pertussis toxoid + 2-4 other virulence factors
    • Diphtheria, Tetanus, acellular pertussis series (DTaP)
      • 5 doses ⇒ 2, 4, 6 m/o, 6 yr, 11-12 y/o
      • Booster during pregnancy @ 27-36 weeks ⇒ passive protection of infant
    • ↓ Neurologic complications
    • Cocooning infant ⇒ boost everyone in close proximity
41
Q

DTap vs Tdap

A

DTaP ⇒ initial and boosters in children

Tdap ⇒ boosters in adolescents and pregnant women

42
Q

Pertussis

Re-emergence

A
  • Immunity wanes over time
    • Adolescent/adults susceptible
      • Reservoir for transmission to infants
  • Many cases in infants prior to or because of delayed immunization
  • Need to boost mother otherwise no maternal passive immunity
  • Vaccine boosters recommended q10 years
43
Q

Corynebacterium

Overview

A
  • C. diphtheriae
    • Pathogenic & highly toxigenic
    • Causes Diphtheria
      • Vaccine preventable illness
      • Effects due to exotoxin
  • Diphtheroids ⇒ commensal organisms
    • C. ulcerans, C. xerosis, C. pseudodiphtericum
    • Normal flora of pharynx, nasopharynx, distal urethra, and skin
44
Q

C. diphtheriae

Characteristics

A
  • Small, pleomorphic club-shaped gram ⊕ rods
    • “Chinese letter” or palisade arrangements
  • Non-spore forming
  • Aerobic
  • ± metachromatic granules ⇒ stains bluish-purple w/ methylene blue
  • Grown on Tinsdale agar
    • Contains potassium tellurite
      • ⊗ normal flora
      • Reduced by C. diphtheriae to produce brown to black colonies
45
Q

C. diphtheriae

Transmission & Epidemiology

A
  • Respiratory droplet or direct skin contact
  • Only reservoir in humans
  • Maintained in population by asymptomatic carriage in oropharynx or skin of immune individual
  • Outbreaks in populations w/o immunization programs
    • Ex. End of Soviet Russia
46
Q

Diphtheria Toxin

(DT)

A

Most important virulence factor of C. diphtheriae

⊗ Protein synthesis ⇒ Cytotoxic effect

A-B type structure

  • B subunit ⇒ binds heparin binding EGF-receptor
    • Receptor mediated endocytosis
    • Facilitates translocation of A subunit into cytosol
    • Highly expressed on cardiac and neural tissue
  • A subunit ⇒ ADP-ribosylation of elongation factor-2 (EF-2)
    • Required for translocation of polypeptidyl-tRNA from A site during protein synthesis
47
Q

Diphtheria Toxin

Regulation

A
  • tox gene codes for DT
  • Carried by lysogenic or temperate β-phage
    • Lysogen required for disease
  • Lysogenic conversion ⇒ non-toxigenic to toxigenic upon phage infection
  • tox gene regulated by DtxR repressor + iron
    • Chromosomally encoded by C. diphtheriae
    • Low iron ⇒ tox gene de-repressed ⇒ DT made
    • Iron critical for virulence
48
Q

C. diphtheriae

Pathogenesis

49
Q

C. diphtheriae

Clinical Manifestations

A
  • Malaise, sore throat, fever
  • Gray-white pseudomembrane on tonsils, uvula, soft palate, or pharyngeal wall
    • Bleeds when scraped
    • May obstruct breathing & detach in young children ⇒ ± suffocation
  • Cervical lymphadenitis and edema ⇒ “bull-neck”
  • DT disseminates w/ varied sx
    • Cardiac ⇒ arryhthmias, myocarditis, CHF
    • Neuro ⇒ neuritis, diaphragm paralysis, coma
50
Q

Cutaneous Diphtheria

A

Infection of the skin w/ C. diphtheriae

Chronic skin ulcer with a dirty-gray membranous base

51
Q

Diphtheroid

Infection

A

Non-toxigenic strains cause non-diphtherial disease.

Mild pharyngitis

Endocarditis

Septicemia

Abscess

52
Q

C. diphtheriae

Lab Diagnosis

A
  • Swab pharynx
  • Culture on Tinsdale agar w/ potassium tellurite ⇒ grey/black colonies
  • Demonstrate toxin activity ⇒ Elek test or PCR
    • Immunodiffusion and tissue culture assays
  • No rapid tests ⇒ initial clinical dx and treatment
53
Q

Diphtheria

Treatment

A
  • Eliminate toxin producing bacteria
    • PCN or erythromycin
  • Neutralize toxin
    • Passive admin of equine anti-toxin
      • Heterologous anti-serum ⇒ risk of serum sickness (type III hypersensitivity)
54
Q

C. diphtheriae

Immunity

A

Largely dependent on presence of Ab that neutralize DT

55
Q

Diphtheria

Prevention

A

Active immunization with diphtheria toxoid

  • Prevents disease
  • Part of DPT series @ 2, 4, and 6 m/o
    • Diphteria, pertussis, tetanus (DTaP)
  • Boosters
    • Between 4-6 y/o
    • Before entering school
56
Q

Childhood Vaccine Schedule

A

24 immunizations in the first 18 months of life

2. HDS Pulmonary (28 decks)

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