HRR: gram negative rods Flashcards

1
Q

What are the three species of Bordetella that infect humans?

A
  1. Pertussis: causes whooping cough
  2. Parapertussis: milder pertussis-like illness
  3. Bronchiseptica: kennel cough in canines and sometimes chronic respiratory tract infection in humans
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2
Q

What are some clinical manifestations of Bordetella pertussis?

A

Black eyes, whooping cough, dehydration, exhaustion

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3
Q

Describe culture of Bordetella pertussis.

A

It requires a special medium and grows slow; antibiotics are needed. It is too late to culture once the cough starts as the bacteria is usually cleared.

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4
Q

Describe the 3 stages of Bordetella pertussis.

A
  1. Catarrhal: 1-2 weeks and causes fever, malaise, profuse rhinorrhea
  2. Paroxysmal: 2-4 weeks and causes coughing, lymphocytosis, and whoop (audible gasps for breath)
  3. Convalescent: symptoms fade
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5
Q

Describe clinical presentation of Bordetella.

A

Bacteremia does not occur. Infants have a high mortality rate. Adult disease is atypical. Bacterial replication is localized to respiratory epithelium. Can cause rib fracture.

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6
Q

What are the virulence factors of B. pertussis?

A

Adhesins (pili and FHA) and exotoxins (pertussis toxin, AC, and TCT)

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7
Q

Describe the pathogenesis of B. pertussis.

A
  1. It adheres to cilia via FHA
  2. PT and pore-forming AC injure cells
  3. TCT damages ciliated epithelium
  4. PT absorbed into bloodstream and causes immune dysregulation
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8
Q

Describe PT toxin.

A

An AB toxin that ADP-ribosylates G proteins that regulate adenylate cyclase; the effect is tissue specific.

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9
Q

What are systemic effects of PT and AC?

A

Lymphocytosis, inactivation of neutrophils/macrophages/lymphocytes, histamine sensitization, insulin secretion

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10
Q

How do we prevent B. pertussis?

A

Acellular pertussis vaccines DTaP and Tdap booster

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11
Q

What can be found in Tdap boosters?

A

Inactivated PT, FHA, and other virulence factors

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12
Q

What are the two human pathogens of Haemophilus?

A

H. influenza and H. ducreyi

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13
Q

What do the Haemophilus require for growth?

A

H. influenza requires hematin and NAD, while H. ducreyi only needs hematin. Blood must be lysed for them to get these.

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14
Q

How is H. influenza typed?

A

If they are encapsulated, they are typed by antibodies specific for the capsular material.

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15
Q

What is the worst strain of H. influenzae? What is the capsule made of?

A

Type B; polyribitol phosphate

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16
Q

What are some common characteristics of encapsulated and non-encapsulated H. influenzae that help cause disease?

A

Adhesins (pili and outer membrane proteins) and endotoxins (LOS and LPS)

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17
Q

What are the virulence factors of Haemophilus?

A

Attachment via pili and HMWs and anti-phagocytic capsules if they are encapsulated. This allows them to enter the bloodstream.

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18
Q

What are clinical manifestations of encapsulated H. influenza?

A

Cellulitis, purulent meningitis, acute epiglottis, pneumonia and septic arthritis, bacteremia

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19
Q

What are clinical manifestations of non-encapsulated H. influenza?

A

Chronic sinusitis, otitis media, chronic bronchitis, pneumonia

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20
Q

How does H. influenzae spread?

A

Through respiratory droplets; only spread person to person.

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21
Q

Describe immunity to H. influenzae.

A

At 0-6 months you’re protected by maternal antibodies. 6-18 months there is a lack of T-independent immune response. Over 18 months there is increasing immunity.

22
Q

What confers protection against H. influenzae?

A

Anti-PRP antibodies

23
Q

How do we diagnose H. influenzae?

A

Clinical presentation, gram stain, growth on chocolate agar.

24
Q

How do we treat H. influenzae?

A

Empiric therapy, beta lactams with beta lactamase inhibition, rifampin prophylaxis.

25
Q

Describe H. ducreyi.

A

It is an STI that causes soft and painful ulcers. You can be infected over and over again, and the ulcers increase HIV transmission.

26
Q

Describe the growth of Pseudomonas.

A

Very minimal growth requirements; can grow in wide temperature range, is salt tolerant, grows readily on common media, and is hemolytic on blood agar.

27
Q

Describe Pseudomonas.

A

Motile, pale-staining, aerobic gram-negative rod.

28
Q

What is the relation between Pseudomonas and lactose?

A

It fails to ferment it.

29
Q

What are distinctive features of Pseudomonas aeruginosa?

A

Colorful water-soluble pigment, strong odor, oxidase positive, and mucoid colonies.

30
Q

What are infection sites for Pseudomonas?

A

Eyes, ears, burns, wounds, catheters (UTI), and in cystic fibrosis.

31
Q

What are the virulence factors of Pseudomonas aeruginosa?

A
  1. LPS
  2. Pili
  3. Flagella
  4. Slime made of secretion of alginate polymer
  5. Exotoxin A that inactivates EF2
  6. Elastase that cleaves elastin, IgA/G, and complement components
  7. Exotoxin S that acts on protein G to affect the cytoskeleton and induce apoptosis.
32
Q

What injection system does exotoxin S use?

A

Type III.

33
Q

What does elastase do?

A

Disrupts blood vessels and lung structures.

34
Q

Which species survives in tap water?

A

Pseudomonas aeruginosa.

35
Q

What are modes of transmission of Pseudomonas aeruginosa?

A

Sinks, nebulizers, humidifiers, contact lens solution, pools.

36
Q

What is the most significant pathogen in cystic fibrosis patients?

A

Pseudomonas aeruginosa.

37
Q

What are clinical presentations of Pseudomonas aeruginosa?

A

Infections of burns and wounds, pneumonia with necrosis/infarct/vascular invasion, otitis externa, folliculitis, eye infection.

38
Q

What temperature does Pseudomonas grow at?

A

42 Celsius.

39
Q

How do we diagnose Pseudomonas?

A

Growth at 42 degrees on almost any media showing pigment production and positive oxidase.

40
Q

How do we treat Pseudomonas aeruginosa?

A

It is pretty resistant to antibiotics, and the only effective agents are given IV. CF patients can be given cipro and aztreonam.

41
Q

Which gram-negative species do not ferment lactose?

A

Pseudomonas and Burkholderia.

42
Q

What are the virulence factors of Burkholderia?

A

Elastase, adhesins, and LPS.

43
Q

Describe Burkholderia cepacia.

A

An opportunistic pathogen found in aquatic environments that colonizes in CF patients and causes rapidly fatal cepacia syndrome with respiratory distress and septicemia.

44
Q

How is Burkholderia cepacia transmitted?

A

Contaminated IV solutions, nebulizers, disinfectant, urinary catheters.

45
Q

How do we treat Burkholderia?

A

It is resistant to many antibiotics, so TMP-SMX is first line.

46
Q

Where do we find Burkholderia pseudomallei?

A

Southeast Asia and aquatic environments.

47
Q

How is Burkholderia transmitted?

A

Inhaled, ingested, traumatic inoculation.

48
Q

What is the clinical presentation of Burkholderia pseudomallei?

A

Melliodosis, acute pneumonia, cutaneous melliodosis.

49
Q

What population might we see Burkholderia pseudomallei in?

A

Vietnam veterans.

50
Q

Describe Burkholderia mallei.

A

Causes glanders in horses and sometimes humans; presents with ulcerative lesions in nasal mucosa and lung nodules.