Haemophilus, Bordetella, Flashcards

(47 cards)

1
Q

Two main classes of H. I.

A

Encapsulated (type able)

Non-encapsulated (non-type able) refers to serotype testing

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2
Q

Ecapsulated H.i.

A

Respiratory tract infections
Bacterial meningitis, mainly in children and elderly

Before vaccine Hib was leading cause of bacterial meningitis
High death and complication rate

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3
Q

Unencapsulated H.i.

A

Respiratory infections
Ear aches
Disseminated disease in comprimised indv

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4
Q

H.i Capsule

A

Made from carbohydrates

Type B most important,

Contributes to VIRULENCE (allows to get to meninges)

  • antiphagocytic
  • prevents complement binding
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5
Q

H.i. Epidemiology

A

Reservoir in nasopharynx of human only

75% indv carry H.i.

Opportunistic

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6
Q

Hib Disease Course

A

Acquired through aerosol
Nasopharyngitis and otitis media

  • > baceteremia -> meningitis
  • > epiglottitis
  • > joint infection
  • > cellulitis
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7
Q

Hib Pathogenisis

A

No known exotoxins, (maybe IgA protease)

Adhesins

Endotoxins (LPS)

  • initially covered by capsule, camouflage
  • bacteria takes host choline and puts on LPS, more camouflage
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8
Q

Hib immunity

A

Passive immunity in very young
-maternally acquired

Active immunity in the absence of vaccine

  • at about 3-4 years
  • usually induced by asymptomatic infections
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9
Q

Hib vaccine

A

Conjugate capsular vaccine

carbohydrates linked to increase effectivity

Recent inc in non Hib Hi infections, vaccinated indv may have reduced protection against other strains?

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10
Q

Hib treatment

A

Different antibiotics dependent on specific disease

Low mortality if caught early

Steroid use reduces damage to inflammation

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11
Q

Unencapsulated Hi (NTHi) targets

A

Restricted to resp tract and ear

  • nasopharynx
  • otitis
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12
Q

NTHi in adults

A

Usually occurs in pts with underlying respiratory problem

Needs predisposing factors

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13
Q

NTHi virulence

A

Adhesins

Both intra and extracellular
-keep in mind for treatment

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14
Q

NTHi immunity

A

No vaccine

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15
Q

Treatment of NTHi

A

Antibiotics (mainly amoxicillin)

Hard to fight biofilms

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16
Q

H.i diagnosis (growth and metabolism)

A

Facultative anaerobe

No fermentation pattern

Fragile, easily killed?

Not grow on blood agar

Fastidious, needs lots of growth factors (x and v)

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17
Q

Bordetella Pertussis

A

Small Gram-negative coccobacillus

Obligate aero be

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18
Q

BP disease course

A

Transmission aerosol droplets

Stage 1 mild respiratory symptoms

Stage 2 narrowed glottis and cough attacks
-infants have small airways and died of hypoxia

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19
Q

BP Infection Steps

A
  1.  Introduction via water droplets
  2. Interactions with ciliated epithelial cells in the trachea and nasopharynx
  3. Adherence
  4. Local multiplication (no dissemination)
  5. Toxin production
  6. Evasion of host defenses (stops beating cilia)
  7. Transmission
20
Q

BP virulence

A
  1. Pertussis toxin
  2. Adenylate cyclase toxin
  3. Dermonecrotic toxin
  4. Tracheal cytotoxin
  5. LPS
21
Q

Pertussis Toxin

A

Leads to increased level of cAMP

-> inc insulin, sensitization of histamine,

22
Q

Dermonectrotic toxin

A

causes local necrosis and inflammation

Through actin polymerization

23
Q

Tracheal cytotoxin (TCT)

A

Peptidoglycan fragment
Kills tracheal epithelial cell
Ciliostasis (reduces clearance)

24
Q

BP virulence summary

A

Ciliary stasis

Adhesins

Toxins

25
BP vaccine
Subunit/component vaccine More effective than old whole cell vaccine (and less side effects)
26
DP diagnosis
``` Classic cough –  Isolation of the organism –  Lymphocytosis (increased lymphocytes in blood) –  History of contacts ```
27
Detection
PCR (only for b pertussis)
28
Treatment of BP
Therapeutic (like oxygen) Antibiotics
29
Corynebacterium
Pleomorphic Gram positive rods (non spore forming) Aerobes
30
Corynebacterium diptheriae
Human only host 2-5 day incubation Local inflammatory response skin or sore throat and fever Pseudo membrane and bull neck (swollen Lymph nodes)
31
Diptheria toxin (general)
Cells localized but toxin becomes systemic Lethal to eukaryotic cells -Heart, kidney, nervous system most susceptible Blocks protein synthesis
32
Diagnosis and treatment of CD
Need special media (forms metachromatic granules) Detect toxin: PCR (or Elek test) Antitoxin available from CDC Antibiotic therapy
33
Dip immunization
Depends on immunity (ab) to TOXIN Led to vaccine that uses toxin
34
Legionella pneumophila
Gram negative rod | Pleomorphic
35
Leg epidemiology
Grows wherever water found (can live in amoebae) -can forms biofilms, difficult to remove Air ventilation system, water towers, etc
36
Legi symptoms
Atypical pneumonia | -diffuse localization in lung
37
Legi Disease
Disseminated, systemic disease
38
Legi pathogenicity
Airborne transmission (not person to person) Usually presents as "cold" Summer and early fall (more air conditioning)
39
Legi targets
Macrophages and alveolar cells Induces apoptosis
40
Legi diagnosis
(Fastidious, grown on charcoal yeast) Direct fluorescent ab test in sputum usual method Antigens in urine
41
Legi prevention
Proper water handling High temp, chlorine, cleanings
42
Mycoplasma (general)
Infects upper respiratory tract Smallest bacterium and smallest genome NO PEPTIDOGLYCAN CELL WALL ->Pleomorphic
43
Mycoplasma survival strategy
Variable lipoproteins and lipid anchors stabilize Increases cell membrane rigidity (by incorporating cholesterol)
44
Mycoplasma epidemiology
"Walking pneumonia" Possibly up to 50% of summer pneumonias -frequency varies by year Outbreaks in close contact groups Hits adolescents and college kids
45
Mycoplasma symptoms
Atypical pneumonia - diffuse throughout lung - doesn't respond to Penicilin Weakness, fever, cough
46
Mycoplasma Diagnosis
Clinical picture PCR detection Cold agglutination test (present in half pts)
47
Haemophilus influenzae general characteristics
Small, gram-negative, pleomorphic, non-motile