Gram Negative Rods - Pseudomonads & Vibrio Flashcards

(31 cards)

1
Q

Features of pseudomonads

A
  1. Mostly found in the environment

2. Not normal flora

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2
Q

Examples of pseudomonads

A
  1. Pseudomonas aeruginosa (PAE)
  2. Stenotrophomonas maltophilia
  3. Burkholderia spp
    - Burkholderia cepacia
    - Burkholderia pseudomallei
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3
Q

Features of PAE

A
  1. Oxidase positive
  2. Non-lactose & non-glucose fermenter
  3. Motile
  4. Aerobic growth
  5. Produce diffusible pigments (commonly green)
  6. Found in moist conditions
  7. Important cause of opportunistic infections (hospitalised & immunocompromised, on antibiotics, community acquired eg contact lenses, spa baths)
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4
Q

Virulence factors of PAE

A
  1. Produces slime/biofilm, allows adherence to implants/lines
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5
Q

Clinical presentations of PAE (10)

A

Hospital acquired

  • infects areas with abnormal stasis of body fluids, exposed wounds or penetrated by poorly maintained instruments/fluids
    1. UTI - related to catheterisation, instrumentation, surgery, residual bladder urine, common after multiple recurrent inf
    2. Pneumonia - diffuse bronchopneumonia or rapidly progressing multi-focal necrotising pulmonary lesions (& bacteremia) esp in cystic fibrosis patients
    3. Septicaemia - esp in neutropenic patients, classically assoc w ecthyma gangrenosum (small skin nodules that hemorrhage, necrose, ulcerate)
    4. GI infection - necrotising enterocolitis, esp in young infants & neutropenic cancer patients, 2 to gut colonisation
    5. SSTI - hemorrhage, necrosis, esp in burns/wounds
    6. Bone & joint infections, meningitis, endocarditis

Community acquired

  1. Ear infections - malignant otitis externa (spreads to face, neck, bone - req systemic treatment), chronic suppurative otitis meda, esp in elderly diabetes
  2. Eye infections - keratitis (corneal ulcer - penetrates/perforates cornea - panophthalmitis), due to contaminated contact lens fluids, ocular medications, minor eye trauma
  3. Skin infections - jacuzzi/whirlpool rash (folliculitis)
  4. Nail infections
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6
Q

Diagnosis of PAE

A
  1. Biochemical tests

2. Mass spectroscopy

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7
Q

Treatment of PAE (4)

A
  1. Piperacillin
  2. Carbapenems, 3G cephalosporins, aminoglycosides, quinolones
  3. HAI usually MDR - check antibiotic sensitivities
  4. Severe infection, neutropenia - use 2 antibiotics eg ceftazidime + gentamicin
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8
Q

Prevention of PAE

A
  1. Prophylactic ciprofloxacin for neutropenic patients, also prevents septicaemia
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9
Q

Treatment of stenotrophomonas maltophilia

A
  • nosocomial pathogen, less common than PAE, MDR
  • produces carbapenemases - resistant to carbapenems
    1. Co-trimoxazole, levofloxacin
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10
Q

Features of burkholderia cepacia

A
  • rare in healthy people, usually after prolonged antimicrobial therapy or in cystic fibrosis patients
  • causes serious & terminal lung infections - poor drainage of respiratory secretions leads to repeated infections & antibiotics that select for resistant organisms
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11
Q

Epidemiology & transmission of burkholderia pseudomallei

A
  • endemic in SEA & northern australia
  • found in soil & surface waters (esp rainy season)
  • immunocompromised eg diabetics & exposure to soil, water eg rice farmers are at risk
  1. Inhalation & contamination of skin abrasions
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12
Q

Clinical presentations of burkholderia pseudomallei (3)

A
  • some show no early signs, but are latently infected & reactive later on (20-80% subclinical)

Melioidosis

  1. Pneumonia - CXR w upp lobe disease with cavitation
  2. Abscesses - acute/chronic
  3. Septicemia
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13
Q

Diagnosis of burkholderia pseudomallei (2)

A
  1. Culture - characteristic wrinkled colonies

2. Serology - test for antibodies/observe rise in antibody titre

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14
Q

Treatment of burkholderia pseudomallei (3)

A
  1. Ceftazidime/Imipenem (at least 2 weeks IV)
  2. Drain abscesses
  3. Oral maintenance ≥ 6 months (combination therapy eg doxycycline) - prolonged due to risk of relapse
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15
Q

Examples of vibrio

A
  1. Vibrio cholerae
  2. Vibrio parahaemolyticus
  3. Vibrio vulnificus
  4. Vibrio alginolyticus
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16
Q

Features of V. cholerae

A
  1. Oxidase positive

2. Sucrose fermenter - produces yellow colonies on TCBS agar

17
Q

Transmission of V. cholerae

A

Faecal-oral

- esp in disasters when sewage contaminate drinking water, LDCs

18
Q

Virulence factors of V. cholerae (3)

A
  1. Cholera toxin
    - A subunit crosse membrane, activates adenylate cyclase - cAMP - inhibits active absorption of electrolytes & osmotic reabsorption of water by enterocytes - increases anion extrusion & decreases Na/H2O uptake + increases Na outflow & H2O secretion - vast fluid loss – causes diarrheal disease
    - B subunit binds to ganglioside receptors on enterocyte membrane – immunogenic
  2. Motility - non flagellated cells are less virulent
  3. Adherence - strains without pili are non virulent
19
Q

Clinical presentations of V. cholerae

A

Cholera

  1. Profuse watery diarrhea
    - rice water stools with fish odour
    - no abdominal pain & fever, sometimes vomiting
    - results in severe dehydration, can cause death <1 day
    - epidemic strains are serotype 01 & 0139, the other non-epidemic strains are usually less severe
20
Q

Diagnosis of V. cholerae

A
  1. Culture on selective medium (thiosulphate-citrate-bile salts-sucrose agar - TCBS) - characteristic short curved rod with single polar flagellum - rapid motility
21
Q

Treatment of V. cholerae (2)

A
  1. Rehydration
    - ORS - replaces fluid & electrolytes
    - severe cases need IV fluids (potassium, bicarbonate & strict monitoring)
  2. Ciprofloxacin/tetracycline
    - reduce period of pathogen excretion & severity of diarrhea
22
Q

Prevention of V. cholerae

A
  1. Vaccine
    - against serotype 01 (inactivated V. cholerae 01 + B subunit of cholera toxin)
    - none against type 0139
23
Q

Features of V. parahaemolyticus

A
  1. Non sucrose fermenter - green colonies on TCBS agar
24
Q

Transmission of V. parahaemolyticus

A

Contaminated seafood (raw/undercooked shellfish) - thrives in salt water environments

25
Virulence factors of V. parahaemolyticus
Secretes enterotoxin, invasive, primarily affects colon
26
Clinical presentations of V. parahaemolyticus
Food poisoning 1. Acute onset explosive watery diarrhea/frank dysentery-like syndrome - seldom causes severe fluid loss/significant intestinal tissue damage - associated with cramping abdominal pain, low grade fever
27
Diagnosis of V. parahaemolyticus
Culture stools
28
Treatment of V. parahaemolyticus
- usually self limiting | - antibiotics do not alter clinical course
29
Transmission of V. vulnificus
1. Contaminated seafood | 2. Contact between sea water & wounds (found in salt water environments)
30
Clinical presentations of V. vulnificus (2)
1. Food poisoning (ingestion of contaminated seafood) - self-limiting diarrhea - immunocompromised: acute septicaemia w high fever, hypotension, 50% mortality, multiple erythematous skin lesions (turn hemorrhagic, necrotic then ulcerating) - high risk in elderly males with alcoholic liver damage 2. Wound infections - cellulitis with edema, erythema & life threatening necrosis - V. alginolyticus - cellulitis & otitis externa (assoc w seawater exposure)
31
Treatment of V. vulnificus
1. Aggressive surgical wound debridement | 2. Combinations of doxycycline/ceftazidine/ciprofloxacin