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microb - bacteria > Gram Negative Rods - Pseudomonads & Vibrio > Flashcards

Gram Negative Rods - Pseudomonads & Vibrio Flashcards

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
Q

Virulence factors of V. parahaemolyticus

A

Secretes enterotoxin, invasive, primarily affects colon

26
Q

Clinical presentations of V. parahaemolyticus

A

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
Q

Diagnosis of V. parahaemolyticus

A

Culture stools

28
Q

Treatment of V. parahaemolyticus

A
  • usually self limiting

- antibiotics do not alter clinical course

29
Q

Transmission of V. vulnificus

A
  1. Contaminated seafood

2. Contact between sea water & wounds (found in salt water environments)

30
Q

Clinical presentations of V. vulnificus (2)

A
  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
Q

Treatment of V. vulnificus

A
  1. Aggressive surgical wound debridement

2. Combinations of doxycycline/ceftazidine/ciprofloxacin

microb - bacteria (11 decks)

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