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MHD 1 > L27 Pseudomonas and Other Gram Negative Rods > Flashcards

L27 Pseudomonas and Other Gram Negative Rods Flashcards

1
Q

What are the key characteristics of glucose non-fermenting gram-negative bacilli?

A
  1. Gram-negative
  2. Non-spore-forming
  3. Rods or coccobacilli
  4. Obligate aerobes
  5. Good growth seen in 24 hours
  6. Glucose not fermented
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2
Q

What is the natural habitat of glucose non-fermenting gram-negative bacilli?

A

Water, soil, plants, moist areas, hospital environment

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3
Q

Pseudomonas aeruginosa is an aerobic Gram ___ ___ (shape).

A

Negative; rod

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4
Q

What are the major virulence factors of P. aeruginosa?

A
  1. Motility with polar flagella
  2. Mucoid polysaccharide slime layer
  3. Pili on the cell surface
  4. LPS
  5. Pyocyanin
  6. Exotoxin A
  7. Exoenzyme S
  8. Elastase
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5
Q

What factors pre-dispose patients to serious infection with P. aeruginosa?

A
  1. Burn patients
  2. CF patients
  3. Patients with hematologic malignancies
  4. Immunocompromised patients
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6
Q

True or false - P. aeruginosa can be part of the microbial flora in hospitalized patients and ambulatory, immunocompromised hosts.

A

True

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7
Q

What skin infections are caused by pseudomonas?

A
  1. Burn wounds
  2. Folliculitis
  3. Nail infections
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8
Q

What pulmonary infections are caused by/associated with pseudomonas?

A
  1. Asymptomatic colonization
  2. CF and chronic lung disease
  3. Severe necrotizing bronchopneumonia
  4. Ventilator associated pneumonia (VAP)
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9
Q

What is the most common cause of VAP?

A

Pseudomonas

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10
Q

What other infections are caused by Pseudomonas?

A

UTI, ear infections (swimmer’s ear, malignant external otitis, chronic otitis media), eye infections, bacteremia with ecthyma gangrenosum, endocarditis, osteomyelitis

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11
Q

What is ecthyma gangrenosum?

A

A well-recognized but uncommon cutaneous infection most often associated with a P. aeruginosa bacteremia; usually occurs in patients who are critically ill and immunocompromised. It is almost always a sign of pseudomonal sepsis. q

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12
Q

What are the symptoms of bacteremia with ecthyma gangrenosum?

A

Characteristic hemorrhagic pustules or infarcted-appearing areas with surrounding erythema that evolve quickly into necrotic ulcers surrounded by erythema

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13
Q

What are the structural virulence factors of P. aeruginosa?

A
  1. Capsule
  2. Pili
  3. LPS
  4. Pyocyanin
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14
Q

How does exotoxin A function?

A

Exotoxin A blocks protein synthesis and contributes to dermatonecrosis in wounds and tissue damage in lungs

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15
Q

How does exoenzyme S function?

A

Exoenzyme S is an ADP-ribosylating toxin that causes epithelial damage, which facilitates bacterial spread, tissue invasion, and necrosis

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16
Q

How does elastase (Las A and Las B) function?

A

Causes tissue destruction and hemorrhagic lesions by degrading elastin and complement components, and inhibiting neutrophil chemotaxis and function

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17
Q

Describe growth of P. aeruginosa.

A

Grows on blood and MacConkey agar, producing spreading colonies with a metallic sheen. It is temperature tolerant and grows at 42 degrees Celcius.

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18
Q

What are some ID aspects of P. aeruginosa?

A
  1. Glucose non-fermenter
  2. Oxidase positive
  3. Grape-like odor
  4. Produces pyocyanin
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19
Q

How are Pseudomonas infections treated?

A

They are resistant to many common antibiotics used for Gram negative infections due to changes in porins. Combination therapy of cell wall active agent + aminoglycosides are needed for serious systemic infection.

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20
Q

What is the habitat of Burkholderia pseudomallei?

A

Soil, water, and vegetation of Southeast Asia

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21
Q

What disease does Burkholderia pseudomallei cause?

A

Melioidosis

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22
Q

B. pseudomallei is a category B ___.

A

Biothreat agent

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23
Q

What are the three types of melioidosis?

A
  1. Acute disease: septicemia with metastatic lesions
  2. Subacute disease: most common; TB-like disease with cellultis and lymphangitis
  3. Chronic disease: localized chronic cellultis
24
Q

How is chronic melioidosis treated?

A

Treat with antibiotics before draining to avoid bacteremia

25
Q

What is the habitat of B. cepacia?

A

Water sources, wet surfaces, detergent solutions

26
Q

What diseases are caused by B. cepacia?

A
  1. Respiratory tract infections (60% isolated from these)
  2. Problematic in patients with CF and CGD
  3. UTIs
  4. Septicemia
27
Q

What is the most common autosomal recessive genetic disease in Caucasians?

28
Q

What causes CF?

A

A mutation in the CFTR gene (CF transmembrane conductance regulator); this gene regulates components of sweat, digestive juices, and mucus

29
Q

How is CF inherited?

A

Autosomal recessive

30
Q

Mutation in CFTR results in defects in innate immunity, including…

A

…decreased NO levels, failure to internalize bacteria in bronchial epithelial cells, increased inflammation of CF airway, and abnormal electrolyte transport, which causes thick, dry, sticky mucus.

31
Q

Abnormal mucus adversely effects mucocilliary clearance and provides and ideal ___ for chronic lung infection.

32
Q

Over 85% of premature deaths in CF are due to…

A

…cardiopulmonary failure secondary to chronic lung infection

33
Q

What is the median life expectancy in US patients with CF?

34
Q

What are pulmonary exacerbations?

A

Cellular defects resulting in thickened viscous mucus layer in the respiratory tract and impaired innate immunity.

35
Q

When does pulmonary exacerbation occur?

A

When there is impaired mucociliary transport and chronic infection with a number of bacterial species

36
Q

What characterizes pulmonary exacerbation?

A

Recruitment of neutrophils, cytokine release, and high level of neutrophil derived elastases causing significant lung pathology

37
Q

Which pathogens are known to cause infection in CF/chronic lung disease?

A
  1. S. aureus
  2. P. aeruginosa
  3. B. cepacia complex
38
Q

What infections are caused by Stenotophomonas maltophilia?

A

Bacteremia, pneumonia, meningitis, wound infections, UTIs

39
Q

What is the habitat of Stenotrophomonas maltophilia?

A

Worldwide distribution, soil, water, animals, vegetation, crops; not park of normal flora but can be recovered from almost any clinical site

40
Q

From which clinical site is Stenotrophomonas maltophilia recovered most frequently?

A

Respiratory tract (60%)

41
Q

> 95% of all clinical infections caused by S. maltophilia are ___.

A

Hospital-acquired

42
Q

S. maltophilia is the second leading cause of ___.

A

Gram-negative non-fermentive bacillary infections.

43
Q

What is the hallmark of S. maltophilia disease?

A

Life-threatening systemic infections in debilitated patients (usually with cancer)

44
Q

Describe the lab features of S. maltophilia.

A

Good growth on BAP and MacConkey, oxidase negative, some strains have yellow pigment

45
Q

How is S. maltophilia treated?

A

This bacteria is very INHERENTLY resistant to beta-lactams, including imipenem and aminoglycosides. The drug of choice is trimethoprim-sulfamethoxazole (SXT).

46
Q

What is the habitat of E. meningoseptica?

A

Soil, water, plants, food-stuffs, may exist in water systems and wet surfaces

47
Q

Nosocomial outbreaks of E. meningoseptica are often traced to ___.

A

Breast pumps used in hospital nurseries

48
Q

E. meningoseptica is associated with neonatal ___.

A

Meningitis

49
Q

What are the lab features of E. meningoseptica?

A
  1. Oxidase positive
  2. Pale yellow pigment on BAP
  3. Poor growth on MacConkey
50
Q

How is E. meningoseptica treated?

A

Very INHERENTLY resistant to beta lactam agents and aminoglycosides; current methods are unreliable

51
Q

What is the habitat of A. baumannii?

A

Free living in water and soil, isolated foods, hospital air, inanimate objects, human sources

52
Q

What is the most common gram-negative organism carried on the skin of hospital personnel?

A

A. baumannii

53
Q

What diseases does A. baumannii cause?

A

Implicated in community acquired and nosocomial infections

54
Q

___ colonizes 45% of inpatient tracheostomy patients.

A

A. baumanii

55
Q

What are the lab features of A. baumannii?

A
  1. Coccobacilli
  2. Good growth on BAP and MacConkey
  3. Oxidase negative
  4. Non-motile
56
Q

How are A. baumannii treated?

A

Imipenem or merepenem, fluroquinolone + amikacin or ceftazidime, ampicillin-sulbactam, colistin

MHD 1 (58 decks)

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