Opportunistic Infections Flashcards

1
Q

What are the frequently encountered opportunistic pathogens?

A
E coli
Staph aureus
Klebsiella pneumoniae
Enterococcus spp
Pseudomonas aeruginosa
Enterobacter spp
Serratia spp
Proteus spp
C. difficile
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2
Q

Which frequently encountered opportunistic pathogens cause nosocomial epidemics?

A
Staph aureus
Klebs pneumo
Enterococcus spp
Pseduomonas aeruginosa
Enterobacter spp
Serratia spp
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3
Q

What local host factors contribute to opportunistic infection?

A
Anatomical defects
Surgical and other wounds
Burns
Catheterisation (bladder, IV)
foreign bodies (sutures etc.)
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4
Q

Opportunistic infections are especially important to recognize because

A

They are a sign that something else is wrong with the patient - always ask WHY the patient has this infection

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5
Q

T/F Sutures reduce the chance of infection

A

False; the presence of a foreign body including sutures increases the chance of infection

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6
Q

Why do foreign bodies predispose to opportunistic infection?

A

They can provide a haven from the immune system for bacteria eg injecting medical students with S aureus and talc - the ability to hide in the talc made the S aureus more pathogenic

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7
Q

T/F Burns are commonly associated with Pseudomonas infection

A

False; previously Pseudomonas infections were more common; now we see more Staph and other bacteria

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8
Q

Catheters are a source of opportunistic infection because

A

they bypass normal host defenses

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9
Q

What systemic host factors contribute to opportunistic infection?

A
Extremes of age
Leucopenia
Malignancy
Malnutrition
Diabetes
Liver disease
Certain infections (HIV, measles)
Tx with antimicrobials (C. diff)
1' congenital immunodeficiency
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10
Q

Leucopenia as a predisposing factor for opportunistic infection is commonly seen in

A

Patients undergoing treatment for malignancy which itself is immunocompromising

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11
Q

Candidiasis (Candida albicans infection) can be an indication of

A

Diabetes

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12
Q

Someone who is treated with antimicrobials is susceptible to infection by

A

C difficile

Fungi (eg post UTI tx co-amoxyclav, then they get thrush)

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13
Q

Why does antimicrobial treatment predispose to fungal infection eg candidiasis post UTI Tx?

A

It alters the normal microbiota that protects against fungal overgrowth

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14
Q

Common types of opportunistic infections seen include

A
wound infection
UTI
intra-abdo infection
pneumonia
septicaemia/sepsis
meningitis (esp neonates)
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15
Q

Why are exogenous sources of OI important to recognize?

A

something has gone wrong with infection control procedures

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16
Q

Sources of OI pathogens can be __________ or __________

A

Endogenous - own microbiota OR own microbiota as acquired in hospital
Exogenous - other people

17
Q

Why are bactericidal agents required in some OIs?

A

If the patient is immunocompromised they not have the necessary immune response to deal with microbes that are alive but not growing (bacteriostatic) and can relapse

18
Q

What is used for epidemiological classification of Pseudomonas?

A

RFLP or multilocus sequence typing

19
Q

What makes Pseudomonas resistant to many ABs?

A

chromosomal encoded beta lactamase that degrades many penicillins (eg amoxycilin) and is not inhibited by clavulanic acid

20
Q

Psuedomonas colonises

A

skin, mucous membranes, gut

21
Q

T/F Pseudomonas colonization is permanent

A

False; transient colonization UNLESS they have CF or other disorder that allows permanent colonization

22
Q

Pseudomonas infections are mostly acquired

A

from the environment

23
Q

Pseudomonas is spread in hospital on

A

hands and fomites (inanimate objects)

24
Q

What is unique about Pseudomonas isolation techniques in the lab?

A

Weak disinfectant agents are used - centrimide agar - that stop other bacteria from growing ie acts as a selective media; allows pseudomonas to flourish

25
What resistance mechanisms does Pseudomonas have?
intrinsic (chromosomal beta lactamase); AND readily acquires resistance from other bacteria via plasmids (clav-acid is effective against plasmid-acquired beta lactamases)
26
Why did Pseudomonas develop resistance to carbenicillin and ticarcillin?
these ABs are not susceptible to the chromosomally-encoded beta lactamase BUT as pseudomonas acquires plasmid-encoded resistance it acquires beta lactamases that these drugs are susceptible to; therefore they need to be used in combination with clavulanic acid which inhibits plasmid-encoded beta lactamases
27
Superficial infections of PA include
wound, otitis externa, folliculitis, keratitis, corneal ulcer, and deep eye infection
28
Deep and systemic infections of PA include
nosocomial pneumonia, chronic pulm infection in CF patients, UTI, endocarditis, osteomyelitis, septicaemia
29
How is PA in biofilm different?
``` non-motile more capsule/hypermucoid more adherent less invasive shorter LPS w/o O Ag slowed growth increased resistance to ABs ```
30
Why do PA in biofilms have greater AB resistance?
slower growth and more capsule makes it harder for AB to penetrate
31
What is the cause of the changes to PA observed in biofilms?
Changes in activation of genes that are regulated by quorum sensing
32
What is quorum sensing?
Cross-talk between bacteria during biofilm formation that leads to the turning on and off of certain genes, causing different properties to be expressed by the bacteria
33
Why do biofilms tend to persist?
They resist mechanical removal (less motile) and they are less visible to the innate immune system (short or no O Ag)