Opportunistic Infections Flashcards

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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
Q

What resistance mechanisms does Pseudomonas have?

A

intrinsic (chromosomal beta lactamase); AND readily acquires resistance from other bacteria via plasmids (clav-acid is effective against plasmid-acquired beta lactamases)

26
Q

Why did Pseudomonas develop resistance to carbenicillin and ticarcillin?

A

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
Q

Superficial infections of PA include

A

wound, otitis externa, folliculitis, keratitis, corneal ulcer, and deep eye infection

28
Q

Deep and systemic infections of PA include

A

nosocomial pneumonia, chronic pulm infection in CF patients, UTI, endocarditis, osteomyelitis, septicaemia

29
Q

How is PA in biofilm different?

A
non-motile
more capsule/hypermucoid
more adherent
less invasive
shorter LPS w/o O Ag
slowed growth
increased resistance to ABs
30
Q

Why do PA in biofilms have greater AB resistance?

A

slower growth and more capsule makes it harder for AB to penetrate

31
Q

What is the cause of the changes to PA observed in biofilms?

A

Changes in activation of genes that are regulated by quorum sensing

32
Q

What is quorum sensing?

A

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
Q

Why do biofilms tend to persist?

A

They resist mechanical removal (less motile) and they are less visible to the innate immune system (short or no O Ag)