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Microbiology and Immunology > Opportunistic Infections > Flashcards

Flashcards in Opportunistic Infections Deck (33):
1

What are the frequently encountered opportunistic pathogens?

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

2

Which frequently encountered opportunistic pathogens cause nosocomial epidemics?

Staph aureus
Klebs pneumo
Enterococcus spp
Pseduomonas aeruginosa
Enterobacter spp
Serratia spp

3

What local host factors contribute to opportunistic infection?

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

4

Opportunistic infections are especially important to recognize because

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

5

T/F Sutures reduce the chance of infection

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

6

Why do foreign bodies predispose to opportunistic infection?

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

7

T/F Burns are commonly associated with Pseudomonas infection

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

8

Catheters are a source of opportunistic infection because

they bypass normal host defenses

9

What systemic host factors contribute to opportunistic infection?

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

10

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

Patients undergoing treatment for malignancy which itself is immunocompromising

11

Candidiasis (Candida albicans infection) can be an indication of

Diabetes

12

Someone who is treated with antimicrobials is susceptible to infection by

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

13

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

It alters the normal microbiota that protects against fungal overgrowth

14

Common types of opportunistic infections seen include

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

15

Why are exogenous sources of OI important to recognize?

something has gone wrong with infection control procedures

16

Sources of OI pathogens can be __________ or __________

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

17

Why are bactericidal agents required in some OIs?

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

What is used for epidemiological classification of Pseudomonas?

RFLP or multilocus sequence typing

19

What makes Pseudomonas resistant to many ABs?

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

20

Psuedomonas colonises

skin, mucous membranes, gut

21

T/F Pseudomonas colonization is permanent

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

22

Pseudomonas infections are mostly acquired

from the environment

23

Pseudomonas is spread in hospital on

hands and fomites (inanimate objects)

24

What is unique about Pseudomonas isolation techniques in the lab?

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)