Flashcards in Opportunistic Infections Deck (33):
What are the frequently encountered opportunistic pathogens?
Which frequently encountered opportunistic pathogens cause nosocomial epidemics?
What local host factors contribute to opportunistic infection?
Surgical and other wounds
Catheterisation (bladder, IV)
foreign bodies (sutures etc.)
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
T/F Sutures reduce the chance of infection
False; the presence of a foreign body including sutures increases the chance of infection
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
T/F Burns are commonly associated with Pseudomonas infection
False; previously Pseudomonas infections were more common; now we see more Staph and other bacteria
Catheters are a source of opportunistic infection because
they bypass normal host defenses
What systemic host factors contribute to opportunistic infection?
Extremes of age
Certain infections (HIV, measles)
Tx with antimicrobials (C. diff)
1' congenital immunodeficiency
Leucopenia as a predisposing factor for opportunistic infection is commonly seen in
Patients undergoing treatment for malignancy which itself is immunocompromising
Candidiasis (Candida albicans infection) can be an indication of
Someone who is treated with antimicrobials is susceptible to infection by
Fungi (eg post UTI tx co-amoxyclav, then they get thrush)
Why does antimicrobial treatment predispose to fungal infection eg candidiasis post UTI Tx?
It alters the normal microbiota that protects against fungal overgrowth
Common types of opportunistic infections seen include
meningitis (esp neonates)
Why are exogenous sources of OI important to recognize?
something has gone wrong with infection control procedures
Sources of OI pathogens can be __________ or __________
Endogenous - own microbiota OR own microbiota as acquired in hospital
Exogenous - other people
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
What is used for epidemiological classification of Pseudomonas?
RFLP or multilocus sequence typing
What makes Pseudomonas resistant to many ABs?
chromosomal encoded beta lactamase that degrades many penicillins (eg amoxycilin) and is not inhibited by clavulanic acid
skin, mucous membranes, gut
T/F Pseudomonas colonization is permanent
False; transient colonization UNLESS they have CF or other disorder that allows permanent colonization
Pseudomonas infections are mostly acquired
from the environment
Pseudomonas is spread in hospital on
hands and fomites (inanimate objects)
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
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)
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
Superficial infections of PA include
wound, otitis externa, folliculitis, keratitis, corneal ulcer, and deep eye infection
Deep and systemic infections of PA include
nosocomial pneumonia, chronic pulm infection in CF patients, UTI, endocarditis, osteomyelitis, septicaemia
How is PA in biofilm different?
shorter LPS w/o O Ag
increased resistance to ABs
Why do PA in biofilms have greater AB resistance?
slower growth and more capsule makes it harder for AB to penetrate
What is the cause of the changes to PA observed in biofilms?
Changes in activation of genes that are regulated by quorum sensing
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