Opportunistic infections Flashcards

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1
Q

What are the main opportunistic infections that cause nosocomial infections?

A
S. aureus
Klebsiella pneumoniae
Enterococcus spp.
Pseudomonas aeruginosa
Enterobacter spp.
Serratia spp.
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2
Q

What are some host factors that may contribute to infection

A

Anatomical defects
Surgical or other wounds (sutures and other foreign material)
Burns (particularly for Pseudamonas or staph)
Catheterisation
Age (young or old)
Immunocompromised
Malnutrition
Co-infection
Antimicrobial infections (Thrush, C.diff and pseudomembranous collitis)

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3
Q

Where do opportunistic pathogens come from?

A

Endogenous - E.coli and UTI

Exogenous - Infection control problems

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4
Q

List some types of specimens that may betaken for diagnosis

A
Wound swab
pus
urine
Sputum
blood
CSF
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5
Q

What does treatment of opportunistic infections depend on?

A

The antibiotic susceptibility (nosocomial strains are often multiresistant).
Often use bactericidal agents especially if the pt is immuno compromised

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6
Q

List some prevention measures

A

Aseptic technique (hand hygiene)
Education
Isolation

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7
Q

What are the key features of pseudamonas

A
GNR
Motile
Facultative anaerobe
Non-fermenting and non-spore forming 
Catalase and oxidase positive
Produce green pus
Widespread, distinctive odour 
Low nutritional requirements
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8
Q

How is Ps. aeruginosa subtyped?

A

based on serotype and biotype (use restriction fragment length polymorphisms)

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9
Q

Why are CF patients easily colonised with Ps. aeruginosa?

A

Host factors: defective CFTR protein, thickened mucus and impaired muco-cilliary escalator.

Bacteria factors: Not inhibited by high salt environments, creates biofilms which resist mechanical removal, secretes DNA which further thickens mucus.

They transiently colonises the mucus membranes, skin and GIT and the CFTR protein is an antigen for Ps. aeruginosa which holds it closer and allows for easier colonisation.
are intrinsically resistant to beta-lactamases

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10
Q

Ps. aeruginosa is associated with what types of hospitalisations?

A

previously with burns and febrile neutropenia

Now mainly UTI, pneumonia and sepsis, CF patients.

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11
Q

How is Ps. aeruginosa spread in the hospital?

A

It is common environmental pathogen but is commonly spread by inanimate objects or on the hands of wrkers

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12
Q

Why is Ps. aeruginsa a problem in hospitals?

A

They are resistant to many antibiotics and to weak disinfectants (can also acquire resistant from other bacteria)

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13
Q

What type of superficial and deep/systemic infections does Ps.aeruginosa cause?

A

Superficial: Skin (wound infection, Otitis externa, folliculitis)

Deep: Pulmonary (especially in CF patients), UTI, endocarditis, septicaemia

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14
Q

How does Ps. aeruginosa adhere and invade the host?

A

In normal unbroken skin, it does not invade but adheres weakly via its LPS (bind CFTR), pilli and flagella (binds to TLR and cause inflammation).
It’s capsule assists in adherence and biofilm production

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15
Q

Describe the biofil produced by Ps. aeruginosa

A

Ps. becomes not motile and alters gene expression such that it adopts a hypermucoid phenotype. It allows it to be more adherent but less invasive (LPS reduces in length).
There is also increased resistance to antibiotics due to the slowed growth.
Quorum sensing - cross talk between bacteria to co-ordinate growth (POTENTIAL THERAPY)

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16
Q

Describe the spread and multiplication of Ps. aeruginosa

A

Secretes exo enzymes (proteases, haemolysins, phospholipases etc) that act on pulmonary tissue and surfactant.
There are exoenzymes that are secreted and inhibit phagocytosis.
LPS-CFTR mediated invasion aggrevates corneal damage

17
Q

Control mechanisms for Ps. aeruginosa

A

It cannot be eradicated from the environment therefore we need to prevent infection.

Treat early, hand hygiene, clean contact lenses, life long monitoring for CF patients