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Hannah's Intersystem > Opportunistic Infections > Flashcards

Opportunistic Infections Flashcards

1
Q

List 9 commonly encountered opportunistic pathogens. Which of these may cause nosocomial epidemics?

A 
E. coli
Staphylococcus aureus*
Klebsiella pneumoniae*
Enterococcus spp.*
Pseudomonas aeruginosa*
Enterobacter spp.*
Serratia spp.*
Proteus spp.
Clostridium difficile
*May cause nosocomial infections
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2
Q

What host factors combat colonisation and penetration by microbes?

A

Physical and chemical barriers

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3
Q

What host factors combat multiplication of microbes and tissue damage caused by microbes?

A

Inflammatory response and phagocytosis

Adaptive immune response

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4
Q

How do microbial virulence and host resistance affect disease outcome?

A

If host resistance is reduced, pathogen does not need to be very virulent to cause overt infection (and vice versa)

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5
Q

Give 5 examples of local host factors that may predispose to opportunistic infection

A 
Anatomical defects
Surgical and other wounds
Burns
Catheterisation (bladder, IV)
Foreign bodies in general (e.g. suture)
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6
Q

Why is it important to recognise opportunistic infections?

A

May be 1st sign that there is something wrong with the host (e.g. immunosuppression, obstruction, etc)

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7
Q

What is the effect of foreign bodies on opportunistic infection?

A

Increases likelihood of infection (allows microbes to evade immunity)

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8
Q

Give an example of a type of infection that is commonly opportunistic

A

UTIs (in females especially)

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9
Q

What might pneumonia that does not respond to conventional treatment suggest?

A

Obstruction or lung disease (pre-disposing factor exists)

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10
Q

List 9 systemic host factors that may predispose to opportunistic infection

A 
Extremes of age
Leucopenia
Malignancy
Malnutrition
Diabetes
Liver disease
Certain infections
Treatment with antimicrobials
Primary (congenital) immunodeficiency
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11
Q

What opportunistic infection does diabetes predispose to?

A

Candida albicans infection (candidiasis; often the 1st presentation of DM)

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12
Q

Give 2 examples of an infection that predisposes to opportunistic infection

A

HIV

Measles (temporary severe immunocompromise)

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13
Q

Give 2 examples of opportunistic infections associated with antimicrobial treatment

A 
Clostridium difficile infection (pseudomembranous collitis)
Fungal infection (e.g. thrush following broad spectrum antibiotic for UTI)
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14
Q

List 6 common presentations of opportunistic infections

A 
Wound infection
UTI
intra-abdominal infection
Pneumonia
Septicaemia
Meningitis (especially in neonates)
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15
Q

How are opportunistic infections diagnosed?

A

By culturing an appropriate specimen (e.g. wound swab, pus, urine, sputum, blood, CSF)

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16
Q

What is the risk with taking antimicrobials in hospital?

A

Patient are susceptible to becoming colonised with resistant organisms

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17
Q

How are opportunistic infections treated?

A

Depends on antibiotic susceptibility (nosocomial strains are often multi-resistant, although multi-resistant strains are now also seen in the community)
May need potent bactericidal agents (due to immunocompromise - may not have neccessary armoury to deal with live microorganisms)

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18
Q

How can opportunistic infections best be prevented?

A

Aseptic technique (especially hand hygiene)

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19
Q

What kind of bacteria is Pseudomonas?

A

Gram negative bacilli

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20
Q

What is the metabolic classification of Pseudomonas?

A

Aerobes or facultative anaerobes

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21
Q

Is Pseudomonas motile?

A

Yes

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22
Q

Does Pseudomonas ferment?

A

No

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23
Q

Does Pseudomonas form spores?

A

No

24
Q

What result does Pseudomonas produce on a catalase test?

A

Catalase positive

25
Q

What result does Pseudomonas produce on an oxidase test?

A

Oxidase positive

26
Q

Does Pseudomonas produce pigments?

A

Some do, including Ps. aeruginosa

27
Q

What is the name of the pigment produced by Ps. aeruginosa?

A

Pyocyanin (greenish pus)

28
Q

What are the nutritional requirements of Pseudomonas?

A

Low nutritional requirements (can survive almost anywhere but love moist environments)

29
Q

Where is Pseudomonas’ favourite place to grow?

A

Moist environments

30
Q

How are Pseudomonas classified?

A

Divided into species based on biochemical tests

31
Q

How is Pseudomonas subtyped for epidemiological studies?

A

RFLP
MLST (multilocus sequence typing)
May use whole genome sequencing as cost comes down

32
Q

Colonisation with which organism is associated with a poor prognosis for CF?

A

Pseudomonas

33
Q

List 3 genera related to Pseudomonas. Which of these are opportunistic pathogens? Which species often colonise the RT of patients with CF and are intrinsically resistant to many commonly-used antibiotics?

A 
Burkholderia capacia (opportunistic)*
Stenotrophomonas maltophilia (opportunistic)*
Burkholderia pseudomallei
*Colonise CF patients (also Ps. aeruginosa)
34
Q

What is a saprophyte? Give an example

A

Organism that grows freely in the environment

E.g. Ps. aeruginosa

35
Q

What organism causes melioidosis, which can lead to pneumonia?

A

Burkholderia pseudomallei

36
Q

What is 1 reason Ps. aeruginosa (and related pathogens) are intrinsically resistant to many commonly-used antibiotics?

A

Due to chromosomal B-lactamase

37
Q

Does Ps. aeruginosa colonise normal healthy individuals?

A

Only transiently colonises skin, mucous membranes and GIT

38
Q

List 6 conditions associated with Ps. aeruginosa

A 
CF
Pneumonia
UTI
Sepsis
Burns (more previously)
Febrile neutropenia (more previously)
39
Q

How is Ps. aeruginosa spread in hospitals?

A

On hands and fomites

40
Q

How can Ps. aeruginosa be isolated in the lab?

A

Grown on cetrimide agar (disinfectant; kills all other organisms but Pseudomonas can grow)

41
Q

What kind of superficial infections can be caused by Ps. aeruginosa?

A

Skin (wound infection, otitis externa, folliculitis)

Eye (keratitis, corneal ulcer - can also invade and cause deep ulcer)

42
Q

What kind of deep and systemic infections can be caused by Ps. aeruginosa?

A 
Pulmonary (nosocomial pneumonia, chronic infection in CF patients)
UTI*
Endocarditis*
Osteomyelitis*
Septicaemia*
*In immunocompromised patients
43
Q

How does Ps. aeruginosa adhere to intact epithelium?

A

Weakly via flagella, pili, LPS

Capsule assists

44
Q

What is a risk factor for eye infection with Ps. aeruginosa?

A

Contact lens use (grows in fluid, forms biofilm, adheres to contact lens)

45
Q

How does Ps. aeruginosa invade?

A

Does not invade intact skin unless in very high numbers

46
Q

What part of Ps. aeruginosa binds to CFTR? What is the result of this?

A

LPS core

Prevents invasion in individuals with normal CFTR - adheres to CFTR and can be phagocytosed by macrophages

47
Q

What is the role of the capsule of Ps. aeruginosa?

A

Assists adherence and biofilm formation

48
Q

List 7 properties of Ps. aeruginosa in biofilms

A 
Non-motile (no flagella)
More capsule material (mucoid phenotype)
More adherent
Less invasive
Shorter LPS (no O-Ag)
Slowed growth
Increased antibiotic resistance
49
Q

What is responsible for the change in the properties of Ps. aeruginosa when in a biofilm?

A

Activation of genes regulated by quorum sensing (also inactivation of some genes)

50
Q

What is quorum sensing?

A

Bacterial “cross-talk” which aids the formation of biofilms

51
Q

What are the stages of biofilm formation?

A 
Bacteria adhere to an innate (or non-innate e.g. respiratory epithelium) surface
Produce mucus material
Form "mushroom-like" structure
Change back into motile form
Break out of mushroom structure
Process repeats
52
Q

List 5 cellular aspects of Ps. aeruginosa that aid it spread through tissues and the body

A 
Reduced PMNs
Flagella
Exoenzymes (act on pulmonary tissues and surfactant)
Exotoxins
LPS-CFTR-mediated invasion
53
Q

List 5 unique aspects of the Ps. aeruginosa infection in CF patients

A

Defect in CFTR causes abnormal ion transport, thickened mucus and impaired mucociliary function
Pseudomonas (and Staph) are not being inhibited by high salt concentrations
Bacteria in biofilms resist mechanical removal and are less visible to the innate immune system
DNA secreted by bacteria and released from dying cells causes thickened mucus, trapping Ps. aeruginosa
Bacterial variants which persist are those with reduced virulence

54
Q

What is the role of type III secreted proteins in Ps. aeruginosa pathogenesis?

A

Act on various host cell targets to interfere with phagocytosis and enhance cytokine production

55
Q

What is the role of exotoxin A in Ps. aeruginosa pathogeneis?

A

Blocks protein synthesis

56
Q

What is the role of LasA and LasB in Ps. aeruginosa pathogenesis?

A

Proteases that act together as elastase

57
Q

What is the role of phospholipase in Ps. aeruginosa pathogenesis?

A

Damages cell membranes, degrades surfactant

Hannah's Intersystem (16 decks)

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