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OD2 - Applied Clinical Training & Research Studies in Vision and Optometry > AED - Infection I & II - Week 3 > Flashcards

AED - Infection I & II - Week 3 Flashcards

1
Q

List 5 mechanisms of tissue injury with bacterial infections.

A

Release of enzymes that aid in invsaion and tissue breakdown
Release of exotoxins which inhibit cellular functions
Release of endotoxins that have detrimental effects on cell function
Collateral tissue damage
Initiation of later hypersensitivity response

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2
Q

Which gram type generally releases exotoxins and endotoxins?

A

Endo - gram negative

Exo - gram positive

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3
Q

List 4 mechanisms of damage in viral infections.

A

Avoids immune surveillance by entering cells and using machinery to self-replicate and burst through the membrane
Viral replication changes cell’s antigenic properties invoking inflammatory/immunes responses
Intracellular replication disrupts cellular function

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4
Q

Are most bacteria able to penetrate an intact cornea or conjunctiva?

A

No

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5
Q

How long would P. auruginosa proteases take to penetrate an intact epithelium? What is this usually prevented by (3)?

A

Needs 3 hours

Prevented by lid action, tear flow and tear antibacterials

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6
Q

What happens if bacteria gain access to basolateral surfaces of the epithelium?

A

Much easier to disrupt junctional complexes

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7
Q

Some bacteria can bind and enter ocular epithelial cells. To what purpose? Give an example.

A

To protect themselves from the inflammatory response.

P. auruginosa

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8
Q

Describe the early histopathology of a bacterial infection.

A

Compromised epithelium allows bacteria invasion - exotoxins aid this process
Replication in the stroma and further exotoxin release damages overlying epithelium - stimulates inflammatory response
Neutrophil enzymes and bacterial exotoxins cause further tissue damage

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9
Q

What cell coordinate further inflammatory cell activity late in infections?

A

Lymphocytes

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10
Q

Describe how daytime contact lens wear can increase susceptibility to infection (5).

A

Contact lenses and an immobile tear film shield bacteria from lip sweeping and tear film protective action
Chronic mild hypoxia of the corneal epithelium promotes bacterial adhesion to the epithelium

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11
Q

How can overnight contact lenses increase susceptibility to bacterial infection?

A

Alters tear levels of pro-inflammatory cytokines - may promote a pro-inflammatory environment

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12
Q

The migration of which cell is stimulated with extended wear contact lenses? To which part of the eye do they migrate? Explain what kind of cells they are and why this migration is so significant.

A

Langerhan’s cells migrate to the central cornea

They are APCs, so if an infection occurs, inflammation is more aggressive than normal

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13
Q

What does chronic dry eye induce? Does dry eye increase susceptibility to ocular infection? Explain.

A

Chronic dry eye induces epithelial apoptosis
This can cause epithelial erosion, improving bacterial adhesion
Reduced tears results in reduced antibacterial activity

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14
Q

Briefly describe the model of pathogenesis for corneal bacterial infection (5).

A

Early destruction of opithelium and bacterial proliferation
Neutrophil chemotaxis from limbal vessels
Release of proteases and ROS
Chemotaxis of lymphocytes - inflammatory cell activity increases
Corneal perforation

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15
Q

What are protozoan infections characterised by?

A

Extreme pain

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16
Q

List the two forms of acanthamoeba.

A

Trophozoites (motile form)

Encysted (cellulose wall)

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17
Q

How are acanthamoeba identified?

A

Confocal microscopy

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18
Q

What are the most common inflammatory cells in an acanthamoeba infection and what is usually seen when this happens?

A

Neutrophils - a ring infiltrate can be seen

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19
Q

What do acanthamoeba preferentially target?

A

Corneal nerves

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20
Q

How can chlamydia spread (2)?

A

Infective particles transmitted by flies
Mostly caused by the eye being exposed to infected genital secretions
( ͡° ͜ʖ ͡°)

21
Q

What are the two most common fungi responsible for eye infections?

A

Candida and Aspergillus

22
Q

In what three cases are fungal infections most common?

A

Post-trauma with vegetative matter
Post-surgery
Immunocompromised individuals (including those on corticosteroids)

23
Q

What are the most common initial cells during a fungal infection?

A

Neutrophils

24
Q

Do fungal infections spread rapidly or slowly?

A

Once they take hold, they spread rapidly

25
Q

What will happen with chronic fungal infections over time?

A

Granulomatous

26
Q

What happens if a fungal infection takes hold in the cornea over a period of time?

A

Perforation is almost certain

27
Q

What may acanthamoeba form in the corneal stroma and why?

A

Cysts for protection

28
Q

Can acahnthamoeba go dormant?

A

Yesd

29
Q

Briefly list the cellular basics of viral infection.

A

Virion fuses with the cell membrane, enters via endocytosis
Uncoats, enters nucleus, replicates
New viral proteins are made, exits cells

30
Q

List 4 pathological consequences of viral infeciton.

A

Vius damages or kills host cell
Persistence of viral infection without cell injury
Cell transformation - unchecked division - neoplasia
Innate system inflammation

31
Q

List 5 possible effects of viruses on target cells.

A 
No effect - latency
Cell death
Cell fusion
Formation of inclusion bodies
Cell proliferation
32
Q

Do primary infections of herpes simplex virus often involve the eye? What part of the eye does it usually involve?

A

It is rare

Those that do are usually sub-clinical blepharoconjunctivitis

33
Q

Can recurrent ocular HSV infection affect any ocular structure or only certain types?

A

Any ocular structure

34
Q

True or false

HSV is not implicated in acquired Horner’s symdrome

A

False

35
Q

Does HSV cause cell death?

A

Yesd

36
Q

Which cranial nerve is involved with HSV infections?

A

Trigeminal (5)

37
Q

Briefly describe the pathogenesis of a primary HSV infection.

A

Primary infection occurs (cold sore)
Virus travels via peripheral nerves to the trigeminal ganglion
Remains there as a latent virus

38
Q

List three factors that can cause reactivation of latent HSV particles in the trigeminal ganglion.

A

Colds
Sunlight (UV)
Menstruation

39
Q

What can a primary HSV infection of the cornea direcly cause?

A

Infection of the ophthalmic division of the trigeminal ganglion.

40
Q

What layer of the cornea is where HSV infection begins?

A

Basal cells

41
Q

What is the earliest clinical sign of HSV infection?

A

Epithelial cysts with raised overlying tissue, prior to patent ulcers

42
Q

Do corneal wing cells need nerve association for viral spread? Explain.

A

No, once epithelial cells are infected, no innervation is needed for lateral speed.

43
Q

Histopathologically, where do HSV virion particles accumulate? What can this be a possible mechanism of?

A

At the apical surface of the epithelium

Possible mechanism for release into tears for person-person transfer

44
Q

What is the cause of corneal ulcers with HSV infection? Is the underlying stroma affected?

A

Progresive cell death following virion infection.

Stroma is unaffected

45
Q

Are stromal keratocytes affected by HSV infection?

A

Yes, but subclinically

46
Q

What is an important manifestation of HSV? When is it often seen?

A

Stromal keratitis, often seen some time after dendrite healing

47
Q

What does the simplest and severest form of HSV induced stromal keratitis cause?

A

Simplest - mild anterior cellular infiltrate

Severest - aggressive necrotising stromal degeneration

48
Q

What is disciform keratitis usually accompanied with (2)?

A

Anterior chamber inflammation (anterior uveitis) and inflammatory cell accumulation on the endothelium (keratic precipitates)

49
Q

Describe how viruses can cause cell division (2) and give an example of such a virus.

A

Human papilloma viruses can express certain oncoproteins while replicating
These proteins immortalise the cell and cause cell division beyond the number of programmed cell passages

OD2 - Applied Clinical Training & Research Studies in Vision and Optometry (174 decks)

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