WEEK 1: Eye infections Flashcards

1
Q

Define normal flora.

A

Resident bacteria – Facilitate inhibition of growth of virulent strains.

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2
Q

Conjunctiva - habitat for various resident microorganisms

State the predominant species found in it.

State other species found in it.

A

Conjuctiva - habitat for various resident microorganisms

Predominant species:
Coagulase negative Staphylococcus i.e.
S. epidermidis
Streptococcus species

Others:
Corynebacterium, Propionibacterium acnes, Staphylococcus aureus, Escherichia coli , Haemophilus & Pseudomonas species

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3
Q

Outline various factors influence indigenous flora.

A

Environmental factors
Age
Contact lens use.
Immunocompromising disease & medications

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4
Q

The eye is a moist, warm tissue, oxygenated & rich in nutrients. So, without effective host defenses, contaminating microbes would infect frequently.

Outline the Mechanical, anatomical & immunological defense mechanisms of the eye.

A
  1. Conjunctiva, eyelids & lacrimal apparatus
    Protective structures
  2. Tears
    Flush foreign particles; also contain - IgA & IgG; antimicrobial proteins-lactoferrin, lysozyme, lipocalin & beta-lysin.

-Tears contain several antimicrobial molecules attained primarily from the lacrimal gland and surfaces of the eye i.e. cornea, & epithelial cells.

There are also: neutrophils; AMPs = antimicrobial peptides; sIgA = secretory Immunoglobulin A; sPLA2 = secretory phospholipase A2; SLPI = secretory leukocyte protease inhibitor; SP-D = surfactant protein D.

-Tears help to physically wash out invading pathogens & they contain several antimicrobial molecules that are inhibitory to the growth of pathogens.

  1. Corneal nerves
    Relay sensory information leading to reflex movements to protect eye.
  2. Epithelium
    Corneal epithelial cells secrete cytokines.
  3. Keratocytes
    Under influence of IL-1 & TNF, can synthesize IL-6 & defensins.
  4. Neutrophils
  5. Cytokines, Complement
  6. Langerhans cells
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5
Q

Outline the different eye infections for the following parts.

Conjunctiva
Cornea
Cornea & Conjunctiva
Soft tissue around the eye
Vitreous & aqueous humor

A

Conjunctiva: Conjunctivitis, trachoma
Cornea: Keratitis (abrasions & ulcers)

Cornea & Conjunctiva: Epidemic keratoconjunctivitis

Soft tissue around the eye: Periorbital & orbital cellulitis

Vitreous & aqueous humor: Endophthalmitis

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6
Q

Define Conjunctivitis – ‘Pink / red eye.’

A

Inflammation of conjunctiva - mucous membrane lining inside of eye lids (tarsal) & sclera (bulbar)

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7
Q

Conjunctivitis can be infectious + noninfectious can be further divided into other types.

Give the examples of the infectious and non-infectious conjunctivitis.

A

Infectious
*Bacterial
*Viral

Non- infectious
*Allergic
*Nonallergic

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8
Q

Discuss the prevalence of conjunctivitis and the treatment options.

A

Prevalence of infectious conjunctivitis differs in paediatric vs. adults. Bacterial more prevalent in children

Infectious conjunctivitis is generally self-limiting, but treatment facilitates reduction of transmission.

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9
Q

Define Allergic conjunctivitis.

Outline the examples of allergic conjunctivitis.

A

Notes: Hypersensitivities to an exposure to an ‘allergen’ on the ocular surface.

It is an IgE mediated hypersensitivity reaction (type I), with resultant mast cell degranulation following direct contact with an allergen on the ocular surface.

Can be acute or seasonal &/or perennial. In many cases the onset of allergic conjunctivitis happens in people younger than 20 years old & then tends to decrease with age i.e. in older populations.

Although allergic conjunctivitis can by itself most times is also associated together with allergic rhinitis, atopic dermatitis &/or asthma.

Allergic conjunctivitis: group of diseases incl.

*Vernal keratoconjunctivitis.
*Seasonal rhinitis.
*Atopic keratoconjunctivitis
*Papillary conjunctivitis

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10
Q

Discuss the following:

*Vernal keratoconjunctivitis.
*Seasonal rhinitis.
*Atopic keratoconjunctivitis
*Papillary conjunctivitis

A

For further reading please refer to article: ‘Allergic Conjunctivitis’ by Baab, S; Le, P. H.and Kinzer, E. E. (https://www.ncbi.nlm.nih.gov/books/NBK448118/)

Vernal Keratoconjunctivitis
Exact mechanism not well understood, it’s suggested that it is an IgE mediated hypersensitivity with some Tcell involvement.
More common during in warm climates
More common in males. In younger people (<10years) with a history of atopy or asthma
Also tends to decrease with age, in many cases it is completely resolved after adolescence

Atopic Keratoconjunctivitis
Type I & delayed type IV hypersensitivity
In contrast to the previous, it is more evident in older years of age (30-50years)
Associated with atopic dermatitis. Like vernal keratoconjunctivitis, there is a male to female predominance

Giant Papillary Conjunctivitis:
Type I & delayed type IV hypersensitivity
Mostly seen as an aggressive allergic response to contact lenses.
Common in teenagers & young adults
Most commonly seen in conjunctionwith soft contact lens use & observed in ~5% of contact lens users

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11
Q

State the symptoms of allergic conjuctivities.

A

Symptoms

-Bilateral redness; intense itching; watery discharge; follicles & papillae in conjunctiva (‘cobblestone appearance’)

In extreme cases: chemosis i.e. bulging, oedematous conjunctiva extending beyond eye lid level & maybe dark patches under eyes)

May occur at specific times of the year e.g. during periods of high levels of pollen or specific allergy e.g. cats

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12
Q

Outline the causative agents and treatment of allergic conjunctivitis.

A

Causative factors:
-Airborne allergens contact eye, causing type I hypersensitivity, triggering local mast degranulation & release of mediators e.g. histamine, eosinophil chemotactic activating factors

Treatment is primarily supportive measures i.e.

*Cold compress
*Artificial tears.
*In some cases, topical or oral antihistamines and mast cell inhibitors may also be prescribed
*Largely supportive but topical corticosteroids beneficial in severe cases

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13
Q

Discuss the causative agents, symptoms and treatment of Non-allergic/ Irritant Conjunctivitis.

A

Cause-usually transient.

Mechanical trauma or chemical exposure or other various irritants causing inflammatory response e.g. smoke, chlorinated pool H2O, shampoos), eyelashes.

Symptoms (usually improve within 24hours)

-Discharge watery
-Intermittent redness

Treatment - cleansing of eye to remove irritant.

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14
Q

The presentation now moves onto microbial infections of the eye, starting with those of the conjunctiva which, can be broadly categorized as:

  1. Bacterial conjunctivitis
  2. Viral conjunctivitis.
A
  1. Bacterial conjunctivitis

-Usually, a bilateral suppurative ocular infection resulting in purulent discharge.
-Treated with antibiotic eye drops.

  1. Viral conjunctivitis
    -Usually starts as a unilateral infection that becomes bilateral after few days.

-Resulting in tears & watery discharge.

-Normally self limiting, with supportive management

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15
Q

Discuss Ophthalmia neonatorum.

A

Ophthalmia neonatorum - treated as an emergency

Rare ocular infection in new-Borns

Acquired via vertical transmission i.e. vaginal delivery from the mother with an untreated sexually transmitted infection

Treated as an emergency to prevent permanent eye damage or blindness.

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16
Q

Outline the major causes of ophthalmia neonatorum.

A
  1. Chemical
  2. Bacterial: Neisseria Gonorrhea, Chlamydia trachomatis, H. Influenza, Step. Pneumoniae
  3. Viral: Herpes simples, adenovirus
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17
Q

Discuss the management of hyperacute conjunctivitis.

A

Gonococcal ocular infection will include treatment would need to include both mother and baby:

-Intramuscular ceftriaxone for adults, children & neonates
&
-Oral azithromycin or doxycycline for adults (& erythromycin –neonates)

Due to increased rates of antimicrobial resistance in N. gonorrhoeae, the Centers for Disease Control & Prevention treatment 2015 guidelines support dual therapy with ceftriaxone & azithromycin.

As with Gonococcal conjunctivitis, neonates are mostly infected with Chlamydial conjunctivitis during delivery (from an infected mother) but they can also be infected after delivery by nursing mother.
Similar treatment as above

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18
Q

Discuss acute conjuctivitis.

Signs and symptoms
Causative pathogens

A

Common, contagious, higher incidence & prevalence in children (particularly infants, school children) & elderly

Symptoms
*Eye redness
*Mucopurulent discharge – thick yellow, white or green (vs. watery in viral). Usually, one eye but may be bilateral.
*Eyes may be ‘stuck shut’ especially in mornings

Causative pathogen

*Staphylococcus aureus – (esp. adults)
*Streptococcus pneumoniae (in children)
*Haemophilus influenzae (in children)
*Moraxella catarrhalis (esp. in children)
*Pseudomonas aeruginosa

~a 1/3rd acute infectious conjunctivitis cases are caused by bacteria: Staphylococci species are the most common pathogens, followed by
followed by Streptococcus pneumoniae and Haemophilus influenzae.

But in children, the leading causes of these infections are S. pneumoniae, H. influenzae, or Moraxella catarrhalis.

Recall: If the onset is hyper acute in neonate, the leading causative pathogens are: Neisseria gonorrhoeae or Chlamydia trachomatis.

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19
Q

Discuss the management of bacterial conjunctivitis.

A

HIGHLY CONTAGIOUS:
Management = prevent spread + treat infection

  1. Standard ‘Infection control measures’ i.e. continual hand sanitization; avoid sharing of hygiene cloths.
  2. Broad spectrum topical antibiotic i.e. eye drops or ointment
    Chloramphenicol
    Fusidic acid

In most cases self-limiting, 60% of cases will resolve within 5 days without antibiotic interventions.

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20
Q

Discuss Viral conjunctivitis.
1. Causative pathogen
2. Transmission
3. Symptoms

A

Causative pathogen
Most common cause (60-90%): Adenovirus
Less common - Herpes simplex virus type 1; Varicella-zoster virus; Measles virus

Contagious especially in first ~2 wks (& may last up to 2-3wks)

May occur with or just after common colds & systemic viral infections
(i.e. measles, chickenpox, rubella & mumps.

Localised viral conjunctivitis without systemic manifestations usually results from adenoviruses

Transmission:
-Direct contact of tears or eye discharge

Symptoms
-Significant eye redness + very watery
-Chemosis ; preauricular lymph node may be swollen
-Tarsal conjuctiva may have follicular or ‘bumpy’ appearance-gritty feeling

Disease often becomes bilateral in 24 - 48hrs.
Self-limiting infection

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21
Q

Discuss clinical presentation in both bacterial & viral conjunctivitis vs keratitis.

A

*Visual acuity is preserved

*Photophobia absent

NB.
Presence of either photophobia or decreased visual acuity triggers concern for corneal involvement.

Corneal involvement has more dire prognosis & requires ophthalmologic consultation.

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22
Q

Discuss Allergic Conjunctivitis - Management.

A

*Diagnosis extensively by clinical history & clinical examination.
*Swabs & laboratory cultures rarely performed.

Focus is on alleviating discomfort.

-Mild cases - cold compresses on eyes & artificial tears
-Vasoconstrictors - antihistamine combination for severe pruritis
-Anti inflammatories i.e. steroid eye drops
Antibiotics

Strict hygiene is vital – hand washing / sanitising
Avoiding sharing personal articles & contact with others

Conjunctivitis often self-limiting BUT early & correct diagnosis vital, to rule out medical emergencies i.e. bacterial keratitis, corneal abrasions, acute closed angle glaucoma.

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23
Q

Discuss Conjunctivitis - Management
1. Viral conjunctivitis (most common):
2. Bacterial conjunctivitis (less common):

A

In certain cases, treatment:
Viral conjunctivitis (most common): no specific
-Antiviral treatments but for Herpes simplex or zoster virus then antivirals are prescribed i.e. Acyclovir ointment or Ganciclovir gel

Bacterial conjunctivitis (less common):
-Antibiotics not generally prescribed

-But if prescribed: chloramphenicol 0.5-1% eye drops -Fusidic acid

They both prevent the synthesis of bacterial protein.

In most cases self-limiting, 60% of cases will resolve within a week without antibiotic interventions.
If condition doesn’t improve in approx. referral to ophthalmologist necessary

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24
Q

Discuss management of Gonococcal ocular infection.

A

Gonococcal ocular infection will need treatment.

If suspected, conjunctival swabs collected for lab testing.
Must be immediately referred to ophthalmologist.

*Intramuscular ceftriaxone recommended for adults, children & neonates
*Patients should lavage infected eye with saline

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25
Q

Discuss management of Chlamydial ocular infection.

A

*Many cases have concurrent genital infection
*If suspected, conjunctival swabs collected for lab testing

  1. Oral azithromycin or doxycycline for adults ( & erythromycin –neonates)

Due to increased rates of antimicrobial resistance in N. gonorrhoeae, the Centers for Disease Control & Prevention treatment 2015 guidelines support dual therapy with ceftriaxone & azithromycin.

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26
Q

Define keratitis.

A

Inflammation of cornea, most often by a bacterial or viral infection.

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27
Q

Why is Viral & Bacterial keratitis considered serious ocular infections?

A

Because can cause of corneal opacifications & if untreated common cause of blindness world-wide after cataracts.

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28
Q

Outline Risk factors: ***Most common pre-disposing factors of Keratitis.

A

*Overuse of contact lenses, esp. overnight
*Ocular surgery
*Use of topical corticosteroids
*Abrasions (physical &/or chemical) on cornea, *Refractive surgery
*Diabetes
*Topical steroids
*Trachoma
*Exposure to intense ultraviolet light,

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29
Q

Outline symptoms of keratitis.

A

*Acute redness
*Tearing
*Painful eye
*Often with a foreign body sensation
*Photophobia
*Decreased vision

Prompt diagnosis, identification of causative agents & treatment paramount. To prevent vision loss due to ulceration, necrosis & scarring***

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30
Q

Outline Common bacterial pathogens for Keratitis.

A

Staphylococcus spp.

Streptococcus pneumoniae

Pseudomonas spp.- esp. amongst contact lens wearers

Moraxella catarrhalis-immunocompromised patients

Neisseria gonorrhea & Chlamydia trachomatis: sexually active patients esp. if conjunctivitis is present:

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31
Q

Outline Common viral pathogens for Keratitis.

A

Adenovirus

Herpes Simplex virus -1

Varicella Zoster Virus

Epstein-Barr Virus

Cytomegalovirus

32
Q

What causes 80% bacterial corneal ulcers?

A

*Staphylococcus aureus
*Streptococcus pneumoniae
*Pseudomonas aeruginosa – NB. most pathogenic, can cause corneal perforation in just 72 hr

33
Q

Discuss the Virulence factors for bacterial pathogens in keratitis.

A

Cell wall associated appendages e.g. fimbriae, pili, glycocalyx envelope (P. aeruginosa & N. gonorrhoea) used in adherence to epithelial cells

Certain bacteria i.e. S. pneumoniae resist effects of lysozyme produced in tears fluid & resists phagocytosis due to their polysaccharide capsule

Expression of proteolytic enzymes i.e. protease, chymase, tryptase cause degradation glycoproteins & epithelial lesions.

34
Q

Discuss Viral Epidemic Keratoconjunctivitis

-Main causative agents
-Symptoms
-Transmission

A

Epidemic keratoconjunctivitis (EKC) is a viral conjunctivitis caused by certain Adenovirus serotypes i.e. types 8, 19 & 37.

Inflammation of conjunctiva & cornea.

Symptoms
*Can also cause pharyngoconjunctival fever characterized by:

-Highfever
-Sore throat
-Conjunctivitis

*Rapid onset of symptoms (4-14days incubation) typical of viral conjunctivitis

-Multiple white & fuzzy infiltrates may be located superficially in cornea reducing acuity

-Pseudo membrane/ pannus (white & smooth) forms on the tarsal conjunctiva

**Potentially vision-threatening

EKC is highly contagious & has a tendency to occur as epidemics.

Transmission
*Direct contact of tears or eye discharge from infected eyes
*Air droplets

35
Q

Discuss the Treatment of EKC.

A

Currently no approved, specific “anti-adenoviral” therapies

So, topical corticosteroids &/or steroid-sparing/non-steroidal anti-inflammatory drugs e.g. cyclosporine eye drops may be prescribed to reduce risk of scarring

But clinical use of topical corticosteroids is restrained & justified only when there is a threat of visual loss due to persistent sub epithelial infiltrates, pseudomembranous conjunctivitis & iris inflammation (iridocyclitis)

NB. steroids may suppress conjunctival & corneal inflammation & provide symptomatic relief but they do not shorten the course of EKC

Commonly palliative treatment is recommended i.e. cool compresses & artificial tears.

36
Q

Discuss Corneal ulcers.

A

An open sore in the epithelial cell layer of the cornea with an inflammatory response

The cornea is avascular, thus posing a challenge for immune cells to access the infection.

Thus, require urgent attention by ophthalmologists & topical antibiotics.

An ocular emergency, as a delay in treatment may result in corneal perforation, endophthalmitis &/or permanent corneal scarring & subsequent visual loss.

37
Q

Outline Corneal layers & injuries.

A

A.Corneal abrasion in epithelium only.

B.Corneal ulceration involving epithelium, Bowman’s layer & stroma.

C.Perforation of entire cornea, which can occur following fulminant infectious ulceration or in trauma, where a foreign body may be present in the cornea or anterior chamber.

38
Q

Discuss HSV Keratitis can be categorized as.

A
  1. Epithelial (primary infection): characterized by dendritic ulcers.
  2. Stromal (recurrent infection with severe morbidity):

-Stromal opacification
-Inflammation of the stroma
-Corneal thinning.

Neovascularization may occur, with leaking of lipids into stroma &/ or stromal scarring.

  1. Endotheliitis/ Endothelial (uncommon):

-Disciform keratitis: stromal & epithelial oedema occurring in a round ‘disc-form’ with precipitates underlying the area of oedema (can also be by herpes zoster viruses)

39
Q

KERATITIS.

Discuss the following.

  1. Risk factors
  2. Clinical symptoms
  3. Physical exam findings.
A

Risk factors:
-Wearing contact lenses, esp. excessive, continuous throughout the night
-May develop secondary to corneal abrasions,
-Blepharitis: An inflammation of the eyelids.
-Ocular trauma
-Subsequent fungal, parasitic, viral or bacterial infection (can also be sterile i.e. auto-immune)

Clinical symptoms:
-Decreased vision
-Severe pain
-Redness
-Light sensitivity

On physical exam:

-Injected/hyperemia conjunctiva
-Dense collection of inflammatory cells “infiltrate” in cornea &/or
-Hypopyon” (dense collection of WBCs in anterior chamber)

40
Q

Corneal ulcers are commonly caused bacteria, viruses, fungi, or a parasite.

Discuss them.

A

Acanthamoeba spp. (protozoa) common cause of corneal ulcers in contact lens users esp. in those who make their own homemade lens cleaning solutions.

Fungal keratitis can occur after a corneal injury involving trauma to the eye with foreign bodies e.g. plant material. Leading to injury of the protecting epithelium. Common causes Fusarium, Aspergillus & Candida spp.

May also result from certain conditions whereby eyelids don’t close completely, resulting in eye dryness & possible ulcer formation e.g. Bell’s palsy

Herpes simplex keratitis is a serious viral infection which may be recurrent. Possibly triggered by any condition that lowers the immune response e.g. stress, inflammatory disorders

41
Q

Discuss Herpes simplex keratitis (causative pathogen).

A

Keratitis (corneal infection & inflammation) caused major cause of blindness worldwide, due to corneal scarring & opacity.

**Causative pathogen: HSV type-1
HSV-I typically affects the orofacial region, whereas HSV-II usually causes genital infections.

However, there are cases whereby both viruses affecting either location or mixed infections occurring

Keratitis most prevalent form of ocular HSV-1 disease but other forms HSV-1 ocular infections incl. eyelid lesions (herpetic blepharitis), conjunctivitis, uveitis, retinitis & rarely, scleritis

42
Q

Discuss Herpes simplex keratitis transmission.

A

Transmission:
-Most ocular HSV disease is a recurrent disease following a primary oro-facial infection

-Primary infection occurs after inoculation of mucosal or skin surfaces by direct contact.

After a primary oro-facial infection, HSV-1 enters sensory nerve endings, travels up the axon & goes into latency (maybe for years) in trigeminal ganglion.

Reactivation may occur, provoked by various of stimuli i.e. stress, febrile illnesses, immunosuppression.

HSV-1 reaches the corneavia the ophthalmic branch of the trigeminal nerve, causing lesions in the corneal epithelium & stroma.

43
Q

Discuss the hallmark of Herpes simplex keratitis.

A

Herpes simplex keratitis typically presents with the following features:

Dendritic Lesions: These are branching ulcerations that resemble the branches of a tree. They are often seen on the surface of the cornea and are caused by the replication of the herpes simplex virus within the epithelial cells.

Terminal Bulb Ends: At the tips of the dendritic lesions, there are usually small rounded or bulbous structures. These terminal bulbs are indicative of active viral replication within the cells.

Epithelial Involvement: The virus primarily affects the epithelial layer of the cornea, causing inflammation, ulceration, and the characteristic dendritic pattern.

Stromal disease occurs i.e. clouding of cornea due to scar formation, resulting in blurred vision (or ultimately no vision) – requires urgent referral to ophthalmology.

44
Q

Discuss Diagnosis of HSV keratitis.

A

Diagnosis of HSV keratitis with characteristic dendritic lesions can often be done by a primary care provider during the initial evaluation

Primary care providers can also start treatment BUT referral of the patient to an ophthalmologist within a few days for follow-up must be done

Especially, if the initial diagnosis is suspected to be stromal disease a prompt ophthalmologic referral is recommended.

Commonly by clinical history & physical examination without lab testing. Slit lamp (specialized magnifying microscope used for eye exam) is usually needed to confirm pathognomonic (characteristic) lesions.

Usually presents with acute onset of eye pain, redness, visual blurring, photophobia & watery ocular discharge. Presentation usually unilateral.

Scrapings of epithelial lesions collected. Three types of tests can be done if available:

*Viral culture (gold standard)
*Detection of viral antigen (viral antigen assay)
*Detection of viral DNA (PCR)

Immunofluorescence fluorescein staining under cobalt blue lighting can also be done.

45
Q

Discuss the management of Herpes simplex keratitis.

A

Since potentially vision-threatening: requires rapid ophthalmologic referral.

-Topical glucocorticoid monotherapy to be avoided
Use of topical glucocorticoid therapy should be administered by the ophthalmologist, in combination with antivirals.

Glucocorticoids: commonlyprednisolone acetate 1% suspension

Oral treatments e.g. oral acyclovir; topical agents: acyclovir (3%) typically preferred (or ganciclovir, 0.15%)

Significant corneal scarring may require corneal transplantation.

46
Q

Define trachoma.

A

Trachoma is an infectious eye disease caused by the bacterium Chlamydia trachomatis.

It is the leading preventable cause of blindness worldwide.

The infection causes roughening and scarring of the inner surface of the eyelids, leading to pain, discomfort, and eventual blindness if left untreated.

Trachoma is characterized by repeated eye infections, which can result in scarring on the inside of the upper eyelid.

This causes the eyelid to retract and the eyelashes to turn inwards, a condition known as trachomatous trichiasis. The inward-turning eyelashes can rub against the eyeball, causing further damage to the cornea.

*Initially a bacterial conjunctival infection

*Repeated episodes lead to keratoconjunctivitis & leading cause of infectious blindness in certain areas of the world

47
Q

Discuss the transmission of trachoma.

A

Direct i.e. via hands (with eye, nose & throat secretions) from affected individuals

Contact with fomites i.e. inanimate objects e.g. handkerchiefs, towels, washcloths contaminated with the secretions

Vector i.e. fly species Musca sorbens can carry & transmit Chlamydia trachomatis.

48
Q

Discuss the epidemiology of trachoma.

A

More in tropical areas and low-income areas to lack of antibiotics for treatment.

Endemic in >50 countries (mainly tropical) i.e. west Africa, Middle East, Asia, Latin America, Pacific Islands & remote Aboriginal communities in Australia (resource limited regions)
>80 million people worldwide with active trachoma

> 7 million with trichiasis (ingrown eyelashes)

> 1 million have blindness due to corneal scarring.

In many endemic regions, women have x2-6 more rates of trachoma vs. men. May be due to women having ongoing exposure to children with C. trachomatis infection.

49
Q

Apart from trachoma, name other diseases caused by Chlamydia Trachomatis.

A

Chlamydia trachomatis mostly known as a prevalent cause of Urogenital infection, STIs.

Can also cause ophthalmia neonatorum & inclusion conjunctivitis.

50
Q

Outline Certain C. trachomatis serotypes and their associated infections.

A

Certain C. trachomatis serotypes:
*D – K associated conjunctivitis (& assoc. genital infections)
-But serotypes A, B, Ba, & C associated with Trachoma.

51
Q

Contagious eye infection
-Leading infectious cause of blindness in certain low resource tropical countries
-Blinding endemic occurs in areas with poor personal & family hygiene.

Name the disease.

A

Trachoma

52
Q

Gram-negative coccoid or rod shaped, non-motile bacteria.

Cytoplasmic membrane & outer membrane similar to Gram-negative bacteria but lack/minimal (debatable) peptidoglycan cell wall.

Thus, resistant to -lactam antibiotics such as penicillin,

Obligate intracellular bacteria of eukaryotic cells with tropism for epithelial cells.

Cannot survive outside of a eukaryotic host.

Name the pathogen.

A

Chlamydia

53
Q

Humans are only known natural host for what Chlamydia?

A

Humans are only known natural host forC. trachomatis.

54
Q

Describe C. trachomatis life cycle.

A
  1. Elementary body: Bacteria initiate uptake by endocytosis into host cell, in the ‘elementary body’ (EB) form.

EB- infectious & non-replicatingdispersal form analogous to a spore, found in secretions, attaches to host cells.

  1. Within the endosome, it inhibits phagosome-lysosome fusion, allowing intracellular survival of the bacteria.
  2. Reticulate body: Within 8 hours EB transforms into a replicating non-infectiousreticulate body (RB).
    Multiplies by binary fission within an isolated area called an inclusion body (detected in diagnosis).
  3. Within 24 hours, the RB transforms back to EB form & released from the cell by exocytosis (host cell wall bursts) to infect adjacent cells.
  4. One phagosome usually produces 100-1000 EB. They are released.
55
Q

Discuss the following:
1. Active trachoma
2. Cicatricial disease

A

Active trachoma (inflammation) affects mostly young children with a peak incidence 4 – 6 yrs.

Subsequent scarring & blindness seen more in adults.

Cicatricial disease due to repeated episodes of infection. Causes recurrent conjunctival inflammation, leading to eyelid scarring, trichiasis (ingrown eyelashes), corneal opacification & subsequent blindness.

56
Q

Discuss Trichiasis & its sequelae.

A

Trichiasis is a medical condition characterized by the abnormal positioning of eyelashes that grow back toward the eye, touching the cornea or conjunctiva.

This can cause irritation, discomfort, and potential damage to the eye.

Repeated inflammation in eyelid causes scar tissue & distortion, Eyelashes rub cornea. (Ingrown eyelash/ Trichiasis)

Pannus - growth of vascular tissue over cornea as a result of oedema & ulceration due to eyelash abrasion. Hallmark of trachoma

Corneal opacity blurring part of the pupil margin.

CAN ALSO CAUSE THE FOLLOWING:
*Corneal Abrasion and Scarring: The misdirected eyelashes in trichiasis can rub against the cornea, leading to corneal abrasion. If the condition persists, scarring of the cornea can occur, which can affect vision.

*Corneal Ulcers: Trichiasis can sometimes result in corneal ulcers, which are open sores on the Cornea. Corneal ulcers can be painful and may cause further damage to the eye.

*Punctate Keratopathy: Punctate keratopathy refers to the presence of small, pinpoint-like lesions on the cornea. Trichiasis can contribute to the development of punctate keratopathy.

*Eye Irritation and Discomfort: The presence of misdirected eyelashes in trichiasis can cause redness, irritation, a foreign body sensation, tearing, sensitivity to light, and sometimes pain in the affected eye

57
Q

Infections of the vitreous &/or aqueous humors.

Where are the aqueous humor and vitreous humor located anatomically and state their respective functions?

A

Aqueous Humor:

-The aqueous humor is a clear fluid that fills both the anterior chamber (front part) and the posterior chamber of the eye.

-It is mainly produced by the ciliary body, a structure supporting the lens of the eyeball.

-The aqueous humor provides nourishment to various ocular tissues, helps maintain the shape of the eye, contributes to refraction, and prevents eye dryness.

-It also plays a role in immune response to defend against pathogens.

The vitreous humor:

*It is a transparent, gel-like substance that fills the space between the lens and the retina within the eye.

*It is located in the posterior segment of the eye and fills the vitreous chamber, which takes up about 80% of the eye.

The vitreous humor is surrounded by a layer of collagen called the vitreous membrane, which separates it from the rest of the eye.

FUNCTIONS
-Maintaining Eye Shape.
-Supporting the Retina
-Allowing Light Transmission TO reach the retina
-Shock Absorption
-Distribution of Oxygen

58
Q

Define Endophthalmitis.

A

Endophthalmitis is an infection that affects the tissues or fluids inside the eyeball.

Damaging infection involving vitreous &/or aqueous humors.

Irreversible damage to retina photoreceptor cells.

Despite aggressive therapeutic & surgical intervention partial or complete vision loss possible.

59
Q

There are two main types of endophthalmitis: exogenous and endogenous.

Discuss them.

A
  1. Exogenous endophthalmitis occurs when an infection is introduced into the eye from an external source, such as after eye surgery, penetrating ocular trauma, or as an extension of corneal infection.

*Post cataracts surgery infection or other ocular surgeries by conjunctival normal flora.

  1. Endogenous endophthalmitis arises from the spread of infection from a distant source in the body through the bloodstream.
60
Q

Discuss Acute post cataract endophthalmitis.

How does it cause damage to the eye and blindness?

A
  1. Acute post-cataract endophthalmitis refers to the development of endophthalmitis, an infection within the eye, following cataract surgery. It is considered a rare but serious complication of cataract surgery.
  2. Surgery performed through anterior chamber may result in bacterial contamination of aqueous humor by conjunctival normal flora.

-Normally this is a low inoculum & cleared BUT if vitreous humor is contaminated, risk of endophthalmitis greatly increases.

-The infection can lead to the destruction of the delicate structures of the eye, including the retina photoreceptors, which is responsible for capturing and transmitting visual information to the brain. Damage to the retina can result in permanent vision loss.

In addition, the infection and inflammation can cause scarring and fibrosis within the eye, leading to distortion and disruption of the normal anatomy. This can further impair vision and contribute to blindness.

If left untreated or not treated effectively, acute post-cataract endophthalmitis can progress rapidly and cause irreversible damage to the eye, resulting in severe visual impairment or blindness.

61
Q

Outline the clinical presentations of Endophthalmitis.

A

*Inflamed conjunctiva
*Hazy cornea
*Hypopyon (pus in anterior chamber).

62
Q

Conjunctiva habitat for various resident microorganisms.

Discuss Normal flora of conjunctiva.

A

Predominant species:
-Coagulase negative Staphylococcus i.e. S. epidermidis
-Streptococcus species

Others:
Corynebacterium, Propionibacterium acnes, Staphylococcus aureus, Escherichia coli, Haemophilus & Pseudomonas species

63
Q

Discuss acute post cataract endophthalmitis.

*Symptoms:
*Causative bacteria:

A

Symptoms
*75% of cases, symptoms occur within a week after surgery
*Decreasing vision
*Eye ache
*Light sensitivity
*Hypopyon (layer of white blood cells in anterior chamber)
*Conjunctival chemosis: Conjunctival chemosis refers to the swelling or edema of the conjunctiva.

Causative bacteria:
-Staphylococcus epidermidis~70%
-Staphylococcus aureus ~10%
-Streptococci ~9%
-Other Gram+ bacteria ~5%
-Gram- bacteria ~6%

64
Q

Discuss Endogenous endophthalmitis.

-Epidemiology
-Population at risk
-Causative pathogens

A

Rare: 2-8% of endophthalmitis cases
Hematogenous spread of bacteria into posterior segment of eye.

Populations at greatest risk
*Immunocompromised patients
*Patients with prolonged indwelling devices
*Intravenous drug abusers

Causative pathogens
*S. aureus, Bacillus cereus
*Gram-ve organisms including Escherichia coli, Neisseria meningitidis & Klebsiella spp.

Fungal pathogen
- Candida albicans

(Bacillus spp. – primary bacterial cause of endogenous endophthalmitis in intravenous drug abusers. i.e. from contaminated injection paraphernalia and drug solutions)

65
Q

Discuss the diagnosis of endophthalmitis.

A

*Must be confirmed by positive aqueous or vitreous culture (but negative culture does not exclude infection)

*Aspirate of vitreous humor

-Gram stain

-Bacterial Culture e.g. blood agar, chocolate agar, anaerobic media & Sabourad agar (for fungi)

-Identification tests & antimicrobial susceptibility tests

-Molecular assays may also be used i.e. PCR

66
Q

Discuss the management of endophthalmitis

A

Medical emergency

  1. Intravitreal/ direct injection of antibiotics into vitreous humor + topical/subconjunctival
  2. Vancomycin + ceftazidime or amikacin (Ceftazidime preferred due toxicity concerns) (systemic antibiotics also given alongside but debatable)
  3. Vitrectomy – surgical debridement of vitreous humor

Management of inflammation in endophthalmitis

*Corticosteroids: anti-inflammatory agents used in the management of endophthalmitis

BUT not for fungal endophthalmitis because enhance fungal growth by weakening defense mechanisms within the body.

*Administered as an intravitreal injection, topical drops or systemically

Supportive Therapy
*Cycloplegic agents’ essential part of treatment to relieves ciliary muscle spasms

*In patients with elevated intraocular pressure, vitreous tap before intravitreal injection also helps reduce intraocular pressure

67
Q

Infections of tissues anterior & posterior to the orbital septum.

Discuss Pre versus Post septal cellulitis.

A

Preseptal cellulitis, also known as periorbital cellulitis, refers to an infection of the tissues localized anterior to the orbital septum.

The orbital septum is a thin membrane that separates the front of the eye from the eyelids and surrounding tissues.

Preseptal cellulitis typically affects the eyelids and periocular region in front of the orbital septum.

It can be caused by minor trauma to the eyelid, such as an insect bite, or the spread of another infection, such as a sinus infection.

Post septal cellulitis, also known as orbital cellulitis:

-It involves infection of the tissue’s posterior to the orbital septum.

-It affects the soft tissues within the bony orbit, including the fat and muscles.

-Orbital cellulitis is often caused by the spread of infection from adjacent structures, such as the paranasal sinuses or teeth, or as a complication of trauma or ocular surgery
.

The key distinction between pre-septal and post-septal cellulitis lies in the location of the infection relative to the orbital septum.

  1. Preseptal cellulitis is localized anterior to the orbital septum, while orbital cellulitis involves the soft tissues posterior to the orbital septum.

May be confused because both cause ocular pain, eyelid swelling & erythema. BUT involve different anatomic sites.

  1. Preseptal cellulitis generally a mild condition, whereas post septal/ orbital cellulitis may cause loss of vision.
68
Q

Discuss pre-septal cellulitis (Peri-orbital cellulitis)

  1. Etiology and route of infection, CAUSATIVE PATHOGENS
  2. Clinical symptoms:
  3. Diagnosis
  4. Management
A

Pre septal / Periorbital cellulitis
-Infection & inflammation of the soft tissues i.e. eyelids & soft tissues anterior to the orbital septum.
-No orbital/ eyeball involvement.
-May initially appear as conjunctivitis prior to tissue swelling.

Causative pathogens

-Streptococcus pneumoniae
-Haemophilus influenzae
-Staphylococcus aureus
-Moraxella catarrhalis

Etiology:
*Sinusitis
*Trauma to eyelids
*Eyelid abscess
*Respiratory infection
*Bacteremia

Clinical symptoms:
-Unilateral ocular pain
-Eyelid swelling
-Erythema

Diagnosis
***Important to establish eyeball movement i.e. can follow a moving finger to distinguish from ‘orbital cellulitis’

Management
Oral (or intravenous) Broad spectrum antibiotics

69
Q

Pre-septal cellulitis can also be caused by skin infections mainly due to S. aureus & S. pyogenes.

Describe the following skin infections:
1. Impetigo
2. Cellulitis
3. Hordeolum (stye)
4. Dacryocystitis:
.

A

Impetigo:

Impetigo is a highly contagious bacterial skin infection that commonly affects children.
-It is characterized by weeping, exudative areas with a honey-colored crust on the surface.

-It is usually caused by Staphylococcus aureus bacteria but can also be caused by group A Streptococcus.
-Impetigo can be spread through direct contact and is often seen on the face and hands
.

  1. Cellulitis:

Cellulitis is a bacterial infection of the skin and underlying tissues.

-It can occur anywhere on the body, including around the eye.

-Cellulitis is typically caused by Streptococcus or Staphylococcus bacteria.

-It is characterized by redness, swelling, warmth, and pain in the affected area.

-Cellulitis requires prompt treatment with antibiotics to prevent the infection from spreading and causing complications
.

  1. Hordeolum (Stye):

A hordeolum, commonly known as a stye, is a localized infection or inflammation of the eyelid.

It usually appears as a red, painful bump on the eyelid, often near the base of the eyelashes.

Styes are typically caused by a bacterial infection, often Staphylococcus aureus. Most styes resolve on their own within a few days, but warm compresses and good eyelid hygiene can help alleviate symptoms.

  1. Dacryocystitis:

Dacryocystitis is an infection or inflammation of the lacrimal sac, which is located in the inner corner of the eye.

It can be caused by bacteria or viruses and is often associated with a blockage or narrowing of the tear drainage system.

Dacryocystitis can result in redness, swelling, pain, and discharge in the area around the tear sac.

Treatment may involve antibiotics, warm compresses, and in some cases, surgical intervention to address the underlying tear duct obstruction.

70
Q

Discuss Post-septal / Orbital cellulitis.

How is it differentiated from pre-septal cellulitis?

Discuss the diagnosis.

Treatment options?

A
  1. Infection involving the contents of the orbit: fat & extraocular muscles. In most cases it is due to extension of paranasal sinus infection into orbital region
  2. Whereas “Preseptal cellulitis” is generally a mild condition ORBITAL cellulitis may cause loss of vision

3.Ophthalmoplegia

Orbital cellulitis distinguished from pre-septal cellulitis by its clinical features:

**Ophthalmoplegia, pain with eye movements, and proptosis)

Diagnosis: CT &/ or MRI by imaging studies.

-In cases in which the distinction is not clear, clinicians should treat patients as though they have orbital cellulitis.

71
Q

Outline Other potential causes of Post-septal / Orbital cellulitis.

A

-Ophthalmic surgery
-Peribulbar anesthesia
-Orbital trauma with fracture or foreign body
-Dacryocystitis
-Bacteremia
-An infected mucocele/ mucous cyst that erodes into the orbit

72
Q

State the 3 main symptoms specific to orbital cellulitis.

A

-Ophthalmoplegia (pain when rolling eyes to different directions)
-Proptosis (bulging eye)
-Double vision (diplopia)

73
Q

State the Hallmarks of orbital cellulitis.

A

**Chemosis (swelling or blistering),

**Decreased visual acuity

**Fever, pain.

**Proptosis/ Exophthalmos – bulging out & complete or partial dislocation of eye from the orbit

**Ophthalmoplegia - paralysis of extraocular muscles, responsible for eye movement. Eyeball does not move.

74
Q

Outline the causative pathogens for orbital cellulitis.

A

Causative pathogens
Staphylococcus aureus & Streptococci species
Streptococcus anginosus
Streptococcus pneumoniae
Non typeable H. influenzae
Beta-haemolytic Streptococci
Anaerobes

Rare:
Fungi- Mucorales or Aspergillus spp (immunocompetent infants)
Mycobacterium tuberculosis

75
Q

Discuss the diagnosis and management of orbital cellulits

A

Diagnosis

-Establish that eyeball does not move (ophthalmoplegia)
-CT & / MRI scan

Management
*Drainage & broad-spectrum antibiotics (intravenous): Vancomycin or cefotaxime

CEFOTAXIME
*Cell wall synthesis inhibitor: cefotaxime binds to and inhibits penicillin-binding proteins (PBPs) in bacterial cell walls. This prevents the cross-linking of peptidoglycan chains, which are essential for the structural integrity of the bacterial cell wall.

76
Q

Outline other diseases that affect the different parts of the eye.

A
  1. Lens abnormalities
    *Cataracts
    *Lens dislocations (acute glaucoma)

Raised intraocular pressure i.e. Glaucoma

  1. Diseases of the uvea
  2. Diseases of the retina
    May be inflammatory, vascular or degenerative.
  3. Diseases of the orbit
    -Lesions to the orbit
    -Including lymphomas