Lecture 54 Eye Infections Flashcards
Orbital Cellulitis characteristics
Painful swelling of the eyelids
Globe looks normal, but has restricted/painful motion
Fever > 102
Orbital Cellulitis causes
Often a spread of infection from another location:
Sinusitis (90%) => Staph/Strep/H. influenzae spread
Fungal
Arthropod bite
Trauma
Complication of dental extraction
Septicemia
Treatment for Orbital Cellulitis
Hospital
IV antibiotics or antifungal
Surgery
Blepharitis signs/symptoms
Inflammation of the eyelid
Red/itchy/gritty/burning/foreign body sensation
Excessive tearing, or dry eye
Eyelashes matted, crusted, missing, or misdirected
Blepharitis Causes
Staph: most common, overgrowth of normal flora, usually bilateral
Virus: HSV, VZV, Molluscum Contagiosum, assoc. with lesions, usually unilateral
Ectoparasite: Follicle Mites, Crab Lice
Blepharitis Treatment
Warm compress Clean eyes regularly Contacts can be worn Antibiotic, antiviral, tea tree oil (mites) Avoid steroids for viral infections
Hordeolum and Chalazion
Hordeolum: infection that is painful to palpation, usually caused by Staph
External Hordeolum: infection of gland of Zeiss
Internal Hordeolum: infection of Meibomian gland
Chalazion: granuloma formation in Meibomian gland, often not painful
can follow an internal hordeolum
Treatment: warm compress, generally resolve within days to weeks; otherwise, antibiotics or surgery can be implemented
Conjunctivitis
Red/Pink Eye Can have viral or bacterial cause Adenovirus is most common Usually self-limited to 2-4 weeks Transmitted by secretions: hand to eye Hand washing important for control Viral infection tends to be >12 y/o, itching, burning, watery, FB sensation, lymphadenopathy, hemorrhaging, longer course Bacterial infection tends to be
Follicular Conjunctivitis
Least severe type
Doesn’t involve the cornea
Usually caused by Adenovirus
Can be caused by HSV, VZV, Molluscum Contagiosum
Pharyngoconjunctival fever (PCF)
Adenovirus caused (Serotypes 3&7)
Follicular conjunctivitis with additional symptoms:
Fever, sore throat, headache, malaise
If bilateral, second eye becomes infected 1-3 days later and is less severe
Most often in kids
Epidemic Keratoconjunctivitis (EKC)
Adenovirus caused (Serotypes 8, 19, 37) Symptoms initially like PCF or the Flu Subepithelial corneal infiltrates Pseudomembrane may form Transmitted on contaminated equipment in clinics Rule of 8
Acute epidemic hemorrhagic conjunctivitis
Viral cause: Coxsackie virus A24, Enterovirus 70, (Adenovirus)
Acute onset, rapid course, self-limited 5-7 days
Subconjunctival hemorrhage prominent
Topical steroid use => bac superinfection
Assoc. with crowding and poor hygiene
More common in developing areas
Bacterial Conjunctivitis
Mucopurulent discharge
Actue: generally self-limited, antibiotics shorten course, but not necessarily needed
Common agents: S. aureus, S. pneumoniae, H. influnzae, Moraxella spp.
Hyperacute: more severe, requires systemic antibiotics
Spreads to cornea if untreated
Neisseria gonorrhoeae, menigitidis
Often concurrent infection with Chlamydia trachomatis
Inclusion conjunctivitis and trachoma
General info
Both caused by Chlamydia trachomatis (gram (-) obligate intracellular bacteria)
IC: serotypes D-K (assoc. with genital infections), named for inclusion bodies seen in infected cells, in neonates called neonatal conjunctivitis
Trachoma: serotypes A-C, can lead to complete vision loss, leading cause of preventable blindness in the world
Adult inclusion conjunctivitis
Usually unilateral, little to no discharge, transmitted by contact with infected fluids
Numerous papillae on lower conjunctival membrane
Scarring of cornea very rare
Trachoma general characteristics
Disease progression is slow
Lymphoid follicles and papillae develop on superior conjunctiva, papillae necrose and lead to scarring of the cornea and inversion of eyelids and lashes
Repeat infections required to lead to end stage blindness
Trachoma epidemiology
Assoc. with poverty and unsanitary conditions
Disease of the creche
Infection spread by vectors like flies, or infected fomites like dirty towels
Clean water and handwashing important to prevent trachoma and IC
Diagnosis of IC and Trachoma
Clinical signs
Scrapings and microscope looking for inclusion bodies
Treatment of IC and Trachoma
SAFE Strategy:
S: Surgery (limits scarring)
A: Antibiotics (Oral azithromycin, Topical Tetracycline) (IC only needs A)
F: Facial Cleanliness
E: Environmental Change (water supply and sanitation, improve community and personal hygiene)
Most likely organism and mechanism of neonatal conjunctivitis (ophthalmia neonatorum
Conjunctivitis in newborns less than 28 days old generally caused by inoculation during delivery by:
Neisseria gonorrhoeae
Chlamydia trachomatis
Ophthalmia neonatorum from Neisseria gonorrhoeae
50% of kids born to infected mothers Appears within 24-48 hours Often bilateral Purulent discharge Rapidly destructive Treat with systemic antibiotics
Ophthalmia neonatorum from Chlamydia trachomatis
70% of kids born to infected mother
5-15 days after birth
Unilateral or Bilateral
Keratitis general characteristics
Infection of the cornea
Unilateral, but can be bilateral
Severe pain, photophobia, impaired vision from scarred or damaged cornea
Correlated with use of immuno-suppressive agents for the eye
Keratitis pathogens
Viral:
HSV 1
VZV (shingles)
Adenovirus
Bacterial:
S. pneumonia
Pseudomonas aeruginosa
Fungal:
Candida
Aspergillus
Fusarium solani
Parasitic:
Acanthamoeba
HSV Keratitis
Leading cause of infectious blindness in developed countries => corneal transplant
Rare in kids, mostly adults
Many kinds: Stromal and Epithelial
Remember that HSV is known to remain latent in the trigeminal ganglia
Stromal HSV Keratitis
More sever of the HSV Keratitis types
Two types:
Non-necrotizing: also known as Immune Stromal Keratitis (ISK)
Necrotizing: immune response to viral infection causes necrotizing damage to the cornea
Epithelial HSV Keratitis
More common of HSV Keratitis types
Usually no pain, but irritation and tearing common
DENDRITIC ULCERS on corneal epithelium
VZV Recrudescence
Shingles outbreak from VZV in trigeminal will affect the eye in 50% of cases
Sharp lines of demarcation on face with lesions
Adenovirus keratitis
Characteristic punctiform lesions on the cornea
punctiform= form of a point
What will be observed if scrapings from the cornea of an HSV infection are observed under a microscope?
Multinucleated giant cells
Treatment and outcomes of viral keratitis
Common treatment is Acyclovir or ganciclovir
HSV keratitis will resolve without treatment, but treatment can minimize corneal damage
Shingle patients need treatment within 3 days of lesion appearance
Why is a central corneal ulcer that is not clearly due to HSV an emergency?
If not clearly due to HSV, it could be a bacterial infection.
Bac. infections of the eye progress rapidly and cause damage quickly.
Causes of bacterial keratitis
S. pneumonia and Pseudomonas aeruginosa
Bacterial infections of the cornea are not common, require a breach of the cornea from:
Surgery=> dry eyes
Abrasions
Or, just wearing contacts and allowing growth of Pseudomonas
Most common bacterial corneal pathogen in developing areas
Strep pneumoniae
Most common bacterial corneal pathogen in developed countries
Pseudomonas aeruginosa
Contact wearers–can live in some disinfectants, can’t otherwise bind to normal cornea without contact lenses
Formation of hypopyon (collection of leukocytes in anterior chamber)
What is quorum sensing
Some bacterial virulence factors are only expressed when the bacteria reach a certain density
What factors of contact lens use lead to increased chance of bacterial keratitis?
Soft contacts worse than others
Extended wear
Decreased O2 transmission
Preserved solutions
Fungal keratitis
Usually only in immunocompromised or those using topical steroids in the eye
Aspergillus
Candida
Fusarium solani
What should be suspected when a chronic case of keratitis does not respond to traditional therapy?
Acanthamoeba keratitis
Usually only possible if there has been an abrasion of the corneal epithelium
Therefore, generally unilateral
Most likely eye infection condition if patient’s first complaint is visual field loss or lost visual acuity, and is most often unilateral
Retinitis or Chorioretinitis
Common infective agents of retinitis and chorioretinits
Viral: CMV, HSV, VZV
Fungal: Histoplasma capsulatum
Parasites: Toxoplama gondii, Toxocara canis/cati, Baylisascaris procyonis
CMV Retinitis
Characteristics: Opportunistic infection of immunocompromised patients
Often an end-stage condition in AIDS patients leading to blindness
Left untreated=> permanent retinal damage and blindness
Diagnosis: Characteristic lesions– “Cheese Pizza” lesions on the retina, these are large patches of red (hemorrhage) and white (necrosis) on the retina
No inflammation in the vitreous humor
Symptoms: Blind spots, blurred vision, floaters, dec visual acuity, loss of peripheral vision, can be asymptomatic
Treatment: Antivirals injected or implanted, often Ganciclovir or Fomivirsen
Surgery to treat retinal detachment
HSV and VZV retinitis
Generally only immunocompromised patients
Poor prognosis for sight retention even if immunocompetent
Ocular histoplasmosis syndrome
Fungal infection of the retina caused by Histoplasma capsulatum
Endemic in the midwest and south central US
Often asymptomatic, symptoms don’t appear until years after infection
Rare condition, resembles macular degeneration
Histo-Spots = tiny scares of inflammation on the retina
Exogenous Endophthalmitis
Infection involving several layers of the eye and the vitreous/aqueous humors
Post-operative: most cases
Coagulase (-) staph–good prognosis
S. aureus, enterococci, Bacillus–poorer prognosis
Post-traumatic:
Staph most common, Bacillus cereus 2nd
Endogenous Endophthalmitis
Usually immune compromised
Most common underlying disease: DM II
2nd most common: IV Drug use
Immunosuppressive meds
Break down of blood-ocular barrier=> infection
Fungal >50% of the time–C. albicans
Bacterial:
Gram (+): coagulase neg Staph, Bacillus
Gram (-): Klebsiella, E. coli,
Components of immune privilege in the eye
Lack of blood and lymph vessels
Lack of MHC I receptors, but expression of HLA-G/E that suppress the function of NK cells
Increased expression of FAS ligand (used to signal apoptosis, helpful to tune down an immune response)
Anti-inflammatory/immunosuppressive proteins in the aqueous humor
ACAID–Anterior Chamber-Assoc. Immune Deviation
