Dacryocystitis and infectious keratitis

• Acute dacryocystitis is infection of the lacrimal sac, usually because the nasolacrimal duct is blocked; the sac becomes a warm, tender swelling below or at the medial canthus, and the usual organisms are Staphylococcus aureus and the streptococci.
• Infectious keratitis is a sight-threatening corneal infection. The main types are herpes simplex, bacterial (often contact-lens related, with Pseudomonas aeruginosa), fungal, and Acanthamoeba, and they look different enough to separate late at night with a slit lamp and fluorescein.
• Bacterial and Acanthamoeba infection must be assumed when a contact lens wearer has a painful red eye with a corneal defect; do not paste a steroid on an undiagnosed ulcer.
• Red flags are central or paracentral ulcer, hypopyon, a ring infiltrate, corneal thinning or perforation, severe pain with photophobia, and any drop in vision; these need same-day ophthalmology referral.
• In low-resource settings the diagnosis is clinical, empiric broad-spectrum topical treatment is started early, and self-medication with steroid drops is a major cause of advanced disease.

By the end of this page you should be able to:

1. Explain how nasolacrimal duct obstruction leads to acute dacryocystitis, name the typical organisms, and outline medical and definitive management.
2. Distinguish herpes simplex, bacterial, fungal and Acanthamoeba keratitis by history, pain level, slit-lamp findings and fluorescein pattern.
3. List the risk factors for each major type of infectious keratitis.
4. Use a simple algorithm to decide which tests to do and when to refer before treatment.
5. State the first-line therapies for each type, including a steroid caution.
6. Recognise sight-threatening red flags and state what must happen next.
7. Describe practical management when culture, confocal microscopy or antifungal drops are not available.

The nasolacrimal duct drains tears from the lacrimal sac into the inferior nasal meatus. When it is blocked, the sac is a closed pouch: stasis follows, the mucosa becomes inflamed (dacryocystitis in the broad sense), and the normal conjunctival and skin flora turn the retained contents into an acute infection. Dacryocystitis can therefore be considered in two stages:

• Chronic or low-grade obstruction, with epiphora and sometimes a mucocoele but little pain.
• Acute infection on top of obstruction, with pain, redness and swelling.

Classification here is by organism, because organism drives treatment:

• Viral: herpes simplex keratitis (epithelial/dendritic, stromal, endothelial/diciform).
• Bacterial: most contact-lens related disease is Pseudomonas aeruginosa; non-contact-lens disease more often Staphylococcus aureus, Streptococcus pneumoniae, or Moraxella.
• Fungal: filamentous (Fusarium, Aspergillus) in tropical trauma and contact-lens cases; yeasts (Candida) in immunocompromised or chronically diseased eyes.
• Protozoal: Acanthamoeba.

Infectious keratitis is a major avoidable cause of monocular blindness. Corneal opacity from all causes is ranked among the leading causes of blindness globally and affects an estimated 4 to 6 million people with unilateral or bilateral visual impairment.^[5] The incidence of microbial keratitis varies widely by climate and lifestyle, from about 2.5 to over 700 cases per 100,000 person-years, with much higher rates in low- and middle-income countries.^[5]

Fungal keratitis is concentrated in the tropics: filamentous fungi account for an estimated 20 to 60% of culture-positive microbial keratitis in tropical and developing regions, and a systematic review estimates a minimum global annual incidence of 1,051,787 cases (range 736,251 to 1,367,323), possibly 1,480,916 if culture-negative infections are presumed fungal.^[3] About 8 to 11% of affected eyes eventually require evisceration or enucleation.^{[3] [5]}

Acanthamoeba keratitis (AK) accounts for only about 5% of infectious keratitis but is responsible for roughly half of the cases of vision loss.^[4] Its global annual incidence is estimated at about 2.3 cases per million, rising to roughly ten times that in contact-lens wearers.^[4]

Uncomplicated acute dacryocystitis is common in all ages and both sexes; exact incidence is not well established in open sources, and it is usually managed in primary or secondary eye care.

The immediate cause is obstruction of the nasolacrimal duct. Common mechanisms:

• Involutional (age-related) narrowing or stenosis of the nasolacrimal duct, the commonest cause in adults.
• Congenital obstruction in infants (dacryostenosis).
• Nasal or sinus disease, turbinate hypertrophy, a deviated septum, or sinus surgery distorting the distal duct.
• Dacryoliths or concretions in the sac or duct.
• Trauma or fracture involving the lacrimal fossa.
• Tumours of the lacrimal sac or adjacent nose (always consider in atypical or recurrent cases).
• Previous facial or nasal surgery.

The organisms that secondarily infect the sac are those of the ocular surface and skin: Staphylococcus aureus and the streptococci are the classic pair taught for acute dacryocystitis. Mixed infection is common.

The risk factor is more useful than the organism name, because it tells you what to look for:

• Contact-lens wear, especially overnight or extended wear, and poor lens hygiene (cleaning with tap water, contaminated cases or solution). This is the dominant risk factor for both Pseudomonas aeruginosa and Acanthamoeba. ^{[7] [4]}
• Ocular trauma, especially with vegetable matter (thorn, branch, husk) in tropical settings: points to fungi.
• Chronic surface disease: dry eye, bullous keratopathy, chronic dacryocystitis, ectropion, entropion, trichiasis, lagophthalmos.
• topical or systemic corticosteroids, and topical anaesthetic abuse.
• Systemic: diabetes, immunosuppression, malnutrition, alcohol and drug misuse, intravenous drug use, malignancy, HIV.
• Previous keratoconjunctivitis, especially herpetic eye disease, raising the risk of recurrent herpes simplex keratitis with triggers such as fever, stress, illness, sun exposure, menstruation, immunosuppression or trauma.

Tears flow from the puncta through the canaliculi into the lacrimal sac and down the nasolacrimal duct into the nose. Obstruction (usually at or below the sac–duct junction) turns the sac into a stagnant reservoir. Retained tears and mucus change its pH and bacterial flora; inflammation thickens and scars the walls, which in turn worsens the obstruction. Once the duct is genuinely occluded, the sac distends with a mucocoele or (if infected) a tense, painful abscess. If the wall ruptures or infection penetrates tissues, preseptal or orbital cellulitis can follow.

A separate, newer entity is acute dacryocystic retention (reversible obstruction): a sudden mechanical block of tears, often with a cast or small dacryolith, producing severe pain and a tense, non-fluctuant sac that resolves spontaneously or with conservative management, sometimes without antibiotics. It can be mistaken for infection.^[1]

After primary mucosal infection the virus becomes latent in the trigeminal ganglion (usually the first division, V1). Reactivation sends virus back to the cornea along the nerve. The result depends on which layer is inflamed:

• Epithelial keratitis: live virus replicates in epithelium, producing the classic dendritic (branching, terminal-bulb) ulcer seen with fluorescein.
• Stromal keratitis (interstitial/necrotising): mainly immune-mediated inflammation driven by viral antigen in the stroma, not active replication.
• Endothelial (disciform) keratitis: an immune reaction targeting endothelium, with corneal oedema and keratic precipitates.

Recurrences are the rule and the visual morbidity comes from stromal scarring, not from any single episode.

Organisms adhere to the epithelium (especially a contact lens), then invade through a micro-defect into the stroma, where they multiply and release enzymes and toxins. Pseudomonas aeruginosa is particularly destructive: it can liquefy stroma and perforate within hours. Because penetration is rapid, therapy must be intensive and started before culture results return.

Fungi are slower than bacteria to grow but harder to eradicate: they penetrate the stroma along lamellae, may reach Descemet's membrane, and respond poorly to standard topical antibacterial drops. Topical corticosteroids allow them to advance. Differentiation from bacterial disease is often clinical plus microscopy and culture.

Acanthamoeba is a free-living protozoan (trophozoite and cyst). It binds to mannosylated glycoproteins on the corneal epithelium, enters stroma, and produces radial neuritis, ring infiltrates and disproportionate pain. The cyst form is highly treatment-resistant and explains relapse and long treatment courses.

• History: epiphora that may precede the acute episode; acute onset of pain, swelling and redness at the inner canthus.
• Pain is usually severe and localised.
• Examination: a warm, tender, erythematous swelling below or at the medial canthal tendon. Purulent reflux from the puncta may be expressed on pressure. Fever may occur.
• If the swelling is above the medial canthal tendon, think of ADR or an orbital/upper sac problem and image it.^[1]
• Red flags: orbital cellulitis signs (proptosis, restricted eye movement, vision loss, fever) or any suspicion of tumour in an older adult.

All types share redness, pain, photophobia, watering and blurred vision, but the pattern differs:

• Onset and course: bacterial is usually rapid (hours to days); fungal slower (days to weeks); herpes reactivates in a previously affected eye.
• Pain: Acanthamoeba is classically out of proportion to findings; herpetic epithelial disease often has surprisingly little pain because corneal sensation is reduced; bacterial disease hurts.
• Discharge: purulent in bacterial; minimal in viral.
• Vision: drop with central disease or oedema.

Slit-lamp and fluorescein findings:

• Herpes simplex epithelial: branching linear ulcer with terminal bulbs (dendrite) that stains brightly with fluorescein; reduced corneal sensation.
• Bacterial: focal stromal infiltrate with an overlying epithelial defect; hypopyon, purulent discharge.
• Fungal: feathery, irregular infiltrate edges, satellite lesions, endothelial plaque, sometimes a raised lesion with hyphate margins.
• Acanthamoeba: radial keratoneuritis (radial lines), ring infiltrate (ring of stromal infiltrate), pseudodendrites.

• Slit-lamp examination with fluorescein staining and documentation (including size and depth of the defect and infiltrate).
• Corneal sensation (cotton wisp): reduced in herpetic disease.
• Scraping and culture before starting antibiotics if the ulcer is large, central, severe, atypical, or in a contact-lens wearer. Plate on blood agar, chocolate agar and Sabouraud dextrose agar; Gram stain and KOH preparation the same day.
• Confocal microscopy where available: high sensitivity for Acanthamoeba (bright cysts) and for filamentous fungi.
• PCR for HSV and for Acanthamoeba where available.
• Imaging (CT) for suspected acute dacryocystic retention, tumour, or orbital extension.
• Lacrimal syringing/dye disappearance after the acute episode to document obstruction.

There is no universal staging score for dacryocystitis. It is diagnosed clinically, supported by imaging when the presentation is atypical or when a mass or orbital extension is suspected.

For Acanthamoeba keratitis, the following staging (Robaei et al.) is often used and explains why outcomes differ:

• Stage 1: corneal epitheliopathy only.
• Stage 2: one or more corneal epithelial defects, perineural infiltrate, stromal infiltrate.
• Stage 3: a corneal ring infiltrate with one or more features of stage 2.^[4]

In one real-world series, 16 of 39 patients (41%) had stage 3 disease at presentation, and 59% had gone more than 30 days from symptom onset to starting treatment.^[4]

• Warm compresses and analgesia.
• Oral antibiotic covering Staphylococcus aureus and the streptococci. An anti-staphylococcal penicillin or a beta-lactam/beta-lactamase inhibitor is the usual choice; one reported case used 1 g oral amoxicillin-clavulanate with topical erythromycin ointment twice daily.^[1]
• Topical antibiotic ointment to the ocular surface is often added.
• If an abscess has formed, incision and drainage.
• Systemic signs or orbital involvement require intravenous antibiotics and imaging.

• A first episode in an older adult often settles and can be observed, but recurrence is common because the obstruction remains.
• Document patency with dye disappearance and lacrimal syringing once inflammation has settled.
• If obstruction persists or episodes recur, dacryocystorhinostomy (DCR), external or endoscopic, is the definitive procedure; an inferior turbinate fracture may help when nasal anatomy contributes.^[1]
• Treat contributing nasal disease (rhinitis, turbinate hypertrophy, septal deviation) before or with DCR.
• In reversible obstruction (acute dacryocystic retention), conservative management may be curative without antibiotics.^[1]

The table summarises the organism-specific therapy.

• Stop contact-lens wear immediately and discard (do not reuse) the lens and case; culture the lens and case if possible.
• Debride loose necrotic epithelium if directed by ophthalmology.
• Cycloplegia (e.g. atropine 1%) for pain and ciliary spasm.
• Lubricants and a protective shield; avoid pressure patching in infection.
• Treat the cause of exposure (ectropion, lagophthalmos) later.

• Bacterial or fungal: therapeutic penetrating keratoplasty for perforation, deep stromal melting, or uncontrolled infection. Amniotic membrane grafts and tissue adhesives for small perforations.
• Herpes: keratoplasty for deep scarring with long antiviral cover; tectonic grafts for perforation.
• Acanthamoeba: keratoplasty in 20 to 25% of patients for perforation or later visual rehabilitation.^[4]
• Dacryocystitis: DCR once the sac is quiet.

• Review bacterial disease daily until improvement; fungal and Acanthamoeba disease weekly then as directed.
• Stop or taper therapy based on epithelial healing and infiltrate resolution, not on a fixed date.
• Photograph the lesion at each visit.

Refer the same day when any of these are present:

• Central or paracentral ulcer
• Hypopyon
• Dense infiltrate larger than about 2 mm, or any stromal thinning
• Suspected perforation or descemetocele
• Severe pain with photophobia
• Reduced vision
• No improvement after 24 to 48 h of appropriate therapy
• Contact-lens wearer with any corneal defect
• Fungal or Acanthamoeba disease suspected
• Acute dacryocystitis with fever, orbital signs, or poor response to oral antibiotics

• Corneal scarring and opacity (the main cause of permanent visual loss).
• Corneal thinning and perforation, most feared with Pseudomonas aeruginosa (hours) and fungal disease.
• Secondary infection or polymicrobial infection.
• Anterior uveitis, posterior synechiae, cataract and glaucoma after severe disease.
• Endophthalmitis and, rarely, loss of the eye.
• Dacryocystitis: orbital cellulitis, abscess, fistula; rarely sepsis.
• Acanthamoeba: severe scarring, need for keratoplasty in 20 to 25%.^[4]

• Bacterial keratitis that is treated early, especially disease confined to the epithelium, usually heals with useful vision. Central ulcers, large infiltrates and delayed treatment predict scarring and grafting.
• Herpes simplex keratitis is recurrent; the prognosis depends on the number and severity of stromal episodes and on how much scarring has accumulated.
• Fungal keratitis has a worse prognosis than bacterial in most series; about 8 to 11% of eyes are lost.^[3]
• Acanthamoeba keratitis treated with PHMB 0.08% achieved medical cure in 35 of 39 patients (89.7%), with a median time to cure of 95 days (interquartile range 63 to 140 days).^[4] Late diagnosis, deeper disease and prior corticosteroid use all worsen outcomes.^[4]

• Counsel contact-lens wearers: no overnight wear unless prescribed, no tap water on lenses or cases, replace cases regularly, wash hands before handling, and stop wearing the lens at the first symptom.
• Trauma prevention (eye protection) and rapid irrigation after chemical or organic injury.
• Prompt referral and treatment of dacryocystitis to prevent orbital extension; treat recurrent episodes definitively.
• In recurrent herpes simplex, long-term antiviral prophylaxis (oral aciclovir or valaciclovir) is often used after specialist assessment.^[2]

• Children: congenital nasolacrimal obstruction is common and usually resolves by 12 months; persistent obstruction or recurrent dacryocystitis warrants probing and (later) DCR. In children, keratitis with trauma is more likely bacterial or fungal.
• Pregnancy: topical treatment is preferred; systemic antivirals and antifungals need obstetric and ophthalmology agreement.
• Older adults: involutional nasolacrimal obstruction and atypical (including neoplastic) lacrimal sac disease; biopsy any suspicious mass.
• Immunocompromised: Candida and other opportunistic fungi, and more aggressive Pseudomonas.

Dacryocystitis and infectious keratitis are more disabling where access to care is late. Practical points from low-resource experience:

• Microbial keratitis can present 2 to 3 weeks after symptom onset, often after self-medication with unidentified drops, including steroids that allow fungal disease to progress.^[5]
• Where scraping and culture are unavailable, treatment is empirical and clinical: for a severe corneal abscess, intensive hourly topical therapy (e.g. a fortified cephalosporin for bacteria, plus natamycin 5% because fungal disease cannot be excluded in the tropics, and ganciclovir when the aetiology is uncertain) can control infection and preserve useful vision.^[5]
• In vivo confocal microscopy and PCR are frequently unavailable; use clinical risk factors and fluorescein patterns to guide therapy.
• The commonest pathogens in tropical settings are different to temperate countries: fungal disease may be 40 to 60% of microbial keratitis.^[5]
• Acanthamoeba is easy to miss and often mis-labelled as herpetic or fungal disease; severe pain, ring infiltrate and contact-lens use in a tropical setting should make you suspicious even when initial smears are negative.
• Self-medication, shortage of trained staff, cost and transport are major barriers; simple education and early referral at primary level save sight.^[5]
• Where DCR is unavailable, refer recurrent dacryocystitis to a regional eye centre rather than repeating short courses of antibiotics.

• Acute dacryocystitis is infection of an obstructed lacrimal sac, typically with Staphylococcus aureus and streptococci; treat the acute episode, then fix the obstruction.
• Warm compresses, an oral anti-staphylococcal antibiotic, and drainage of any abscess control the acute episode. DCR is definitive for recurrent disease.
• Infectious keratitis is an emergency. Separate the types by risk factor, pain, and fluorescein pattern.
• Herpes simplex gives dendritic ulcers with terminal bulbs and reduced sensation; antivirals (topical ganciclovir 0.15%, and oral agents for stromal/endothelial disease) plus a cautious, antiviral-protected use of steroid.
• Bacterial and Pseudomonas disease is rapid and destructive: remove the lens and start intensive topical therapy the same day.
• Fungal disease is slower and feathery, worsened by steroids; natamycin 5% is first-line for filamentous fungi.
• Acanthamoeba causes disproportionate pain, ring infiltrates and radial keratoneuritis; PHMB 0.08% gave a medical cure in about 9 in 10 patients, but treatment runs to months. ^[4]
• Red flags (central ulcer, hypopyon, perforation risk, vision loss, deterioration) always mean same-day referral.
• In low-resource settings, empirical broad-spectrum topical therapy started early preserves sight.

Plain-text follow-ons (no verified topics are linked, so these are listed for use once those topics exist): bacterial endophthalmitis after keratitis; ocular herpes zoster; corneal transplantation; orbital cellulitis; allergic and vernal keratoconjunctivitis; contact lens complications.