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Infectious Scleritis

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Title: Infectious Scleritis
Authors: Andrew Nelson, MSIV, Keck School of Medicine of USC
Photographer: James Gilman, COA, FOPS; Roger Harrie, MD
Date: 08/23/19

Figure 1. Pseudomonas infectious scleritis after pterygium surgery. A) Slit-lamp photo showing deep episcleral injection, subconjunctival and episcleral infiltration, and areas of necrosis. Also present is an inferonasal, crescent-shaped area of corneal thinning.


Figure 1. Pseudomonas infectious scleritis after pterygium surgery. B) B-scan ultrasound biomicroscopy showing serous retinal detachment in posterior infectious scleritis.


Figure 2. Resolved infectious scleritis with mild conjunctival injection, multiple areas of scleral thinning, and persistent inferonasal corneal thinning.


Keywords/Main Subjects: Scleritis, Infectious Scleritis, Pseudomonas Scleritis
Diagnosis: Infectious Scleritis

Case Presentation:

A 67-year-old female presented with 1-2 months of left eye pain and redness. She had had pterygium surgery 10 months prior, after which a persistent episcleral plaque was noted. When the patient starting experiencing pain and redness, this plaque was removed and cultured. She had been started on topical steroids and cyclopentolate for presumed autoimmune scleritis, but symptoms continued to worsen over the ensuing two weeks. She steroid treatment was augmented to 60 mg oral prednisone, but the culture results came back, growing Pseudomonas aeruginosa. She decided to seek out a second opinion.

Examination Findings:

On exam, the left eye nasal to the limbus showed deep episcleral and subconjunctival injection as well as multiple nodules, areas of necrosis and scleral thinning (Figure 1A). An inferonasal crescent-shaped area of corneal thinning and inferior posterior synechiae were also present in the left eye. There was no anterior chamber cell or vitreous cell on exam. Fundus examination was limited due to discomfort, but choroidal folds were seen in the left eye. B-scan ultrasound revealed a nasal serous retinal detachment (Figure 1B).

Clinical Course:

The differential diagnosis of acute post-surgical scleritis includes traumatic activation of autoimmune scleritis, infectious scleritis, and surgically-induced necrotizing sclerokeratitis (SINS). Given culture positivity for Pseudomonas and the patient’s lack of response to corticosteroid therapy, treatment was initiated for infectious scleritis with oral levofloxacin, topical moxifloxacin, topical cyclopentolate, and topical difluprednate. Oral prednisone was tapered and discontinued. Patient also received a subconjunctival injection of ceftazidime two weeks later. Laboratory examination for uveitis was performed with all results returning negative. Inflammation gradually resolved with antimicrobial therapy and the patient retained temporal scleral thinning and inferonasal corneal thinning following resolution of the infection (Figure 2).


Scleritis refers to inflammation of the sclera, or the white portion of the eye between the uvea and Tenon’s layer, and most commonly occurs due to immune-mediated inflammation. Infectious scleritis is much less common given the lack of an external point of entry for pathogens with an intact conjunctiva. While only about 5-10% of patients with acute scleritis have an infectious etiology4, infectious scleritis must always be considered before treatment for presumed inflammatory scleritis with steroids.

On examination, scleritis must be distinguished from conjunctivitis and episcleritis, where inflammation occurs superficial to the sclera. Pain and tenderness upon palpation of the globe are present in scleritis but not in conjunctivitis or episcleritis. Furthermore, injected scleral vessels have a crosshatched appearance and are adherent to the sclera, while injected conjunctival and episcleral vessels may be moved relative to the sclera with a cotton-tipped applicator. Conjunctival and episcleral vessels may also blanch with pressure or application of topical phenylephrine while scleral vessels do not. Scleritis may be differentiated into anterior scleritis, in which inflammation occurs anterior to the insertion of the extraocular muscles (EOM), versus posterior scleritis being posterior to the EOM insertion. Autoimmune scleritis is typically anterior, and may be complicated by vasculitis, infarction, and necrosis of the sclera. Distinct nodules of scleral edema may be present. Necrotizing anterior scleritis may result in exposure of the choroid and is characterized by severe pain, except in the rare case of scleromalacia perforans, where necrosis is present without pain. Posterior scleritis is difficult to detect and may instead manifest as serous retinal detachments or choroidal folds.

Infectious scleritis is typically necrotizing and can have both anterior and posterior involvement. Infectious scleritis may also be associated with calcific plaques, microabscesses, and tissue involvement extending beyond obvious margins of infection on clinical examination4. The cornea and vitreous should also be closely examined for signs of concomitant keratitis or endophthalmitis.


Ocular surgery, particularly pterygium excision, and ocular trauma are the most likely inciting factors for infectious scleritis. It is suggested that excessive intraoperative cautery or use of adjuvant radiation or antimetabolites may increase the risk of infectious scleritis2. Notably, there is often a delayed presentation of months to years after the inciting surgery or trauma. The mechanism behind this apparent dormant period is unclear. Endogenous infectious scleritis, in which there is no inciting factor, is also possible and immunosuppression is likely to be a risk factor.

In a recent retrospective analysis of 73 cases of infectious scleritis, 87% were due to bacteria and 11% were due to fungi2. Pseudomonas aeruginosa was the most common offending organism, having been isolated in nearly half of all bacterial cases. Of note, Nocardia and mycobacterial species were also isolated, and the risk of infection with these acid-fast organisms was increased following retina surgery with either vitrectomy or scleral buckle5. There was a greater delay between symptom onset and treatment for fastidious organisms due to the negative initial gram stain, and greater time required for acid-fast positivity. Therefore, suspicion for fastidious organisms should be increased in the setting of infectious scleritis after retina surgery, as well as when there is no improvement with fluoroquinolone therapy. Acid-fast cultures should be considered at initial presentation.


Scleral scraping and culture on blood and chocolate agar, brain–heart infusion broth, thioglycolate broth, nonnutrient agar with E. coli overlay, and Sabouraud dextrose agar is recommended4. Eyes with infectious scleritis must be closely examined and followed for signs of keratitis or endophthalmitis. Ultrasound biomicroscopy or optical coherence tomography are useful to evaluate scleritis-associated retinal or choroidal detachment, or choroidal folds.


Treatment of infectious scleritis involves antimicrobial therapy appropriate for the isolated organism. Optimal methods of medical treatment of infectious scleritis are not entirely clear, however aggressive therapy with both topical and systemic antimicrobial therapy is generally performed. There is some evidence that subconjunctival antibiotics or subpalpebral antibiotic lavage may provide a benefit1. Intravitreal antimicrobial injection should be performed when endophthalmitis is suspected. Topical or oral corticosteroids may provide an additional benefit to visual outcomes, but these agents should be used with caution in Nocardial scleritis.

There is also evidence to suggest that patients benefit from adjuvant surgical treatment with early and repeated surgical debridement3. Debridement provides debulking of necrotic tissue and increases local drug penetration. Additional intervention with cryotherapy, conjunctival recession, or extirpation may also be performed when the inflammation is refractory to conventional therapy. Ultimately, evisceration or enucleation may be necessary, and the risk for this outcome is increased when concomitant keratitis or endophthalmitis is present.


In general, the prognosis of infectious scleritis is worse than autoimmune scleritis, possibly due to delay in diagnosis and initiation of antimicrobial therapy. Visual acuity remains poorer than 20/200 in approximately 50% of eyes with infectious scleritis2. Visual acuity at the time of diagnosis is the strongest prognostic factor for visual outcomes.


  1. Ahmad S, Lopez M, Attala M, et al.Interventions and Outcomes in Patients with Infectious Pseudomonas scleritis: A 10-Year Perspective. Ocular Immunology and Inflammation. 2019;27(3): 499-506,
  2. Hodson K, Galor A, Karp C, et al. Epidemiology and Visual Outcomes in Patients with Infectious Scleritis. April 2013; 32(4): 466-472.
  3. Huang FC, Huang SP, Tseng SH. Management of infectious scleritis after pterygium excision. 2000;19:34–39.
  4. Ramenaden ER, Raiji VR. Clinical characteristics and visual outcomes in infectious scleritis: a review. Clin Ophthalmol. 2013;7:2113–2122.
  5. Rich RM, Smiddy WE, Davis JL. Infectious scleritis after retinal surgery. Am J Ophthalmol. 2008;145:695–699.


Faculty Approval by: Akbar Shakoor, MD

Identifier: Moran_CORE_26915

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