Fungal Endophthalmitis

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Article initiated by:
Arman Saeedi, MPH, Eric Weldy, MD, Galia Deitz
All contributors:
Florence Valcourt, Ghazala D. O'Keefe, MD, Eric Weldy, MD, Galia Deitz, Neelakshi Bhagat, MD, FACS, Kevin Yang Wu, MD. DMD.
Assigned editor:
Neelakshi Bhagat, MD, FACS, Olena Hurzhii, MD
Review:
Assigned status Up to Date
 by Neelakshi Bhagat, MD, FACS on December 17, 2024.


Disease Entity

Fungal endophthalmitis is a rare, purulent fungal infection involving the intraocular fluids (vitreous and aqueous).

Etiology and Risk Factors

The etiology depends on the mode of transmission of the fungus:

Endogenous fungal endophthalmitis

Endogenous endophthalmitis is due to hematogenous ('blood-borne') seeding.  Of all cases of endogenous endophthalmitis including bacterial, over half are due to fungus[1]. 

Bloodstream seeding secondary to fungus may result from yeast (fungus consisting of single celled organisms) or saprophytic mold (fungus consisting of multicellular filaments called hyphae). The incidence of endophthalmitis in presence of candidemia is

The yeast species Candida albicans is the most common fungal microbe implicated in endogenous fungal endophthalmitis [2][3], followed by the mold species Aspergillus in the US.

Risk factors for endogenous fungal endophthalmitis

Any cause of fungemia can lead to endogenous endophthalmitis. Risk factors for fungemia include: [4][5][6]

  • IV drug use
  • immunosuppression*
    • corticosteroid use
    • history of solid organ transplant
    • neutropenia
    • diabetes mellitus
    • chemotherapy
  • gastrointestinal procedures (especially Candida)
  • chronic lung disease (especially disseminated Aspergillosis)
  • central venous catheter or other indwelling line
  • hematologic malignancies with or without prior history of stem cell transplantation
  • pyogenic liver abscess
  • prolonged ICU stay
  • mechanical ventilation

Fraility, chronic diabetes, IV drug abuse, endocarditis, immunosuppression increase the odds of developing endophthalmitis in Candidemic patients. [7] [8]


Risk factors specific to each fungal species include:

  • Candida species:
    • Recent major gastrointestinal surgery, bacterial sepsis, systemic antibiotic, chronic catheters, hyperalimentation, chronic disease, immunomodulatory therapy, prolonged neutropenia, organ transplantation, hospitalized neonates, and intravenous drugs abusers[5]
  • Aspergillus species:
    • Patients with chronic lung disease, cancer endocarditis, severe immunosuppression, past liver transplantation, and intravenous drugs users[9]
  • Coccidioides species:
    • Endemic in California, southwest of the United States, Mexico, Argentina
  • Cryptococcus neoformans:
    • Immunocompromised and particularly HIV/AIDS patients


*Molds (e.g. Aspergillus) have been shown to be significantly associated with immunosuppression and history of organ transplantation when compared to yeast (e.g. Candida). [10][11]

Exogenous endophthalmitis

Among cases of fungal endophthalmitis, exogenous sources are less common. Reported cases have been linked to eye surgery, trauma, or extension of infectious keratitis. [12] The most common causative organism is Aspergillus, in 56-74% of cases, followed by Candida, in 11-19% of cases.[13][14]

Following cataract surgery in the United States, the incidence of fungal endophthalmitis has reported to be 0.002% to 0.005%, considerably lower than reported incidence of 0.06% for postoperative bacterial endophthalmitis. [15] Risk factors for development of post-cataract surgery fungal endophthalmitis include intraoperative complication and old age and are usually seen in more tropical climates. [16] It is rare to see a fungal post-cataract endophthalmitis.

Fungal keratitis is uncommon in the US comprising <2% of all microbial keratitis.[17] Multivariate analysis has revealed revealed topical steroid use, previous corneal laceration suturing , large corneal ulcer size, hypopyon , and aphakia to be risk factors for developing endophthalmitis in cases with fungal keratitis with Fusarium and Aspergillosis being the most common type of fungal pathogens in China. [18]

Prevalence and Incidence

Over half of all cases of infectious endogenous endophthalmitis are due to fungus. [1]

In hospitalized patients with fungemia, the overall incidence of fungal endogenous endophthalmitis remains quite low. Specifically in patients with Candidemia, the incidence of chorioretinitis is much higher than that of endophthalmitis. One large study reported a rate of 11% of chorioretinitis while only 1.6% had endophthalmitis. [19]

Endogenous endophthalmitis is frequently unilateral but may progress to bilateral involvement in a quarter to a third of patients.[20] [21]

Pathophysiology

In cases of fungemia, the fungal embolus typically seeds the highly vascular choroid and retina in the posterior pole, acting as a nidus for infection extending into surrounding ocular structures. [22][23] When the fungal infection is limited to the choroid and retina alone, these lesions are defined as fungal chorioretinitis as opposed to endophthalmitis, given the lack of vitreous involvement. During this stage, patients may remain asymptomatic.

As the fungal chorioretinal lesions progress, the infectious infiltrates may progress into the retina lead to compromise of the blood-ocular barrier, and seeding into the vitreous resulting in endophthalmitis.

In cases of exogenous post-operative fungal endophthalmitis, previous studies have shown Candida, Aspergillus and, Fusarium are ubiquitous airborne contaminants found on the human conjunctiva, especially in warmer climates. [24][25] Introduction of fungal contaminants via the conjunctival surface or surgical equipment may play a role in pathogenesis.

Diagnosis

Fungal endophthalmitis is a clinical diagnosis suspected on exam findings of vitreous inflammation in the setting of epidemiologic risk factors. The diagnosis is confirmed by microbiology cultures.

Blood Cultures

Blood cultures have reported to be positive in only one-third to one half of confirmed cases of endogenous fungal endophthalmitis. [26][21][27] This may be partially explained by the difficulty in culturing from blood samples and the transient nature of fungemia, whereby no systemic infection may be pressed at the time the eye is seeded.

Microbiology

Aqueous or vitreous samples are helpful in confirming the diagnosis and assessing for antimicrobial susceptibilities. Posterior chamber paracentesis is more reliable and sensitive than aqueous samples.[28] Furthermore, undiluted samples from vitrectomy have even higher diagnostic yield than posterior chamber paracentesis.[29]

Although culture of intraocular fluids is gold standard, it has poor sensitivity and slow rate of growth. PCR of common organisms (ie Candida, Fusarium, Aspergillus) has emerged as a relatively rapid method of identifying fungal species, even in culture negative samples.[21]

Symptoms

  • Floaters
  • Vision loss
  • Eye pain
  • Eye redness
  • Fever (if fungemic)
  • Systemic symptoms due to liver or lung involvement (as in disseminated Aspergillosis)


Endogenous fungal endophthalmitis tend to show a more gradual onset of symptoms than with bacterial etiology.  Symptoms of endogenous Aspergillus endophthalmitis tend to be more acute compare to other fungal species with relatively rapid progression of severe vision loss due to large area of macular involvement and dense vitritis.[30] In contrast, symptoms of endogenous Candidal endophthalmitis are generally more insidious, with vision loss occurring over a period of days to weeks with minimal pain until later in the progression of the disease.[31]

Symptoms of exogenous fungal endophthalmitis often present as a sub-acute to chronic endophthalmitis. There is a wide range of latency with onset of symptoms occurring several weeks to months following the initial inoculation, depending on the burden of implicated fungus. [32][33][34]

Physical Exam Findings

In endogenous fungal endophthalmitis, dilated exam reveals yellowish fluffy chorioretinal infiltrates with ill-defined, irregular borders predominantly involving the posterior pole associated with varying degrees of vitritis. Vitritis must be present to make the diagnosis of fungal endophthalmitis. In the absence of vitritis, fungal chorioretinitis is a more fitting diagnosis. Intraretinal hemorrhages may also be present.

If left untreated, endogenous fungal endophthalmitis can gradually expand to the anterior segment resulting in keratic precipitates, hypopyon and cellular aggregates. Iris nodules and rubeosis may also been seen in more severe cases. When comparing clinical manifestations of differing fungal organisms in endogenous sources, there are a couple of notable differences:

  • Classically Candida endophthalmitis presents with slowly progressive focal vitritis overlying chorioretinal lesions. These discrete areas of vitritis may present with consolidated fungal abscess balls adjacent to one another in a "string of pearls" configuration. Lesions are often numerous, bilateral, white, small and well circumscribed.[35]
  • Aspergillosis tends to have more rapidly progressive and large macular lesions.
  • Aspergillosis tends to be more hemorrhagic due to angiocentric invasion of the mold hyphae. This invasion leads to retinal and choroidal vessels causing retinal vessel occlusion and choroidal ischemia. Vitreous involvements are milder compared to Candida disease.[36]
  • Coccidioides species produces multifocal granulomatous chorioretinal lesions similar to those seen in Candida diseases, but granulomatous anterior uveitis can be seen just as frequently. Ocular surfaces are more often affected so that conjunctivitis, superficial keratitis, scleritis and episcleritis are observed more often.
  • Cryptococcus eye involvement is frequently seen in association with fungal meningitis and therefore papilledema, optic atrophy and cranial nerve palsies can be associated findings. The most common sign of ocular infection, with or without increased intracranial pressure, is multifocal chorioretinitis with larger and fewer lesions than with Candida infections.[37]


Exogenous fungal endophthalmitis predominantly presents with vitritis that may be focal or diffuse. [38]

Imaging

OCT

In Candidal endophthalmitis, OCT imaging of retinal lesions have demonstrated involvement of all layers of the retina (pre-retinal, subretinal, intraretinal, full-thickness)[39].

Alternatively, Aspergillus endophthalmitis classically preferentially demonstrates subretinal involvement with relatively normal overlying retinal architecture. [40]

B-Scan

Signs of endophthalmitis on b-scan include vitritis as well as chorioretinal thickening.   

Choroidal or retinal detachments can also occur, both of which are poor prognostic factors.  

Differential Diagnosis

Management

Medical Therapy

Anti-fungal therapy for fungal endophthalmitis can be administered systemically and/or intravitreally depending on the severity of intraocular involvement. Intravitreal therapy should be considered in patients with vitritis or endophthalmitis, chorioretinitis involving the macula, or any patient persistently worsening on systemic therapy alone.  

There are four classes of medications used to treat disseminated fungal infections today, however, not all have equal effect in treating intraocular fungal infections. Amphotericin B was the first anti-fungal medication to be developed in the 1950s and belongs class of antifungals known as polyenes. While Amphotericin B has broad-spectrum coverage, it has limited intraocular penetrance when used systemically, as well as numerous risks and side effects such as infusion reactions, electrolyte abnormalities, and renal failure. [41] Liposomal amphotericin, however, has much improved ocular penetrance. The preferred method of drug delivery for Amphotericin B in these cases is intravitreal, though there is a potential risk of retinal toxicity and necrosis at high doses.[42]

The first generation of triazoles, which includes fluconazole, demonstrate excellent activity against Candida species however does not cover invasive filamentous fungal infections such as aspergillosis or mucormycosis. Systemic fluconazole is generally well tolerated and has superior intraocular penetrance compared to most other antifungals. Voriconazole is a second generation triazole and has added activity against filamentous fungi compared to first generation triazoles as well as fluconazole-resistant Candida species such as Candida glabrata and Candida krusei. Like fluconazole, it also has excellent intraocular penetrance. [41] Voriconazole can also be given as an intravitreal injection and may be safer than amphotericin B given the lack of demonstrated dose-dependent toxicity in animal studies. [43] A point to note, voriconazole has a short half-life in vitreous.

Ultimately, diagnosis of endogenous endophthalmitis warrants a systemic workup and assistance from infectious disease specialists. Per the most recent IDSA guidelines, echinocandin is often started as the initial therapy in candidemia. [44] However, it is important to note that the ocular penetrance of echinocandin is poor, and in instances of endogenous intraocular Candidiasis, an alternative systemic therapy such as an azole should be recommended to the primary treating team. [45]

The length of treatment with systemic anti-fungal therapy is typically 4-6 weeks, with the final duration depending on treatment response as well as presence of other organ involvement. Serial examinations should be performed on patients to assess treatment response. [44]

Surgical Therapy

There is no current consensus regarding the role of surgery, such as pars plana vitrectomy (PPV), in treating fungal endophthalmitis. Because the Endophthalmitis Vitrectomy Study (EVS) did not enroll patients with endogenous endophthalmitis, it cannot be directly applied to patients with endogenous endophthalmitis for fungi. However, there has been evidence of the benefits of performing a PPV to aid in both diagnosis and treatment of endogenous fungal endophthalmitis. [46] Vitrectomy can debulk the infection and assist in better diffusion of antibiotics in the infectious vitreous. Though the treatment benefit may not necessarily be reflected in final visual acuity, instead PPV may hasten time to recovery and reduce risk of retinal detachment. [47]

Potential treatment modalities according to microbiologic results

  • Candida endophthalmitis[48]
    • Chorioretinitis without vitreal involvement can be treated with oral fluconazole or voriconazole or liposomal amphotericin for two to four weeks.
    • Intravitreal injections of amphotericin or voriconazole in addition to pars plana vitrectomy should be considered when vitreous is affected.
    • If severe, intravenous amphotericin B and oral voriconazole are needed.
  • Aspergillus endophthalmitis[49]
    • Aggressive treatment with pars plana vitrectomy with intravitreal injection of amphotericin B or voriconazole in conjunction with oral voriconazole or caspofungin.
  • Coccidioidomycosis
    • Oral treatment with fluconazole or itraconazole if localized disease and larger dose or intravenous amphotericin or oral voriconazole if systemic disease
    • Surgical treatment such as pars plana vitrectomy and debulking of anterior chamber granulomas may be required. There is a poor visual prognosis even with aggressive treatment and most patient suffer from severe pain and blindness requiring enucleation.
  • Cryptococcus endophthalmitis
    • Intravenous amphotericin B and oral flucytosine are the mainstay of treatment.

Complications

Complications from fungal endophthalmitis are largely secondary to the complications caused by the intraocular inflammation. They can include retinal detachments, chorioretinal scarring, epiretinal membrane, cataract formation, and persistent vitreous opacification.  [50] A possible increase in endogenous fungal endophthalmitis in post COVID-19 patients treated with steroids has been reported. [51]

Prognosis

The prognosis for fungal endophthalmitis, as with other forms of infectious endophthalmitis, is generally poor. Though outcome can vary depending on location of lesions and virulence of fungus. Factors associated with a poorer prognosis include delay in treatment, traumatic etiology of infection, and infection with Aspergillus species. 

Follow-up

Follow up patterns vary by institution, as there is no clearly defined protocol. At the authors' institution, for non-verbal (i.e. intubated) fungemic patients with a normal initial dilated fundus exam, a repeat dilated fundoscopic exam is performed two weeks after the initial exam due to the slowly progressive nature of fungal endophthalmitis and proportion of cases that can be missed on initial evaluation (13% by one study). [52] In contrast, patients that are asymptomatic at presentation with a normal eye exam and remain asymptomatic may be followed on an as-needed basis.  

If abnormal findings are present on the initial exam, a repeat exam should be done in one week or sooner if new visual symptoms should develop, to assess for evolution.  

In patients who have confirmed fungal endophthalmitis, depending on intervention (PPV, intravitreal injection, systemic antifungal therapy) close observation is often appropriate for the initial several days to assess response to treatment. Fundus examinations can later be spaced out once improvement is documented. 

References

  1. ↑ 1.0 1.1 Schiedler V, Scott IU, Flynn HW Jr, Davis JL, Benz MS, Miller D. Culture-proven endogenous endophthalmitis: Clinical features and visual acuity outcomes. Am J Ophthalmol 2004;137:725-31
  2. ↑ Lingappan A, Wykoff CC, Albini TA, Miller D, Pathengay A, Davis JL, Flynn HW Jr. Endogenous fungal endophthalmitis: Causative organisms, management strategies, and visual acuity outcomes. Am J Ophthalmol 2012;153:162-6.e1. doi:10.1016/j.ajo.2011.06.020. Epub 2011 Sep 13.
  3. ↑ Sridhar J, Flynn HW Jr, Kuriyan AE, Miller D, Albini T. Endogenous fungal endophthalmitis: Risk factors, clinical features, and treatment outcomes in mold and yeast infections. J Ophthalmic Inflamm Infect 2013;Sep 20;3(1):60. doi: 10.1186/1869-5760-3-60.
  4. ↑ Dimitrios P. Kontoyiannis, Irfan Vaziri, Hend A. Hanna, Maha Boktour, Jack Thornby, Ray Hachem, Gerald P. Bodey, Issam I. Raad, Risk Factors for Candida tropicalis Fungemia in Patients with Cancer, Clinical Infectious Diseases, Volume 33, Issue10, 15 November 2001, Pages 1676–1681
  5. ↑ 5.0 5.1 Shah CP, McKey J, Spirn MJ, Maguire J. Ocular candidiasis: a review. Br J Ophthalmol.2008;92(4):466–468.
  6. ↑ Kato H, Yoshimura Y, Suido Y, et al. Prevalence of, and risk factors for, hematogenous fungal endophthalmitis in patients with Candida bloodstream infection. Infection. 2018;46(5):635-640. doi:10.1007/s15010-018-1163-z
  7. ↑ Henry RK, Uppuluri A, et al. The Impact of Frailty Syndrome on Endogenous Endophthalmitis Development and Outcomes: A Population-Level Analysis. Ophthalmology. 2022 Dec;129(12):1440-1447.
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  9. ↑ Hariprasad SM, Mieler WF, Holz ER, et al. Determination of vitreous, aqueous, and plasma concentration of orally administered voriconazole in humans. Arch Ophthalmol.2004;122(1):42–47
  10. ↑ Sridhar J, Flynn HW Jr, Kuriyan AE, Miller D, Albini T. Endogenous fungal endophthalmitis: risk factors, clinical features, and treatment outcomes in mold and yeast infections. J Ophthalmic Inflamm Infect. 2013;3(1):60. Published 2013 Sep 20. doi:10.1186/1869-5760-3-60
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  34. ↑ Wykoff CC, Flynn HW Jr, Miller D, Scott IU, Alfonso EC. Exogenous fungal endophthalmitis: microbiology and clinical outcomes. Ophthalmology. 2008;115(9):1501–7.
  35. ↑ Rao NA, Hidayat AA. Endogenous mycotic endophthalmitis: variations in clinical and histopathologic changes in candidiasis compared with aspergillosis. Am J Ophthalmol.2001;132(2):244–251.
  36. ↑ Hariprasad SM, Mieler WF, Holz ER, et al. Determination of vitreous, aqueous, and plasma concentration of orally administered voriconazole in humans. Arch Ophthalmol.2004;122(1):42–47.
  37. ↑ Kestelyn P, Taelman H, Bogaerts J, et al. Ophthalmic manifestations of infections with Cryptococcus neoformans in patients with the acquired immunodeficiency syndrome. Am J.Ophthalmol. 1993;116(6):721–727.
  38. ↑ Vilela RC, Vilela L, Vilela P, Vilela R, Motta R, Po ˆssa AP, de Almeida C, Mendoza L. Etiological agents of fungal endophthalmitis: diagnosis and management. Int Ophthalmol. 2014;34(3):707–21.
  39. ↑ Zhuang, H., Ding, X., Gao, F. et al. Optical coherence tomography features of retinal lesions in Chinese patients with endogenous Candida endophthalmitis. BMC Ophthalmol 20, 52 (2020). https://doi.org/10.1186/s12886-020-01337-9
  40. ↑ Adam CR, Sigler EJ. Multimodal imaging findings in endogenous Aspergillus endophthalmitis. Retina 2014;34(9):1914-1915. https://www.ncbi.nlm.nih.gov/pubmed/24695061
  41. ↑ 41.0 41.1 Nett, J. E. and D. R. Andes (2016). "Antifungal Agents: Spectrum of Activity, Pharmacology, and Clinical Indications." Infect Dis Clin North Am 30(1): 51-83. 
  42. ↑ Cottreau JM, Barr VO. A review of antiviral and antifungal use and safety during pregnancy. Pharmacotherapy. 2016;36(6):668-678. 
  43. ↑ Kernt M, Neubauer AS, De Kaspar HM, Kampik A. Intravitreal voriconazole: in vitro safety-profile for fungal endophthalmitis. Retina. 2009;29:362–70. 
  44. ↑ 44.0 44.1 Pappas, P. G., et al. (2016). "Clinical Practice Guideline for the Management of Candidiasis: 2016 Update by the Infectious Diseases Society of America." Clin Infect Dis 62(4): e1-50. 
  45. ↑ Livermore, J. L., et al. (2013). "Pharmacokinetics and pharmacodynamics of anidulafungin for experimental Candida endophthalmitis: insights into the utility of echinocandins for treatment of a potentially sight-threatening infection." Antimicrob Agents Chemother 57(1): 281-288. 
  46. ↑ William A, Spitzer MS, Deuter C, Blumenstock G, Partsch M, Voykov B, Ziemssen F, Bartz-Schmidt KU, Doycheva D. Outcomes of Primary Transconjunctival 23-Gauge Vitrectomy in the Diagnosis and Treatment of Presumed Endogenous Fungal Endophthalmitis. Ocul Immunol Inflamm 2017;25(2):239-245. 
  47. ↑ Sallam A, Taylor SR, Khan A, McCluskey P, Lynn WA, Manku K, Pacheco PA, Lightman S. Factors determining visual outcome in endogenous Candida endophthalmitis. Retina (Philadelphia, Pa.). 2012 Jun;32(6):1129-34. 
  48. ↑ Breit SM, Hariprasad SM, Mieler WF, Shah GK, Mills MD, Grand MG. Management of endogenous fungal endophthalmitis with voriconazole and caspofungin. Am J Ophthalmol.2005;139(1):135–140.
  49. ↑ Hariprasad SM, Mieler WF, Holz ER, et al. Determination of vitreous, aqueous, and plasma concentration of orally administered voriconazole in humans. Arch Ophthalmol.2004;122(1):42–47.
  50. ↑ Dave VP, Pathengay A, Relhan N, Sharma P, Jalali S, Pappuru RR, Tyagi M, Narayanan R, Chhablani J, Das T, Flynn HW, Jr. Endophthalmitis and Concurrent or Delayed-Onset Rhegmatogenous Retinal Detachment Managed With Pars Plana Vitrectomy, Intravitreal Antibiotics, and Silicone Oil. Ophthalmic Surg Lasers Imaging Retina2017;48(7):546-551. 
  51. ↑ Shroff, Daraius; Narula, Ritesh1; Atri, Neelam; et al. Endogenous fungal endophthalmitis following intensive corticosteroid therapy in severe COVID-19 disease. Indian Journal of Ophthalmology 69(7):p 1909-1914, July 2021.
  52. ↑ Shah, C. P., McKey, J., Spirn, M. J., & Maguire, J. (2008). Ocular candidiasis: a review. Br J Ophthalmol, 92(4), 466-468. doi:10.1136/bjo.2007.133405 
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