AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Fungi are eukaryotic organisms that are ubiquitous in nature. The following 3 classes of fungi are important ocular pathogens: molds, yeasts, and diphasic fungi. Molds, also known as filamentous fungi, are multicellular organisms that form a tangled mass known as the mycelium. From this mass, filamentous projections, known as hyphae, branch out. The hyphae may be septate or nonseptate. Septate hyphae have true divisions, subdividing them into several cells, while nonseptate hyphae have no true divisions. Common septate filamentous fungi are Aspergillus, Fusarium, Cephalosporium, Paecilomyces, and Penicillium species. The nonseptate filamentous fungi include the Mucor species.

Yeasts are unicellular organisms that may develop pseudohyphae. Candida and Cryptococcus are the important ocular pathogens. The diphasic fungi exist in 2 forms, yeast and mold. Important ocular pathogens include Histoplasma, Blastomyces, and Coccidioides.

Endophthalmitis refers to intraocular inflammation involving the vitreous and anterior chamber of the eye. In most cases, endophthalmitis results from an infectious organism. Fungal endophthalmitis can be divided into the less common endogenous infections and the more common exogenous infections.

Endogenous fungal endophthalmitis is frequently an ocular manifestation of a systemic disease. Endogenous infections usually occur in patients with 1 or more of the following risk factors: immunosuppression, intravenous drug abuse, bacterial sepsis, prolonged hyperalimentation, systemic antibiotics, corticosteroid therapy, recent abdominal surgery, malignancy, alcoholism, diabetes mellitus, trauma, and hemodialysis. Candida albicans is by far the most common pathogen isolated in endogenous fungal endophthalmitis. Other pathogens include Aspergillus, Coccidioides, Cryptococcus, Blastomyces, and Sporothrix species.

Exogenous infections usually are secondary to trauma or surgery. A variety of fungi, including Paecilomyces, Acremonium, and Sporothrix species, have been associated with endophthalmitis following intraocular surgery or trauma.

Pathophysiology

Candida endophthalmitis

C albicans is by far the most common cause of endogenous endophthalmitis. They are commensal organisms that reside in the human body and are found normally in the female genital tract, the gastrointestinal tract, and the respiratory tract.

These fungi are kept in check by the host's normal immune response. When a breakdown in the host's immune system occurs, fungi may spread throughout the body. Many organs, including the eye, can be affected by this spread of fungi through the bloodstream. However, immunosuppression alone does not increase significantly the risk of fungi entering the bloodstream. For instance, candidal chorioretinitis is an uncommon ophthalmic condition in AIDS patients. Neutrophils are apparently important in the first-line defense against candidal organisms. Infection probably starts in the choroid and spreads to the retina and vitreous.

Patients who are at risk include patients with longstanding indwelling catheters; persons who use intravenous drugs; postpartum women; premature infants; patients undergoing hyperalimentation; patients with a history of recent abdominal surgery; and patients with debilitating diseases, such as diabetes mellitus, postorgan transplantation, or malignancies.

Aspergillus endophthalmitis

Of the more than 200 species of aspergilli, Aspergillus flavus and Aspergillus fumigatus are the most common pathogenic organisms in humans. They are ubiquitous organisms found in soil, decaying matter, water, and organic debris. Its conidia are airborne, so inhalation is an important route of entry into the human body. In patients who are at risk, such as those patients with chronic pulmonary diseases or those patients with orthotopic liver transplants, renal transplants, and bone marrow transplants, disseminated aspergillosis may result. In these patients, the fungus usually spreads from the lungs to the eye. Persons who use intravenous drugs may present with ocular symptoms only.

Aspergillus infections are characterized by the breakdown of neutrophil and mononuclear phagocytic defenses. The first line of defense is the mononuclear phagocyte, which engulfs the conidia, the asexual spores of aspergilli organisms. Neutrophils constitute the second line of defense, which kill the mycelia. Most likely, the choroid is the first ocular site where aspergilli organisms gain access to the eye.

Cryptococcus endophthalmitis

Pigeons play an important role in the pathogenesis of cryptococcosis. Cryptococci spores can survive up to 2 years in pigeon droppings. Spores gain access to the human body through inhalation. From the lungs, the fungus is disseminated hematogenously and preferentially affects the central nervous system. It is the most common cause of fungal meningitis. Cryptococci organisms reach the eye through either direct extension from the optic nerve sheath or hematogenously from a distant focus. The choroid is probably the first site of ocular infection.

Coccidioides endophthalmitis

Coccidioides endophthalmitis results from the inhalation of Coccidioides immitis arthroconidia, which are found in the dust of endemic areas. Agricultural workers and constructions crews are at risk. In most patients, the inhalation of the spores leads to a self-limited respiratory disease. In few patients who are reexposed to the fungus, a chronic respiratory disease ensues. Hematogenous dissemination to the eye can occur.

Frequency

United States

Compared to previous decades, the incidence of endogenous endophthalmitis appears to have increased in the past few decades. This may be secondary to an increase in intravenous drug use; the advent of chemotherapy for cancer patients; and the increased ability to care for more debilitated patients with hyperalimentation, indwelling catheters, and potent antibiotics.

Prospective studies of hospitalized patients with candidemia reveal that 9-37% of patients developed candidal endophthalmitis. In studies where prompt treatment of a systemic fungal infection is instituted, only 3-9% patients developed endogenous fungal endophthalmitis.

International

Because it is commensal in the human body, Candida species are found throughout the world. Cryptococci and aspergilli also are present worldwide and found in both urban settings and rural settings.

C immitis is endemic in the southwestern United States (the San Joaquin Valley) and Northern Mexico. It also has been reported in Honduras, Venezuela, and Colombia.

Mortality/Morbidity

• The prognosis of fungal endophthalmitis depends on the virulence of the organism, the extent of intraocular involvement, and the timing and mode of interventions.
• Prompt therapy following early diagnosis helps to reduce significant visual loss in all forms of fungal endophthalmitis.
• The visual outcome of Aspergillus endophthalmitis usually is poor because of the preferred macular involvement by the fungus.

Race

No racial predisposition has been observed.

Sex

A male preponderance is reported for endogenous fungal endophthalmitis.

Age

With regard to endogenous fungal endophthalmitis, there are 2 incidence peaks: one in patients younger than 1 year, and the other in middle-aged patients.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Risk factors for Candida endophthalmitis
  
  
  • The most common risk factor for the development of endogenous Candida endophthalmitis is intravenous drug abuse.
  • Other risk factors include patients with long-standing indwelling catheters; postpartum women; premature infants; patients undergoing hyperalimentation; patients with a history of recent abdominal surgery; and patients with debilitating diseases, such as diabetes mellitus, postorgan transplantation, or malignancies.
• Risk factors for Aspergillus endophthalmitis
  
  
  • Patients with a history of renal transplantation who are receiving corticosteroids, leukemia and other hematological disorders, Goodpasture syndrome, alcoholism, and prematurity.
  • The most common predisposing factor is intravenous drug abuse.
  • Notably, chest x-ray film findings are normal in up to 20% of patients with invasive pulmonary aspergillosis.
  • Aspergillus endogenous endophthalmitis tends to present more acutely than Candida endophthalmitis and to progress more rapidly.
  • Aspergillus endocarditis is often found together with Aspergillus endophthalmitis; therefore, a thorough cardiac workup is necessary.


• Risk factors for Cryptococcus endophthalmitis
• • Patients who are known to be at risk of developing this condition are those with lymphoproliferative diseases, collagen vascular diseases, sarcoidosis, tuberculosis, diabetes mellitus, Cushing syndrome, or AIDS; those who are pregnant or abuse drugs; and those who have had organ transplants.
  • A few cases of cryptococcosis have been reported in individuals with no known risk factors or immune deficiencies.
  • Since the arthroconidia of C immitis are found in the dust of endemic areas, agricultural workers and construction crews are at risk of acquiring the infection. 
• Symptoms include the following:
• • Visual loss may be present; however, several studies have shown that visual acuity is not a useful factor in assessing the presence of endogenous fungal endophthalmitis in patients who are at risk. 
  • In addition, patients may be asymptomatic if the lesion is in the peripheral retina or if the patient is moribund. 
  • Red eye 
  • Photophobia 
  • Pain 
  • Floaters 
  • Scotoma

Physical

• Candida endophthalmitis
  
  
  • Candida chorioretinitis typically presents as several, small, creamy white, circumscribed chorioretinal lesions with overlying vitreous inflammation.
  • In certain cases, these chorioretinal lesions may be surrounded by hemorrhage, giving them the appearance of a white-centered hemorrhage (Roth spot). 
  • In the area of the lesion, the retinal vessels may be sheathed.
  • The vitreous opacities resemble fluffy balls, and they may be linked to each other by strands giving them the so-called string of pearls appearance. 
  • If the infection is not suspected and the disease advances, epiretinal membranes may develop, leading to vitreoretinal traction and retinal detachment. 
  • As the lesions heal with treatment, chorioretinal scarring evolves in the areas of prior inflammation. 
  • Choroidal neovascular membranes may develop at the site of these scars. 
  • Two thirds of patients have bilateral disease, and more than one half of patients have vitreous involvement. 
  • Iridocyclitis often is present, and a hypopyon also may be present. 
  • Infection of the iris and ciliary body is rare. 
• Aspergillus endophthalmitis
• • In Aspergillus endophthalmitis, an iridocyclitis with or without a hypopyon may be present; yellow subretinal and retinal infiltrates that preferentially affect the macula are observed. 
  • Inflammatory cells within the infiltrate may layer secondary to gravity, thereby creating a pseudohypopyon. 
  • As the disease progresses, the vitreous becomes severely involved, concealing all fundus details. With time, the macular lesions scar. 
  • In addition, Aspergillus species have a propensity for vascular invasion, leading to thrombosis and necrosis. 
  • If the fungus invades the choroidal vessels, an exudative retinal detachment may result. 
  • When the retinal vessels become involved, retinal necrosis may occur.
• Cryptococcus endophthalmitis
• • Cryptococcus neoformans usually presents intraocularly as a multifocal chorioretinitis characterized by discrete yellow-white lesions of different sizes. 
  • Retinal vessels may be sheathed, and a vitritis of variable intensity may develop. 
  • Retinal necrosis accompanied by retinal hemorrhage and exudative retinal detachments also have been known to occur. 
  • If the central nervous system is involved, papilledema is present. 
  • A mild inflammatory reaction is present in the anterior segment. 
  • If treatment is not instituted, iris neovascularization and cataract may result. 

• Coccidioides endophthalmitis

• Ocular coccidioidomycosis is an uncommon finding in patients with disseminated disease.
• Usually, a severe granulomatous iridocyclitis characterized by mutton-fat keratic precipitates is present.
• Multifocal choroiditis, typified by several, scattered, discrete, yellow-white lesions measuring less than the disc diameter in size, is observed. 
• Occasionally, vascular sheathing, vitreous haze, serous retinal detachment, and retinal hemorrhage also may be seen.

Causes

• C albicans is by far the most common cause of endogenous fungal endophthalmitis.
• Other organisms that can cause fungal endophthalmitis include the following:
  
  
  • Aspergillus species
  • Cryptococcus neoformans
  • Coccidioides immitis

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• The diagnosis of endogenous fungal endophthalmitis should be considered in patients who present with vitritis accompanied by a chorioretinal focus in the clinical setting of a recent or current debilitating illness. Clinical suspicion plays an important role in identifying patients who may have fungal endophthalmitis.
• A presumptive diagnosis of fungal endophthalmitis can be made if the fungus is isolated from anywhere in the body and the typical intraocular findings are present.
• Blood cultures, urine cultures, sputum cultures, and cerebrospinal fluid (CSF) cultures should be obtained in patients suspected of endogenous endophthalmitis. In addition, direct examination of fungi with Giemsa, Gomori-methenamine-silver (GMS), and periodic-acid Schiff (PAS) stains should be obtained.
• Culture of the fungus confirms the diagnosis. However, the fungus may not always be detected, even clinically, in certain cases or in cases where the fungus has grown from another site. Fungal cultures can be positive in 44-70% of patients diagnosed clinically. Vitrectomy samples are more sensitive for fungal cultures than vitreous needle biopsies.
• Part of the delay in making a diagnosis is because many laboratory isolates are considered contaminants by laboratory personnel. Laboratory personnel should be told to consider all fungal growth as significant and to report these findings. In addition, the culture must be kept at the laboratory for at least 4-6 weeks to ensure that slow-growing or fastidious fungal organisms are not missed.
• A useful, recently introduced diagnostic tool for fungal endophthalmitis is the polymerase chain reaction (PCR). The main advantages of PCR over conventional fungal cultures are the higher sensitivity and the rapid results obtained with PCR. Although PCR does not replace conventional mycologic methods, it helps to make an early differentiation between bacterial endophthalmitis and fungal endophthalmitis.
• Candida species grow well on Sabouraud media without cycloheximide.
  
  
  • The colonies are white and pasty.
  • PCR has been used successfully to identify Candida species from an intraocular sample.
• Aspergilli species are observed best with GMS or PAS stains.
  
  
  • Culture is the most reliable means of identification.
  • The fungus grows readily in Sabouraud and Czapek solutions.
  • Aspergilli cultures are initially flat, white, and filamentous.
  • Within 48 hours, conidia are produced with a concomitant change in pigmentation.
  • Blood cultures are often negative for aspergilli organisms.
• Cryptococci also grow well in Sabouraud agar.
  
  
  • Cryptococci may be identified by India ink.
  • C immitis can be diagnosed using a 10% KOH mount and identifying endospores that contain spherules.

Imaging Studies

• Fluorescein angiography: The chorioretinal lesions appear hypofluorescent in the early phases of the study; leakage occurs in the later phases.

Procedures

• Anterior chamber tap
• • Anterior chamber (AC) specimens are unreliable in the diagnosis of Candida species.
  • Coccidioidomycosis has been diagnosed in a handful of cases by analyzing the AC taps.

• Pars plana vitrectomy
• • Pars plana vitrectomy is important in obtaining undiluted specimens for culture and sensitivity.
  • Vitreous samples should be concentrated either by centrifugation or by millipore filtration.
  • If C neoformans is suspected, the sample should be stained with mucicarmine and undergo membrane filtration cytology.

Histologic Findings

Candida endophthalmitis: Candida organisms can be seen as budding yeasts with pseudohyphae within the lesions. The lesions contain few organisms, but they are surrounded by an intense granulomatous and suppurative inflammatory reaction.

Aspergillus endophthalmitis: Identification of branching septate hyphae in the choroid, retina, and vitreous characterizes Aspergillus endophthalmitis. Vessel thrombosis characterized by perivasculitis and necrotizing vasculitis often is observed in the retina and the choroid. Acute and chronic inflammatory cells are present in the anterior chamber and the vitreous.

Cryptococcus endophthalmitis: Cryptococci organisms usually are found in the choroid. They also have been identified in the retina, subretinal space, vitreous, and optic nerve. Typically, a diffuse or focal granulomatous inflammatory reaction that leads to a noncaseating necrosis is elicited. However, the number of inflammatory cells involved is much less than the expected given inflammatory reaction.

Coccidioides endophthalmitis: C immitis has been isolated from the limbus, iris, ciliary body, retina, choroid, and optic nerve. Typically, a granulomatous inflammatory reaction is present.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

In vitro, minimum inhibitory concentration (MIC) data do not always correlate with in vivo MIC values. Therefore, these should only be used as a guideline.

• The following drugs are used in treating of fungal endophthalmitis:
  
  
  • Amphotericin B
  • Fluconazole
  • Ketoconazole
  • Miconazole
  • Flucytosine
  • Itraconazole
• Systemic amphotericin has been the treatment of choice because of its broad-spectrum coverage; however, the penetration of the vitreous cavity is poor. Doses of 5- to 10-mg intravitreal amphotericin have been used. Retinal toxicity has been reported in animal models at these doses. Fluconazole and flucytosine have good intraocular penetration, but Candida species show high resistance to flucytosine.
• A new systemic treatment is voriconazole; when administered orally or intravenously, it has good intravitreal concentrations. Intravitreal administration of voriconazole also seems safe without evidence of retinal toxicity with concentrations up to 25 mg/mL.

Surgical Care

• The advent of pars plana vitrectomy has improved the treatment results of fungal endophthalmitis.
• The advantages of pars plana vitrectomy are that it provides material for culture, removes viable organisms and inflammatory end products from the infected vitreous, and provides intravitreal access to antifungal agents (eg, amphotericin B).
• Vitrectomy and intravitreal amphotericin B should be considered in those cases of endogenous fungal endophthalmitis where the disease is progressing despite initial therapy with an appropriate systemic antifungal agent.
• As a general rule, moderate-to-severe vitreous involvement requires vitrectomy because most systemic antifungals have poor vitreous penetration.
• Endogenous fungal endophthalmitis without evidence of disseminated disease can be treated successfully with vitrectomy and intravitreal amphotericin B.
• Given the narrow therapeutic range of amphotericin B, it should not be given in a gas-filled eye.
• Some authors have advocated the use of 400 µg of intravitreal dexamethasone as an adjuvant.

Consultations

Because endogenous fungal endophthalmitis is frequently an ocular manifestation of a systemic disease, the patient requires a multidisciplinary approach.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The best initial therapy for patients with endogenous fungal endophthalmitis has not been established. However, a broad-spectrum systemic antifungal agent, such as amphotericin B or fluconazole, is recommended as first-line therapy.

Drug Category: Polyene antibiotics

They are classified based on the number of conjugated double bonds. Fungicidal agents bind to sterols in the cell membrane of susceptible fungi and change the permeability of the cell membrane, leading to leakage of cellular constituents and consequently cell death.

Drug Category: Imidazoles

Bind to the fungal cell membrane and induce permeability changes that alter intracellular electrolyte levels, leading to fungal cell damage. These agents are fungistatic.

Drug Name	Ketoconazole (Nizoral)
Description	Fungistatic activity. Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. Active against Blastomyces dermatitidis, C immitis, and Candida and Fusarium species, and exhibits some activity against Aspergillus species.
Adult Dose	200 mg PO qd/bid
Pediatric Dose	<2 years: Not recommended >2 years: 3.3-6.6 mg/kg/d
Contraindications	Documented hypersensitivity; fungal meningitis
Interactions	Isoniazid may decrease bioavailability of ketoconazole; coadministration decreases effects of either rifampin or ketoconazole; may increase effect of anticoagulants; may increase toxicity of corticosteroids and cyclosporine (cyclosporine dosage can be adjusted); may decrease theophylline levels
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Hepatotoxicity may occur; may reversibly decrease corticosteroid serum levels (adverse effects avoided with dose of 200-400 mg/d); administer antacid, anticholinergics, or H2-blockers at least 2 h after taking ketoconazole

Drug Name	Itraconazole (Sporanox)
Description	Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.
Adult Dose	200 mg PO tid loading dose, followed by 200-400 mg PO qd
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; coadministration with cisapride may cause adverse cardiovascular effects (possibly death)
Interactions	Antacids may reduce absorption of itraconazole; edema may occur with coadministration of calcium channel blockers (eg, amlodipine, nifedipine); hypoglycemia may occur with sulfonylureas; may increase tacrolimus and cyclosporine plasma concentrations when high doses are used; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (lovastatin or simvastatin); coadministration with cisapride can cause cardiac rhythm abnormalities and death; may increase digoxin levels; coadministration may increase plasma levels of midazolam or triazolam; phenytoin and rifampin may reduce itraconazole levels (phenytoin metabolism may be altered)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in hepatic insufficiencies

Drug Name	Miconazole (Absorbine, Femizol)
Description	Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in fungal cell death. The lotion is preferred in intertriginous areas. If the cream is used, apply sparingly to avoid maceration effects. Administered intravenously due to poor absorption from the gastrointestinal tract. Used as a second-line drug in the treatment of Candida, Cryptococcus, and Aspergillus species and coccidioidomycosis. Use in cases that are resistant to treatment with amphotericin B.
Adult Dose	600-3600 mg/d divided tid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	If sensitivity or chemical irritation occurs, discontinue use; use only externally; avoid contact with eyes

Drug Name	Voriconazole (Vfend)
Description	Used for primary treatment of invasive aspergillosis and salvage treatment of Fusarium species or Scedosporium apiospermum infections. A triazole antifungal agent that inhibits fungal cytochrome P-450-mediated 14 alpha-lanosterol demethylation, which is essential in fungal ergosterol biosynthesis.
Adult Dose	Loading dose: 6 mg/kg IV q12h infused over 2 h for 2 doses Maintenance: 4 mg/kg IV q12h infused over 2 h and switch to 200 mg PO q12h when able to tolerate; may increase to 300 mg PO q12h if inadequate response <40 kg: Average maintenance dose is 100 mg PO q12h (may increase to 150 mg PO q12h) Up to 25 µg/mL (final vitreous concentration) of voriconazole has been reported to cause no retinal toxicity in rats
Pediatric Dose	<12 years: Not established >12 years: Limited data exist, administer as in adults
Contraindications	Documented hypersensitivity; CrCl <50 mL/min if administering IV (due to decreased excretion of IV vehicle); coadministration with rifampin, rifabutin, carbamazepine, barbiturates, sirolimus, pimozide, quinidine, cisapride, ergot alkaloids
Interactions	CYP450 2C19 (highest affinity), 2C9, and 3A4 (minor) substrate and inhibitor; CYP450 inducers (eg, rifampin) have shown to decrease steady state peak plasma levels by up to 93%; may increase serum levels of drugs metabolized by CYP450 2C19 or 2C9, of which some are contraindicated (eg, sirolimus, pimozide, quinidine, cisapride, ergot alkaloids), other may need more frequent monitoring (eg, cyclosporine, tacrolimus, warfarin, HMG CoA inhibitors, benzodiazepines, calcium channel blockers)
Pregnancy	D - Unsafe in pregnancy
Precautions	Decrease maintenance dose in hepatic dysfunction; common adverse effects include visual disturbances, fever, rash, vomiting, nausea, diarrhea, headache, sepsis, peripheral edema, abdominal pain, rash (including Stevens-Johnson syndrome and phototoxicity), and respiratory disorder; rare cases of severe hepatotoxicity reported; administer PO dosage form 1 h ac or pc

Drug Category: Corticosteroids

Some have advocated the use of intravitreal dexamethasone as an adjuvant. Inflammation is believed to play a role in the destructive nature of this disease.

Drug Category: Chemotherapeutic agents

Inhibit cell growth and proliferation.

Drug Category: Echinocandins

Inhibit cell wall synthesis.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Many patients with this condition are hospitalized. Patients may require intravenous medications.

Further Outpatient Care

• Patients should receive follow-up care as needed.

Deterrence/Prevention

• Once a positive fungal culture is obtained, the patient should be started on systemic antifungals. At the same time, an ophthalmologic consultation should be obtained. In 2 different studies using this protocol, the incidence of endogenous fungal endophthalmitis was reported to be only 3-9%.

Complications

• Choroidal neovascularization at the site of chorioretinal scars
• Epiretinal membranes
• Tractional retinal detachment

Prognosis

• The prognosis following fungal endophthalmitis depends on the virulence of the organism, the extent of intraocular involvement, and the timing and mode of interventions.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Early recognition is important for preservation of vision.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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• Anand A, Madhavan H, Neelam V, Lily T. Use of polymerase chain reaction in the diagnosis of fungal endophthalmitis. Ophthalmology. Feb 2001;108(2):326-30. [Medline].
• Blumenkranz MS, Stevens DA. Therapy of endogenous fungal endophthalmitis: miconazole or amphotericin B for coccidioidal and candidal infection. Arch Ophthalmol. Jul 1980;98(7):1216-20. [Medline].
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• Essman TF, Flynn HW Jr, Smiddy WE, et al. Treatment outcomes in a 10-year study of endogenous fungal endophthalmitis. Ophthalmic Surg Lasers. Mar 1997;28(3):185-94. [Medline].
• Gao H, Pennesi ME, Shah K, Qiao X, Hariprasad SM, Mieler WF, et al. Intravitreal voriconazole: an electroretinographic and histopathologic study. Arch Ophthalmol. Nov 2004;122(11):1687-92. [Medline].
• Griffin JR, Pettit TH, Fishman LS, Foos RY. Blood-borne Candida endophthalmitis. A clinical and pathologic study of 21 cases. Arch Ophthalmol. Jun 1973;89(6):450-6. [Medline].
• Gross JG. Endogenous Aspergillus-induced endophthalmitis. Successful treatment without systemic antifungal medication. Retina. 1992;12(4):341-5. [Medline].
• Henderson DK, Edwards JE Jr, Montgomerie JZ. Hematogenous candida endophthalmitis in patients receiving parenteral hyperalimentation fluids. J Infect Dis. May 1981;143(5):655-61. [Medline].
• Hunt KE, Glasgow BJ. Aspergillus endophthalmitis. An unrecognized endemic disease in orthotopic liver transplantation. Ophthalmology. May 1996;103(5):757-67. [Medline].
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Article Last Updated: Jul 24, 2007