Microbial Organisms and the Eye: From Everyday Irritations to Rare Threats (2025)

Microbial Organisms and the Eye: From Everyday Irritations to Rare Threats

Learn to recognize these common and uncommon infections so that you can initiate early and effective care.

By Theresa Jay, OD, Steve Njeru, OD, Daniel Grangaard, OD, and William Hileman, OD

Jointly provided by the Postgraduate Institute for Medicine (PIM) and the Review Education Group

Release Date: May 15, 2025

Expiration Date:May 15, 2028

Estimated Time to Complete Activity: two hours

Target Audience:This activity is intended for optometrists interested in identifying various microbial threats to the eye, in order to start treatment and safeguard their patients’ vision.

Educational Objectives: After completing this activity, participants should be better able to:

• Identify common and uncommon microbial organisms that cause ocular infections, including their key clinical features.

• Differentiate between mild, self-limiting eye infections and serious, vision-threatening conditions that require urgent intervention.

• Understand the mechanisms by which microbes invade ocular tissues and the eye’s immune response to infection.

• Apply evidence-based strategies for the management of patients who present with microbial eye infections.

Disclosure of Conflicts of Interest: PIM requires faculty, planners and others in control of educational content to disclose all their financial relationships with ineligible companies. All identified conflicts of interest are thoroughly vetted and mitigated according to PIM policy. PIM is committed to providing its learners with high-quality, accredited CE activities and related materials that promote improvements or quality in health care and not a specific proprietary business interest of an ineligible company.

Those involved reported the following relevant financial relationships with ineligible entities related to the educational content of this CE activity: Faculty -Drs. Jay, Njeru, Grangaard and Hileman have nothing to disclose.Planners and Editorial Staff - PIM has nothing to disclose. The Review Education Group has nothing to disclose.

Accreditation Statement: In support of improving patient care, this activity has been planned and implemented by PIM and the Review Education Group. PIM is jointly accredited by the Accreditation Council for Continuing Medical Education, the Accreditation Council for Pharmacy Education and the American Nurses Credentialing Center to provide CE for the healthcare team. PIM is accredited by COPE to provide CE to optometrists.

Credit Statement: This course is COPE-approved for two hours of CE credit. Activity #130714 and course ID97918-GO. Check with your local state licensing board to see if this counts toward your CE requirement for relicensure.

Disclosure of Unlabeled Use: This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the FDA. The planners of this activity do not recommend the use of any agent outside of the labeled indications. The opinions expressed in the educational activity are those of the faculty and do not necessarily represent the views of the planners. Refer to the official prescribing information for each product for discussion of approved indications, contraindications and warnings.

Disclaimer: Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patient’s condition(s) and possible contraindications and/or dangers in use, review of any applicable manufacturer’s product information and comparison with recommendations of other authorities.

The eye is in constant contact with the external environment, making it an easy target for microbes. From common conditions like conjunctivitis to rare but potentially sight-threatening infections such as endophthalmitis, a wide range of pathogens—including bacteria, viruses, fungi, and parasites—can pose serious risks. Understanding how these invade and affect the eye can help optometrists catch signs early to provide prompt treatment. This article highlights various microbial threats to the eye, equipping optometrists with the knowledge needed to safeguard their patients’ vision.

A Demodex infestation that can be seen by the sleeves at the base of the lash line.Photo: Cecelia Koetting, OD.Click image to enlarge.

Bacterial

Ocular bacterial infections are a common cause of inflammation and discomfort, ranging from mild conjunctivitis to severe endophthalmitis or keratitis. Prompt diagnosis and treatment are key to successful treatment and preservation of vision.

Staphylococcus aureus. This is one of the most common bacterium, with about 30% of the general population and 50 to 66% of hospital workers carrying Staphylococcus aureus.¹ The bacterium spreads through direct contact, contaminated surfaces and airborne particles, which contributes to its widespread presence in both community and hospital environments. S. aureus uses several virulence factors, including exotoxins like alpha-toxin and leukocidins, biofilm formation and coagulase production, to evade the immune system.² Methicillin-resistant Staphylococcus aureus (MRSA) is a strain of S. aureus that has developed resistance to methicillin and other beta-lactam antibiotics, which makes it more challenging to treat. This resistance is due to the acquisition of the mecA gene, which encodes a modified penicillin-binding protein (PBP2a) that reduces the efficacy of beta-lactam antibiotics.

Ocular infections from S. aureus can lead to bacterial conjunctivitis, blepharitis, keratitis and postoperative endophthalmitis. Blepharitis affects 37% to 47% of adults and can cause symptoms like redness, burning, itching, foreign body sensation, crusting, blurry vision and irritation.³ It has been reported that 8% to 36% of bacterial keratitis is due to S. aureus, which can lead to vision loss if not treated.⁴ S. aureus is also a leading cause of post-operative endophthalmitis, which can lead to vision loss if not treated urgently. S. aureus accounts for 6% to 16% of all postoperative endophthalmitis and 10% of endophthalmitis following cataract surgery; of all S. aureus-associated postoperative endophthalmitis, about 40% are MRSA.²

Staphylococcus epidermidis. While this bacterium is normally found as part of the skin’s microflora, it can become pathogenic when introduced into the body through surgery or trauma. It primarily spreads through direct contact or by contaminated medical devices, such as contact lenses. One of the key virulence factors that make S. epidermidis so harmful is its ability to form biofilms, which allow it to stick to devices like intraocular lenses and survive even in the face of immune defenses. Ocular infections caused by this bacterium can include bacterial conjunctivitis, keratitis, blepharitis and postoperative endophthalmitis. Over 90% of all cases of endophthalmitis after surgery are caused by bacteria, and the most common causative agent following cataract surgery is Staphylococcus epidermidis.⁵

Streptococcus pneumoniae. This bacterium is capable of causing a wide range of ocular infections, from mild to potentially visually impairing such as bacterial conjunctivitis, keratitis, endophthalmitis and orbital cellulitis.⁶ In pediatric populations, Streptococcus pneumoniae is a leading cause of bacterial conjunctivitis and accounts for up to 41% of pediatric bacterial conjunctivitis cases.⁶ Fortunately, more sight-threatening infections like bacterial keratitis are relatively rare with S. pneumoniae responsible for an estimated 1.8% to 10.7% of bacterial keratitis cases. However, the bacterium poses a notable risk for postoperative infections, contributing to 57.1% of bleb-associated endophthalmitis following trabeculectomy.⁶

The virulence of S. pneumoniae is largely driven by its polysaccharide capsule and an array of factors that aid in host infection.⁴ Key traits include pneumolysin, neuraminidases and zinc metalloproteinases, which work together to promote bacterial survival and invasion. Pneumolysin, a pore-forming toxin, disrupts lipid-rich host cell membranes, leading to cell lysis and increased bacterial spread.⁴ Additionally, surface proteins such as neuraminidases and zinc metalloproteinases enhance adhesion and facilitate deeper tissue invasion, which furthers the infection process.⁴

A case of endogenous endophthalmitis seeded by an undiagnosed liver abscess.Photo: Rami Aboumourad, OD.Click image to enlarge.

Pseudomonas aeruginosa. A common opportunistic pathogen, Pseudomonas aeruginosa is a leading cause of bacterial keratitis, responsible for 10% to 39% of cases and nearly 70% of cases among contact lens wearers.⁷ The increased risk in contact lens users is due to P. aeruginosa’s ability to form biofilms on contact lenses and storage cases.⁷ This biofilm is a self-generated matrix of extracellular polymeric substances that encases the bacteria, providing protection from environmental stressors such as temperature fluctuations and nutrient deprivation.⁷

Beyond biofilm formation, P. aeruginosa possesses several virulence factors that contribute to its pathogenicity. Its outer membrane is rich in endotoxins called lipopolysaccharides and features multiple cell surface proteins known as porins.⁸ These porins not only facilitate bacterial adhesion to host cell receptors but also contribute to toxic cellular damage.⁸ By disrupting host tissues, porins trigger inflammation and tissue damage.⁸

Treponema pallidum. This bacterium is responsible for syphilis and transmitted primarily through sexual contact or congenital transmission in utero.⁹ Ocular syphilis can affect nearly all ocular structures and often mimics other eye diseases, making diagnosis challenging. It is this ability to mimic other disease processes that has led to the common moniker, “The Great Imitator,” when referring to ocular syphilis. The most common manifestation is uveitis (can involve any portion of the uveal tract with granulomatous or non-granulomatous inflammation), but it can also produce interstitial keratitis or scleritis.⁹

Symptoms of ocular syphilis typically include eye pain, redness, blurred vision, floaters and photophobia.⁹ The virulence of T. pallidum is largely due to its unique cellular membrane, which is rich in lipoproteins that help the bacterium evade immune detection and resist phagocytosis.¹⁰ Additionally, like many pathogenic bacteria, T. pallidum produces protease enzymes that contribute to tissue damage and destruction during infection.¹⁰

Bartonella henselae. This is the bacterium responsible for cat scratch disease, a zoonotic infection transmitted from animals to humans.¹¹ Cats serve as the primary reservoir host with transmission occurring via bites or scratches. The most common ophthalmic manifestation is multifocal chorioretinitis. This typically manifests unilaterally with optic nerve edema, peripapillary hemorrhages, cotton-wool spots and a macular star pattern of exudates. Symptoms often include an enlarged blind spot and decreased vision with central or paracentral scotomas.¹²

While B. henselae can infect individuals of all ages, the disease tends to be more severe in immunocompromised patients.¹² Two key bacterial traits contribute to its virulence. First, adhesion to host cells is facilitated by a surface protein called BadA.¹¹ Second, B. henselae uses a type IV secretion system to infect and invade host cells. These secretion system proteins trigger inflammatory cascades, which leads to tissue damage.¹¹

Haemophilus influenzae. This bacterium is best known for causing upper respiratory infections, but Haemophilus influenzae can also lead to a variety of ocular infections, particularly in children. The most common ocular manifestation is bacterial conjunctivitis, especially in pediatric populations. However, more severe infections such as orbital cellulitis, keratitis, endophthalmitis and dacryocystitis can also occur. Like many bacterial pathogens, H. influenzae possesses several virulence factors that enhance its ability to cause infection.¹³ One key trait is its ability to be classified into subgroups based on the presence of a polysaccharide capsule.¹³^,¹⁴ In polysaccharide capsule-producing strains, this protective barrier helps the bacterium evade phagocytosis by immune cells while also promoting adhesion to host tissues.¹³^,¹⁴

Neisseria gonorrhoeae. This bacterium is transmitted through direct physical contact, primarily as a sexually transmitted infection affecting the genitourinary tract.¹⁵ Ocular infections most commonly result from autoinoculation but can also occur through direct exposure to infected urinary or genital secretions.¹⁶ The most frequent ocular manifestations are conjunctivitis and preseptal cellulitis. Gonococcal conjunctivitis, most common ocular manifestation, is characterized by severe, hyperacute, mucopurulent discharge with associated eyelid swelling and pain. Unrecognized and untreated gonococcal conjunctivitis can rapidly produce to keratitis with a high risk of a corneal perforation in the absence of appropriate intramuscular/intravenous (IV) antimicrobial therapy.¹⁶

Globally, N. gonorrhoeae is estimated to cause over 78 million infections annually.¹⁶ As a mucosal pathogen, it adheres to epithelial cells using a variety of virulence factors.¹⁵ Cell surface proteins, such as porins and type IV pili, help to facilitate adhesion to host tissues.¹⁶ In addition to promoting bacterial attachment, porins play a role in host cell invasion and tissue damage, contributing to the infection’s severity.¹⁶

Borrelia burgdorferi. The bacterium responsible for Lyme disease, Borrelia burgdorferi is transmitted through bites from Ixodes ticks. The infection begins when larval ticks feed on small rodents carrying the bacteria. Once a tick has attached for at least 24 hours, the bacteria enter the skin and can spread through the bloodstream and lymphatic system to other organs. If left untreated, it can stay in the body for years, causing both systemic and ocular complications.¹⁷ While ocular involvement is rare, Lyme disease can affect several parts of the eye, including the conjunctiva, cornea, retina and optic nerve. Early Lyme disease may cause non-specific follicular conjunctivitis in 7% to 11% of patients.¹⁸

As the disease progresses, patients may experience episcleritis, keratitis and/or uveitis. Lyme disease-associated keratitis may present as nummular stromal opacities within months of Lyme disease onset. Lyme disease-associated uveitis typically presents with granulomatous keratic precipitates. Additionally, Lyme disease can cause neuro-ophthalmic symptoms such as neuroretinitis, cranial nerve paralysis, optic atrophy and orbital myositis. Interestingly, Lyme disease has been linked to around 25% of new cases of Bell’s palsy in endemic regions, leading to facial paralysis (cranial nerve VII) and potential complications like neurotrophic keratitis due to exposure keratopathy.¹⁹

Chlamydia trachomatis. Chlamydia is a sexually transmitted infection caused by the bacteria Chlamydia trachomatis, which is one of the most reported bacterial infections.²⁰ This bacterium has a unique life cycle, with two forms: the elementary body and the reticulate body.²⁰ The elementary body is metabolically inactive and enters host cells. Once inside, it transforms into the active, metabolically active reticulate body. These reticulate bodies gather energy sources and amino acids to replicate and produce new elementary bodies that go on to infect other host cells.²⁰ Chlamydia trachomatis is transmitted through direct contact with infected tissue during vaginal, anal or oral sex, and can also be passed from an infected mother to her newborn during childbirth.²⁰

Ocular manifestations of Chlamydia trachomatis include neonatal conjunctivitis, adult inclusion conjunctivitis and trachoma. Neonatal conjunctivitis, which occurs in newborns, can be caused by bacterial infections such as chlamydia after a vaginal birth. Newborns are at higher risk due to their underdeveloped immune systems, low levels of IgA in tears and reduced lysozyme activity.²¹ When caused by chlamydia, the condition typically appears within the first two weeks of life, with symptoms such as mucopurulent discharge and eyelid swelling. Between 2% to 40% of neonatal conjunctivitis cases are related to Chlamydia trachomatis.²¹

Adult inclusion conjunctivitis can occur through autoinoculation or sexual transmission. It leads to follicular conjunctivitis, which can persist for weeks or even months if untreated, potentially causing conjunctival scarring. This form of conjunctivitis accounts for 1.8% to 5.6% of all acute conjunctivitis cases, and most of these cases are unilateral.²² Patients with adult inclusion conjunctivitis often have a concurrent genital infection.

Finally, Chlamydia trachomatis is the leading infectious cause of blindness worldwide due to trachoma. This condition is caused by repeated episodes of active infection that lead to conjunctival inflammation, scarring and trichiasis, ultimately resulting in blindness from corneal scarring. It is responsible for approximately 1.3 million cases of blindness globally.²³

An advanced case of Acanthamoeba keratitis with a large central ring infiltrate.Photo: Christine W. Sindt, OD.Click image to enlarge.

Nontuberculous mycobacteria (NTM). These are a type of atypical mycobacteria commonly found in the environment. The most common ways they are transmitted include contaminated water sources, trauma and post-surgical infections. NTM has a complex cell wall component, such as mycolic acids, that contribute to their resistance to desiccation and chemical treatments.²⁴ Additionally, the bacteria can manipulate host immune responses and lead to chronic inflammation, tissue damage and difficulty in treating infections. NTM keratitis is slow-progressing and often misdiagnosed as it can be mistaken for fungal, herpetic or Acanthamoeba keratitis. It typically presents with a “cracked windshield” appearance of the cornea due to a central ulcer with radiating infiltration.²⁴

Risk factors for NTM keratitis include contact lens use, trauma, penetrating keratoplasty and LASIK; of note, NTM keratitis is the most common organism implicated in late-onset post-LASIK infections.²⁴ Infectious scleritis can also develop following trauma (e.g., laceration), surgery (e.g., pterygium excision) or as local spread from adjacent keratitis. Although NTM is not a common cause of infectious keratitis, it can be challenging to treat due to delayed diagnosis, inadequate drug penetration and slow or poor response to therapy.

Endophthalmitis caused by NTM is rare, but it carries a poor prognosis since diagnosis is often delayed. Clinicians should be on alert if they encounter low-grade, prolonged intraocular inflammation that is persistent or recurrent, particularly following intraocular surgeries or when there is a poor response to topical corticosteroids.²⁴

Enterobacteriaceae. The Enterobacteriaceae family, including Escherichia coli and Klebsiella pneumoniae, is commonly associated with healthcare settings but has become increasingly resistant to antibiotics that were once effective. Transmission can also occur through contaminated contact lenses and poor hygiene. These bacteria use adhesins to bind to host cells and have a lipopolysaccharide capsule that helps them evade phagocytosis, which can trigger an inflammatory response and potentially lead to sepsis.²⁴ Additionally, they produce beta-lactamase, which breaks down the beta-lactam ring in certain antibiotics, such as penicillin or cephalosporins, rendering them less effective. Ocular manifestations include bacterial keratitis and endophthalmitis, with one study reporting an incidence of Enterobacter endophthalmitis at 3.24%.²⁵

Moraxella. The Moraxella species was first discovered as an ocular pathogen and includes Moraxella catarrhalis and Moraxella lacunata. These bacteria are typically found in the respiratory tract and spread through direct contact or respiratory droplets. There are several virulence factors that enhance their ability to cause infection, including adhesins like ubiquitous surface proteins.²⁶ A classic manifestation of infection with Moraxella species is angular blepharoconjunctivitis, which involves the canthal angle and often causes irritation at the outer corners of the eyes and chronic redness.²⁶ Moraxella-related keratitis is more commonly seen in colder climates, as well as in immunocompromised patients and chronic alcoholics. This condition carries a risk of corneal thinning and even perforation. Although rare, Moraxella can cause endophthalmitis in immunocompromised individuals.²⁷

Viral

Herpetic viral ocular infections are a common cause of eye irritation, redness, pain and ocular surface disease. Although the anterior segment is most commonly impacted, these viruses can affect all structures of the eye. Therefore, it is critical to accurately diagnose with proper treatment to prevent longstanding visual reduction or recurrences.

Herpes simplex virus. Herpes simplex ophthalmicus is due to neurotropic herpes simplex virus (HSV) type 1 and type 2. This condition can impact all the structures of the eye and is most caused by the HSV-1 virus. In rare cases, HSV-2 is transmitted to newborns via vaginal birth of infected mothers. The virus first spreads through the cutaneous nerves where it remains latent in the trigeminal ganglion.²⁸ Triggers for viral replication include stress, steroid use, immunocompromised status, secondary infections, menstruation, radiation and fever.²⁹ Ophthalmic manifestations can involve any ocular structures (e.g., ICE syndrome, Possner-Schlossman syndrome, Fuchs heterochromic iridocyclitis) but classically presents as an epithelial keratitis.

Herpetic keratitis is actually a broad category that can involve the epithelium, stroma, and endothelium either in isolation or combination, and the stromal keratitis can be described as necrotizing versus non-necrotizing; common sequelae include scaring, lipid keratopathy and neurotrophic keratopathy. The most visually devastating manifestation is acute retinal detachment in immunocompetent individuals and progressive outer retinal necrosis in immunocompromised patients, both with risk of retinal detachment.

Varicella-zoster virus (VZV). This pathogen is transmitted via airborne, droplet and direct contact pathways. Herpes zoster results from reactivation of the latent VZV within a sensory nerve ganglion, often presenting decades after the initial infection. The disease typically presents as a unilateral maculopapular or vesicular rash in an isolated dermatome.^30-32 Herpes zoster ophthalmicus (HZO) is specifically defined by the involvement of the ophthalmic division (V1) of the trigeminal nerve (V). V1 is subdivided into three branches: the frontal nerve branch, the nasociliary nerve branch and the lacrimal nerve branch. Classification of HZO may include the involvement of just one or potentially all these nerve branches. It is reported that approximately 50% of cases are associated with ocular manifestations.^30-32

A case of herpes simplex epithelial keratitis as noted by a paracentral dendritic lesion stained with fluorescein.Click image to enlarge.

Major risk factors for HZO include immunocompromised status, autoimmune diseases requiring corticosteroids or other immunosuppressants, anti-TNF α use, statin use, irritable bowel syndrome, reconstitution inflammatory syndrome, status post-transplant, age greater than 50 years old and chemotherapy treatment.³² Ocular manifestations are similar to HSV-1 and HSV-2 with stromal keratitis being the most common cause of vision loss in these patients and acute retinal necrosis being the most visually devastating.^32-35 Elevated eye pressure due to secondary to zoster-induced trabeculitis or synechiae formation may lead to secondary glaucoma.³⁶

Adenoviruses. This large group of highly contagious double-stranded DNA viruses are distinguished by various serotypes.³⁷ The risk of inter-familial infection rates has been estimated up to 50%.³⁸ Transmission can occur through direct touch contact and possible airborne nasal droplets. There are four accepted clinical presentations for adenoviral conjunctivitis: epidemic keratoconjunctivitis, pharyngoconjunctival fever, acute non-specific follicular conjunctivitis and chronic keratoconjunctivitis.

Epidemic keratoconjunctivitis (EKC) is the most severe and is associated with adenovirus serotypes 8, 4, 19 (now 64 by whole genome sequencing), and 37. Additionally, serotypes 53 and 54 have been identified as the causative agent in a few recent outbreaks of EKC.³⁹ This condition usually presents unilaterally with no systemic involvement. Patient presentation includes foreign body sensation, photophobia, conjunctival hyperemia, serous discharge, conjunctival follicles, conjunctival edema, subconjunctival hemorrhages, pseudomembranes and preauricular lymphadenopathy.^39-41

Pharyngoconjunctival fever is associated with adenovirus types 3, 4 and 7. It is also highly contagious and usually presents predominately with systemic symptoms including pharyngitis, tender pre-auricular lymphadenopathy, fever and bilateral follicular conjunctivitis.^37,42

Acute non-specific follicular conjunctivitis is caused by a multitude of serotypes. It is milder in nature, with a self-limiting seven to 10-day presentation of conjunctival hyperemia, serous discharge, follicles and a lack of corneal involvement.

Chronic keratoconjunctivitis is a rare, prolonged course of intermittent conjunctival hyperemia, photophobia and serous discharge. It can be difficult to differentiate between other conjunctival infections as presentation demonstrates conjunctival papillae more than follicles.^43-45

Cytomegalovirus (CMV). This occurs in patients lacking primary T-cell response against the virus, or immunocompromised carriers of CMV. These patients are usually immunocompromised secondary to status post-transplant, AIDS or cancer treatments (such as chemotherapy).^46-48 Like HSV and VZV, CMV can impact both the anterior and posterior segment. CMV endothelitis demonstrates endothelial cell loss, localized stromal edema and keratic precipitates. Occasionally, increased eye pressure or iris atrophy may present.⁴⁹ Diagnosis must be confirmed to rule out HSV or VZV reactivation. CMV anterior uveitis typically presents with a recurrent acute or chronic unilateral anterior uveitis and increased eye pressure in immunocompetent adults.⁵⁰

Active CMV retinitis presents with retinal whitening and hemorrhage areas spreading along the arcades with subsequent retinal necrosis and atrophy; visual loss is mainly due to direct involvement of the macula, optic nerve head or retinal detachment.^46-48 Confirmatory diagnosis of CMV ocular involvement is obtained through PCR amplification of viral DNA in specimens of aqueous, reported sensitivity nearing 100%.^46-48

Epstein Barr virus (EBV). A herpesviral DNA virus, EBV is the most common cause of infectious mononucleosis syndrome. EBV transmission occurs by the sharing of saliva which spreads to mucosal surfaces and lymph tissues.⁵¹ Typical symptoms and signs of active infection include fever, pharyngitis, lymphadenopathy and splenomegaly.⁵² Ocular symptoms are most associated with acute mononucleosis.⁵² EBV can impact all ocular structures from anterior to posterior segments such as conjunctivitis, dry eye syndrome, dacryoadenitis, keratitis, uveitis, choroiditis, retinitis, papillitis, optic neuritis, facial nerve palsy, oculoglandular syndrome and ophthalmoplegia.^{51, 53-57} EBV infection is most accurately diagnosed using heterophile antibody tests for those with primary EBV infections and serology tests for asymptomatic patients.^52,54

Fungal

Although rare, fungal infections can cause a variety of serious ocular conditions. Identification of fungal pathogens is key to initiating proper treatment and limiting vision loss.

Fusarium. This species is a common cause of fungal keratitis. Fusarium is a filamentous fungus that is found in soil associated with plants. Fungal keratitis is found in all parts of the world with the highest prevalence of Fusarium keratitis found in tropical and subtropical climates.⁵⁸ The estimated annual incidence of fungal keratitis is between 736,251 and 1,367,322 cases/year with the highest rates in Asia and Africa.⁵⁸ Risk factors for Fusarium keratitis include ocular trauma with organic material, ocular surface disease, topical steroid use and contact lens use.⁵⁹ Infections occur when corneal epithelial integrity is broken allowing Fusarium to gain access to the tissue. Fungal antigens and toxins are released into the cornea resulting in necrosis and damage to the surrounding cornea. Fusarium also forms a biofilm increasing its virulence and antifungal resistance.⁶⁰

Initially, Fusarium keratitis may have a non-specific appearance as a non-healing corneal abrasion, but over time matures into a stromal infiltrate with feathery edges and satellite lesions that is susceptible to stromal necrosis.⁵⁹ Symptoms include pain, blurry vision, tearing, foreign body sensation and photophobia. Diagnosis is made through history and slit lamp examination. Cultures and cytologic testing using corneal scrapings are used for a definitive diagnosis.⁶¹ Recently fungal PCR testing has also been used to aid in faster detection.⁶¹

Aspergillus. Another filamentary fungus, Aspergillus has been implicated in keratitis, orbital infections and endophthalmitis. Like Fusarium, Aspergillus is most commonly found in tropical areas and following trauma involving organic matter. Aspergillus is also the most common cause of exogenous fungal endophthalmitis and the second leading fungal cause of endogenous endophthalmitis.⁶² It has also been implicated in post-surgical infections and has been shown to account for up to 74% of all cases of fungal endophthalmitis post-cataract extraction.⁶³

A case of POHS as noted by the punched-out lesions, area of peripapillary atrophy and pigmentary changes within the fovea.Click image to enlarge.

Key differences between endogenous Aspergillus endophthalmitis and those caused by Candida are a more acute onset, increased retinal hemorrhages, vascular occlusions, macular lesions and less vitreal involvement.⁶² Aspergillus keratitis is similar in appearance and follows a similar clinical course to Fusarium. Distinction is best made through microbiological sampling such as corneal culture. Aspergillus is also the most common cause of fungal orbital infection and orbital cellulitis.⁶⁴

Candida. A yeast fungus, Candida is among the normal flora of the human body. Candidemia is commonly contracted in hospital-based settings as a complication of surgery and indwelling catheters.⁸ Exogenous routes are due to direct inoculation from surgery or due to trauma with organic material and endogenous candidiasis is found mostly in immunocompromised individuals.

Risk factors for developing candidemia include infection with Candida albicans, abdominal surgery, trauma, long-term IV therapy and catheters, immunosuppression, diabetes and IV drug use.^65,66 Ocular candidiasis can present as chorioretinitis or endophthalmitis. Ocular signs include single or multiple yellow-white chorioretinal lesions. Other signs include corneal haze, anterior chamber cells, retinal hemorrhages, cotton wool spots, retinal detachment and vitreal lesions that appear as a “string of pearls.” In endophthalmitis, hypopyon, scleritis and optic neuropathy can occur.

Patients may present with symptoms of blurred vision, floaters, photosensitivity and ocular pain or be asymptomatic. Diagnosis is made by completing an extensive history with an emphasis on risk factors, clinical presentation, blood, urine, IV and catheter cultures and vitrectomy with cultures and smears. Due to the low prevalence of endophthalmitis (1%) in patients with candidemia, routine screening is no longer recommended in fully asymptomatic patients. Patients with any ocular symptoms or have any clinical concern for infection should continue to have routine screenings completed.^67,68

Histoplasma capsulatum. This dimorphic fungus is found worldwide and endemic to certain parts of the world especially associated with river valleys. In the United States, H. capsulatum is endemic to the Ohio and Mississippi river valleys and found in the soil. Infection occurs through inhalation of spores in contaminated soil. Initial infection can be asymptomatic or cause a flu-like illness. The connection between H. capsulatum and presumed ocular histoplasmosis syndrome (POHS) comes from epidemiological studies in POHS patients who tested positive for a histoplasmin skin antigen test.⁶⁹ The exact pathophysiology is ill-defined, but hematogenous spread to the choroid then causes an inflammatory reaction. This inflammation produces a classic triad of multifocal chorioretinal scars (“punched out lesions”), peripapillary atrophy and a risk of developing choroidal neovascular membrane at any point thereafter primary infection.

Other diagnostic criteria include the absence of inflammation in the anterior chamber and vitreous. Although an accepted pathophysiology for choroidal neovascular membrane formation has not been agreed upon, smoking has been associated with a three-times greater chance of developing one in POHS than in a non-smoker.⁷⁰ POHS is a clinical diagnosis that does not require supporting serological titers.

Parasitic

Parasitic infections in the eye can lead to a variety of ocular findings ranging from redness and mild irritation to severe pain and vision loss. Early detection and intervention are essential to improve visual outcomes.

Acanthamoeba. A genus of amoeba, Acanthamoeba is found in many habitats including soil and fresh water. In the eye, Acanthamoeba most commonly causes microbial keratitis. Acanthamoeba adheres to the corneal surface using several proteins including mannose-binding protiens.⁷¹ The adhesion sets off phagocytosis and prompts the release of enzymes and toxins causing epithelial destruction and apoptosis allowing invasion into the stroma.⁷¹ Risk factors for contracting Acanthamoeba keratitis (AK) include exposure to contaminated water, poor contact lens hygiene and swimming with contact lenses in contaminated water.⁷²

A filamentary fungal keratitis as noted by the necrotic lesion, feathery borders and satellite lesions.Click image to enlarge.

Initial AK diagnosis can be challenging as it presents with non-specific signs similar to other forms of microbial keratitis.⁷² Although there may be decreased corneal sensation in very early stages, one factor that can assist in diagnosis is that AK is marked by severe ocular pain which may be worse than initial signs of infection. Lesions are slowly progressive and radial keratoneuritis (late sign) and ring infiltrates can develop. Diagnosis is aided by history including contact lens history and clinical examination. Diagnosis of AK is confirmed by cultures, cytologic testing, PCR and biopsy before treatment for AK is initiated.⁷²

Toxoplasma gondii. While cats are the definitive host for this obligate intracellular protozoan parasite, other animals and humans serve as intermediate hosts. There are three forms of the parasite: the oocysts found in soil and cat feces, the tachyzoites which is the infectious form, and the bradyzoite or tissue cyst which is the latent form.⁷³ T. gondii can be contracted by ingesting food or water contaminated by cat feces, eating raw or undercooked meat, or transmitted congenitally from the mother to the fetus.⁷⁴ Toxoplasmosis is the most frequent infectious cause of posterior uveitis in humans worldwide.⁷³

The classic presentation is a focal white necrotizing retinitis with overlying vitritis resulting in the “headlights in the fog” appearance. Satellite lesions found near a chorioretinal scar are common and may be a sign of recurrent disease. Toxoplasmosis has recurrence rates of up to 79%.⁷⁴ Other ocular findings associated with toxoplasmosis are retinal neovascularization, retinal detachment and optic neuritis. Diagnosis is usually made by clinical presentation and examination alone but may be aided by serological testing with anti-toxoplasma IgM and IgG antibodies or by anterior chamber or vitreous tap especially in atypical cases.

Mite

Demodex mites are a commonly overlooked cause of ocular surface disease. Although these mites are typically commensal in nature, overgrowth can lead to significant ocular surface discomfort through blepharitis and keratitis. Therefore, identification of these mites and proper treatment can help improve ocular comfort while preventing anterior segment complications.

Demodex folliculorum. This ectoparasite inhabits the eyelash follicles and base of eyelashes. It carries a higher transmission rate than Demodex brevis due to its anterior structural location.⁷⁵ Clinical signs may include blepharitis, conjunctivitis, keratitis or dry eye syndrome. The multifactorial condition of eyelid inflammation also termed blepharitis causes foreign body sensation, ocular irritation, ocular itching, meibomian gland dysfunction and dry eye symptoms. In cases where the condition is not managed, complications can arise including corneal neovascularization, ulceration, trichiasis and eyelid anatomy changes.⁷⁶ Cylindrical sleeves at the base of the eyelash is highly indicative of the D. folliculorum presence. Diagnostic confirmation can be made via microscopy of an epilated lash or in vivo confocal microscopy.⁷⁷

Demodex brevis. In contrast to Demodex folliculorum, Demodex brevis resides within the meibomian and sebaceous glands therefore contributing to chalazion development.^78,79 D. brevis are also found commonly elsewhere on the body including the neck and chest.⁸⁰ These ectoparasites also contribute to blepharitis symptoms leading to conjunctivitis, keratitis, meibomian gland dysfunction and dry eye syndrome.

Takeaways

The eye is constantly exposed to a variety of microbes in our everyday lives. A range of microbes including bacteria, viruses, fungi, parasites and mites can lead to a wide variety of ocular diseases. While many infections can be relatively easy to treat, some can become serious if not addressed promptly. Recognizing signs early and starting treatment as soon as possible is essential to help patients maintain good eye health.

Staying informed about these risks is the best way to protect our patients’ vision. Remember that even minor irritations can sometimes signal something more significant. So, encouraging regular eye exams and open communication with your patients can make a big difference in their overall eye care.