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Keratitis

Keratitis is the inflammation of the cornea, the clear, dome-shaped tissue covering the front of the eye that protects the iris and pupil.^[1] It can result from infectious agents such as bacteria, viruses, fungi, or parasites, or from noninfectious causes like injury, autoimmune conditions, or exposure to irritants.^[2] If untreated, keratitis may lead to corneal scarring, ulceration, or permanent vision loss, making it a significant cause of ocular morbidity worldwide.^[1] Infectious keratitis, the most common form, accounts for a substantial portion of cases and is often associated with risk factors including contact lens wear, ocular trauma, and compromised ocular surface integrity.^[3] Bacterial keratitis, frequently caused by pathogens like Pseudomonas aeruginosa or Staphylococcus aureus, is prevalent among contact lens users, with an incidence rate up to 130 cases per 100,000 person-years in this group compared to 14 per 100,000 in non-wearers (as of 2010).^[3] Viral keratitis, particularly from herpes simplex virus (HSV), affects the corneal epithelium and stroma, leading to recurrent episodes and dendritic ulcers.^[4] Fungal and parasitic forms, such as those caused by Aspergillus species or Acanthamoeba, are more common in agricultural settings or with exposure to contaminated water, and they pose challenges due to delayed diagnosis.^[2] Noninfectious keratitis may stem from systemic diseases like rheumatoid arthritis or nutritional deficiencies such as vitamin A shortage, resulting in stromal inflammation without microbial involvement.^[2] Emerging antimicrobial resistance in bacterial pathogens has complicated treatment in recent years.^[5] Epidemiologically, keratitis contributes to corneal blindness, affecting an estimated 1.3 million individuals globally due to infectious keratitis as of 2015, and ranks as the fifth leading cause of blindness, particularly in developing regions like South Asia where incidence can reach 799 per 100,000 in high-risk areas (as of 2007).^[3] More recent estimates as of 2020 indicate that corneal opacities, largely from keratitis, cause blindness or moderate/severe visual impairment in approximately 5.5 million people bilaterally and 6.2 million unilaterally worldwide.^[6] In the United States, it prompted over 1 million annual visits to eye care professionals as of 2010.^[3] Common symptoms include eye pain, redness, photophobia, excessive tearing, blurred vision, and a sensation of a foreign body, which can vary in severity based on the underlying etiology.^[1] Diagnosis typically involves clinical examination, corneal scrapings for culture and sensitivity, polymerase chain reaction (PCR) testing, or confocal microscopy to identify the causative agent.^[2]^[3] Treatment strategies are tailored to the type and severity of keratitis, emphasizing prompt intervention to prevent complications.^[2] Bacterial cases are managed with topical fortified antibiotics like vancomycin or fluoroquinolones, while viral infections require antivirals such as acyclovir.^[2] Fungal keratitis responds to topical natamycin or voriconazole, and parasitic infections like acanthamoeba keratitis necessitate biguanides such as polyhexamethylene biguanide.^[2]^[7] For noninfectious forms, corticosteroids or immunosuppressive agents may be used cautiously to reduce inflammation, alongside addressing underlying conditions; recent advances include nerve growth factor therapies for neurotrophic cases.^[2]^[8] Prognosis depends on early detection, with scarring occurring in many cases but vision preservation possible through timely therapy or surgical options like corneal transplantation in advanced scenarios.^[2]

Clinical Presentation

Symptoms

Patients with keratitis typically present with a range of subjective ocular symptoms, primarily involving pain and visual impairment due to inflammation of the cornea.^[1] Ocular pain is a hallmark complaint, often described as ranging from mild irritation or a gritty foreign body sensation to severe, sharp discomfort that worsens with blinking or eye movement.^[9] This pain may be accompanied by significant photophobia, making exposure to light intensely uncomfortable and prompting patients to keep their eyes closed.^[10] Visual disturbances are central to the experience of keratitis, with blurred or hazy vision being the most common report, resulting from corneal edema and irregularity that scatters light entering the eye.^[2] Reduced visual acuity, particularly in the affected eye, can occur rapidly, and some patients notice halos around lights, especially at night, due to corneal swelling.^[11] These symptoms are specific to corneal involvement and may lead to difficulty with daily activities like reading or driving. Associated discomforts include excessive tearing, a sensation of eye redness (though subjective), and discharge that can feel sticky or watery.^[12] Symptom severity and onset vary by underlying cause; for instance, bacterial keratitis often presents with acute, intense pain and purulent discharge, whereas viral keratitis, such as herpes simplex, tends to have a more gradual onset with milder discomfort and watery discharge.^[13]^[4] Fungal keratitis may initially cause subtler symptoms, with less pronounced pain compared to bacterial forms.^[14] In untreated cases, symptoms typically progress rapidly, with pain and visual blurring intensifying within hours to days, potentially leading to profound vision loss if the inflammation spreads or causes corneal thinning.^[15] This progression correlates briefly with observable signs like corneal opacity, underscoring the urgency of symptom recognition.^[1]

Signs

Clinical signs of keratitis are primarily identified through slit-lamp biomicroscopy, which reveals characteristic corneal abnormalities and associated ocular changes.^[2] Epithelial defects appear as punctate erosions or ulcers that stain with fluorescein, often overlying stromal infiltrates that manifest as focal opacities ranging from small, gray-white lesions to larger, denser areas of inflammation.^[16] Stromal involvement may include edema and cellular infiltration, while anterior chamber reaction typically presents as cells and flare, indicating inflammatory response in the aqueous humor.^[2] Specific slit-lamp findings vary by keratitis type. In herpes simplex virus (HSV) keratitis, dendritic ulcers are hallmark features, appearing as branching, linear epithelial lesions with terminal bulbs that enhance under cobalt blue light after fluorescein staining.^[17] Acanthamoeba keratitis often shows a ring-shaped stromal infiltrate in advanced stages, accompanied by radial keratoneuritis—linear opacities extending from the limbus—and epitheliopathy resembling pseudodendrites.^[18] Bacterial keratitis typically exhibits an epithelial defect overlying a suppurative stromal infiltrate with irregular, undermined edges, while fungal keratitis displays dry, elevated lesions with feathery margins and satellite infiltrates.^[2] Severity of corneal involvement is assessed using standardized grading systems. The Oxford grading scheme evaluates the extent of corneal staining post-fluorescein application on a 0–5 scale, where grade 0 indicates no staining and grade 5 represents confluent staining across the entire corneal surface.^[19] Ulcer depth is measured via slit-lamp pachymetry or optical coherence tomography, often categorized as superficial (limited to epithelium), stromal (involving mid-layers), or deep (approaching Descemet's membrane), with depths exceeding 50% of corneal thickness signaling high risk for perforation.^[20] Associated ocular signs include conjunctival injection, which may be focal (ciliary flush around the limbus) or diffuse, reflecting vascular response to corneal inflammation.^[2] Lid edema contributes to periorbital swelling, particularly in herpetic cases, while hypopyon—a layered collection of white blood cells and debris in the anterior chamber—involves up to 20–30% of cases, most commonly in bacterial or fungal infections, and appears as a dependent, yellowish level on upright slit-lamp view.^[21]

Etiology and Risk Factors

Infectious Causes

Infectious keratitis arises from a variety of microbial pathogens that invade the corneal epithelium, leading to inflammation and potential vision loss. These infections typically occur following corneal trauma, contact lens overuse, or exposure to contaminated environments, allowing opportunistic microbes to breach the ocular surface barrier.^[2] Bacterial keratitis is predominantly caused by gram-positive and gram-negative organisms, with Staphylococcus aureus and Pseudomonas aeruginosa being among the most common pathogens. S. aureus often colonizes the ocular surface in cases of chronic blepharitis or after surgical interventions, while P. aeruginosa is frequently implicated in contact lens-related infections due to its ability to thrive in moist environments and form biofilms on lens surfaces, which protect it from host defenses and disinfectants. These biofilms contribute to outbreaks, as seen in increased incidence among extended-wear contact lens users exposed to contaminated solutions. Other notable bacteria include Staphylococcus epidermidis and Streptococcus pneumoniae, which exploit epithelial defects to initiate infection.^[13]^[22]^[23]^[24] Viral keratitis is primarily driven by herpesviruses, with herpes simplex virus type 1 (HSV-1) accounting for the majority of cases through recurrent epithelial and stromal infections. HSV-1 establishes latency in trigeminal ganglia and reactivates due to triggers like stress or immunosuppression, leading to dendritic ulcers and neurotrophic effects that impair corneal sensation and healing. Varicella-zoster virus (VZV), reactivating as herpes zoster ophthalmicus, similarly damages corneal nerves, causing neurotrophic keratitis with pseudodendrites and stromal involvement. Adenovirus contributes to epidemic keratoconjunctivitis, featuring superficial punctate keratitis that can progress to subepithelial infiltrates. These viruses evade immunity by inhibiting interferon responses and persisting in neuronal tissues.^[4]^[25]^[26]^[2] Fungal keratitis involves opportunistic pathogens such as Candida species and Fusarium species, often following ocular trauma with vegetative matter like plant material, which introduces spores into the corneal stroma. Fusarium and Aspergillus species predominate in agricultural settings, where hyphal forms invade stromal layers, eliciting a robust inflammatory response. Candida typically affects immunocompromised individuals or those with prior steroid use, penetrating via endothelial routes in severe cases. The hyphal invasion by filamentous fungi like Fusarium disrupts collagen architecture and promotes necrosis through enzymatic degradation.^[14]^[27]^[28] Parasitic and protozoal causes include Acanthamoeba species and microsporidia, both associated with exposure to contaminated water sources. *Acanthamoeba* keratitis arises from trophozoites or resilient cysts entering via contact lens storage in tap water or during swimming, with cysts exhibiting exceptional durability—surviving desiccation for years and resisting standard multipurpose solutions due to their double-walled structure. This leads to ring-shaped infiltrates and radial neuritis. Microsporidia, spore-forming protozoa, cause punctate epitheliopathy after ocular exposure to water or soil, embedding spores in corneal cells and evading phagocytosis. Water-related risks are heightened in contact lens wearers, where poor hygiene facilitates protozoal adhesion.^[29]^[7]^[30]^[31] The general pathogenesis of infectious keratitis involves microbial adhesion to the corneal epithelium via adhesins or pili, followed by evasion of innate immunity through capsule formation or toxin-mediated suppression of antimicrobial peptides. Pathogens like P. aeruginosa and S. aureus produce exotoxins (e.g., alpha-toxin) and proteases that degrade epithelial tight junctions and extracellular matrix, causing ulceration and neutrophil influx that amplifies tissue destruction. Fungi and protozoa employ hyphal or cyst penetration to invade deeper layers, while viruses induce cell lysis and immune dysregulation. This cascade results in corneal opacity if unchecked.^[22]^[32]

Non-Infectious Causes

Non-infectious keratitis encompasses a range of conditions where corneal inflammation arises from immune-mediated, mechanical, chemical, or neurological disruptions rather than microbial invasion. These etiologies often result in sterile corneal infiltrates characterized by epithelial defects, stromal haze, and ulceration without suppuration, distinguishing them from infectious forms that typically exhibit purulent discharge and rapid progression.^[2] Autoimmune and inflammatory processes play a significant role in non-infectious keratitis, particularly through mechanisms involving immune complex deposition and hypersensitivity reactions. In rheumatoid arthritis, peripheral ulcerative keratitis (PUK) develops when immune complexes activate the complement system, recruiting neutrophils and macrophages that release collagenase and proteases, leading to stromal degradation and crescent-shaped limbal ulcers.^[33] Similarly, Sjögren's syndrome contributes via lymphocytic infiltration of lacrimal glands, causing aqueous tear deficiency and keratoconjunctivitis sicca, which manifests as filamentary keratitis due to disrupted tear film stability and elevated proinflammatory cytokines like IL-6 and TNF-α.^[34] These conditions highlight immune-driven sterile inflammation, often requiring systemic evaluation to address underlying collagen vascular diseases.^[2] Nutritional deficiencies, particularly vitamin A deficiency, can lead to xerophthalmia and keratomalacia, resulting in corneal drying, melting, and ulceration due to impaired epithelial integrity and increased susceptibility to secondary infections.^[2] Traumatic and chemical injuries represent common external triggers for non-infectious keratitis, initiating sterile inflammatory responses through direct corneal damage. Abrasive injuries from foreign bodies, scratches, or trichiasis cause epithelial denudation and subsequent stromal infiltration without initial microbial involvement, though secondary infection risk exists.^[1] Chemical burns and ultraviolet (UV) exposure, as in photokeratitis or "snow blindness," damage the corneal epithelium via photochemical reactions, leading to punctate erosions and transient inflammation that resolves without antibiotics if uncomplicated.^[35] These mechanisms emphasize the cornea's vulnerability to environmental insults, resulting in self-limited sterile keratitis unless exacerbated by ongoing exposure.^[10] Neurotrophic and exposure-related keratitis stem from impaired corneal innervation or inadequate eyelid closure, promoting epithelial breakdown through reduced protective reflexes. Trigeminal nerve damage, such as post-herpetic neuralgia following herpes zoster ophthalmicus, diminishes corneal sensation and trophic support, fostering persistent epithelial defects and neurotrophic ulcers via halted cell migration and healing.^[36] Lagophthalmos, often from facial nerve palsy or proptosis, causes incomplete eyelid closure, leading to exposure keratopathy where desiccated corneal surfaces develop superficial punctate keratitis and potential ulceration from chronic drying.^[37] These forms underscore the role of neural and mechanical factors in maintaining ocular surface integrity, yielding sterile changes that mimic infection but lack microbial elements.^[2] Iatrogenic causes arise from medical interventions that compromise corneal health, often through overuse or procedural trauma. Postoperative complications following LASIK or other refractive surgeries can induce diffuse lamellar keratitis via epithelial disruption or inflammatory debris under the flap, presenting as sterile central infiltrates.^[38] Prolonged use of topical anesthetics, such as in abuse cases, toxic to the epithelium, results in anesthetic keratopathy with ring-shaped infiltrates and delayed healing due to inhibited cellular proliferation.^[39] These iatrogenic insults produce non-suppurative inflammation, contrasting with infectious keratitis by the absence of pathogens and reliance on resolution through intervention cessation.^[2] In summary, non-infectious keratitis features sterile infiltrates driven by immune, traumatic, or neurotrophic mechanisms, differing from infectious suppuration by the lack of microbial proliferation and purulent response, though clinical overlap may necessitate diagnostic differentiation.^[40]

Classification

By Chronicity

Keratitis is classified by chronicity into acute, chronic, and recurrent forms based on the duration and pattern of corneal inflammation. Acute keratitis is typically defined as an episode lasting less than 3 months, characterized by rapid onset and progression that can lead to severe complications such as corneal thinning and perforation if not addressed promptly.^[41]^[42] This form is exemplified by bacterial corneal ulcers, where aggressive inflammatory responses cause swift tissue destruction, often within days to weeks.^[43] Chronic keratitis, in contrast, persists for more than 3 months, involving ongoing inflammation that may result in corneal scarring and vascularization over time.^[41] Examples include herpetic stromal keratitis, an immune-mediated condition following initial viral infection, and marginal keratitis associated with prolonged blepharitis, both of which maintain low-grade but sustained corneal involvement.^[44]^[45] These cases often stem from unresolved acute episodes or underlying immune dysregulation, leading to protracted healing.^[4] Recurrent keratitis manifests as episodic flares separated by periods of quiescence, with new episodes occurring at least 3 months after resolution of the prior one or within 3 months of healing.^[46] This pattern is common in viral infections like herpes simplex or autoimmune-related cases, triggered by factors such as psychological stress, fever, hormonal changes, or ultraviolet light exposure.^[47]^[48] Without timely intervention, acute keratitis can transition to chronic forms through persistent stromal inflammation and inadequate epithelial repair, particularly in cases involving viral agents that establish latency and provoke repeated immune responses.^[49] Bacterial agents predominate in acute presentations, while viral pathogens are more typical in chronic and recurrent types.^[50]

By Infective Agent

Infectious keratitis is classified by the causative microbial agent, with viral, bacterial, fungal, protozoal, and parasitic subtypes each presenting distinct clinical features and epidemiological patterns. Viral keratitis encompasses several subtypes, primarily herpetic caused by herpes simplex virus (HSV), adenoviral from human adenovirus (HAdV), and cytomegalovirus (CMV) infections, particularly in immunocompromised individuals. Herpetic keratitis, the most common viral form, is subdivided into epithelial, stromal, neurotrophic, and endothelial types based on the affected corneal layer; the epithelial subtype characteristically exhibits a dendritic pattern of branching ulcers visible on fluorescein staining, resulting from direct viral replication in corneal epithelial cells.^[51] Adenoviral keratitis, often manifesting as epidemic keratoconjunctivitis (EKC), is typically caused by HAdV serotypes 8, 19, and 37, leading to subepithelial infiltrates that can persist and cause chronic visual impairment; it spreads rapidly in community settings like schools or healthcare facilities.^[52] CMV keratitis, though rarer, predominantly affects immunocompromised patients such as those with AIDS or post-transplant immunosuppression, presenting as corneal endotheliitis with endothelial cell loss, occasionally associated with iris atrophy in cases involving anterior uveitis, often confirmed via polymerase chain reaction on aqueous humor.^[53] Bacterial keratitis is differentiated by Gram staining characteristics, with Gram-positive and Gram-negative organisms requiring culture-based identification for targeted therapy. Gram-positive bacteria, such as coagulase-negative staphylococci and Staphylococcus aureus, predominate in cases linked to ocular surface colonization or contact lens overuse, forming central ulcers with stromal infiltrates and hypopyon; these are identified through growth on blood or chocolate agar, showing positive Gram staining and catalase positivity.^[54] In contrast, Gram-negative bacteria like Pseudomonas aeruginosa are more aggressive, often associated with contact lens wear or trauma in humid environments, producing rapid corneal thinning and ring abscesses due to exotoxin production; cultures on MacConkey agar reveal lactose-nonfermenting colonies, with Gram-negative rods confirming the diagnosis.^[55] This Gram-based differentiation guides initial empiric antibiotics, as Gram-negatives like Pseudomonas exhibit higher resistance to certain agents.^[56] Fungal keratitis is categorized into filamentous and yeast forms, with regional variations influenced by environmental exposure. Filamentous fungi, including Aspergillus and Fusarium species, are prevalent in tropical and agricultural regions, frequently following trauma with vegetative matter like plant material, which introduces spores into the corneal stroma; these cause feathery-edged infiltrates with satellite lesions, diagnosed via potassium hydroxide smears showing septate hyphae.^[14] Yeast-like fungi, such as Candida species, are more common in temperate climates and immunocompromised hosts, often presenting as fluffy white plaques in the stroma without a history of trauma; they grow as budding yeasts on Sabouraud dextrose agar and are associated with endogenous spread from systemic candidiasis.^[57] Agricultural workers in developing countries face elevated risk for filamentous infections due to frequent ocular exposure to soil and plant debris during farming activities.^[27] Protozoal and parasitic keratitis involves free-living amoebae and helminths, each tied to specific environmental or vector-borne exposures. Acanthamoeba keratitis, caused by the free-living protozoan Acanthamoeba species, arises from contaminated water sources or improper contact lens hygiene, progressing through pseudodendrites, radial keratoneuritis, and ring infiltrates due to trophozoite invasion; it is diagnosed by confocal microscopy revealing double-walled cysts.^[58] Helminthic keratitis, exemplified by onchocerciasis from Onchocerca volvulus, contributes to river blindness in endemic African and Latin American regions, where microfilariae carried by blackfly bites induce sclerosing keratitis with pannus formation and corneal opacity; this chronic process leads to blindness in untreated cases.^[59] Post-2020, emerging infectious agents in keratitis include SARS-CoV-2-associated cases and drug-resistant bacterial strains, reflecting pandemic-related shifts. SARS-CoV-2 has been linked to secondary bacterial or fungal superinfections exacerbating keratitis in hospitalized patients, potentially via direct viral conjunctival invasion or immune dysregulation, though primary viral keratitis remains uncommon.^[60] Drug-resistant strains, such as extensively drug-resistant Pseudomonas aeruginosa, have surged in outbreaks tied to contaminated products like artificial tears, causing severe necrotizing keratitis with poor response to standard antibiotics; genomic sequencing identifies multi-locus sequence types like ST244 in these resistant isolates.^[61] These trends underscore the need for vigilant surveillance in high-risk settings.^[62]

By Disease Stage

Keratitis progresses through distinct stages characterized by increasing depth of corneal involvement and inflammatory response, typically beginning with superficial epithelial changes and potentially advancing to deep stromal damage if untreated.^[2] In the early stage, the disease primarily affects the corneal epithelium, manifesting as superficial punctate keratitis with small, scattered areas of epithelial erosion and minimal underlying stromal alteration, often accompanied by mild edema and inflammatory cell infiltration.^[2] This phase is marked by symptoms such as ocular discomfort and blurred vision, but structural integrity remains largely preserved.^[20] As the condition advances to the intermediate stage, stromal infiltration becomes prominent, leading to localized suppuration, ulceration of the epithelial and anterior stromal layers, and the initial onset of neovascularization as blood vessels begin to invade the peripheral cornea to support immune response.^[13] Ulceration in this stage involves tissue necrosis and sloughing, with surrounding stromal edema and possible anterior chamber reaction, increasing the risk of deeper extension.^[20] Neovascularization emerges as fine, looping vessels at the ulcer margin, aiding in the delivery of inflammatory cells but potentially contributing to persistent opacity.^[13] In the advanced stage, progressive stromal thinning occurs due to ongoing enzymatic degradation and inflammation, heightening the risk of corneal perforation and forming a descemetocele, where the thin Descemet's membrane bulges forward through the weakened stroma.^[63] This phase features severe corneal haze, significant visual impairment, and potential hypopyon, necessitating urgent intervention to prevent rupture.^[2] During the resolution stage, active inflammation subsides, leading to re-epithelialization and stromal remodeling, often resulting in corneal scarring, persistent superficial vascularization, and long-term visual sequelae such as irregular astigmatism or central opacity.^[13] Scar tissue may contract over time, further altering corneal curvature, while residual vessels can regress partially but contribute to chronic haze.^[20] Staging systems for keratitis severity aid in assessing progression and guiding management; for instance, the modified Jones grading for bacterial keratitis categorizes cases as mild (superficial with minimal stromal involvement), moderate (deeper stromal changes with moderate inflammation), or severe (extensive ulceration and thinning).^[13] These systems emphasize epithelial defects, infiltrate depth, and ulcer size to track evolution from early epithelial disruption to advanced stromal compromise.^[13]

By Environmental Exposure

Keratitis can arise from various environmental exposures that compromise the corneal surface or introduce pathogens. Contact lens wear is a prominent risk factor, where poor hygiene practices, such as inadequate cleaning or storage, allow bacterial contamination, leading to microbial keratitis; overwearing lenses reduces oxygen supply to the cornea, increasing susceptibility to infections like Pseudomonas aeruginosa. Solution contamination further exacerbates this, with multipurpose solutions sometimes failing to eradicate Acanthamoeba, resulting in severe cases. Occupational exposures heighten vulnerability in specific professions. Agricultural workers face elevated risks of fungal keratitis due to corneal trauma from plant materials, such as vegetable matter harboring Fusarium species, which penetrate minor abrasions during fieldwork. Similarly, swimmers and those using tap water for lens care are prone to Acanthamoeba keratitis, as the amoeba thrives in chlorinated water and biofilms on storage cases. Geographic and climatic factors influence keratitis incidence by altering environmental stressors. In arid regions, dry winds and low humidity contribute to exposure keratitis by desiccating the ocular surface, often seen in desert climates where ultraviolet radiation intensifies epithelial damage. Tropical areas, with their warm, humid conditions, foster parasitic infections like microsporidial keratitis from soil or water exposure during daily activities. Iatrogenic exposures occur in healthcare settings, where contaminated instruments during ocular procedures can transmit bacteria, leading to postoperative keratitis. Immunosuppression following corneal transplants or systemic therapies heightens infection risk from environmental opportunists like airborne fungi. Post-2023 research highlights how climate change amplifies these risks, with rising temperatures and altered precipitation patterns increasing UV exposure and trauma events, potentially leading to increased incidence of infectious keratitis in vulnerable regions, with projections estimating up to a 36.5% rise in ocular disease prevalence as of 2025.^[64] Such exposures often favor infectious agents like bacteria and fungi, as detailed in classifications by infective agent.

Diagnosis

Clinical Evaluation

Clinical evaluation of keratitis begins with a detailed history to identify potential risk factors and guide suspicion toward specific etiologies. Patients are queried about the onset and progression of symptoms, such as acute pain, photophobia, or blurred vision, which may suggest infectious causes like bacterial or viral keratitis.^[2] A history of ocular trauma, including foreign body injury or chemical exposure, is crucial, as it predisposes to bacterial, fungal, or atypical mycobacterial infections.^[13] Contact lens use is a major risk factor, particularly for Pseudomonas or Acanthamoeba keratitis, with details on wear duration, overnight use, hygiene practices, and activities like swimming in lenses being essential.^[65] Travel history to regions with soil or water exposure may indicate fungal or parasitic risks, while queries about immunosuppression—such as HIV, diabetes, or corticosteroid use—raise concern for opportunistic infections like herpes simplex virus or microsporidial keratitis.^[2] Visual acuity assessment forms the cornerstone of the initial evaluation, providing a baseline measure of functional impact. Standard Snellen chart testing is performed, often supplemented by pinhole occlusion to differentiate refractive errors from corneal pathology; significant reduction in acuity correlates with central or deep stromal involvement.^[65] This testing helps quantify vision loss, which is a common presenting complaint in moderate to severe cases.^[13] The physical examination relies on basic bedside tools to detect corneal abnormalities. Penlight inspection reveals ciliary injection, lid edema, blepharospasm, and purulent discharge, indicating anterior segment inflammation confined to the cornea.^[13] Fluorescein staining under cobalt blue light highlights epithelial defects, revealing patterns such as linear abrasions from trauma, dendritic figures in herpetic keratitis, or punctate erosions in viral cases; the stain uptake delineates the infiltrate's size, depth, and location, aiding in severity assessment.^[2] Differential diagnosis during evaluation emphasizes corneal exclusivity to distinguish keratitis from mimicking conditions. Unlike conjunctivitis, which features diffuse conjunctival hyperemia without stromal involvement, keratitis presents with focal corneal infiltrates, edema, or ulceration.^[65] In contrast to uveitis, characterized by anterior chamber cells and flare but intact corneal epithelium, keratitis shows primary epithelial or stromal changes with possible secondary chamber reaction like hypopyon.^[13] These clues, linked to the hallmark symptoms of pain and photophobia, direct further suspicion toward keratitis when corneal signs predominate.^[2]

Laboratory and Imaging Tests

Laboratory tests for keratitis primarily involve obtaining corneal scrapings to identify infectious agents through staining and culture techniques. Corneal scrapings are collected under topical anesthesia using a sterile blade or spatula from the ulcer base and edges, followed by Gram staining to detect bacterial morphology and arrangement, which aids in presumptive identification of pathogens like Gram-positive cocci or rods. Giemsa stain is particularly useful for visualizing intracellular organisms, protozoa, or viral inclusions, enhancing detection in cases of suspected Acanthamoeba or viral keratitis. Cultures from these scrapings are inoculated onto media such as blood agar for bacteria, Sabouraud agar for fungi, and chocolate agar for fastidious organisms, with subsequent sensitivity testing via disk diffusion or broth microdilution to guide antibiotic selection; however, culture sensitivity varies, achieving positive yields in 60-80% of bacterial cases but lower for fungi at around 40-50%.^[20]^[66]^[67]^[68] Molecular diagnostics, such as polymerase chain reaction (PCR), provide rapid and sensitive detection of viral pathogens in keratitis. Real-time PCR assays target viral DNA or RNA, including herpes simplex virus (HSV) types 1 and 2, and varicella-zoster virus (VZV), with multiplex panels allowing simultaneous detection of multiple agents from corneal scrapings or tear samples; these tests exhibit sensitivities exceeding 90% and specificities near 100% for HSV in epithelial keratitis. For instance, multiplex PCR panels like those for HSV and VZV enable quantification of viral load, correlating with disease severity and treatment response. These tests are particularly valuable when clinical suspicion guides sampling, as in dendritic ulcers suggestive of herpetic involvement.^[69]^[70]^[71] In vivo confocal microscopy offers non-invasive imaging of corneal microstructures to identify specific pathogens without tissue removal. This technique uses a laser scanning confocal microscope to visualize Acanthamoeba cysts, appearing as double-walled, ovoid structures measuring 10-25 μm in the epithelium and stroma, facilitating early diagnosis with sensitivity up to 80% in suspected cases. For fungal keratitis, it detects branching hyphae as highly reflective, linear elements, often 5-10 μm wide, outperforming traditional stains in speed and specificity for non-responsive ulcers.^[72]^[73]^[74] Anterior segment optical coherence tomography (AS-OCT) provides high-resolution cross-sectional imaging to assess keratitis structural changes. It quantifies stromal depth involvement, revealing hyporeflective areas in infectious infiltrates and measuring thinning, where central corneal thickness may reduce to below 300 μm in severe cases, aiding in perforation risk assessment. AS-OCT delineates epithelial defects, stromal edema, and hyperreflective debris, with resolution down to 5-10 μm, supporting monitoring of progression without contact.^[75]^[76]^[77] Recent advancements in 2024-2025 have integrated artificial intelligence (AI) with microscopy for accelerated pathogen identification in keratitis. Deep learning models applied to confocal microscopy images achieve over 90% accuracy in classifying fungal and Acanthamoeba keratitis by analyzing hyphal branching patterns and cyst morphologies. Systems like DeepIK, developed in 2024, use convolutional neural networks on slit-lamp data to differentiate infectious types in real-time, reducing diagnostic time from days to minutes and improving accessibility in resource-limited settings. These AI tools, validated on diverse datasets, enhance specificity to 95% for rapid triage.^[78]^[74]

Management

Pharmacological Treatment

Pharmacological treatment of keratitis is etiology-specific, aiming to eradicate the infectious agent, reduce inflammation, and support corneal healing while minimizing complications such as scarring or perforation.^[79] For infectious cases, anti-infective agents form the cornerstone, with adjunctive therapies addressing pain and secondary inflammation.^[2] Treatment selection relies on clinical suspicion, culture results, and sensitivity testing to combat rising antimicrobial resistance.^[79] In bacterial keratitis, broad-spectrum topical antibiotics are initiated empirically, with fortified preparations preferred for severe or central ulcers. Common regimens include alternating hourly drops of fortified tobramycin (14 mg/mL) and cefazolin (50 mg/mL), or monotherapy with fluoroquinolones such as moxifloxacin 0.5% or gatifloxacin 0.3% every hour while awake.^[80] For methicillin-resistant Staphylococcus aureus (MRSA) infections, fortified vancomycin (25-50 mg/mL) is recommended, often combined with tobramycin.^[16] Dosing typically starts hourly and tapers based on clinical improvement, with cultures guiding de-escalation after 48-72 hours; monitoring involves daily slit-lamp exams for infiltrate resolution and avoidance of overtreatment to prevent toxicity. A Cochrane review found no significant efficacy differences among common topical antibiotics, emphasizing broad coverage initially.^[79] Viral keratitis, particularly herpes simplex virus (HSV), is managed with antivirals to inhibit replication. For epithelial HSV keratitis, topical acyclovir 3% ointment five times daily or oral acyclovir 400 mg five times daily for 7-10 days is standard, with oral valacyclovir 500 mg twice daily as an alternative.^[81] Stromal involvement requires concomitant oral antivirals and cautious topical corticosteroids (e.g., prednisolone acetate 1% four times daily) after epithelial healing to reduce inflammation, per Herpetic Eye Disease Study (HEDS) results showing faster resolution without increased perforation risk.^[4] Monitoring includes weekly follow-up for recurrence, with prophylactic oral acyclovir 400 mg twice daily reducing stromal keratitis relapse by 50% over one year.^[81] Fungal keratitis treatment centers on topical antifungals, with natamycin 5% suspension as first-line for filamentous fungi like Fusarium, applied hourly initially then tapered over weeks.^[82] For yeast infections such as Candida, amphotericin B 0.15% is preferred, while voriconazole 1% serves as an adjunct for deeper penetration in non-responsive cases, though the Mycotic Ulcer Treatment Trial (MUTT I) showed it inferior to natamycin for smear-positive ulcers.^[83] Oral voriconazole (200 mg twice daily) may be added for scleral extension, but MUTT II reported higher adverse events without superior outcomes.^[79] Therapeutic monitoring entails confocal microscopy or cultures to assess response, with poor stromal penetration necessitating adjunctive debridement.^[82] Acanthamoeba keratitis requires prolonged anti-parasitic therapy targeting both trophozoites and cysts. Dual topical therapy with polyhexamethylene biguanide (PHMB) 0.02% and propamidine isethionate 0.1% (or dibromopropamidine 0.15%) is initiated hourly day and night for the first 3-5 days, then every 2 hours while awake, continuing for 6-12 months with slow tapering.^[18] Chlorhexidine 0.02% may substitute for PHMB in dual regimens, and voriconazole 1% is added for refractory pain or scleritis.^[84] Multi-month regimens are essential due to cyst persistence, with monitoring via in vivo confocal microscopy for cyst clearance and clinical signs of resolution; pain often precedes visible improvement.^[29] Anti-inflammatory agents like topical corticosteroids (e.g., prednisolone acetate 1%) are used cautiously in infectious keratitis after 24-48 hours of effective anti-infective therapy and organism identification, to mitigate corneal scarring. The Steroids for Corneal Ulcers Trial (SCUT) demonstrated no overall vision or healing benefit but improved visual acuity in certain subgroups such as those with low baseline vision or central ulcers, with worsening in Nocardia cases; risks of worsening also apply to fungal infections.^[79] In non-infectious keratitis, such as autoimmune or exposure-related, corticosteroids are primary, starting at low doses and tapering per response.^[2] Adjunctive therapies include cycloplegics like atropine 1% or cyclopentolate 1% two to four times daily to relieve ciliary spasm and pain, particularly in anterior chamber involvement.^[13] For neurotrophic keratitis, preservative-free lubricants (e.g., hypromellose or carbomer gels) are applied every 1-2 hours to protect the epithelium and promote healing.^[85] Resistance patterns, such as fluoroquinolone resistance in 80% of MRSA isolates, necessitate vigilance and culture-directed adjustments.^[79] Overall, close ophthalmologic monitoring ensures therapeutic drug levels and prevents complications like resistance or toxicity.^[2]

Surgical Interventions

Surgical interventions are reserved for severe cases of keratitis where medical therapy has failed, particularly when there is significant stromal involvement, impending or actual perforation, or intraocular complications such as endophthalmitis.^[86] These procedures aim to preserve ocular integrity, promote healing, and restore visual function, with timing critical to prevent irreversible damage—often indicated when the ulcer involves more than 50% of stromal depth or progresses despite antimicrobial treatment.^[87] Preoperative preparation typically involves optimizing pharmacological control of infection to minimize intraoperative risks.^[88] Therapeutic penetrating keratoplasty (TPK) is the gold standard for managing perforated corneas or deep stromal ulcers in infectious keratitis, involving full-thickness replacement of the diseased cornea with a donor graft to excise infected tissue and restore structural stability.^[88] It is particularly indicated for bacterial, fungal, or acanthamoeba keratitis with descemetocele formation or perforation, where medical therapy alone cannot eradicate the pathogen.^[89] Graft survival rates for TPK in infectious keratitis vary, with studies reporting approximately 70-80% anatomical success at one year, though functional outcomes depend on the underlying etiology and timely intervention.^[90] Amniotic membrane transplantation (AMT) serves as an adjunctive or primary surgical option for non-perforated keratitis with persistent epithelial defects, leveraging the membrane's anti-inflammatory, anti-scarring, and growth-promoting properties to facilitate re-epithelialization and reduce stromal melting.^[91] It is commonly used in bacterial or fungal keratitis unresponsive to topical agents, applied as a graft or patch over the ulcer bed to enhance healing without full-thickness excision.^[92] Clinical outcomes demonstrate improved visual acuity and epithelial healing in over 80% of cases, with lower rates of progression to perforation compared to conservative management alone.^[93] Photoactivated chromophore corneal cross-linking (PACK-CXL) is an emerging adjunctive procedure for severe infectious keratitis, involving riboflavin application and UV-A irradiation to strengthen the cornea and enhance antimicrobial effects, halting melting and preventing perforation in nearly all treated cases as of 2024 reviews.^[94] Conjunctival flap procedures or tarsorrhaphy provide protective coverage for chronic or exposure-related keratitis, where ongoing ulceration threatens corneal integrity due to inadequate lid closure or neurotrophic changes.^[95] A conjunctival flap involves advancing bulbar conjunctiva over the cornea to shield it from desiccation and promote vascularized healing, indicated in recalcitrant infectious or bullous keratopathy cases.^[96] Tarsorrhaphy, by partially suturing the eyelids, reduces exposure in severe keratitis with lagophthalmos, achieving healing success in about 90% of non-healing epithelial defects.^[97] Common complications across these interventions include graft rejection in TPK (up to 20% in infectious cases), recurrence of infection particularly in fungal keratitis (10-30% post-transplant), and flap-related issues such as retraction or melt in conjunctival procedures (1-5%).^[98]^[99] Other risks encompass intraocular pressure elevation, cataract formation, and endothelial failure, necessitating close postoperative monitoring.^[100]

Supportive Care

Supportive care in keratitis management focuses on alleviating symptoms, promoting corneal healing, and preventing complications through non-specific interventions that complement primary treatments. Pain management is a key component, as keratitis often causes significant discomfort due to corneal inflammation and exposure. Oral analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or acetaminophen combinations, are commonly recommended to control pain without interfering with healing. Cold compresses applied to the closed eyelid for 10-15 minutes several times a day can reduce swelling and provide symptomatic relief by constricting blood vessels and numbing the area. Long-term use of topical anesthetics, such as proparacaine, must be avoided, as they can delay epithelial repair, increase infection risk, and lead to toxic keratopathy.^[84]^[101]^[39] Protective strategies aim to shield the cornea, maintain moisture, and facilitate epithelial regeneration during the acute phase. Eyelid patching or pressure patches may be used short-term to immobilize the lid, reduce friction on the healing epithelium, and promote re-epithelialization, particularly in cases of persistent epithelial defects; however, patching is contraindicated in active infectious keratitis to avoid trapping pathogens. Moisture chambers, such as specialized goggles or spectacles that create a humid environment around the eye, help prevent desiccation and support corneal repair by retaining natural tears and reducing evaporation, especially beneficial in exposure-related or neurotrophic forms. These measures are typically combined with frequent lubrication but should be monitored to ensure they do not exacerbate underlying issues.^[102]^[103]^[37] Nutritional support is particularly relevant in regions where vitamin A deficiency contributes to xerophthalmia and secondary keratitis, common in developing countries with malnutrition. Supplementation with high-dose vitamin A (e.g., 200,000 IU orally for adults) can reverse early corneal changes, restore epithelial integrity, and prevent progression to ulceration or perforation by supporting goblet cell function and mucin production. In deficiency-related cases, dietary improvements incorporating vitamin A-rich foods like liver, carrots, and leafy greens are advised alongside supplements to sustain ocular surface health. This approach is most effective when initiated promptly upon diagnosis of deficiency.^[104]^[105]^[106] Follow-up protocols are essential to track healing, adjust care, and educate patients on hygiene to minimize recurrence risks. Patients typically require daily or every-other-day clinic visits during the initial week to assess epithelial progress, pain levels, and response to therapy, with intervals extending to weekly thereafter until resolution. Education emphasizes hand hygiene, avoiding eye rubbing, proper contact lens care if applicable (e.g., daily cleaning and no overnight wear), and recognizing signs of worsening such as increased redness or discharge to prompt immediate return. These measures empower patients to maintain ocular hygiene and adhere to self-care routines.^[80]^[16]^[107] Holistic aspects address the broader impact of keratitis, including the psychological burden of potential vision impairment. Vision loss from scarring or complications can lead to anxiety, depression, and reduced quality of life, with studies showing higher rates of emotional distress in affected individuals. Referrals to vision rehabilitation services, such as low-vision aids training or counseling, are recommended for patients with persistent visual deficits to improve adaptation, independence, and mental well-being through strategies like magnification devices and psychosocial support. Integrating these elements ensures comprehensive care beyond physical symptoms.^[108]^[109]^[110]

Prevention

General Measures

Maintaining proper eye hygiene is a cornerstone of preventing keratitis, particularly for individuals who wear contact lenses or are prone to corneal irritation. Regular handwashing with soap and water before handling contact lenses significantly reduces the risk of introducing bacteria to the ocular surface, as unclean hands can transfer pathogens directly to the cornea. ^[111] Avoiding rubbing the eyes prevents mechanical trauma to the corneal epithelium, which can create entry points for infectious agents and exacerbate vulnerability to inflammation. ^[107] For contact lens users, safe handling practices are essential; this includes never rinsing lenses or cases with tap water, which may contain Acanthamoeba, a rare but severe cause of keratitis, and always using fresh, sterile solution for disinfection. ^[112] Protective eyewear plays a vital role in shielding the eyes from environmental and occupational hazards that could lead to keratitis. Sunglasses with 100% UVA and UVB protection are recommended to prevent photokeratitis, a painful corneal inflammation triggered by ultraviolet exposure during outdoor activities like sunbathing or skiing. ^[113] In sports such as basketball or racquetball, polycarbonate-framed protective eyewear reduces the risk of corneal trauma by up to 90%, minimizing opportunities for secondary infections. ^[114] For occupational risks, such as welding or chemical handling, safety glasses compliant with ANSI Z87.1 standards provide impact and splash resistance, preventing corneal abrasions that predispose to keratitis. ^[115] Addressing general health conditions that compromise corneal integrity further supports keratitis prevention. Individuals with dry eye syndrome should use preservative-free artificial tears multiple times daily to maintain ocular surface lubrication and reduce epithelial breakdown, which heightens infection susceptibility. ^[116] For those with diabetes, rigorous blood glucose management—targeting an A1C below 7%—helps mitigate diabetic keratopathy, a condition involving delayed corneal healing and increased keratitis risk due to neuropathy and poor wound repair. ^[117] Public health education campaigns emphasize compliance with these practices to curb keratitis incidence, especially among contact lens wearers. Initiatives like the CDC's Contact Lens Health Week highlight that approximately 99% of wearers engage in at least one risky behavior, such as topping off solution or sleeping in lenses, contributing to nearly one million annual U.S. health care visits for keratitis or contact lens complications. ^[118] Non-compliance with lens care regimens is associated with increased risk of contact lens-related keratitis, underscoring the need for ongoing awareness efforts. ^[119]

Specific Prophylaxis

Specific prophylaxis for keratitis targets high-risk subtypes and populations through tailored interventions to mitigate infection risks. For contact lens users, who face elevated chances of bacterial keratitis due to microbial contamination, recommendations emphasize the use of daily disposable lenses to minimize accumulation of pathogens and reduce disease severity compared to reusable lenses.^[120] Additionally, multipurpose contact lens solutions containing antimicrobial agents, such as polyhexamethylene biguanide or hydrogen peroxide, are advised for effective disinfection during cleaning, thereby providing prophylactic protection against bacterial adhesion.^[121] These measures build on general hygiene practices by addressing subtype-specific vulnerabilities in lens wearers. In cases of recurrent herpetic keratitis caused by herpes simplex virus, oral antiviral prophylaxis with acyclovir at 400 mg twice daily for up to 12 months significantly reduces the recurrence rate of epithelial and stromal disease by approximately 50% in at-risk patients.^[122] This long-term suppressive therapy is particularly recommended for individuals with a history of multiple episodes, as it prevents viral reactivation and associated corneal damage.^[17] For acanthamoebic keratitis, a subtype linked to exposure to contaminated water, preventive strategies for swimmers and contact lens wearers include avoiding lens wear during water activities and using approved disinfecting solutions for lens care to eliminate amoebic cysts.^[7] Although chlorhexidine is primarily employed in therapeutic regimens, its antimicrobial properties support its consideration in enhanced disinfection protocols for high-risk exposures, such as rinsing storage cases in contaminated environments, though standard prevention prioritizes water avoidance.^[84] Vaccinations play a role where applicable, notably the varicella vaccine administered to children at 12-15 months and 4-6 years to prevent primary varicella-zoster virus infection, thereby reducing the lifetime risk of herpes zoster ophthalmicus, which can lead to keratitis in 50-70% of cases.^[123] This immunization is especially critical for preventing zoster-related ocular complications in pediatric populations.^[124] Among immunosuppressed groups, such as those with HIV or on systemic corticosteroids, routine ophthalmic screening through regular eye examinations is essential to detect early signs of keratitis, given their heightened susceptibility to opportunistic infections.^[125] Post-ocular surgery, povidone-iodine prophylaxis at 5% concentration applied preoperatively reduces the incidence of postoperative infections, including keratitis, by broadly targeting microbial flora in these vulnerable patients.^[126]

Prognosis and Complications

Short-Term Outcomes

Short-term outcomes in keratitis primarily revolve around the resolution of acute epithelial defects and restoration of visual function following initial treatment. In mild cases, particularly bacterial keratitis, complete epithelial closure typically occurs within 7-14 days with prompt initiation of topical antimicrobial therapy, as early intervention minimizes stromal invasion and promotes rapid re-epithelialization.^[20] Factors such as the organism's virulence and host immune response further modulate this timeline; for instance, superficial ulcers respond faster than those with deeper involvement.^[127] Visual recovery in the immediate post-treatment period is often substantial, with many patients achieving best-corrected visual acuity of 20/40 or better in bacterial keratitis when antibiotics are started within 24-48 hours of symptom onset. Randomized prospective studies demonstrate an average improvement of 2.9 logMAR lines in visual acuity from presentation to three weeks post-treatment, reflecting the efficacy of fortified antibiotics in halting progression and allowing corneal repair.^[128] This early gain is most pronounced in central ulcers, where timely scraping and culture-guided therapy prevent scarring in the visual axis.^[129] Treatment failure is indicated by persistence of the epithelial defect beyond two weeks, often signaling antimicrobial resistance, inadequate penetration, or underlying misdiagnosis such as fungal etiology in presumed bacterial cases. In such scenarios, re-evaluation including repeat cultures is essential, as non-resolution rates in uncontrolled studies exceed 15% without adjustment.^[130]^[131] Recent time-to-resolution metrics from randomized controlled trials up to 2025 underscore these patterns; for example, a 2022 trial comparing photoactivated chromophore cross-linking (PACK-CXL) to standard antimicrobials reported maximum epithelial healing of 28 days in the CXL group versus 50 days in controls for moderate infectious keratitis, highlighting adjunctive options for faster resolution in select cases.^[132] Similarly, a 2025 systematic review of amniotic membrane transplantation in corneal ulcers found consistently shorter healing times (reductions of several days, such as 2-3 days in some studies) compared to medical therapy alone, with success rates ranging from 73% to 93%, often above 85% in select studies in non-perforated cases.^[93] These data emphasize that while mild episodes resolve predictably, moderate-to-severe keratitis may require multimodal approaches to achieve short-term endpoints within 4-6 weeks.^[127]

Long-Term Effects

One of the primary long-term effects of keratitis is corneal scarring and opacity, which can distort the corneal surface and lead to irregular astigmatism, resulting in permanent vision loss in approximately 14-20% of cases depending on the severity and etiology.^[133]^[134] These scars reduce corneal transparency, impairing light transmission to the retina and often necessitating interventions like corneal transplantation to restore function.^[79] Recurrence poses another significant risk, particularly in herpetic keratitis, where rates can reach up to 50% within five years, leading to cumulative corneal damage and progressive visual decline with each episode.^[135] Untreated or recurrent inflammation exacerbates fibrosis, further compromising visual acuity over time.^[44] Severe cases may also develop secondary complications such as glaucoma, cataract formation, or endophthalmitis due to corneal perforation, each contributing to additional intraocular pressure elevation, lens opacification, or intraocular infection that can cause irreversible vision impairment.^[136]^[137] These issues arise from prolonged inflammation or structural compromise, with secondary glaucoma occurring in up to 38% of advanced infectious cases.^[136] The functional impacts of these long-term effects are profound, including driving restrictions due to reduced visual acuity or field defects that fail to meet legal standards (e.g., 20/40 or better in many jurisdictions), alongside psychological burdens like anxiety and depression from monocular vision loss.^[138]^[139] Patients often require ongoing rehabilitation, such as low-vision therapy or adaptive aids, to manage daily activities and maintain independence.^[140] Recent longitudinal data from tropical regions highlight persistent vision impairment in post-fungal keratitis cases, with over 50% of patients experiencing monocular blindness and central axis involvement affecting 54% at presentation, underscoring the need for enhanced follow-up in high-risk areas.^[83]^[141]

Epidemiology

Global Incidence

Keratitis imposes a substantial global health challenge, with infectious forms predominating in many regions. Fungal keratitis has a worldwide incidence of 23.6 cases per 100,000 people, equating to approximately 1.2 million cases annually, with the highest burdens in Asia and Africa.^[142]^[143] Overall infectious keratitis is estimated to cause around 1.5-2 million cases of unilateral blindness annually, though total incidence may be higher due to underreporting.^[144] In developing countries, infectious causes comprise approximately 70-90% of all keratitis cases, contrasting with higher rates of non-infectious forms in developed settings.^[145] According to World Health Organization (WHO) data as of 2020, corneal opacities—often resulting from untreated keratitis—affect about 5.5 million people with bilateral blindness and 6.2 million with unilateral blindness globally.^[146] Recent trends indicate a rise in contact lens-related keratitis in urban areas, driven by increased lens usage and associated hygiene challenges, particularly in developed and rapidly urbanizing regions.^[142] Conversely, fungal keratitis remains prevalent in agriculture-heavy regions, where ocular trauma from plant matter facilitates infection by filamentous fungi.^[143] Meta-analyses highlight these patterns, with variations in etiology by region. The COVID-19 pandemic led to fewer reported cases and potential underreporting due to healthcare disruptions.^[147] Underreporting significantly skews incidence figures, especially in low-resource settings where limited access to microbiology labs and ophthalmologic services leads to misdiagnosis or overlooked cases.^[108] Projections suggest climate change will drive increases in parasitic forms, such as Acanthamoeba and microsporidial keratitis, through expanded vector habitats, warmer temperatures, and more frequent extreme weather events that heighten exposure risks.^[148] These trends underscore the need for enhanced surveillance in vulnerable areas.

Risk Group Distribution

Keratitis affects various demographic and clinical groups disproportionately, with risk profiles varying by age, geography, comorbidities, and socioeconomic status. Among age groups, young adults aged 18-40 are particularly vulnerable to infectious keratitis due to contact lens wear, which accounts for up to 32% of cases in this demographic in developed countries.^[149] In contrast, elderly individuals over 65 face heightened risks from non-infectious forms such as exposure keratitis, often linked to lagophthalmos or reduced blink rate, with studies showing increased incidence in this group due to age-related ocular surface changes.^[150] Children under 12, especially those under 2 years, are more prone to traumatic keratitis, where ocular trauma is a common risk factor, comprising 20-60% of pediatric cases in various cohorts.^[151]^[152] Geographically, infectious keratitis shows elevated rates in Asia and Africa, particularly among agricultural workers exposed to plant matter and soil, leading to fungal and bacterial etiologies that account for a significant portion of cases in these regions.^[153] For instance, in rural India and sub-Saharan Africa, trauma-related infections predominate due to occupational hazards in farming, contrasting with higher non-infectious keratitis prevalence in arid climates like the Middle East, where dry eye exacerbates exposure risks.^[154] In Western countries, contact lens-associated cases are more common, reflecting lifestyle differences.^[13] Comorbidities substantially elevate keratitis risk across groups. Patients with diabetes mellitus experience approximately 1.3 times the risk of corneal ulcers and neurotrophic keratitis compared to non-diabetics (adjusted HR 1.31), attributed to impaired corneal innervation and delayed wound healing.^[155] Individuals with HIV face opportunistic infections, including herpes simplex keratitis recurrences and rare bacterial or fungal forms, affecting about 5% of cases and often compounded by immunosuppression or drug abuse.^[156] Post-transplant patients, particularly those on immunosuppressive therapy following organ or corneal transplantation, show increased susceptibility to infectious keratitis, with graft infection rates reaching 4-6% due to epithelial defects and steroid use.^[157] Socioeconomic factors further stratify risk, with low-income populations exhibiting 3-5 times higher incidence rates of infectious keratitis, driven by poor hygiene, limited access to protective eyewear, and delayed care.^[153] Migrant agricultural workers face elevated risks of trauma-related eye infections from occupational exposures without adequate safety measures, particularly in regions like Southeast Asia and North America.^[153] Socioeconomic disparities in access to care exacerbate outcomes in underserved areas.^[158]

Veterinary Aspects

In Domestic Animals

Keratitis in domestic animals manifests differently across species, often sharing etiological overlaps with human cases such as bacterial and viral infections, though adapted to veterinary contexts. In dogs and cats, ulcerative keratitis is a common presentation, frequently triggered by corneal trauma from scratches or foreign bodies, leading to epithelial defects that predispose to secondary bacterial infections.^[159] In cats specifically, feline herpesvirus-1 (FHV-1) serves as a primary cause, inducing dendritic ulcers and persistent epithelial erosions, particularly in young or stressed individuals.^[160] Treatment for these cases typically involves topical antibiotics such as oxytetracycline or triple antibiotic ointments to address secondary infections, alongside antivirals like famciclovir (40 mg/kg orally three times daily) for FHV-1, and supportive measures including oral L-lysine to reduce viral shedding.^[159]^[160] In horses, keratitis often arises in association with equine recurrent uveitis (ERU), an immune-mediated condition where repeated episodes of anterior uveal inflammation lead to secondary corneal edema, ulceration, and opacification, potentially causing vision impairment if unmanaged.^[161] Fungal keratitis, or keratomycosis, is another prevalent form, commonly resulting from corneal abrasion by plant material such as hay or bedding, allowing opportunistic fungi like Aspergillus spp. to invade the stroma.^[162] Management includes topical antifungal agents (e.g., natamycin or voriconazole), systemic non-steroidal anti-inflammatories for pain and inflammation control, and subconjunctival or intrastromal injections in severe cases to promote healing and prevent perforation.^[163] Cattle and other livestock are particularly susceptible to infectious bovine keratoconjunctivitis (IBK), commonly known as pinkeye, a highly contagious condition primarily caused by Moraxella bovis bacteria, exacerbated by face flies and ultraviolet light exposure during summer months.^[164] This leads to rapid herd outbreaks, with clinical signs including corneal ulceration, purulent discharge, and blepharospasm, potentially resulting in temporary blindness and reduced productivity.^[165] Effective herd management strategies encompass prompt isolation of affected animals, fly control with insecticides, and vaccination against M. bovis strains, alongside topical oxytetracycline ointments or long-acting tetracyclines for treatment to minimize transmission and economic losses.^[164]^[165] Veterinary diagnostics for keratitis across species employ slit-lamp biomicroscopy to visualize corneal defects, depth of ulcers, and anterior segment inflammation, enabling precise assessment similar to human ophthalmology but tailored to animal restraint challenges.^[166] Species-specific pathogens require targeted identification; for instance, in goats, Mycoplasma conjunctivae is a key etiologic agent in infectious keratoconjunctivitis, diagnosed via PCR on conjunctival swabs or culture on special media to confirm its role in outbreaks.^[167]^[165] Zoonotic transmission of keratitis-related pathogens is rare but documented, such as Chlamydia felis from infected cats causing chronic follicular conjunctivitis in humans through direct ocular contact with secretions.^[168]

In Wildlife

In wild primates, such as free-ranging rhesus macaques, traumatic injuries to the cornea represent a significant cause of keratitis, often resulting from environmental hazards like urban encroachment that increase encounters with sharp objects or aggressive interactions. These injuries can lead to corneal opacity and impaired vision, compromising foraging efficiency and predator evasion essential for survival in natural habitats.^[169] Parasitic infections also contribute to keratitis in wildlife, notably through eyeworms of the genus Thelazia. In wild birds, Thelazia species, particularly those in the subgenus Thelaziella, infest orbital cavities and conjunctival sacs, inducing conjunctivitis that may progress to keratitis with symptoms including lacrimation and corneal ulceration. Similarly, in cervids like deer, Thelazia gulosa and related species cause ocular infestations leading to epiphora, pruritus, and keratitis, with corneal opacity hindering visual acuity critical for detecting threats in forested environments.^[170]^[171]^[172] Among marine mammals, environmental factors exacerbate keratitis risks in wild populations. Seals and sea lions experience keratopathies linked to ultraviolet (UV) radiation exposure from environmental factors, causing edema and superficial damage that affects underwater navigation and hunting. Bacterial keratitis in these species can arise from pollution-related stressors, such as contaminated coastal waters harboring opportunistic pathogens like Vibrio spp., leading to corneal ulcers that impair vision in foraging dives.^[173]^[174]^[175] In reptiles, fungal keratitis occurs sporadically in wild individuals, as documented in a gopher tortoise (Gopherus polyphemus) infected with an unidentified fungus, resulting in severe corneal ulceration and vision loss potentially tied to habitat degradation that weakens immune responses. For amphibians, while direct fungal keratitis cases are rare, habitat loss increases susceptibility to fungal pathogens like Batrachochytrium dendrobatidis, contributing to overall health decline in fragmented wetlands.^[176] Field studies on corneal health in endangered species highlight the prevalence of infectious keratitis. In wild koalas (Phascolarctos cinereus), chlamydial infections by Chlamydia pecorum cause keratoconjunctivitis in up to 47% of examined individuals, with ocular disease severity correlating directly with bacterial load in conjunctival swabs, leading to corneal scarring that reduces eucalyptus detection and mobility. These investigations, conducted in Queensland habitats, underscore how vision impairment exacerbates vulnerability in declining populations. In 2025, a vaccine against Chlamydia pecorum was approved for rollout in Australia, offering hope for reducing infection rates and aiding conservation efforts.^[177]^[178]^[179] From a conservation perspective, keratitis contributes to wildlife population declines by amplifying mortality in visually dependent species. In koalas, chlamydial keratitis is a key driver of the species' endangered status, with infections facilitating broader ecosystem disruptions through reduced reproduction and heightened predation risk. Emerging 2025 monitoring technologies, such as AI-enhanced camera traps and drone-based thermal imaging, enable non-invasive assessment of koala populations and general health in wild cohorts, informing habitat restoration and targeted interventions.^[180]

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Conclusions : Multiplex real-time PCR reliably detects high copy numbers of HSV1/2 and VZV DNA in patients with clinical viral keratitis and the DNA level is ...Missing: molecular panels
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Australia's iconic koalas are under threat of extinction from several directions, including two infectious diseases; chlamydia and koala retrovirus.<|separator|>
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May 29, 2025 · The aim of our work was i) to develop a clinical observation protocol, easy to use by biologists in charge of monitoring, who can suspect ...Missing: technology | Show results with:technology