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Microbiology, Lens Care and Maintenance


Effective care and maintenance of contact lenses is central to the safety and success of contact lens wear ( , ). Ineffective and noncompliant lens care are two of many reasons for cessation of wear contributing to the number of so-called contact lens dropouts. However, over the last three decades there has been a significant decline in the perceived importance of lens care due largely to:

  • ▪

    The advent of frequent replacement and disposable lenses with lower complication rates ( ).

  • ▪

    Market advances of daily disposable contact lenses that require minimal lens care.

  • ▪

    Convenience lens care products (e.g. one-step disinfectants) and the advent of one-bottle systems (OBSs).

  • ▪

    Manufacturers' ill-conceived promotion of no-rub products.

This diminished focus on lens care is unfortunate because:

  • ▪

    Although DD lenses require no conventional lens care and may eventually dominate the market, it is unlikely that all future lenses will be disposable or worn on an extended-wear (EW) or continuous-wear (CW) basis. High ametropes, those requiring unusual prescriptions and orthokeratology lenses are unlikely to be catered for by disposable lenses in the foreseeable future. A review of microbial keratitis in orthokeratology patients by suggested that most were the result of inexperience and/or use of tap water as part of the care regimen.

Compounding these issues is the relatively high cost of lens care products generally. As the market for nondisposable lenses diminishes, the relative cost of care products increases owing to the loss of previous economies of scale.

Initial contact lens solutions targeted physiological issues (e.g. Sattler's veil), rather than lens care per se . Hind (co-founder of Barnes-Hind, an early market leader in lens care [ ]) first became involved with lens solutions and their problems in the 1940s for cleaning glass, polymethylmethacrylate (PMMA), or hybrid scleral lenses. The earliest attempts at altering the physical condition of contact lenses were intended to improve lens wetting and employed polyvinyl alcohol. Subsequently, it was realised that if the lens surface was unclean ( Fig. 4.1 ), the wetting solution was less effective, and so work began on an effective lens ‘cleaner’.

Fig. 4.1
Rigid lens showing anterior surface lipid and mucus deposition along with numerous surface scratches (shown in specular reflection).

(Courtesy of D. Goldsbury)

Eventually, a suite of products that cleaned, disinfected and wetted lenses was produced ( ), and true contact lens care had ‘arrived’.

The roles of lens care

Lens care will ideally:

  • ▪

    disable and remove all live and dead microorganisms from contact lenses to eliminate the possibility of lens-related infection, inflammation or irritation

  • ▪

    remove all other biological and nonbiological lens contaminants

  • ▪

    restore and maintain the lens in as-new condition.

Unfortunately, these ideals are not realisable in practice, but the minimum requirement is a lens that is safe and comfortable to wear.

Efficacy, safety and convenience are necessary in developing lens care regimens that should:

  • ▪

    remove lens contaminants.

  • ▪

    clean

  • ▪

    rinse

  • ▪

    disinfect

  • ▪

    maintain/store

  • ▪

    rewet/rehydrate

  • ▪

    lubricate

Other considerations when formulating or prescribing care regimens include:

  • ▪

    efficacy

  • ▪

    safety

  • ▪

    convenience (a factor in compliance).

Maintaining good vision and comfort and keeping the lens storage case clean are other important factors.

Lens contaminants

Contact lenses should arrive in sterile, sealed and durable packaging. Once this is opened, ‘contaminants’ can access the lens from:

  • ▪

    the environment

  • ▪

    the wearer's (or carer's) fingers and hands during handling/insertion/removal.

  • ▪

    lens care products.

Contaminants can include:

  • ▪

    viable and dead microorganisms

  • ▪

    viruses

  • ▪

    prions

  • ▪

    cellular debris

  • ▪

    tear components:

    • ▪

      proteins

    • ▪

      mucus

    • ▪

      lipids

    • ▪

      other tear film components

  • ▪

    skin lipids

  • ▪

    finger-borne debris

  • ▪

    eye and other cosmetics

  • ▪

    environmental contaminants

  • ▪

    care products and/or their derivatives

  • ▪

    by-products of any interactions between lens, care products, and contaminants.

In this chapter, challengers (microorganisms and other biological entities) and challenges (everything else) are treated separately.

General Microbiology

Microorganisms consist of nucleic acids, proteins, lipids and carbohydrates (sugars). The nucleic acids may be either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA). DNA codes genetic information that determines the phenotype (physical manifestation) of the microorganism, and RNA molecules participate in protein synthesis. Each microorganism also contains enzymes that determine its metabolic activity. These enzymes regulate cellular reactions and the biosynthesis of macromolecules from nutrients derived from the environment.

The structural unit of fungi, algae and mammalian cells is a eukaryotic cell, and it is more complex than the prokaryotic cell of bacteria. Table 4.1 summarises the differences between these types of cell.

Table 4.1
Characteristics of Eukaryotic and Prokaryotic Cells
Eukaryotic Cells Prokaryotic Cells
Nuclear membrane present No nuclear membrane
Multiple chromosomes Single chromosome
Membrane-bound organelles present (mitochondria, lysosomes) Membrane-bound organelles absent
Intracellular digestive vacuoles present Intracellular digestive vacuoles absent
Cells divide by mitosis Cells divide by binary fission
Bacterial cells have an average diameter of approximately 1–2 µm, viral cells <0.5 µm, fungal cells 3–5 µm, and protozoa 15–30 µm.

Microorganisms are commonly unicellular or acellular and include most bacteria, algae, viruses, protozoa and some fungi. All except algae can produce systemic and ocular disease. Most of these cells are enclosed by a cytoplasmic membrane, a double-layered structure of lipid and protein that encloses all structures and molecules for the maintenance of biological function. It acts as a semi-permeable membrane and controls the passage of solutes between the cell and external environment. Many of the antimicrobials and preservatives in lens care products target the cytoplasmic membrane.

While multicellular microorganisms may originate from a single cell, single cells may also attach to one another to form threads or filaments while still functioning as a single cell. Some bacteria and algae exist in this form.

Bacteria

Bacteria are classified according to their morphology, staining characteristics, growth requirements, biochemical type or antigenic structure as follows ( ).

Morphology (see Fig. 4.2 )

  • ▪

    Spherical (cocci). The morphology of cells depends on how single cells divide. Possible options include:

    • ▪

      if cocci divide in a single plane, they form pairs ( diplococci , e.g. Neisseria spp.) or chains (e.g. Streptococcus spp.).

    • ▪

      if cocci divide in two planes, they form a group of four ( tetrads , e.g. Micrococcus spp.).

    • ▪

      if cocci divide in three planes, they form a cluster of eight either as a cube ( sarcinae ) or as a cluster (e.g. Staphylococcus spp.).

  • ▪

    Cylindrical ( bacilli or rods , e.g. Pseudomonas spp.). Again these may take several forms:

    • ▪

      Coccobacilli are short rods with a more rounded appearance (e.g. Acinetobacter spp.).

    • ▪

      Filamentous rods that grow as elongated forms.

    • ▪

      Vibrios that look like commas (e.g. Vibrio cholerae ).

  • ▪

    Helical, known as spirochaetes.

These different morphologies are illustrated in Fig. 4.2a and b . *

* For further information see: http://www.cdc.gov/od/ohs/biosfty/bmb14/bmb14s7d.htm

Fig. 4.2, Morphology of (a) bacterial cocci and (b) rods.

Bacteria may also be differentiated by their carbohydrate metabolism, protein metabolism, enzyme production or other specific biochemical reactions (biotyping). For microorganisms that are biochemically similar, other methods of typing include:

  • ▪

    Antibiogram typing . This method is based on the microorganism's susceptibility to different antibiotics.

  • ▪

    Bacteriophage typing. Differentiation on the basis of the microorganism's susceptibility to various bacterial viruses, which is used commonly to differentiate between strains of Staphylococcus aureus .

  • ▪

    Bacteriocin typing . Differentiation on the basis of inhibitory protein (bacteriocin or pyocin) production. Certain microorganisms, including Pseudomonas aeruginosa, produce proteins that inhibit the growth of other members of the same species.

  • ▪

    Serotyping. Differentiation on the basis of antigenic structure. This method is used to differentiate between strains of, for example, P. aeruginosa and Legionella pneumophila .

  • ▪

    Molecular typing. These techniques involve differentiation between microorganisms at the DNA level and have been used for a wide range of species. Such molecular biology methods include random amplified polymorphic DNA (RAPD) and restriction fragment length polymorphism (RFLP) techniques. Both methods have been used in differentiating species of organisms derived from the ocular surface. The polymerase chain reaction (PCR) provides a means for amplification of DNA sequences of microorganisms.

Cell Wall

The Gram staining procedure involves sequentially staining a heat-fixed smear of bacterial cells with crystal violet and iodine, then decolourising with an organic solvent and counterstaining. Gram-positive bacteria resist decolourisation and remain stained purple. Gram-negative bacteria decolourise and take up a red/pink counterstain. Fig. 4.3 illustrates Gram-positive and Gram-negative bacilli and cocci. Table 4.2 shows the difference between the two.

Fig. 4.3, Gram stain of Gram-positive and Gram-negative rods and cocci.

Table 4.2
Differences Between Gram-Positive and Gram-Negative Staining Cells
Gram Positive Cells Gram Negative Cells
Colour Stained Remain Purple Become Red/Pink
Cell wall Cytoplasmic membrane surrounded by thick peptidoglycan layer, a mucopeptide cross-linked with peptide subunits that give rigidity to the structure, interspersed with (lipo-) teichoic or teichuronic acid Cytoplasmic membrane has smaller peptidoglycan layer, surrounded by an outer protein membrane and lipopolysaccharide (LPS) enclosing the periplasmic space
In eye defence Lysozyme cleaves peptidoglycan, causing bacterial death Less able to cleave to small peptidoglycan
Peptidoglycan damage More of a problem to cells Less of a problem to cells
Effect of lysozyme More effective Less effective

Bacteria are grouped by their Gram-staining reaction, which reflects the structure of the cell wall. The cell wall of Gram-positive microorganisms comprises a cytoplasmic membrane surrounded by a thick peptidoglycan layer (a mucopeptide) cross-linked with peptide subunits that give rigidity to the structure and interspersed with (lipo-) teichoic or teichuronic acid.

In contrast, Gram-negative microorganisms have a cytoplasmic membrane with a smaller peptidoglycan layer, surrounded by an outer protein membrane and lipopolysaccharide (LPS) enclosing the periplasmic space. In the eye, this difference is important in defence since the tear protein lysozyme cleaves peptidoglycan and causes bacterial death, either by allowing other bactericidal proteins to penetrate the cell or by causing osmotic death. Peptidoglycan damage is more of a problem for Gram-positive microorganisms, and lysozyme is much less effective against Gram-negative bacteria that are protected by their outer wall (that is impermeable to enzymes).

Outside the cell wall, there may be other external structures present such as flagella, pili and capsules. Flagella are filaments of the protein flagellin, responsible for bacterial motility. Pili are shorter filaments of the protein pilin that emerge from the cytoplasmic membrane which are responsible for bacterial adhesion and the transfer of nonchromosomal genetic material, such as plasmids, †

† Plasmid – a small circle of DNA found within bacteria.

between bacteria. These are general gene-carrying, mobile DNA elements found in the cell cytoplasm that are not essential for bacterial survival but that provide some selective advantage (e.g. antimicrobial resistance).

Capsules are frequently a polysaccharide matrix composing the outermost layer of certain bacteria. Capsules are a major determinant in the virulence of a microorganism that act by protecting the bacteria from phagocytosis and from other antimicrobial agents. Capsules also play a role in the binding to host tissue.

Growth Requirements

Bacteria can be further classified according to their environmental requirements for growth. These could include growth temperature, oxygen requirements, pH, salinity and micronutrients.

The temperature ranges for optimal growth are as follows:

  • ▪

    thermophilic microorganisms: 55–80°C

  • ▪

    mesophilic microorganisms: 25–40°C

  • ▪

    psychrophilic microorganisms: below 20°C

Atmospheric requirements can be classified as follows:

  • ▪

    aerobic microorganisms that require oxygen for growth

  • ▪

    facultative anaerobic microorganisms that grow in the presence or absence of oxygen

  • ▪

    anaerobic microorganisms that grow only in the absence of oxygen

  • ▪

    microaerophilic microorganisms that grow in the presence of trace oxygen and carbon dioxide.

External ocular infections tend to be caused by mesophilic microorganisms that may be aerobes, facultative anaerobes or microaerophilic microorganisms.

Bacteria and Disease

Bacteria may cause disease either by:

  • ▪

    direct invasion of tissue and subsequent replication of microorganisms

  • ▪

    toxin or enzyme production that may in turn activate the immune system causing an inflammatory tissue response. Dead or dying bacteria also release toxins.

In diseases associated with Gram-negative microorganisms, endotoxin has been implicated as a cause of major tissue damage. Endotoxin is an outer membrane component of Gram-negative microorganisms composed of lipopolysaccharide that is known to cause antibody and cytokine production, neutrophil migration and complement activation.

Fungi

Most fungi are found in soil where they degrade organic matter. They rarely cause disease in healthy humans but are a major cause of eye infections in immunocompromised individuals or in association with ocular trauma in rural areas.

All fungi are either aerobes (moulds) or facultative anaerobes (yeasts). Structurally, fungi are larger than bacteria and contain multiple chromosomes, and the cytoplasm contains mitochondria and endoplasmic reticulum. Their cell walls are quite different from bacteria, are very thick and contain no peptidoglycan, making them resistant to host defences and difficult to eliminate once infection is established.

Fungi and Disease

Fungi release spores into the environment that are carried by air or water. Spores are highly resistant to environmental factors and can survive extremes of temperature and pH. This resistance is due partly to surface components, such as hydrophobic glycoproteins or lipoglycoproteins, that also help dissemination. They are ubiquitous in the environment, are found on skin and are ingested or inhaled frequently. Despite their frequency in the environment, fungal disease is rare and requires the spores to penetrate the host tissue and germinate.

Species pathogenic in the eye include filamentous fungi, Aspergillus spp., Fusarium spp. and the yeast Candida spp. Historically, fungi have not been associated with contact lens–related infections; however, an international outbreak of Fusarium spp. keratitis in 2006–2007 was attributed to limited antimicrobial efficacy of a specific contact lens solution ( ) (See: Product Recalls (2006/2007) in Section 8 , History, available at: https://expertconsult.inkling.com/ ).

Actinomycetes

Actinomycetes are a group of bacteria that share some common characteristics with fungi and in the eye can cause similar disease to fungi. They are able to form hyphae, usually considered a trait of fungi only. Structurally, in all other ways, they are prokaryotic cells that resemble bacteria and are susceptible to penicillin, which fungi are not.

Examples of Actinomycetes include Streptomyces spp. These are an important group of soil bacteria used in the synthesis of antibiotics such as streptomycin. Species that are pathogenic in the eye include Corynebacterium spp. and Mycobacterium spp.

Viruses

Viruses are responsible for many human, animal and plant diseases, including disease at all ocular sites. Viruses are small (20–250 nm), acellular obligate parasites that are different structurally from cellular microorganisms such as bacteria with different chemical composition and mode of growth.

One useful definition of a virus is ‘a subcellular agent, consisting of a core of nucleic acid surrounded by a protein coat (and sometimes an outer protein and lipid envelope) that must use the metabolic machinery of a living host to replicate’.

Viruses can exist in either an extracellular or intracellular form. The extracellular form, or virion, comprises either single- or double-stranded DNA or RNA molecule(s) (nucleocapsid) within a protein coat or capsid. Viruses can be differentiated by how their nucleic acid is packaged, i.e. rod shaped, helical, spherical or isometric. The virion contains no structures for growth or multiplication. It therefore requires a host cell to undergo replication ( ) and must be released subsequently from the host cell after replication.

Ocular infections may be caused by the herpes virus (cytomegalovirus, varicella-zoster virus, Epstein-Barr virus [MSV], and human virus-6) and adenoviruses, although infections may be caused by other groups.

Viruses and Disease

Viruses can produce disease in several ways:

  • ▪

    Directly by inhibiting cell metabolism and synthesis. Cells infected by viruses lyse, and this can lead to temporary or permanent loss of function.

  • ▪

    Indirectly by compromising host defences so that opportunistic microorganisms such as bacteria can colonise. One example of this is the influenza virus that damages the respiratory epithelium and cilia so that the surface cannot be cleared of bacteria. Bacteria such as Haemophilus influenzae are then able to adhere to the damaged tissue and to colonise and produce disease.

  • ▪

    By inducing tumour formation ( oncogenic viruses). This is controversial, but both DNA and RNA viruses carry genes closely related to host cell genes that are able to transform cells and alter their physiological properties.

Protozoa

Protozoa comprise a number of diverse groups of unicellular microorganisms that range from 5 µm to 1 mm in diameter. Most are aquatic and may live as parasites in a range of species or may be free living. Under certain environmental conditions, many protozoa become encysted as a means of protection. This allows the cell to survive adverse environments and to survive outside the host until they can enter a new host. From the perspective of the contact lens environment, this enables them to resist lens care products and wait until conditions are more suitable.

There are approximately 40,000 species of protozoa, but only a few cause disease in humans.

Ocular infections may be caused by Toxoplasma spp. and by Acanthamoeba spp. Further, there is a strong association between Acanthamoeba spp. and contact lens-related disease ( ).

Prions

Prions are unconventional infectious agents that cause transmissible fatal brain disease in humans and animals. They are not living microorganisms in the conventional sense ( Table 4.3 ).

Table 4.3
Comparison of Biochemical Characteristics of Eukaryotes, Prokaryotes, Viruses and Prions
Biochemical Trait Eukaryotic Cells Prokaryotic Cells Viruses Prions
Protein ✓ ✓ ✓ ✓
Nucleic acids ✓ ✓ ✓(DNA or RNA, not both) ✗
Carbohydrates ✓ ✓ ✓/✗ ✗
Lipids ✓ ✓ ✓/✗ ✗
Ribosomes ✓ ✗ ✗ ✗
Chloroplasts/mitochondria ✓ ✗ ✗ ✗
Nuclear membrane ✓ ✗ ✗ ✗
Multicellular ✓ ✗ ✗ ✗
Intracellular growth ✓/✗ ✓/✗ ✓ ✗

Prions are an aberrant isoform of a normal cellular protein (PrP c ) that exists in normal human and animal neuronal tissue. Prions enter brain tissue and, through mechanisms that are not yet fully understood, cause the conversion of the normal PrP c into copies of the aberrant prion protein PrP sc in a self-propagating process. Conversion to the prion protein PrP sc appears to be associated with abnormal protein folding, rendering the protein insoluble, resistant to protease degradation, resistant to many biocides and transmissible.

Prions and Disease

Prions cause cross-species neurodegenerative diseases known as transmissible spongiform encephalopathies in humans and animals. The most common acquired human prion diseases include Creutzfeldt-Jakob disease (CJD) and new variant Creutzfeldt-Jakob disease acquired through eating infected cattle meat and kuru (ritual cannibalism in New Guinea). Iatrogenic CJD has been reported following administration of prion-containing growth hormone and transplantation of prion-containing nervous system grafts. There was one proven case ( ) and three possible cases following corneal transplantation ( , , ). *

* For further information see: https://www.cdc.gov/prions/cjd/index.html

For a comparison of eukaryotes, †

† Eukaryote – can be single-cell or multi-cellular and contain a nucleus surrounded by a membrane that contains DNA. Eukaryotes also contain other organelles.

prokaryotes, ‡

‡ Prokaryote – single cells that do not contain a nucleus and contain few cell components other than pieces of DNA.

viruses and prions, see Table 4.3 .

Microbiology of the Eye

Normal Ocular Biota (Living Organisms Within the Eye)

Historically, it has been accepted that the external ocular surface is sparsely colonised by culturable organisms, and microorganisms are removed by the normal ocular defence mechanisms rather than leading to persistent and increased colonisation over time.

The most common microorganisms isolated from the eyelids and conjunctiva are Gram-positive bacteria, specifically coagulase-negative staphylococci, Propionibacterium spp. and Corynebacterium spp. Other bacterial species include Staphylococcus aureus, Micrococcus spp., Bacillus spp. and Bacteroides spp. ( , , , , , ). The conjunctival fornices may harbour small numbers of anaerobic organisms, with Propionibacterium and Peptostreptococcus being the most common genera ( , ). Gram-negative microorganisms are isolated in less than 5% of cases and tend to be present as transient microorganisms rather than persistent colonisers in normal healthy eyes. The cornea and anterior chamber have been considered to be sterile, although more recently, molecular surveillance techniques challenge this assumption for the cornea.

Fungi are less common, although regional variations have been reported, with fungal recovery from the eyelids occurring in 2–52% of samples and in 2–28% of conjunctival samples ( , ). An increased recovery rate of fungi from the ocular surface has been reported using PCR for the detection of fungal DNA ( ).

The advent of molecular techniques, particularly 16S ribosomal DNA amplification and sequencing, have shown a much more diverse microbiome §

§ Microbiome – the microorganisms in a particular environment; in this case the eye.

at the ocular surface than revealed by conventional culture of viable organisms ( , , , ). Interpretation of these findings is challenging given the impact of possible DNA contamination from transient and other organisms. With the development of high-throughput DNA-sequencing techniques, there is likely to be further exploration of the ocular surface microbiome and a better understanding of whether a stable microbiome exists and how this may change over time and in different states of the disease ( , ).

Microorganisms and Eye Disease

Table 4.4 summarises the common causative microorganisms for different ocular diseases.

Table 4.4
Common Causative Organisms in Ocular Infections
Sources: , , , , , , , , , , , , , .
Ocular Site Disease Microorganisms
Lacrimal drainage Canaliculitis Propionibacterium sp.
Lid margin Blepharitis, blepharoconjunctivitis, blepharokeratoconjunctivitis S. aureus
Conjunctiva Acute bacterial conjunctivitis (adult) S. aureus
Strep. pneumoniae
H. influenzae
Strep. pyogenes
Proteus spp.
Moraxella spp.
Enteric Gram-negative bacteria
Less commonly anaerobic species
Conjunctiva Acute bacterial conjunctivitis (childhood) H. influenzae
Neisseria gonorrhoeae
Neisseria meningitidis
S. aureus
Strep. pneumoniae
Conjunctiva Phlyctenular conjunctivitis Mycobacterium tuberculosis
S. aureus
C. albicans
Conjunctiva Membranous conjunctivitis Strep. pyogenes
Neisseria spp.
Corynebacterium spp.
Conjunctiva Follicular conjunctivitis Chlamydia trachomatis
Adenovirus 1, 2, 4–6, 19
Conjunctiva Viral conjunctivitis Herpes simplex
Adenovirus (pharyngoconjunctival fever) 3, 7
Herpes zoster
Epstein–Barr virus
Measles, mumps, hepatitis A virus
Conjunctiva Acute haemorrhagic conjunctivitis Adenovirus 11
Coxsackie virus 24
Enterovirus 70
Cornea Microbial keratitis S. aureus
Coagulase-negative staphylococci
Strep. pneumoniae
Strep. pyogenes
Strep. viridans
P. aeruginosa
Moraxella sp.
Proteus sp.
Klebsiella sp.
Serratia sp.
Other Gram-negative bacteria
Chlamydia trachomatis
Herpes simplex
Herpes zoster
Adenovirus
Aspergillus sp.
Fusarium sp.
C. albicans
Cornea Contact lens-related microbial keratitis P. aeruginosa
S. marcescens
Other Gram-negative bacteria
S. aureus
Strep. pneumoniae
Acanthamoeba spp. (Group 2)
Sclera Scleritis Strep. pneumoniae
Acanthamoeba spp. (Group 2)
Anterior chamber Acute endophthalmitis S. aureus
Strep. pyogenes
Strep. pneumoniae
Enteric microorganisms
Anterior chamber Chronic endophthalmitis Coagulase-negative staphylococci
Propionibacterium sp.
Corynebacterium sp.
Haemophilus spp.
Pseudomonas spp.
C. albicans
Fusarium spp.
Aspergillus sp.
Herpes simplex
Herpes zoster

The effect of lens wear on ocular biota

Alterations to the normal ocular biota during lens wear may, theoretically, suppress the ocular defence mechanism and enable colonisation by pathogenic organisms. There is considerable controversy in the literature as to the effect of contact lens wear. Much of this confusion is likely to reflect differences in methodology, sampling techniques, subject groups, lens types, wear modality and type and duration of wear. Increased conjunctival biota has been reported in daily hydrogel lens wearers ( , , , ) although the spectrum of organisms was not found to differ. This increase in conjunctival biota may be secondary to quantitative changes in lid margin biota ( ). In one study, the conjunctival biota could be related to the contaminants of the lens storage case ( ) although no such association was confirmed in a later study ( ). An alteration in the spectrum of organisms was found to occur in a mixed group of rigid and soft lens wearers ( ) and in extended-wear hydrogel wearers ( ), where increased numbers of both sterile cultures and Gram-negative organisms were isolated. However, other studies have reported no differences in conjunctival biota between lens wearers and non–lens wearers ( , , ).

Increased conjunctival colonisation by pathogenic nonresident organisms has been demonstrated during extended wear of rigid gas permeable (RGP) lenses ( ). Adherence and colonisation of lenses by pathogenic organisms has been reported in association with lens-related keratitis ( ), and high numbers of pathogenic organisms have been recovered from lenses during episodes of acute adverse responses ( , ). One possibility is that pathogenic organisms adhere and easily colonise lenses and are not removed as easily as normal biota. Inhibition of the clearing of pathogenic organisms from the eye during lens wear may be one of several factors modulating this alteration in biota with lens wear. This alteration in biota has been reported as persisting subsequent to cessation of lens wear ( ). It is not clear, however, whether this effect is limited to wearers discontinuing wear due to adverse responses.

There is a paucity of studies of the ocular microbiome in contact lens wearers, and those published are often limited by small sample size. There is, however, some evidence to suggest that the conjunctival microbiome is altered in contact lens wear with the conjunctiva more closely matching skin biota ( ).

The Interaction Between Lenses and Microorganisms

In asymptomatic lens wear, a contact lens is frequently colonised by small numbers of microorganisms ( ) derived from:

  • ▪

    the hands ( )

  • ▪

    lids ( )

  • ▪

    lens care solutions ( )

  • ▪

    storage cases ( , , , , )

  • ▪

    the domestic water environment ( )

  • ▪

    environmental sources ( ).

Storage cases have also been implicated as a source of lens contamination by bacteria, fungi and amoebae. Microbial contamination of storage cases has been reported in 18–100% of cases sampled, with heavily contaminated cases showing up to 6 log units of organisms per case well ( ). Differences in rates can be attributed to the study location, study design, methodological differences and differences between subject groups ( ). Bacteria make up the majority of species, and fungal contamination of storage cases has been reported in up to 24% of cases in asymptomatic wearers showing contamination by filamentous fungi and yeasts ( , ). Species isolated most commonly included Cladosporidium spp., Candida spp., Fusarium solarni, Aspergillus spp., Exophiala spp., and Phoma sp. Contamination of storage cases by Acanthamoeba has been shown in 4–10% of wearers ( , , ). However, where tap water rinsing of cases was avoided and cases were replaced monthly, no amoebic contamination was reported ( ). Amoebic contamination of lenses in asymptomatic wearers appears rare ( ). Table 4.5 summarises studies of case contamination by subject group, lens type and by disinfection system (adapted from ).

Table 4.5
Summary of Studies of Storage Case Contamination (Modified from )
Country Author/Study Type Sample Size and Type Lens Type Used (% of Users Using Each Category) Disinfection Systems Used (% of Users Using Each Category) Frequency of Case Contamination Frequently Recovered Microorganisms NR = Not Reported
Bacteria Fungi Protozoa
Canada ( ) (cross-sectional study) 58 asymptomatic lens wearers Soft Various chemical 72% S. epidermidis
Moraxella spp.
Enterobacter spp.		 NR NR
USA ( ) (cross-sectional study) 100 asymptomatic lens wearers Soft (62%)
Rigid (38%)		 Chemical
Peroxide
Heat		 44%
44%
32%		 Coagulase-negative
Staphylococcus, Bacillus spp.		 Fusarium NR
UK ( ) (cross-sectional study) 102 asymptomatic lens wearers Soft (66%)
Rigid (34%)		 Chemical (61%)
Peroxide (20%)
Heat (19%)		 Overall: 42% Environmental pseudomonads,
Gram-negative bacilli
Serratia marcescens
(range: 0–10 6 CFU)		 NR Acanthamoeba (9%)
USA ( ) (cross-sectional study) 53 lens wearers Soft Peroxide (74%)
MPS (16%)		 18%
21%		 Pseudomonas spp. NR NR
USA ( ) (cross-sectional study) 118 asymptomatic lens wearers Soft
Rigid		 Chemical
Peroxide
Saline
Miscellaneous		 Overall: 54%
11%
8%
40%
61%		 Staphylococcus epidermidis
Micrococcus spp.
Serratia marcescens
Pseudomonas aeruginosa
(range: 0–10 5 CFU)		 NR NR
UK ( ) (cross-sectional study) 178 asymptomatic lens wearers Soft (74%)
Rigid (26%)		 Peroxide (22%)
Chemical (42%)
Chlorine release (30%)
Chlorhexidine tablet (3%)
Others: Unknown		 Overall: 53% Serratia marcescens
Pseudomonas fluorescens
Acinetobacter spp.		 Yeast Acanthamoeba (4.5%)
Hartmanella (0.75%)
New Zealand ( ) (cross-sectional study) 101 asymptomatic lens wearers Soft (85%)
Rigid (15%)		 Chemical (23%)
Peroxide (75%)		 Overall: 81% Pseudomonas spp.
Serratia spp.
Diphtheroids
(72% had mixed bacterial contamination)		 Cladosporium spp.
Candida spp.		 Acanthamoeba spp.
Naegleria spp.
Norway ( ) (cross-sectional study) 21 asymptomatic medical students Soft (95%)
Rigid (5%)		 Chemical
Peroxide		 Overall: 24% Xanthomonas maltophilia
Pseudomonas cepacia
Serratia liquefaciens
Serratia plymuthica 		NR NR
Spain ( ) (clinical trial) 126 lens cases Soft Polyaminopropylbiguanide Overall: 81% Staphylococcus epidermidis
Staphylococcus aureus
Streptococcus viridans
Pseudomonas aeruginosa 		NR NR
UK ( ) (cross-sectional study) 20 microbial keratitis patients Various Chlorine release
Hydrogen peroxide
Thiomersal
Polyhexamethylene		 Overall: 85% Staphylococcus aureus
Pseudomonas aeruginosa
Enterobacter spp.		 NR Acanthamoeba spp.
UK ( ) (clinical trial) 155 lens wearers Soft MPS
Peroxide		 78%
58%		 Gram +
Gram −
(range: 0–10 4 CFU)		 NR NR
Hong Kong ( ) (clinical trial) 47 asymptomatic lens wearers Orthokeratology Boston Advance and
Simplicity		 Overall: 70% Acinetobacter spp.
Pseudomonas aeruginosa
Serratia
Staphylococcus aureus 		0 0
Hong Kong ( ) (cross-sectional study) 101 asymptomatic lens wearers Various Multipurpose solution Overall: 34% Staphylococcus aureus
Pseudomonas aeruginosa
Serratia marcescens 		0 0
Brazil ( ) (cross-sectional study) 81 lens wearers NA NA Overall: 80% Gram+ cocci
Gram+ rod
Gram− rods (range: 0–10 6 CFU)		 NR Acanthamoeba spp.
Australia ( ) (clinical trial) 232 asymptomatic lens wearers Silicone hydrogel lenses Polyhexanide (35%)
Polyquaternium (36%)
Hydrogen peroxide (35%)		 92%
76%
81%		 Staphylococcus aureus
Staphylococcus epidermidis
Staphylococcus saprophyticus
Streptococcus viridans
Delftia acidovorans
Serratia marcescens
Stenotrophomonas maltophilia 		Overall: 14%
Australia ( ) (cross-sectional study) 64 asymptomatic lens wearers Soft (95%)
Rigid (5%)		 RGP disinfecting solution (3%)
Hydrogen peroxide (13%)
Multipurpose solution (83%)		 Overall: 58% Bacillus spp.
Coagulase-negative
Staphylococci
Propionibacterium acnes
Micrococcus spp.
Serratia marcescens
Pseudomonas aeruginosa
Achromobacter xyloxidans 		Filamentary fungi 0
USA ( ) (cross-sectional study) 28 microbial keratitis
9 asymptomatic lens wearers		 Soft NA Overall: 61% Achromobacter spp.
Stenotrophomonas
Delftia
Enterobacter
Serratia
Escherichia
Ewingella
Shigella
Pseudomonas aeruginosa 		NR NR
Croatia ( ) (cross-sectional study) 52 asymptomatic lens wearers Soft (48%)
Rigid (52%)		 Polyhexanide (33%)
Polyquaternium (8%)
Hydrogen peroxide (8%)
RGP disinfecting solution (45%)
Unknown (6%)		 Overall: 58% Coagulase-negative
Staphylococci
Bacillus spp.
Proteus mirabilis
Enterobacter sp.
Acinetobacter spp.
Serratia spp.
Staphylococcus aureus
Corynebacterium spp.
Klebsiella pneumoniae 		Chrysosporium sp.
Penicillium spp.
Candida parapsilosis 		0
Australia ( ) (cross-sectional study) 119 asymptomatic lens wearers Soft (92%)
Rigid (8%)		 Polyhexanide (43%)
Polyquaternium (33%)
Hydrogen peroxide (8%)
RGP disinfecting solution (8%)
Unknown (8%)		 Overall: 66% Coagulase-negative staphylococci
Bacillus spp.
Micrococcus spp.
Stenotrophomonas maltophilia
Achromobacter
xylosoxidans
Delftia
acidovorans
Serratia marcescens 		Molds
Yeast		 NR
Canada ( ) (Clinical trial) 38 asymptomatic lens wearers Randomised to 2 SiHy and 1 hydrogel contact lens Randomised to 3 MPS and 1 one-step hydrogen peroxide solution Overall: 79–100% NR NR NR

Under certain circumstances, a contact lens may act as a vector by presenting organisms to the cornea, either by prolonging retention of organisms on the ocular surface or by organisms colonising the lens surface in-eye or during storage. Large numbers of bacteria have been recovered from lenses during corneal inflammation and infection.

Colonisation of lenses by large numbers of Gram-negative bacteria ( P. aeruginosa, Serratia marcescens, and H. influenzae ) ( , ) or Streptococcus pneumoniae ( ) has been reported in contact lens–induced acute red eye (CLARE). Contact lens–induced peripheral ulcer (CLPU) has been associated with Gram-positive contamination of lenses, particularly S. aureus ( ) and Streptococcus pneumoniae ( ). In microbial keratitis, concordance between the corneal isolate and contact lens isolate is reported frequently ( , ).

Bacteria can adhere to both unworn and worn lenses ( , , , ). There is a large amount of literature on the effect of adsorbed tear components, lens material and surface properties, bacterial species, strain, phenotypic characteristic and growth requirements on adhesion, which is a necessary step in retaining organisms on a lens surface sufficiently for colonisation to occur. The predominant mode of growth for bacteria within natural ecosystems is within glycocalyx-enclosed microcolonies, forming a biofilm on inert surfaces ( ), on mucosal surfaces such as in osteomyelitis and on the surfaces of prostheses ( ). Motile bacterial cells lacking this protective mechanism (swarmer or planktonic cells) are released from the body of the biofilm to invade surrounding tissues or to colonise further surfaces ( Fig. 4.4 ).

Fig. 4.4, Schematic of biofilm formation.

Within this favourable adherent environment, propagation of organisms is enhanced and enclosed organisms are protected from host defences (Gristina & Costerton 1984) and antibiotics ( ). Formation of such a bacterial biofilm on lenses will result in increased numbers of organisms and prolonged exposure to the cornea. This has been demonstrated in an animal model ( ) on lenses incubated with bacteria in vitro ( ), on worn lenses in vivo ( ) and on lenses from wearers with culture-proven microbial keratitis ( , , ). The role of biofilm formation in lens-related disease is unclear. However, a bacterial biofilm on a contact lens or within a storage case ( Fig. 4.5 ) renders organisms more resistant to the antimicrobial effects of lens care systems ( , , , ) and enables the organisms to persist on a lens surface with the potential for tissue damage, either directly or via toxin production.

Fig. 4.5, Scanning electron micrograph showing polymicrobial biofilm on a lens storage case.

Sterilisation, disinfection and decontamination

Key Point

Disinfection describes the process by which vegetative microorganisms are killed or their growth is inhibited on a surface, object, or in liquid.

Antiseptics remove or kill vegetative microorganisms on tissue.

Sterilisation refers to killing of all living microorganisms, including bacterial endospores and cysts.

Disinfection is the most important safety issue in lens care. Lens and storage case contamination is associated with both corneal infection ( , , ) and inflammation ( ).

Sterilisation of soft lenses by manufacturers may take place via:

  • ▪

    autoclaving (a process which uses pressure to achieve a temperature of 121°C for 10–15 minutes) that destroys critical enzymes and disrupts DNA

  • ▪

    gamma irradiation that ionises and denatures proteins

  • ▪

    ethylene oxide gas that alkylates, i.e. it attaches C2H5 to biochemical molecules.

Rigid lenses are not supplied sterile following manufacture and cleaning and disinfection are required prior to their use.

Table 4.6 describes the mode of action of commonly used systems ( ).

Table 4.6
Mode of Action of Common Disinfection Agents
Agent Mode of Action Antimicrobial Effect
Alcohol (ethanol or isopropyl alcohol) Lipid solvent causing membrane damage and protein denaturation Broad spectrum – vegetative bacteria, viruses, fungi. Not sporicidal
Quaternary ammonium compounds (QACs) Interaction with lipids in cell wall. Surface active predominantly at the cytoplasmic membrane. Damage to outer membrane of Gram-negative bacteria Broad spectrum – bactericidal, sporostatic, lipid enveloped viruses, enveloped viruses but not non-enveloped viruses. Limited effect on fungi and Acanthamoeba
Biguanides
Chlorhexidine (CHX) Damage to outer membrane, diffusion across cell wall and cytoplasmic and inner membrane damage Broad spectrum – vegetative bacteria (e.g. S . marcescens ), viruses, fungi, Acanthamoeba trophozoites and some effect against cysts. Not sporicidal
Polymeric biguanides (PHX) Initially binds to phospholipids of outer membrane and subsequently cytoplasmic membrane causing altered cell permeability and loss of membrane function Broad spectrum. Variable resistance against fungi, yeasts, Acanthamoeba
Chlorine release compounds Free chlorine acts as an oxidising agent that destroys the cellular activity of proteins, lipids and bacterial DNA Bactericidal activity, some effect on spores, limited effect on Acanthamoeba and fungi
Hydrogen peroxide Hydroxyl (OH) radical acts as an oxidising agent that destroys the cellular activity of proteins, lipids and bacterial DNA Broad spectrum. Depending on the available concentration and duration of exposure, activity against bacteria, spores, viruses, fungi and Acanthamoeba
Heat Disruption of tertiary structures of DNA, proteins and cell membrane Nonspecific. Activity dependent on duration and temperature. Sterilisation results in removal of all organisms including spores

General Concepts in Disinfection Efficacy

The efficacy of many chemical systems is related to the concentration of the active agent, its contact time and the form of delivery. There is invariably a trade-off between antimicrobial activity and ocular toxicity, and comfort and convenience.

Many disinfectants, including contact lens solutions, are neutralised by organic materials ( ) so that binding to organic material effectively reduces the concentration of the antimicrobial agent. Bacterial endospores are more resistant to disinfectants than are vegetative organisms due to their lower water content and slower metabolism. Not all microorganisms are equally susceptible to disinfection. Generally, susceptibility is as follows: viruses with lipid envelopes > vegetative bacteria > fungi > non-enveloped viruses > mycobacteria > bacterial spores > cyst > prions.

Note: a lipid virus has an envelope (or membrane) which is largely lipid and prone to desiccation so more susceptible to sterilisation.

Microorganisms can acquire resistance to disinfectants:

  • ▪

    through transfer of nonchromosomal genetic material on plasmids

  • ▪

    altering the binding sites for antimicrobials as happen through phosphorylation (adding phosphate to an organic compound)

  • ▪

    altering the drug enzymatically

  • ▪

    developing effective pumps for removal of the drug.

Organisms with a complex cell wall composition tend to be more resistant than those with a simple cell wall structure. Certain bacteria (e.g. staphylococci) and fungi produce the enzyme catalase, which neutralises hydrogen peroxide. This may account for higher contamination rates with Gram-positive organisms in one-step peroxide systems ( ). Acquired resistance of Serratia marcescens to solutions containing chlorhexidine and benzalkonium chloride in rigid lens solutions has been documented ( , ), and reported resistance of cytotoxic strains of Pseudomonas aeruginosa to hydrogel lens solutions containing polyaminopropyl biguanide (PAPB) and polymeric quaternary ammonium compounds (QAC).

Solution licensing requirements

Lens care systems are mainly designed to reduce microbial contamination introduced during wear and handling. The safety and efficacy requirements for marketing approval of care products are described by the US Food and Drug Administration (FDA 510[k]; Services 1997) and the International Organisation for Standardisation (ISO-14729; Standardisation 2001 and ISO 18259 – 2014).

Following outbreaks of severe keratitis in contact lens wearers in the mid-2000s, the FDA acknowledged that ‘user error’ and/or ‘real world’ scenarios need to be incorporated into contact lens solution testing regimens before marketing approval was given. *

* https://wayback.archive-it.org/7993/20170406203359/https://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/MedicalDevices/MedicalDevicesAdvisoryCommittee/OphthalmicDevicesPanel/ucm125428.htm , accessed: 1 May 2016.

That requirement means incorporating contact lenses in premarket testing of solutions as well as the addition of Acanthamoeba spp. to the panel of microorganisms that manufacturers use to demonstrate solution efficacy to satisfy the ISO standard and to bring a contact lens care product to market.

In 2014, the ISO standard for contact lens care products was updated from ISO 14729 to ISO 18259. This standard specifies that contact lens care products be evaluated in the presence of contact lenses and a lens case. In addition, they advise the addition of organic soil to testing regimens. Organic soil is designed to replicate organic contamination when handling lenses. These changes to the ISO standard replicate more closely the environment in which contact lens products are used. However, there is still no licensing requirement for efficacy against Acanthamoeba spp .

Acanthamoeba species did not feature in earlier ISO organism test panels because it was believed that the growth of Acanthamoeba would be limited by adequate antibacterial activity against the protozoan's usual food sources. Additional factors, and the AK outbreaks in the mid-2000s, have demonstrated gaps in that belief: in particular, the high rate of culture-positive contact lens storage cases despite adherence to manufacturer guidelines ( ) and the lack of standardised recommendations for contact lens case hygiene ( ).

Standardising the method of testing effectiveness has been a challenge, especially in relation to efficacy against Acanthamoeba spp. that can be applied reliably and repeatedly. Although the contact lens industry tests their products routinely against various strains and species of Acanthamoeba, there is a lack of consistency in the testing regimens employed leading to variability in the results reported. Variables include:

  • ▪

    species and strains tested

  • ▪

    method of culturing Acanthamoeba trophozoites

  • ▪

    methods for inducing encystment.

The more recent ISO 19045 : 2015 specifies a method for evaluating the potential for encystment of Acanthamoeba spp. However, because the method excludes the evaluation of oxidative systems (mostly hydrogen peroxide–based systems) requiring a special lens case (vented), at the time of writing it has yet to be adopted by the FDA.

Product Recalls (2006/2007)

For outbreaks of Fusarium spp. and Acanthamoeba spp., see Section 8 , History, available at: https://expertconsult.inkling.com/ .

Research by suggests that a solution’s formulation plays a significant role in the induction of Acanthamoeba spp. encystment. While they implicated propylene glycol, the fact that not all solutions containing propylene glycol induce encystment implies that the situation might be multifactorial.

Environmental factors that promote the growth of Acanthamoeba spp. were implicated in case-control studies in the UK where Acanthamoeba keratitis (AK) is associated with ‘hard’ water ( ) and loft-located water tank storage systems. It is likely that in those conditions, bacterial biofilms form that are a food source for Acanthamoeba spp.

The avoidance of tap water in all contact lens use has been a consistent safety message in recent years ( ). Furthermore, advice included in contact lens solution patient instruction inserts advocates complete replacement of CL solutions after each and every disinfection cycle ( ). A campaign by the British Contact Lens Association (BCLA) against the use of tap water has also been instigated ( Fig. 4.6 ).

Fig. 4.6, BCLA-sponsored ‘No Tap Water’ stickers.

In-Office Disinfection of Trial Lenses *

* See ISO/TS 19979 : 2014 (E) Ophthalmic optics – contact lenses – Hygiene management of multi-patient use trial contact lenses.

To limit the transfer of microorganisms among patients, trial lenses ideally should be used once and discarded. Where this is not possible, in-office disinfection needs to be effective against bacteria, fungi, viruses and Acanthamoeba .

Another concern is the theoretical risk for transmission of vCJD via trial lens fitting or through other ophthalmic procedures.

Although it appears that the risk for transmission of prion infections by contaminated lenses is negligible ( ), the Department of Health and the College of Optometrists in the UK recommend soaking the lenses in 1% sodium hypochlorite for 10 minutes. For the complete recommendations see https://guidance.college-optometrists.org/guidance-contents/safety-and-quality-domain/infection-control/the-re-use-of-contact-lenses-and-ophthalmic-devices/

It is not clear whether soft lens parameters are stable with this process, although RGP lenses do appear to be. For patients in a high-risk category for vCJD, disposal of the device or lens following use is recommended.

Heat Disinfection

Removal of agents other than prions can be achieved with heat disinfection using sterile saline. This provides:

  • ▪

    a rapid, cheap and effective method of lens and vial disinfection

  • ▪

    an effective method against bacteria, fungi, viruses and Acanthamoeba, including cysts, utilising temperatures of 78–90°C for 20 minutes to 1 hour ( , ).

Drawbacks of heat disinfection of trial lenses include:

  • ▪

    regrowth of organisms over time

  • ▪

    the stability of lens parameters, particularly high–water-content lenses

  • ▪

    reduced lens life

  • ▪

    the periodic requirement to ensure that the disinfection cycle for in-office heating units maintains the required temperature for an appropriate period (i.e. procedure validation).

Hydrogen Peroxide

A 3% concentration of hydrogen peroxide is an effective method for the removal of bacteria, fungi, viruses and Acanthamoeba including cysts ( ). Exposure periods ranging from 10 minutes to 4 hours have been recommended, depending on the organism type. Non-neutralised peroxide has activity against organisms within a biofilm ( , ).

Drawbacks of hydrogen peroxide in trial lens disinfection include:

  • ▪

    the requirement for a neutralisation step before use

  • ▪

    leakage of fluid from one-step cases ( )

  • ▪

    regrowth of organisms in neutralised peroxide ( , )

  • ▪

    the need for a vented case (see later).

Recommended Methods of Disinfection

The US Centers for Disease Control and Prevention (CDC) recommends disinfection of trial lenses with hydrogen peroxide or heat to prevent transmission of HIV ( ). For hydrogel lenses, there are no recommended decontamination procedures for removal of prions, and the consensus appears to be to discard the lenses wherever possible. If this is not possible, patients should be informed of the risks associated with multiple-use lenses, and this should be documented.

The recommended procedure for hydrogel trial lenses is as follows:

  • ▪

    Clean and rinse on removal. Rub lenses for at least 20 seconds on each side of the lens with an alcohol-based cleaner, such as Oté (Oté Pharma), or a mildly abrasive cleaner followed by a sterile-saline rinse. This is associated with at least a 2-log unit reduction in viable organisms ( , ) and also removes HIV from lens surfaces ( ).

  • ▪

    Soak in 3% hydrogen peroxide for at least 2–3 hours, and then neutralise for 10–60 minutes.

  • ▪

    Store in a cold chemical system with redisinfection every 30 days ( ). To prevent contamination while handling, use the same storage container and refill with the chemical system ( ).

  • ▪

    Replace lenses annually or as specified by the manufacturer.

For rigid trial lenses ( ), rub lenses for at least 20 seconds on each side of the lens with an alcohol-based or mildly abrasive cleaner, followed by a sterile-saline rinse.

Then do either of the following:

  • ▪

    Soak in 2% hypochlorite for 1 hour followed by rinsing with sterile saline.

  • ▪

    Soak in 3% hydrogen peroxide for at least 5–10 minutes. Remove and rinse with sterile saline.

Store dry, and, prior to reuse, clean and rinse lenses as above.

Lens Deposits

Lens deposits may be adsorbed onto or absorbed into lens materials, regardless of type. Daily disposable contact lenses are intended to be discarded before any problems can arise from deposits. However, acute lens deposit problems (e.g. an industrial issue such as embedded metallic particles) apply as much to DD lenses as to conventional lenses. Table 4.7 shows the clinical classification of deposits.

Table 4.7
Lens Deposit Classification System (Modified Rudko ( ))
Data from .
Class Degree of Deposit
I Clean
II Visible under oblique light when wet using 7× magnification
III Visible when dry without special lighting, unaided eye
IV Visible wet or dry with the unaided eye
Class Type of Deposit
C Crystalline
G Granular
F Filmy
P Plaque
D Debris
Co Coating
Class Extent of Deposit
a 0–25% of lens
b 26–50% of lens
c 51–75% of lens
d 76–100% of lens

Variables affecting lens deposition (after ) include:

  • ▪

    material chemistry (especially if a conventional hydrogel)

  • ▪

    material water content and polymer ionicity (especially protein deposition)

    • ▪

      protein deposition largely material-dependent

    • ▪

      lipid deposition largely wearer-dependent

    • ▪

      however, silicone hydrogel (SiHy) contact lenses are susceptible to lipid deposition that rubbing removes only partially.

  • ▪

    differences between wearers:

    • ▪

      least for proteins

    • ▪

      depend on protein adhesion ( ).

  • ▪

    differences within wearers:

    • ▪

      differences of up to 30% in lipid levels between eyes ( )

    • ▪

      differences in protein adhesion ( )

    • ▪

      the presence of confounding factors such as dry eye/marginal dry eye/meibomian gland dysfunction, ocular pathology and systemic disease.

Common lens deposits

The following are categorised by broad type:

Organic

  • ▪

    tear proteins – mostly protein deposition remains a problem of hydrogel lens materials, and SiHy contact lenses have relatively little susceptibility to protein deposits.

  • ▪

    lipids – although having only limited solubility in water, some have greater solubility in the lens polymers themselves ( ). The core component of SiHy lenses is poly[dimethyl siloxane]) (pDMS), which is lipophilic and a lipid solvent ( ). This means that deposits may be both on and in the lens matrix. Lipid deposition is greatest with materials containing vinyl pyrrolidone ( , ) and silicones, and many current SiHy lens polymers contain both.

  • ▪

    mucin

  • ▪

    other tear components

  • ▪

    discolourations

  • ▪

    finger-borne contaminants (skin lipids, dirt, microorganisms, other)

  • ▪

    airborne contaminants.

Inorganic

  • ▪

    occupational/industrial

    • ▪

      metallic:

      • ▪

        colours are often characteristic of the metal cation involved

      • ▪

        metal may corrode in situ (e.g. iron), leading to rust spots, pitting, and deposit protrusion.

    • ▪

      nonmetallic:

      • ▪

        may be inactive (e.g. asbestos dust)

      • ▪

        nonasbestos brake linings, disc-brake pad dust

      • ▪

        discolourations.

  • ▪

    clothing residues (lint)

  • ▪

    accumulation of lens care products or their derivatives

  • ▪

    finger-borne contaminants

  • ▪

    air-borne contaminants.

Environmental issues include:

  • ▪

    workplace location and activities

  • ▪

    residential location and environmental factors (e.g. proximity of accommodation to roadways, railways, factories, smokestacks)

  • ▪

    commuting/travelling environment.

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