Fungal and Parasitic Infections of the Eye

November 13, 2005

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=88956

Clin Microbiol Rev. 2000 October; 13(4): 662–685.

A. Klotz,1,2* C. Penn,3 Gerald J. Negvesky,4 and

Salim I. Butrus4

Section of Infectious Diseases, Veterans Affairs Medical Center,

Kansas City, Missouri1; University of Kansas School of Medicine,

Kansas City,2 and Lawrence Memorial Hospital, Lawrence,3 Kansas; and

Department of Ophthalmology, Washington Hospital Center, Washington,

D.C.4

*Corresponding author. Mailing address: Research, Veterans Affairs

Medical Center, 4801 Linwood Blvd., Kansas City, MO 64128. Phone:

(816) 861-4700, ext. 6713. Fax: (816) 922-4687. E-mail:

klotzs@....

This article has been cited by other articles in PMC.

ABSTRACT

The unique structure of the human eye as well as exposure of the eye

directly to the environment renders it vulnerable to a number of

uncommon infectious diseases caused by fungi and parasites. Host

defenses directed against these microorganisms, once anatomical

barriers are breached, are often insufficient to prevent loss of

vision. Therefore, the timely identification and treatment of the

involved microorganisms are paramount. The anatomy of the eye and

its surrounding structures is presented with an emphasis upon the

association of the anatomy with specific infection of fungi and

parasites. For example, filamentous fungal infections of the eye are

usually due to penetrating trauma by objects contaminated by

vegetable matter of the cornea or globe or, by extension, of

infection from adjacent paranasal sinuses. Fungal endophthalmitis

and chorioretinitis, on the other hand, are usually the result of

antecedent fungemia seeding the ocular tissue. Candida spp. are the

most common cause of endogenous endophthalmitis, although initial

infection with the dimorphic fungi may lead to infection and

scarring of the chorioretina. Contact lens wear is associated with

keratitis caused by yeasts, filamentous fungi, and Acanthamoebae

spp. Most parasitic infections of the eye, however, arise following

bloodborne carriage of the microorganism to the eye or adjacent

structures.

This is a comprehensive review of the fungal and parasitic diseases

of the eye. Numerous fungi and parasites infect the eye either by

direct introduction through trauma or surgery,by extension from

infected adjacent tissues, or by hematogenous dissemination to the

eye. The majority of the clinically important species of fungi and

parasites involved in eye infections are reviewed in this article.

The fungi are discussed in relation to the anatomical part of the

eye involved in disease, whereas parasites are discussed by the

diseases they cause. Emphasis has been placed on literature

published within this decade, but prior noteworthy reviews and case

reports are included. A glossary of the ophthalmologic terms used is

provided at the end of the paper (Appendix A). We suggest that the

works of Beard and Quickert (26a) and Snell and Lemp (252a) be

consulted as references concerning the anatomy of the eye.

FUNGAL INFECTIONS OF THE EYE

Epidemiology of Fungal Eye Infections

Ophthalmologists and optometrists, in particular, and clinicians, in

general, must be knowledgeable of the pathogenesis of fungal eye

infections. Mycotic eye infections are commonplace. For example, the

yeast Candida albicans is the most common cause of endogenous

endophthalmitis. Filamentous fungi, such as Fusarium solani and

Aspergillus flavus, may constitute up to one-third of all cases of

traumatic infectious keratitis (157). Furthermore, patients with

AIDS may contract many different fungal infections of the eye and

adjacent structures (Table 2).

In fungal eye disease, the pathogenesis of the infections is

inextricably linked to the epidemiology. Therefore, in discussing

the epidemiology of fungal eye infections, it is worthwhile at the

outset to state several proposed pathogenetic principles of fungal

eye disease. (i) It is likely that sustained fungemia with even

saprophytic fungi will lead to endophthalmitis. (ii) At the time of

initial infection with some of the dimorphic, pathogenic fungi, such

as Histoplasma capsulatum and Coccidioides immitis, an unrecognized

fungemia occurs and often leads to endophthalmitis. (iii) The

paranasal sinuses, because of their direct communication with the

ambient air, harbor saprophytic fungi, which may erode the bony

walls of the sinus and invade the eye in certain circumstances,

e.g., in a patient with neutropenia. (iv) Trauma, either from

vegetable matter or surgery, may introduce saprophytic fungi into

the cornea and/or adjacent tissue, giving rise to invasive disease.

The epidemiology of endogenous endophthalmitis reflects both the

natural habitats of the involved fungi and the habits and health

status of the patients (Table 3). Candida endogenous endophthalmitis

occurs as a direct result of the success of modern medical practice

that sustains patients' lives with broad-spectrum antibiotics,

indwelling central venous lines, parenteral nutrition, abdominal

surgery, and cytotoxic chemotherapy. The recent origin of this

disease is established by the fact that Candida endophthalmitis was

first recognized clinically in 1958 (275). Candida and Aspergillus

spp. also cause endophthalmitis in intravenous drug users. Virtually

any intravascular prosthesis or device may become contaminated by

bloodborne opportunistic fungi, and fungemia arising from such

infection may lead to endogenous endophthalmitis.

Endogenous endophthalmitis occurring as part of disseminated disease

with the dimorphic fungi H. capsulatum, Blastomyces dermatitidis,

and C. immitis is uncommon. Patients with disease from these fungi

have resided in or traveled through the respective areas of

endemicity. These are the Ohio and Mississippi river valleys for H.

capsulatum; the Lower Sonoran Life Zone for C. immitis, including

southern parts of California, Arizona, New Mexico, West Texas, and

parts of Mexico and Argentina; and the Southeast and Midwest of the

United States for B. dermatitidis. Residence along a waterway may be

another important association for exposure to B. dermatitidis (67).

H. capsulatum may flourish in bird and bat droppings; therefore,

exposure to the fungus may occur through one's occupation, for

example, demolition of old bird-infested buildings, or one's hobby,

such as camping or spelunking.

Exogenous endophthalmitis, on the other hand, results from trauma to

the globe or preceding keratitis. It may also occur as a

postoperative complication of lens removal, prosthetic lens

implantation, or corneal transplantation. The vast majority of

postoperative eye infections are due to coagulase-negative

Staphylococcus; however, outbreaks of fungal exogenous

endophthalmitis continue to occur episodically. These have been due

to perioperative contamination of lens prostheses (204) or

contamination of fluids used for irrigation (260) of the

perioperative and postoperative eye. Candida species are

particularly likely to occur in this setting, and infection may be

enhanced by the pre- and postoperative use of topical

corticosteroids and antibacterial agents.

Mycotic keratitis is usually caused by filamentous fungi and occurs

in conjunction with trauma to the cornea with vegetable matter. In

the tropics it is common in male agricultural workers. The fungal

genera causing keratitis in the tropics are more diverse and include

some, such as Lasiodiplodia theobromae, that do not grow in

temperate regions. Eye trauma is the cause of fungal keratitis in

temperate areas as well, but the common fungal genera involved are

Fusarium, Alternaria, and Aspergillus (71, 293). Keratitis caused by

yeasts such as the Candida spp. almost always occur in previously

abnormal eyes, e.g., in patients with dry eye, chronic corneal

ulceration, or corneal scarring.

Bloodborne Infections: Endogenous Endophthalmitis

Endogenous endophthalmitis is uncommon; however, fungi cause this

disease more often than gram-positive or gram-negative bacteria. The

term endogenous endophthalmitis implies that bloodborne spread of

microorganisms to the eye has occurred. Therefore, infection in the

eye is the result of metastatic spread of infection from a distant

site, for example, infected heart valves or the urinary tract. In

this manner the eye becomes the site of numerous microabscesses.

This mechanism of infection is to be contrasted to exogenous

endophthalmitis (see below), which arises from the direct

introduction of a microorganism(s) into the eye during trauma or

surgery. Endogenous endophthalmitis is further distinguished from

exogenous endophthalmitis by occurring in a greater number of

immunocompromised patients, e.g., patients receiving chemotherapy or

total parenteral nutrition, or intravenous drug abusers (Table 4).

Endophthalmitis is recognized clinically by the presence of one or

more creamy-white, well-circumscribed lesions of the choroid and

retina, often accompanied by inflammatory infiltrates in the

vitreous. These lesions can be detected using an ophthalmoscope

after dilating the pupils. Often, there is inflammation in the

anterior chamber manifested by the presence of a hypopyon. Typical

lesions of chorioretinitis are shown in Fig. 2, left. Patients

complain of eye pain and may have blurred vision or spots in their

visual fields. Patients with endogenous endophthalmitis may have

positive blood cultures antedating eye symptoms or signs. In the

absence of a positive blood culture or characteristic clinical

syndrome, aspiration of the vitreous (or biopsy) may be necessary to

establish the causative microorganism.

Why the eye is a common end organ target of fungemia is unknown.

However, in a rabbit model of C. albicans endophthalmitis, more

fungal elements are found in the eye per gram of tissue than are

found in the kidneys of the same animals. Since C. albicans is

believed to have a marked tropism for the kidneys and endothelium,

the great number of organisms in the eye bespeak a tropism for the

eye as well (142, 143). The candidal lesions in the rabbit are

identical to those found in humans demonstrating a focal

chorioretinitis (Fig. 2, middle left), with a mixture of

granulomatous and suppurative host reactions (76). The infection

likely begins in the choroid and progresses anteriorly to the

retinal layers (226). This may be related mechanistically to the

fact that the outer retinal layers, i.e., those considered to be

infected first, receive blood from a high-flow system (150 mm/s),

whereas the inner layers receive blood from a low-flow system (25

mm/s). It should be noted that drainage from the retinal layers is

entirely through the venous system as there is no lymphatic system

serving the inside of the globe.

The most common cause of endogenous fungal endophthalmitis is C.

albicans (287). Endogenous fungal endophthalmitis by definition

follows fungemia; therefore, it is important to note that Candida

species are the fourth most common cause of positive nosocomial

blood cultures in the United States, exceeding the number of

positive cultures of any single gram-negative bacterial genus (21).

It is estimated that some 120,000 patients contract disseminated

candidiasis (i.e., candidemia) per year in North America (58), and

the usual estimates of the incidence of candidal endophthalmitis in

patients with candidemia are around 30% (32, 196; J. R. , R.

Y. Foos, and T. H. Pettit, presented at the 22nd Concilium

Ophthalmologicum, 1974); thus, the disease is fairly common. If the

definition of chorioretinitis is more stringent, i.e., if

nonspecific lesions such as cotton wool spots and retinal

hemorrhages are eliminated, the incidence is much less, on the order

of 9.3% (70, 226).

The pathogenesis of candidemia remains unknown but is likely

multifactorial. There are characteristic clinical features of

patients with candidemia, with one or another feature being found in

each patient. These include the use of broad-spectrum antibiotics

that eliminate competing normal microbiota of the host, the presence

of central venous catheters, the administration of total parenteral

nutrition, prior abdominal surgery, and/or neutropenia (164). One or

all of these factors are sufficient to place a patient at risk for

candidemia and, hence, for endophthalmitis. Neutropenia, although a

risk factor for candidemia, reduces the incidence of candidal

endophthalmitis in the rabbit model (122) and perhaps in patients as

well (78). This suggests that the chorioretinal lesions are probably

a reflection of a vigorous host response rather than just the sheer

number of infecting microorganisms.

During the introduction of total parenteral nutrition in the 1970s

there was a marked increase in the number of patients with Candida

endophthalmitis (77), which is likely related to the prolonged use

of central venous catheters. Candida endophthalmitis has also been

reported to occur after induced abortion (49), in the postpartum

state (43), following treatment of toxic megacolon (123), and as a

consequence of intravenous drug abuse. An addict's use of

intravenous brown heroin often leads to a characteristic syndrome,

at one time common in Europe, that includes pustular cutaneous

lesions, endophthalmitis, and osteomyelitis. C. albicans can be

isolated from all of these lesions (74). The microorganisms in this

syndrome may be acquired from the drug abuser's own skin surface

(79). Candida endophthalmitis may also occur after intravenous

placement of a foreign device, such as a pacemaker (243), and

following repeated intramuscular injections of medications, such as

anabolic steroids (285). Species of Candida other than C. albicans

are capable of causing endogenous endophthalmitis and may do so in

proportion to their ability to cause candidemia (20, 53, 133, 243).

Although Candida species are clearly the most-common causes of

endogenous endophthalmitis, other fungi are occasionally

encountered. Aspergillus species are the second most-common cause of

fungal endophthalmitis (291). Aspergillus spp. may be less capable

of causing endophthalmitis than Candida spp.; an example of this is

the rabbit endogenous endophthalmitis model, in which larger inocula

of Aspergillus spp. are required to cause the disease than with C.

albicans (93). Many species of Aspergillus have been reported to

cause endophthalmitis, but Aspergillus flavus is probably the most

common (219), followed by Aspergillus fumigatus, Aspergillus niger,

Aspergillus terreus, Aspergillus glaucus (281), and Aspergillus

nidulans (271). Endogenous Aspergillus endophthalmitis may be

encountered in neutropenic patients or in patients taking

pharmacologic doses of corticosteroids, often for chronic lung

disease. Aspergillus endophthalmitis has even been reported to occur

following severe periodontitis, although entry of Aspergillus spp.

into the bloodstream through the mouth certainly is not common

(172). Intravenous drug addicts are at particular risk for

disseminated aspergillosis (69). Aspergillus endophthalmitis has

been reported in addicts abusing a mixture of intravenous cocaine,

pentazocine, and tripelennamine. Three such individuals from

Louisville, Ky., were infected with A. flavus in this manner (23).

Patients receiving large doses of corticosteroids for lung disease

may have negative blood cultures but evidence of severe Aspergillus

endogenous endophthalmitis. Endophthalmitis, therefore, is the sole

manifestation of disseminated disease and must be established by

aspiration of the vitreous (281). Aspergillus endophthalmitis has

also arisen in recipients of solid-organ transplants, in which the

donated organ was the likely source of the fungus (16, 139).

Pathologic specimens of invasive aspergillosis usually demonstrate

angioinvasion by the hyphae, and thus Aspergillus species may

possess a tropism for vascular tissue (279).

The emerging pathogens of the genus Fusarium have been reported to

cause endophthalmitis in neutropenic hosts (160), in an intravenous

drug abuser (94), and in a patient with AIDS (106). Penicillium spp.

also have caused endogenous endophthalmitis in an intravenous drug

abuser (265). As mentioned in connection with C. albicans,

endogenous endophthalmitis may occur from fungi seeding the

bloodstream from a catheter or endocarditis. Pseudallescheria boydii

has caused endophthalmitis from an infected porcine allograft of the

aortic valve (259) and even in a patient without risk factors for

the disease (193).

The four dimorphic fungi H. capsulatum (165), B. dermatitidis (158),

Sporothrix schenckii (2), and C. immitis (96) as well as

Cryptococcus neoformans (59) may cause endogenous endophthalmitis as

part of disseminated disease. Within the region of H. capsulatum

endemicity in North America, roughly the Ohio and Mississippi river

valleys, there is a well-described syndrome attributed to infection

with H. capsulatum. This entity is known as presumed ocular

histoplasmosis (POH), which occurs in immunocompetent individuals

and is recognized by the presence of multiple diskiform atrophic

chorioretinal scars without vitreous or aqueous humor inflammation.

POH is said to affect 2,000 new individuals a year in areas of

endemicity and in some cases may lead to visual loss and blindness

(165). The lesions are usually burned out, but not all of them are

static and some may reactivate (41). The lesions are thought to

arise from the hematogenous spread of the fungus following initial

infection. The initial infection, acquired by inhalation of

microconidia into the lung, spreads throughout the body, including

the eye, and is soon controlled by a competent host immune response

(175, 249). H. capsulatum is not detectable in the scars of POH.

However, there is strong epidemiological evidence, principally

deriving from skin test surveys, linking the scars to histoplasmosis

(95, 252). A primate model demonstrates pathology identical to that

found in humans (250, 251). Similar lesions to those of POH are,

however, observed in Europe, where histoplasmosis is rare (264), and

therefore, it is likely that similar chorioretinal lesions are the

end result of several different infectious agents. Active

endophthalmitis in patients with disseminated histoplasmosis

secondary to AIDS or immunosuppression occurs and is associated with

numerous budding yeast cells in the choroidal tissue and endothelium

(41, 88, 231). In some cases the endophthalmitis is accompanied by

yeast cells in the anterior chamber angle structures such as the

iris, ciliary muscle and canal of Schlemm (41, 88). Two cases of

disseminated histoplasmosis, established by elevated H. capsulatum

antigen in blood and urine and high complement fixing antibodies,

occurred in immunocompetent brothers. Their disease was associated

with choroiditis, which appears to progress to typical POH lesions

(136). Thus, the link between active histoplasmosis and POH may be

made by these and similar cases.

Disseminated blastomycosis is common in dogs and is often

accompanied by endophthalmitis (28); for example, 78 eyes in 74 dogs

with disseminated disease had endophthalmitis. Canine blastomycosis

of the eye always involves the choriocapillaries, and organisms are

abundant in the choroid. The disease often progresses to

panophthalmitis (38, 39, 246). Endophthalmitis is also seen in

humans with disseminated blastomycosis (223), as evidenced by the

presence of chorioretinal lesions (108, 223).

Coccidioidomycosis is associated with lesions throughout the eye,

including endogenous endophthalmitis (96). Chorioretinal scarring is

common in individuals within the region of endemicity with positive

skin tests to coccidioidin, a situation reminiscent of

histoplasmosis. The chorioretinal lesions presumably occur at the

time of initial infection and are usually clinically quiescent and

asymptomatic. On the other hand, active chorioretinitis has been

described in patients with disseminated disease (96). Anterior

chamber disease has been documented in patients with disseminated

disease, including iritis and large inflammatory masses in the

anterior chamber (61, 96, 180, 298). It is interesting that

disseminated coccidioidomycosis in dogs often starts in the

posterior chamber and spreads to involve the anterior chamber (15).

As previously mentioned, this is believed to be the same route of

extension of disease with Candida and B. dermatitidis

endophthalmitis.

C. neoformans frequently causes visual symptoms when associated with

meningitis. These symptoms are usually due to the swollen brain

compressing the optic nerve or edema of the optic nerve itself.

However, cryptococcosis may be associated with endophthalmitis

manifesting as chorioretinitis, retinal tears, and overlying

vitritis (59, 62, 108, 242). Pneumocystis carinii is also an

infrequent cause of chorioretinitis in patients with AIDS (Fig. 2,

middle right).

Exogenous Endophthalmitis

As the name implies, exogenous endophthalmitis occurs by

introduction of microorganisms into the eye from trauma or surgery.

It can also be the end result of preexisting scleritis or keratitis

(29). Zygomycosis in the surrounding soft tissue and cryptococcal

neuroretinitis may also lead to exogenous endophthalmitis. Patients

with exogenous endophthalmitis are rarely immunocompromised.

Cataract removal followed by placement of a prosthetic lens and

corneal transplantation are the surgical procedures most often

associated with postoperative fungal exogenous endophthalmitis.

One report describes 19 patients from one hospital with exogenous

endophthalmitis, and there was an approximately equal distribution

of patients between the categories of postsurgical endophthalmitis,

posttrauma endophthalmitis, and endophthalmitis following keratitis

(205). Exogenous endophthalmitis may have a period of latency of

weeks to months before clinically detectable disease occurs. Even

then the infection is often confined to the anterior chamber,

pupillary space, or anterior vitreous. Eighty-four percent of

patients in one series received topical corticosteroids before

diagnosis, and this may have potentiated the disease by reducing

local host immunity (205). The most-common causes of postsurgical

exogenous endophthalmitis are gram-positive bacteria, including

coagulase-negative Staphylococcus, diphtheroids, and

Propionibacterium acnes (287). The mycotic causes of exogenous

endophthalmitis, such as yeasts (principally Candida species,

including Candida glabrata [42] and Candida famata [211]), were

found only in the postsurgical group, whereas Fusarium species were

found only in the posttraumatic and postkeratitis groups (205).

Other Candida spp. have caused exogenous endophthalmitis after lens

surgery (211, 294). An epidemic of postsurgical endophthalmitis with

Candida parapsilosis has been reported following the placement of

anterior and posterior chamber lenses (260). Fifteen patients had

ocular surgery over a 3-month period of time. At the time of surgery

all eyes were irrigated with a solution from the same lot that was

contaminated with C. parapsilosis.

Paecilomyces lilacinus is a ubiquitous soil saprophyte implicated in

cases of keratitis and endophthalmitis after trauma (191, 283).

However, a large outbreak of P. lilacinus exogenous endophthalmitis

followed intraocular lens implantation; the lenses had been

contaminated by a bicarbonate solution used to neutralize the sodium

hydroxide sterilant added to the lenses. P. lilacinus was cultured

from the bicarbonate solution (204). Such fungi as Aspergillus

species (29, 64, 194) and Acremonium kiliense (92) have caused

infections following lens surgery. These infections, like

postoperative P. lilacinus infections, may arise because of fungal

contamination of operative and postoperative irrigating solutions

(174, 190, 260).

Fungal pathogens in posttraumatic endophthalmitis are legion and

similar to those causing fungal keratitis. Recent reports include

Fusarium moniliforme (257), Exophiala jeanselmei (114), P. boydii

(44), A. niger (129), Scytalidium dimidiatum (9), Helminthosporium

spp. (65), S. schenckii (292), Penicillium chrysogenum (82), and L.

theobromae (29).

Infections of the Cornea

Fungal infections of the cornea (fungal keratitis or keratomycosis)

may constitute 6 to 53% of all cases of ulcerative keratitis,

depending upon the country of origin of the study (269). The

majority of fungal keratitis occurs after trauma to the cornea in

agricultural workers, usually, but not always, with fungus-

contaminated plant material (leaves, grain, branches, or wood). The

disease may also occur in gardeners and following corneal trauma

from indoor plants as well. Occasionally the object striking the

cornea is metal. The trauma to the cornea may be so slight as to be

forgotten by the patient. Fungal keratitis also occurs with contact

lens wear, and this will be discussed later.

Trauma to the cornea with vegetable matter either introduces the

fungus directly into a corneal epithelial defect or, alternatively,

the defect may become infected following the trauma. The vast

majority of cases of fungal keratitis are due to septate,

filamentous, saprophytic fungi. Occasionally zygomycetes such as

Absidia (168) or Rhizopus (233) spp. may be implicated in keratitis.

On the other hand, the abnormal or compromised cornea, e.g., chronic

dry eye, is subject to infection with yeasts, usually Candida

species. Such uncommon Candida species as Candida lipolytica and

Candida humicola have, however, been reported to cause posttraumatic

keratitis (187, 188) and Candida guilliermondii after corneal

transplant (3). More than 70 species representing 40 genera of fungi

have been reported to cause fungal keratitis (269). The most common

cause of fungal keratitis is F. solani and other Fusarium species,

Aspergillus species, and Curvularia species (269). There may be a

hierarchy of fungi capable of producing keratitis, e.g., from most

to least capable, Fusarium, Acremonium, and Phialophora spp. This

hierarchy is predicated upon their individual ability to invade and

destroy the cornea (156).

Fungal keratitis is recognizable by the presence of a coarse

granular infiltration of the corneal epithelium and the anterior

stroma (Fig. 2, right). The corneal defect usually becomes apparent

within 24 to 36 h after the trauma. There is minimal to absent host

cellular infiltration. The absence of inflammatory cells is likely a

good prognostic finding, since products of polymorphonuclear

leukocytes contribute to the destruction of the cornea. The

infiltrate is often surrounded by a ring, which may represent the

junction of fungal hyphae and host antibodies (156). Descemet's

membrane, an interior basement membrane near the aqueous humor, is

impermeable to bacteria but can be breached by fungal hyphae,

leading to endophthalmitis (212). Even so, endophthalmitis is a rare

consequence of fungal keratitis (29). Pathologic specimens of

filamentous fungal keratitis demonstrate hyphae following the tissue

planes of the cornea, i.e., laying parallel to the corneal collagen

lamellae. Examination of multiple scrapings of the cornea establish

the agent of fungal keratitis. In some cases a biopsy may need to be

performed. Since many of the filamentous fungi grow slowly, the

disease often remains unrecognized and untreated for days or weeks

until growth is visually detected, and this delay may contribute to

a poor response to therapy.

The abnormal cornea in patients with dry eye syndrome, chronic

ulceration, erythema multiforme, and perhaps human immunodeficiency

virus (HIV) infection (particularly those with AIDS) is subject to

fungal infection, most commonly with Candida species. Candida

keratitis usually appears as a small demarcated ulcer with an

underlying opacity of the cornea resembling bacterial keratitis. C.

albicans was found to be the most common cause of microbial

keratitis in a series of 13 AIDS patients (121). Candida keratitis

has occurred as well in patients who chronically abused corneal

anesthetics (49).

The wearing of hard and soft extended-wear contact lenses is

associated with infectious keratitis usually caused by Pseudomonas

aeruginosa. Both P. aeruginosa (36) and C. albicans (34) adhere to

contact lenses, and the adherence of the former to lens surfaces is

greatly enhanced in the presence of tear deposits (35), some of

which could conceivably serve as carbohydrate receptors for the

microorganisms (147). Adherent microorganisms secrete an extensive

exopolymer that is virtually impenetrable to antibiotics and

difficult to remove. Contact lenses coated with such biofilms likely

increase the risk of infectious keratitis (80). The wearing of

contact lenses leads to a relative hypoxia of the corneal epithelium

that may lead to measurable changes in the cell surface

glycoproteins (145). Perhaps microscopic defects are introduced by

lens wear that enhance microorganism adherence to the otherwise

nonadherent corneal epithelium (144). Fungal keratitis in

association with contact lens wear is almost always due to Candida

spp., although Cryptococcus laurentii (217) has been reported.

Filamentous fungal keratitis occurs less often with lens wear (200,

261, 296), but the filamentous fungi can actually penetrate the lens

matrix (141, 200, 245, 261, 289, 296). Fungi and the bacteria

adherent to contact lenses arise from patient handling, including

the cleaning and storage of the lenses. These adherent

microorganisms also derive from the normal flora of the conjunctiva

(181).

Infections of Adjacent Structures

November 14, 2005

thanks, kc, that's VERY informative!

victoria

[] Fungal and Parasitic Infections of the Eye

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=88956

Clin Microbiol Rev. 2000 October; 13(4): 662-685.