THE TREATMENT AND MANAGEMENT OF
MICROBIAL KERATITIS
Joseph P. Shovlin, O.D., F.A.A.O.
This presentation begins with a review of the epidemiology and pathogenesis of
ulcerative keratitis in contact lens wear. Several recent landmark studies will
be analyzed in order to cite the risk factors associated with the increased
incidence of infection. Preventive measures in minimizing these occurrences
will be stressed. The organisms most likely to be encountered will be reviewed
along with the key measures used to make the important differential diagnosis
between a sterile versus an infectious keratitis.
As a primary care provider, the optometrist must be familiar with the
appropriate treatment protocols in suspected and confirmed cases of ulcerative
keratitis and what to do when these accepted standards of initial therapy fail.
Finally, a few rare corneal pathogens will be reviewed as a cause of microbial
keratitis.
TOPICS:
I. RISK FACTORS AND THE PATHOGENESIS OF
ULCERATIVE KERATITIS
II. THE DIFFERENTIAL DIAGNOSIS OF INFILTRATIVE
KERATITIS
III. TREATMENT PROTOCOLS FOR BACTERIAL
ULCERATIVE KERATITIS
IV. FUNGAL AND PROTOZOAN INFECTIONS OF THE EYE
I. RISK FACTORS AND THE PATHOGENESIS OF ULCERATIVE
KERATITIS IN CONTACT LENS WEARERS
RISK FACTORS FOR BACTERIAL CORNEAL ULCERS
EXOGENOUS: contact lenses, especially extended wear, contaminated cases and solutions,
patching a contact lens abrasion; trauma including foreign body, chemical and thermal
injury; previous ocular surgery including loose sutures; medicamentosa, contaminated
medications and make-up.
OCULAR ADNEXAL DYSFUNCTION: misdirection of lashes; abnormal lid anatomy &
function; tear deficiencies, conjunctivitis; neuropathy involving cranial nerve(s) III, V and
VII; blepharitis, canaliculitis/dacryocystitis.
CORNEAL ABNORMALITIES: hypesthesia, bullous keratopathy, erosive disorders, viral
keratitis.
SYSTEMIC DISEASE: diabetes mellitus; debilitating illness, especially malnutrition or respirator
dependence; collagen vascular disorders, substance abuse, mental illness; exfoliative skin
disease; immunocompromised patient; atopic dermatitis, vitamin A or B deficiency.
IMMUNOSUPPRESSIVE THERAPY: systemic corticosteroids; topical immunosuppressive
agents; systemic chemotherapy for malignancy, organ transplant or collagen vascular
disease.
PATHOGENESIS
Epithelial Compromise- hypoxic, mechanical, osmotic
Contact Lens Contamination- lens care products, case,cosmetics, skin flora,
adherence to lens
Cascade of Events- adherence of microorganism to surface of cornea, invasion
of the cornea, spread and multiplication, induction of the host inflammatory
response, encounter of microorganisms with host immune factors, tissue
damage, tissue repair and recovery
EPIDEMIOLOGY [Adapted from O.D. Schein]
RELATIVE RISK
Population at risk- approximately 24 million lens wearers
Overnight wear the overwhelming risk
Relative risk of extended wear vs daily wear: 10-15:1
Overnight wear of disposable lenses equal risk
Additional risk factors- aphakia, smoking, lens case cleaning, minimal protective effect of
hygiene
INCIDENCE
Daily Wear: approximately 1/2,500/year
Overnight wear of extended wear lenses: estimates range
from one case among 150-300 wearers/year
Population at risk- probably 12,000-15,000 cases /year in U.S.
PREVENTION
Minimizing overnight wear with careful patient selection
Host Factors- diabetes, age, personal hygiene, unknown role of
conjunctival flora
Contact Lens Induced Changes- compromised/injured epithelium,
tear film stagnation and reduced oxygen tension, elevated surface
temperature
Minimizing lens care contamination- wash hands, remove lenses
at pre-determined intervals, clean and disinfect using
FDA approved regimens, small bottles of solution to
avoid contamination, lens case replacement and care, prophylactic
antibiotics not recommended
Warning signs: vision, comfort, appearance (observe < 2 hrs.)
II. THE DIFFERENTIAL DIAGNOSIS OF INFILTRATIVE KERATITIS
BACTERIAL FLORA OF THE NORMAL EYE
Staphylococcus epidermidis
Diphteroids (C. xerosis)
Staphylococcus aureus
Streptococcus (S. viridans)
Hemophilus influenza
Streptococcus pneumoniae
Gram negative rods
Pseudomonas aeruginosa
75-90%*
20-33%
20-25%*
2-6%
3% or more
1-3%*
1% or more*
0-5%*
*Dominant organisms for microbial keratitis
CLINICAL FEATURES
Symptomotology- pain, photophobia, decreased acuity, foreign body
Signs-significant lid edema and reactive ptosis, conjunctival and ciliary injection,
discharge, papillary response, stromal infiltration, surrounding edema, epithelial
defect, anterior chamber reaction, cellular debris of the tear meniscus, and hypopyon
DISTINCTIVE SIGNS
Epithelium
Stromal inflammation
Site of inflammation
Typical
Atypical
ulcerated
suppurative
focal*, diffuse
intact
non-suppurative
multifocal
*multifocal, suppurative keratitis suggestive of mixed infection
INDICATIONS FOR CULTURES
Mandatory
Recommended
Rarely Helpful
corneal ulcers
neonatal conjunctivitis
hyperacute conjunctivitis
dacryocystitis
chronic conjunctivitis
chronic blepharitis
hospital acquired infections
ulcerative conjunctivitis
epidemic conjunctivitis
atypical external disease
follicular conjunctivitis
dendritic ulcer
acute blepharitis
papillary conjunctivitis
hordeolum/chalazian
corneal abrasion
allergic conjunctivitis
LABORATORY CONFIRMATION/SCRAPINGS
Smears- Gram, Giemsa, acridine orange, acid fast, methenamine silver, calcofluor white
Cultures- blood agar, chocolate agar (heated blood), thioglycolate broth, Sabouraud’s,
Lowenstein-Jensen, non-nutrient agar, and others like Thayer-Martin medium for
suspected Neisseria infections
Methods of obtaining material-corneal swabing & scraping, superficial keratectomy, biopsy,
lamellar keratoplasty
Equipment-Bunsen burner, magnification, anesthetic, swabs, spatula, glass
slides, culture media, fixative, stains, lab form
Suggestions for increasing value of lab tests- follow the same technique regardless
of the clinical impression, use fresh media removed from refrigeration several minutes
prior to plating, do not use transport media, use unpreserved anesthetic (lidocaine),work
with magnification, multiple samples on multiple media, fix slides promptly, culture each
site as indicated by location of disease, recognize any growth as potentially important,
when relevant culture contact lens paraphernalia, in-use medications (micro-antibiotic
removal devices may be helpful in patients who have received therapy prior to culturing)
Reasons to culture before treatment- reveal sensitivities of organisms to eliminate ineffective
drugs to reduce toxicity, discriminate between static and cidal properties of antibiotics
and guide modification in therapy, ineffectively treated organisms are often difficult to
isolate, medico-legal component of the patient’s record.
CORNEAL BIOPSY
Corneal biopsy is indicated if there has been a poor response to treatment or if
cultures have been negative on more than one occasion, and the clinical picture
continues to suggest infection. Also, used where a deep suppurration is not
accessible by scraping. The specimen should be sufficiently large to allow
bisection; one section for culture and the other for histopathology. Specimen
should be delivered to the technician without delay.
DOCUMENTATION
DESCRIPTION OF THE ULCER:
Document- size and shape of the epithelial defect, depth and location of the
infiltrate and surrounding stromal inflammation, presence or absence of anterior
chamber and cellular debris of the tear meniscus, and scleral involvement
GRADING OF THE ULCER:
Mild
Moderate
Severe
Size of the defect (mm.)
Depth of ulcer (%)
Infiltrate
<2
< 20
superficial
Sclera
not involved
2-5
20-50
dense, midstromal
not involved
>5
> 50
dense, past
mid-stroma
may be involved
III. TREATMENT PROTOCOLS FOR MICROBIAL KERATITIS
ASSESSMENT OF SEVERITY/ INITIAL PLAN
OBJECTIVES
To distinguish severe suppurative keratitis from non-severe
Implications of virulent versus lesser virulent organisms
Definition of latitudes of initial therapy
GUIDELINES [Adapted from J. McCulley]
Feature
Suppurative/Severe
Non-suppurative/Mild-Mod.
Onset/progression
acute/ rapid
Virulence
Laboratory Studies
Laboratory Materials
Initial Antibiotics
highly likely
immediate, urgent
standard
based on smears/broad
antimicrobial agents
sub-acute, chronic/slowly
progressive
uncertain, doubtful
may delay
special
based on smears + biopsy/
latitude for deferral
PRINCIPLES
Broad spectrum of initial coverage: single agent (fluoroquinolones) vs. multiple agents
Rapid, intensive topical therapy
Daily evaluation
Tailor antibiotic choice by culture results and clinical response
DESIGN FOR DRUG PENETRATION
Topical- every 15 min.- 1 hr. for initial 24-48 hrs. or altered loading dose
Collagen shield- 12 hr. shield reconstituted in water soluble fortified
antibiotic
Subconjunctival injections- once or twice daily for 1-2 days
Intravenous antibiotics- only for impending perforation or scleral
suppuration
MECHANISMS OF ACTION OF ANTIBIOTICS
1. Inhibition of bacterial cell wall synthesis (Penicillins, Cephalosporins, Bacitracin
and Vancomycin)
2. Increasing the permeability of the bacterial cell wall (Polymixin B, Colistin,
Gramicidin)
3. Inhibition of bacterial protein synthesis (Aminoglycosides, Tetracycline,
Erythromycin, Chloramphenicol and Clindamycin)
4. Inhibition of bacterial intermediary metabolism (folic acid synthesis)(Sulfonamides, Pyrimethamine and Trimethoprim)
5. Interference with bacterial DNA synthesis (Quinolones and Nalidixic acid)
INITIAL THERAPY OF INFECTIOUS KERATITIS [Adapted from A. Matoba]*
*depends on severity, individual risk factors, initial gram stain results and clinical impression
Organism
Antimicrobial
Topical Dose
Subconj. Dose
Gram + cocci
Cefazolin
50 mg/ml, every
15-30 minutes
100 mg in 1/3 ml
Gram - rods
Tobramycin or
gentamicin
13.6 mg/ml, every
15-30 minutes
20 mg in 1/2 ml
No organism or
multiple organisms
Cefazolin and
tobramycin
see above dosages
for each agent
Gram + rods
Penicillin and
gentamycin
100,000 units/ml, every
15-30 minutes, see above
for gentamycin
Gram - cocci
Ceftriaxone or
ceftazidime
50 mg/ml, every 1530 minutes
Acid-fast bacilli
Amikacin
20 mg/ml, every 1530 minutes
20 mg in 1/2 ml
MODIFICATION OF THERAPY
Objectives- eliminate replicating bacteria, avoid adverse reaction to the
medication, control the destructive components of the inflammatory
process
Guidelines- avoid abrupt changes in therapy until the response can
adequately be assessed and until the sensitivity tests are completed
at the lab
Expected response despite proper/ effective therapy:
Organism
Response
S. aureus, S. pneumoniae
may be relatively unchanged, then improve
rapidly after 24-48 hrs.; organisms generally
eliminated in 7-10 days
Pseudomonas aeruginosa
generally appears worse at 24 hrs.; organism
may persist for 14 days or longer
Bacteria of low virulence
(ie. S. epidermidis)
generally improve rapidly in 24-48 hrs.;
organisms eliminated in 5-7 days
Mycobacterium, Filamentous fungi
slow response; may persist for weeks
RESISTANT BACTERIA*
Methicillin resistant Staphylococcus aureus
Enterococcus fecalis (group D Streptococcus)
Aminoglycoside resistant Pseudomonas aeruginosa
Beta lactamase producing Neisseria
Atypical Mycobacteria
Current antibiotic recommendation for suspected resistance: Vancomycin
20-30 mg/ml (Vancocin) and Ceftazidine 50 mg/ml (Fortaz/Pentacef)
Gram positive organisms: Vancomycin 20-30 mg/ml (Vancocin) or Cefazolin
50 mg/ml (Ancef), .28% Lysostaphin
Gram negative organisms: Amikacin 10-20 mg/ml (Amikin)
FLUOROQUINOLONE RESISTANCE*
Some concern for streptococcus species, enterococci, non-aeruginosa
pseudomonas, and some MRSA
UCSF Study (1996) Hwuang et al.: topical ciprofloxacin qid. staph. aureus
resistance rose from 12%-50% with in-vitro testing
Wills Eye Hospital Study (1996) Rodman et al.:
Staphylococcus aureus resistance1992: 4%
1996:13%
Streptococcus resistance1992:20%
1996:26%
LV Prasad Eye Institute Study (1999) Kunimoto et al.:
30.7% of isolates from corneal infections were not sensitive to
ciprofloxacin in India; Garg et al.: true pseudomonas resistance to
ciprofloxacin is emerging
*significant increase in in-vitro resistance with ciprofloxacin; clinical
significance is uncertain/fewer pseudomonas infections in CL wearers.
(geographical differences remain)
ADJUVANT THERAPY
Cycloplegia- for comfort and to prevent synechiae
Collagenase inhibitors (ie. EDTA, TCN, Galardin)- to minimize
stromal destruction
Heat (40 degrees C)
Steroids- hazardous early in treatment, safety and efficacy not well
established in most forms of microbial keratitis; helpful in reducing
harmful destruction due to host response
NSAIDs/ Analgesics- reduces inflammation and pain, may enhance antimicrobial(s)
efficacy (NSAIDs) *anecdotal reports suggest very effective for pain in
mycobacteria infections
Tissue adhesives- for impending and actual perforations if small/ bacteriostatic
Glaucoma medication- if needed, beta-blockers is drug of choice
Debridement/ Biopsy- may improve antibiotic penetration
Cryotherapy- possible role in sclerokeratitis
Bandage lens/ Collagen shield- may promote re-epithelialization and
allow for slow concentrated release of antibiotic
Continuous antibiotic infusion devices- possible benefit in extensive
sclerokeratitis
Therapeutic keratoplasty- for large perforations, central/deep medically
recalcitrant keratitis
INDICATIONS FOR HOSPITALIZATION
Inability of patient/ family to deliver high frequency, 24 hr. treatment
Inability to return initially for daily follow-up
Threatening perforation or scleral involvement
TERMINATION OF THERAPY
Elimination or substitute antibiotics only if directed by lab results
Elimination of the less effective agent if combined microbial therapy
initiated for monobacterial keratitis after lab results
Measures of improvement:
Blunting of the perimeter of stromal suppuration
Reduction in the density of suppuration
Reduction in cellular infiltrate and edema in surrounding stroma
Reduction in the anterior chamber reaction
Progressive re-epithelialization
Reducing antimicrobials and adjuvants:
Avoid abrupt cessation; prolonged therapy needed for
Pseudomonas, Mycobacterium, Nocardia, anaerobes
Reduce by “halving method”, substitute regular/commercial
strength for fortified antibiotics when possible
Penetrating Keratoplasty
Progressive suppuration despite appropriate therapy
Persistent infection
Corneal perforation not managed by other methods
IV. FUNGAL AND PROTOZOAN INFECTIONS IN
CONTACT LENS WEAR
FUNGAL KERATITIS
Fungi are primitive non-motile plant-like organisms. Yeast are uni-cellular and
molds are multi-cellular filamentous structures. In the past 10 years there has been a
definite increase in the prevalence of fungal keratitis in certain geographic areas, although
nationwide there are probably only 300 cases per year. There are 40 different genera that
cause keratomycoses; most are saprophytic.
CLASSIFICATION/MOST COMMON ORGANISMS (Adapted from J. McCulley)
Filamentous fungi; Molds
Septate- most common cause of fungal keratitis, variable geographic
distribution, mostly in the southern and southwestern United States,- Nonpigmented: Fusarium (most virulent due to complex enzymes + toxins),
Aspergillus, Pigmented:Curvularia, Paecilomyces, Phialophora
Non-septate- Mucoraceae (rare corneal pathogen)
Risk Factors: corneal injury (frequently a tree branch or vegetative matter
in an agricultural setting), soft contact lens wear (extended
wear/therapeutic), chronic topical medication, systemic steroids,
diabetes mellitus, radial keratotomy.
CLINICAL FEATURES
Epithelium
Type of stromal
inflammation
Site of inflammation*
Typical
Atypical, severe
intact or ulcerated
non-suppurative,
feathery infiltrate(s)
focal or multi-focal,
satellite infiltrates
ulcerated
suppurative
diffuse
*typically accompanied by a mild iritis, endothelial plaque and hypopyon in severe
infections; hypopyon is of no diagnostic value
Yeasts- worldwide distribution: Candida- C. albicans, C. parapsilosis,
C. tropicalis
Risk Factors- protracted ulceration of the epithelium, topical steroid
therapy, penetrating keratoplasty, bandage soft lenses
Epithelium
Type of stromal
inflammation
Site of inflammation
Typical, common
Atypical, rare
ulcerated
suppurative
intact
non-suppurative
focal or diffuse
multifocal
Note: ring infiltrates or abscess is possible with an intact epithelium
KERATOMYCOSES
DIAGNOSIS- clinical suspicion, corneal scraping, superficial keratectomy
(paracentesis)
Diagnostic stains- Gram, Giemsa, GMS, PAS, KOH, acridine orange,
Schwartzman’s, calcofluor white
Culture media- Sabouraud dextrose agar (with gentamicin, without
Confocal
cyclohexamide), blood agar, brain-heart infusion agar
with gentamicin @ 25 + 37 C
microscopy- identifies hyphae, poor for Candida, a guide to therapeutic
response
ANTIFUNGAL DRUG MECHANISMS OF ACTION1.
Sterol Binding- Polyene drugs like Amphotericin B, Nystatin and Natamycin
2.
Inhibition of Sterol Synthesis- the Imidazoles including Miconazole, Ketoconazole,
Clotrimazole, Fluconazole
3.
Interference with RNA Synthesis- Flucytosine (fluorinated pyrimidine) and
Itraconazole (antimetabolites)
4.
Inhibition of Mitosis- Griseofulvin
INITIAL THERAPY- drugs are generally not introduced until definitive
diagnosis is made.
Topical*-HYPHAE-Natamycin 5% (Natacyn) suspension (every hr. for 2448 hrs.) YEAST OR PSEUDOHYPHAE- Amphotericin B .1-.5%
(Fungizone) (every 15-20 minutes for 24-48 hrs.), Miconazole 1%
(Micatin, Monistat) (every hr., but very toxic) as an alternate therapy.
Clotrimazole (cream or powder) and Flucytosine (Ancobon tablets)
converted to a 1% solution have been effective against Candida
infection.
Oral- Ketoconazole (Nizoral) (200-400 mg/day) or Fluconazole (Diflucan)
(100-200 mg/day) [generally used for hyphae and endophthalmitis;
Candida generally responds to topicals alone]; Itraconazole
(Sporanox) is more effective against filamentous fungi especially
Aspergilli .Reserve systemic treatment for deep keratitis, impending
perforation, scleritis, endophthalmitis and post penetrating keratoplasty.
Sub-conjunctival injection-Fluconazole (Diflucan) .5ml = 1mg daily
pending initial response and identification of the organism.
Other agents- atropine 1% or hyoscine .25% 4x/day; glaucoma medication
as needed; role of collagen shield as a delivery device not well
defined. Avoid steroids in fungal keratitis since mold/yeast
replicate more freely and microbial agents are generally only
fungistatic.
*topicals are often continued for 6 wks. or longer; watch for toxicity
Note: excimer ablation may be of some value unless there is deep penetration.
PREVENTION-minimize extended wear, therapeutic lens application whenever
possible, avoid indiscriminate use of topical steroids.
ACANTHAMOEBA KERATITIS
Acanthamoeba keratitis remained a curiosity in the past; however recently
this pathogen affecting primarily the cornea and sclera is recognized with
increased frequency. Early detection will alter the course of therapy and ultimately
affect outcome, therefore early diagnosis is critical. The risks factors that have
been identified by epidemiologic studies, specifically as they relate to contact lens
wear will be examined.
THE ORGANISM- "a free living" protozoan (motile) with worldwide distribution;
isolated from fresh water, well water, sea and brackish water, sewage, hot tubs, air, soil,
wheat and barley; there may be high incidence areas following disasters (ie. Sacramento
floods and hurricane, "Hugo")
Acanthamoeba: >7 species show ocular parasitology [A. castellani, A. quina,
A. culbertsoni, A. lugdunesis, A. polyphaga, A. hatchetti, A. rysodes, A
griffini] Note: Sequence types are recommended as much less
ambiguous units of classification than currently used species names.
Forms: cyst (sessile)*and trophozoite (motile)
*makes the organism resistant to freezing, desiccation, standard chlorination and a
variety of antimicrobial agents
OCULAR INFECTION
Clinical features-initial signs are non-specific; they include: patchy epithelial
involvement (irregularity or pleomorphic focal or stellate epitheliopathy),
suppurative/granulomatous or non-suppurative stromal keratitis, “bull’s eye” lesions,
pseudo-guttata and iritis. More advanced signs include: a radial kerato-neuritis, ring
infiltrate, nodular episcleritis, scleritis and hypopyon or hyphema; there may be a
pseudo-membrane or adenopathy present. A remarkable lack of vascularization; often the
only feature to help differentiating this infection from herpes simplex. Recently, early
signs identified include a bull’s-eye lesion and the appearance of randomly distributed
white spots on the cornea. Persistent epithelial defects immediately following
penetrating keratoplasty may signal early amoebic infection.
Symptomatology-usually unilateral pain disparate to ocular findings, often history to
trauma +/or contact lens wear, symptoms generally wax and wane over time with
chronicity.
LABORATORY CONFIRMATION
Corneal scrapings*- examined with Giemsa or tri-chrome stains, also culture with
heated killed E. coli on non-nutrient agar or activated charcoal/yeast extract; other
valuable tests include immunofluorescent techniques which include: calcofluor white
and indirect immunofluorescent antibody testing. Standard culture negativity for
bacteria, fungi, and virus expected. Cysts can sometimes be seen on soft lenses with high
magnification. Confocal microscopy is an aid to early differential diagnosis.
Polymerase chain reaction may be more sensitive than cultures as a diagnostic test. PCR
analysis of the tears and epithelium may prove a useful tool in confirming an early
diagnosis.
*biopsy with intact epithelium or graft histology
THERAPY
Reported improvement*Antibiotic/Aminoglycoside: paromomycin (Humatin), neomycin
Antifungal: clotrimazole, ketoconazole (Nizoral), itraconazole (Sporanox),
miconazole (Monistat, Micatin), fluconazole (Diflucon)
Antiparasitic/Aromatic Diamidine: propamidine isethionate (Brolene),
hydroxystilbamidine (Pentamidine),hexamidine di-isethionate (Desomedine)
Biocide/Cationic Antiseptic: polyhexamethylene biquanide (PHBG, Baquacil,
Cosmocil), chlorhexidine digluconate, povidone-iodine (Betadine)
*use one agent from at least two of the four categories above, plus oral
ketoconazole or fluconazole, apply topicals every 30-60 minutes; for
recalcitrants with significant ocular toxicity use drops in a three day cycle
(hexamidine, paromomycin, and either PHBG or chlorhexidine)
Supportive and adjunct therapy-debridement, conjunctival flaps, bandage lenses,
debulking procedures, cryotherapy and steroids with caution**; grafts show a high
recrudescence (NSAIDs seem to have little benefit in pain reduction when radial
keratoneuritis is present)
**inhibits metamorphogenesis
Success has been reported by Seals (1995) using .02% chlorhexidine digluconate & .1%
propamidine isethionate has been reported.
CONTACT LENS RELATED RISK FACTORS/ PREVENTION
Accouterment- use of distilled water, tap/well water*, or saliva;
bacterial contamination of case and care system a common factor
*recent concern especially with rigid lens wear
Disinfection- some resistance to chemical disinfection
Corneal trauma- hypoxia, mechanical trauma with lens wear
Note: should avoid swimming and using hot tubs with contact lens wear
ADDITIONAL PROTOZOAN
Other amoeba- A similar infection may be caused by another amoeba besides
Acanthamoeba, such as Naegleria, Hartmanella or Vahlkampfiid.
Microsporidia- an obligate intracellular protozoan recently found on corneal scrapings
of HIV infected patients from nasopharyngeal or urinary colonization. Generally it
presents as a superficial punctate, multifocal keratitis (may be confined to the superficial
cornea for months) in immuno-incompetent patients (genus-Encephalitozoon); a stromal
keratitis is possible following trauma especially in immunocompetent individuals (genus-
Nosema). A slight improvement has been noted with trimethoprim/sulfisoxazole.
Recently itraconazole, propamidine isethionate, albendazole (benzimidazole), and
especially topical fumagillin bicyclohexylammonium salt (Fumadil B), a bacteriostatic
antibiotic secreted by Aspergillus, have shown some promise. Diagnosis is made by
Gram’s stain, cytology with chromotrope-based stain, or by using electron or confocal
microscopy.
SELF ASSESSMENT QUIZ
1. T F Studies have shown that the majority of bacterial corneal ulcers in
an outpatient setting are caused by gram + organisms.
2. T F Pseudomonas is the most common isolate responsible for ulcerative
keratitis in contact lens wearers.
3. T F Microsporida infection is often associated with a punctate keratitis
in HIV positive patients.
4. T F Most experts agree that contact lens related abrasions should not be
patched.
5. T F Tetracaine is recommended for topical anesthesia when scraping
the cornea as it is less bacteriostatic than proparacaine.
6. T F Sabourauds agar supports most fungi and yeast while inhibiting
bacterial growth.
7. T F Regardless of the nature of the infecting agent, the cornea is
usually best treated by frequent, topical application of antimicrobials.
8. T F The use of collagen shields has proven beneficial in delivering
sustained concentration of antibiotics to the cornea and anterior chamber.
9. T F All the currently available fluoroquinolones are effective in treating
keratitis regardless of the organism causing the disease.
10. T F Using a culturette tube is as effective as in-office plating on
various media for retrieval and growth of microorganisms common to
infection to contact lens wearers.
1. T 2. F 3. T 4. T 5. F 6. T 7. T 8. T 9. F 10. F
Current Controversies In Managing Microbial Keratitis
TRANSCRIPT QUALITY ASSESSMENT
1. Which of the following is not a risk factor for developing bacterial
keratitis?
A.
B.
C.
D.
ICU care
the use of steroids
sleeping with contact lenses
aspirin therapy
2. In the landmark CLI relative risk study (extended wear) by Schein and
co-workers, which of the following statement(s) is/are true?
A.
B.
C.
D.
overnight wear is the overwhelming risk in contact lens wear
smoking and aphakia are additional risk factors
24 million lens wearers are at risk
A, B and C are correct
3. The following are symptoms or signs of corneal infection except:
A.
B.
C.
D.
pain, redness and photophobia
discharge and foreign body sensation
anterior chamber reaction
all are possible signs or symptoms of corneal infection
4. When culturing a presumed bacterial keratitis, the following media are
generally plated:
A. chocolate
B. Sabouraud’s media
C. non-nutrient agar
D. A & C are correct
5. Which of the following is not a reason for mandatory culture?
A.
B.
C.
D.
acute blepharitis
dendritic ulcer
dacryocystitis
A &B are not considered mandatory reasons for culturing
6. There are many reasons to culture corneal ulcers. Which of the
following is not one of them?
A. should be a medico-legal component of your record in case the
ulcer doesn’t respond to empiric treatment
B. reveals sensitivities of the organism(s)
C. no single agent is generally effective for most infections
D. ineffectively treated organisms are difficult to isolate
7. Currently the most effective/complete treatment plan for resistant
bacterial infection is:
A.
B.
C.
D.
Vancomycin and Ceftazidime
Tobrex and Ciloxan
Gentamycin and Kefzol
Ocuflox and Erythromycin
8. A patient with a severe corneal infection should be hospitalized if there
is/are:
A.
B.
C.
D.
inability of patient or family to deliver high frequency treatment
inability to return initially for daily follow-up
threatening perforation or significant scleral involvement
all of the above are potential reasons requiring hospitalization
9. Which of the following statements is true regarding fungal keratitis?
A. may account for over 40% of the corneal infections in some
geographic area
B. Natamycin is the only FDA approved drug for the treatment of
fungal keratitis
C. sub-conjunctival injections of Diflucon are started immediately
upon first suspicion of yeast infection
D. topical agents are rarely needed after the first week of treatment
10. Which of the following has generally not been used in the initial
treatment acanthamoeba keratitis once a definitive diagnosis is made?
A.
B.
C.
D.
anti-fungal agents (clotrimozole, ketoconazole, itraconazole)
anti-parasitics (propamidine isethionate, hydroxystilbamidine)
biocides (polyhexamethylene biquanide)
all can be used for the initial treatment of acanthamoeba keratitis
since it is often difficult to eradicate
ANSWERS
1. D 2. D 3. D 4. D 5. D 6. D 7. A 8. D 9. B 10. D